Cardio Summaries:

Contents
ECG diagnosis aid: .................................................... 2
Heart Failure .......................................................... 10
Hypertension treatment: ....................................... 14
Ischaemic HD (See Weich notes) ........................... 18
Approach to Chest pain.......................................... 21
Pathogenesis of IHD: .............................................. 22
Lipid lowering Therapy:.......................................... 26
Vavlular Disease: .................................................... 29
Heart valve surgery ................................................ 32
Infective Endocarditis............................................. 36
Pericarditis and myocarditis................................... 40
Myocarditis: ........................................................... 45
Non - atherosclerotic Aortic disease ..................... 46
ATHEROSCLEROSIS ................................................. 56
BIOCHEMICAL MARKERS OF HEART DISEASE ........ 60

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 ECG diagnosis aid: 7. QRS complex: Tall R wave in V1:
Normal PR interval = 120-200mm/sec o Less than 100ms in width. o RVH
Normal QRS <120ms o >120ms = BBB o RBBB
QT 440ms or less. o When assessing QRS, record: o WPW
do V7,8,9 on
(Small blocks: 0.04s, Big blocks = 0.2 s each.) Axis o True posterior infaction back
When given note the: Width o Duchennes muscular dystrophy
1. Name Height
2. Date Presence of Pathological Q waves Q waves:
3. Calibration o Axis: Pathological Q wave:
o 1mV = 10mm axis is at 90 Normal: -30 - +90 Width > 1 block OR
o 25mm/sec degrees to the Right axis: more than +90 Depth >/= 3 blocks OR
most Left axis: Less than -30 25% of subsequent R wave.
equiphasic
Generalised Small complexes: Northwest axis: Bw +180 and -90 To be infarction: Need to be present in 2/more adjacent (anatomically)
lead
Look at SI and aVF both pos, then normal. leads.
Calibration = sinus rhythm - atrial contraction Causes of Left axis deviation Causes of Right Axis Deviation
Emphysema caused by de polarization of sinus WPW in the WPW Any Q-wave in leads V2V3 0.02 s or QS complex in leads V2
inferior
Obesity node Deep Q wave inf. Infarct leads (II, Antero-lateral infarct and V3
Pericardial effusion sinus nide is at the junction of SVC and Left anterior hemi-block aVF, III) Left-Posterior Hemiblock Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II,
right atrium Premium ASD Right Ventricular
Hypothyroidism aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping
4. Det. HR:
primum ASD due to endocardial cushion defect Hypertrophy (I, aVL,V6; V4V6; II, III, and aVF)
positive in inf leads and displacement of conduction defect
a) Count QRS complexes then X6 o Width R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive
b) 300/(blocks bw R waves) only if RR constant. RBBB = > 120msecs or 3 blocks. T-wave in the absence of a conduction defect
c) Rhythm To dist from LBBB, comp V1 to V6
5. P waves before QRS WiLLiaM MaRRoW ventricular rhythm Sign of Previous myocardial infarction.
W in V1 and M in V6 in LBBB paced rhythm
o SII, SIII + aVF all should have positive P wave pre excitation
deflections. Inverted in AVR and V1. biphasic in V1 M in V1 and W in V6 in RBBB Any Q wave in leads
o P wave best assessed on SII and V1. Normal < 2.5mm RBBB LBBB
QRS > 120ms Greater than 120ms 8. ST segment
and <0.12sec in duration. General: Not bigger/broader
Tall, slurred R wave in V1, Pred neg QRS complex in septal
than 2 blocks.
resulting in chracteristic rSR region sharp r wave in V2 Bw end of QRS and Start of T wave stretches from J point to ST-T
but must o Enlarged P wave: RA enlargement. (P pulmonale) pattern. Deep S in V1 <40ms wave junction. NB in assess presence of Ischaemia/infarction on ECG.
be tall or o Enlarged 2nd half of P wave (M-appearance) = P mitrale Deep slurred S waves in V6 and SI Tall late R wave in V6 and SI
broad! Normally slopes up gradually and merges into the proximal leg of the T
LA enlarge Inverted T waves in V1-V3 Broad predominantly positiv, M
wave, which is less steep than the distal leg of the T wave gives rise to
o V1 normally rec a biphasic deflection. If the 2nd Tall late R wave in V1 shaped complex in V6 + high later
T wave inversion in V5-6 _ hight typical asymmetrical T wave. T waves are normally pos with a rounded
(negative) part is longer/larger than first = LA
lateral apex.
hypertrophy.
Bisfascicular block term used to describe combo of RBBB w left axis Horisontal ST depression is hallmark of Ischaemia.
6. PR segment:
deviation. ST elevation is earliest indicatior of myocardial injury during infarction.
o From start of P wave to start of QRS complex.
o Height
Therefore reflects atrial depolarisation + subsequent
Left Ventricular Hypertrophy: Causes of ST Depression:
delay of impulse in AV node.
Standard voltage criteria:
o Normal: bw 120-200mm/sec thus 3blocks<PR<5blocks MI
Sum of R wave in V6 + S wave in V1 > 35mm o
o Shortened PR seg = WPW/ectopic atrial focus Non ST elevation MI (NSTEMI)
+/- T wave inversion in V5-6 + High lateral Leads o
originating near AC node. Posterior Infarction
Right ventricular hypertrophy o
Prolongation: see Heart Block. Catecholamines - make AV

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o Reciprocal changes of an infarction in opposing wall
node more able to conduct Criteria not strictly defined suspect if large R waves observed in V1. o

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impulses. can shorten PR. May be accomp by T wave inversion in V1-3 and Right axis deviation. o Digoxin
RBBB sometimes present. dominant R wave in V1 with r o Ventricular Hypertrophy
axis
Causes of ST Elevation: Influenced by HR. QTc (corrected) = QT/ 2 In a classic, fully evolved STEMI:
Normal QT < 440 ms <460 in females
o AMI o Necrosis is represented by a pathological Q wave.
QT should be less than half of the RR interval
o Pericarditis Prolonged QT: Necrotic tissue electrically inactive
o Prinzmetal angina (ischaemia from coronary spasm Full thickness electrode will register elec act of
o Ventricular aneurysm. (suspect when ST elevation persists o Congenital genetic defect of K+ channels opposing wall.
following a prev MI) o Hypomagnesaemia Thus necrotic tiss serve as window.
o Hypocalcaemia All elec act away from electrode registered as
NB to note not only Shift of ST up or down, but also normal shape. o Hypokalaemia negative deflection Q wave.
Shape of Normal ST See notes p20. o Drugs inc Tricyclic antidep and anti-arrhythmic drugs. o Injury represent by ST elevation
o Ischaemia infarction. Earliest sign of MI straghtening of (norm
9. T wave
concave ST sebment eliminating curved junc
Shortened = Hypercalcaemia bw ST segment and T wave)
Normally positive.
Early ST elevation =slope-elevation
Inverted T waves can be normal in aVR, standard lead III and V1 That is all general, here are some specific conditions:
Followed by Elevation of J point w prog elevation
T waves are asymmetrical w the ascending limb being less steep than
of ST segment characteristically w a convex
descending. Lead Anatomical area Coronary Artery
SII, SIII, aVF Inferior Right/circumflex surface.
Apex of T wave is usually round.
V1/2/3 Antero-septal Proximal LAD o Ischaemia is represented by inversion of T wave.
Abnormalities: V4,5,6 Lateral Distal LAD Fully evolved ST elevation MI ischaemia is
Flattened T waves V1-6 Antero-Lateral Proximal LAD reflected by inverted T waves earliest sign of
SI, aVL High lateral First diagonal of LAD MI is increase in size of T wave w giant peaked T
o Ischaemia Definition: waves. As ST elevation prog T waves eventually
High Lateral invert. Inverted T waves may persist for
o Myocarditis
S1 Q3 T3 pattern: days/weeks after MI. On average the T waves will
o Pericarditis
o Hypercalcaemia return to normal at abt 2 weeks post-infarct.
S wave in SI, Q wave in SIII, inverted T in Lead III
If MI changes including ST seg elev and T wave
Peaked T waves: inversion persist indefinitely myocardial
Myocardial Infarction:
aneurism suspected.
o Hyperacute MI o W modern thrombolytics NB to diagnose early via ST slope
Hallmark: Horizontal depression of the ST segment.
o Hyperkalaemia elevation and T wave size incr so that therapy can improve
Signs of Ischaemia outcome.
T wave inversion. o ECG helps to localize infarct.
o ST segment becomes horizontal Inferior
o BBB
o ST-T wave junction becomes angular
o MI
o T wave becomes more symmetrical
o Myocardial myopathy
o T wave apex becomes sharp
o Ventricular hypertrophy
o ST segment can be displaced horizontally downwards.
o WPW
o ST segment elevation may also indicate ischaemia
o Verntricular rhythms
(Prinzmetal angina)
o In septal leads can be normal in Black pt.
o T wave may become flattened or inverted.
10. QT interval:
o Ischaemia may cause a left or right BBB
Measured from start of QRS to end of T wave and prepresent

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Infarction: Central necrotic area devoid of Electrical activity. Surrouned
depolarisation and repolarization.

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by an area of myocardial injury, which is surrouned by an area of
ischaemia.
Cardiac Arrhythmias: Classify
Abnormality in cardiac rhythm normal HR bw 60-100 pm. Regular/irregular
Broad/narrow
Tachycardias: (3 basic mechs) Regular, narrow Irregular, narrow
Sinus tachycardia Atrial fibrilation
1. Enhanced automaticity Extopic atrial tachycardia Atrial fibrilation
a. Normal mech or rhythmic depol of heart is due Atrial flutter Atrial fibrilation
to slow depol of trans membrane voltage during AV nodal re-entry (AVNRT) Atral flutter w variable block
pahse 4 of action poential until it reaches AV re-entry (AVRT) Multifocal atrial tachycardia
threshold pot.Automaticity may be nehanced by (MAT)
incr slope of phase 4 of action pot. Eg: Regular, broad complex Irregular, broad complex:
Ventricular tachycardia AF w BBB
i. Sinus tachycardia
SVT w BBB AF w Aberant Conduction
ii. Accelerated AV nodal rhythms
SBT w Aberrant Conduction AF w exxentric conduction
iii. Idio-ventricular rhythms (tachycardia inuced BBB) Multifocal ventricular
2. Triggered activity SVT w eccentric conduction rhythm
a. After-depols that reach threshold pot in diseased Ventricular pacemaker Torsade de Point
myocardium. Eg
i. Atrial tachycardia seen w digitalis See table 13.8 K&C p719.
toxicity Consideration for Anti-coagulation therapy:
ii. Initiation of ventricular tachycardia in CHADS 2 (2>/= then therapy required)
long QT syndrome.
3. Re-entry: Congestive heart failure
a. Commonest cause of sustained tachycardias Hypertension
b. Substrates characterizing: Age >75
i. Presence of more than one Diabetes Mellitus
conduction tract Previous Stroke, TIA (Value = 2)
ii. Unequal conduction velocities in the
two tracts General management of Cardia tachyrhythmis:
iii. Unequal refractory periods in the two Antiarrhythmic drugs
conducation tracts causing uni- ablation therapy
diractional block in the one limb. Device therapy
c. If limb A blocked for anterograde conduction
impulse will go down B. Now A no longer Drug Classes:
refractory retrograde conduction along limb A I Membrane Depressants
initiating circular conduction. II Anti-sympathetic
III Action potential lengtheners
Depending on Origin, classified as Supreventricular(SA node, AV node,
atrium) or Ventricular. Catheter Ablation:

AVNRT
AVRT (incl WPW)
Normal heart VT
Atrial Flutter

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Atrial tachycardia

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Atrial fibrillation
Pulmonary Embolism:
o Sinus Tachycardia
o Atrial Arrythmias, including A-fib
o RVH
o RBBB
o S1Q3T3 pattern
Hyperkalaemia
o Flat/absent P waves
o Broadened QRS complexes
o Large, peaked T waves
o Arrhythmias
Condition
Sinus Tachycardia
Atrial Flutter
if unsure of duration need to TOE . if clot
or unsure anticoagulate for a month. give
beta blockers.
check again. if clear.
cardiovert and anticoagulate for month
afterwards.due to atrial stunning
(Ectopic) Atrial tachycardia
Atrioventricular nodal re-
entry tachycardia (AVNRT)
Atrioventricular re-entry
Tachycardia (AVRT)
COPD Mitral Stenosis Mitral Incompetence:
o Generalised small complexes o LAH if in sinus rhythm o LAH if in sinus rhythm
o Right atrial hypertrophy (P o A-fib commonly present o A-fib commonly present
pulmonale) o RVH o LVH
o Right Axis Deviation o R axis Deviation o RVH may be present (pulm
o Right Ventricular hypertrophy hypertension)
o RBBB
Hypokalaemia Hypercalcemia Hypocalcaemia
o Flat T waves Shortened QT Prolonged QT
o Prominent U waves
o 1st/2nd degree heart block
o ST Depression
Arrhythmias
Classification ECG Causes Treat/Manage
Regular narrow Where each QRS complex is preceded by a P wave. NB: Thryotoxicosis Find underlying cause,
As rhythm originates from SA node P wave has normal Exercise Cardiac failure trat.
axis (positive inferior leads) Pregnancy Shock If nec. Beta blockers to
Fever Pulm embolism slow sinus rate.
Anaemia Alcoholwithdrawal
Regular Narrow Saw-tooth pattern bw QRS complexes Re-entry circuit in atria activatin atria at a rate of 300pm Sim to atrial fib.
IF flutter not clearly visible unmask by slowing AV Most often every second flutter beat is blocked by the AV node gives rise to Sinus rhythm usually be
conduction through vagal stim/ admin of adenosine (blocks vent rate of 150 bpm. obtained through electrical
AV conduction. Usually ass w structural heart disease cardioversion.
If not re-entry parthway
can be treated w radio-
frequency catheter ablation.
Regular Narrow Organized atrial activity w P wave morphology diff from Enhanced automaticity of extopic focus in the atria.
sinus thythm preceding QRS. Fortunately rare often resistant to treatment. Usually in Pt. w struct HD. adenosine can
Often result of Digitalis poisoning precipitate asthma
Regular Narrow Narrow complex Re-entry circuit in the AV node Commonest cause of supra-ventricular Can be interrupted by vagal
Regular tachycardia (150-250) tachycardia in young pt w structurally normal hearts. stim (carotid sinus massage)
P waves often not visible as they are hidden in QRS Paroxysmal sudden onset/termination or Adenosine. 6 to 12 mg
complexes Two pathways in AV node: Fast conducting, longer effective refractory period and Recurrent Can be
Slow conducting shorter refractory period. Impulse travels along fast conducting effectively cured by radio-
normally. If too early (when fast still refractory, slow is taken and then onto fast= frequenxy catheter ablation.
AVNRT.
Regular Narrow Sinus rhythm will iID underlying accessory pathway by In the presence of an accessory parthway connecting atria and ventricle. (See Risk increased by AV node
demonstrating pre-excitation (WPW) WPW) inhibitors:
P wave visible bw QRS and T wave. Re-entry circuit involves both accessory parthway and AV node most commonly Verapamil
reaching ventricle through AV node and returning to atria via accessory pathway. Digoxin CI in WPWS
(Orthodromic conduction) Effectively treated - ablating
Uncommonly direction of conduction reveresed, activating ventricles through accessory pathway. (Treat
accessory pathway giving rise to reg, broad complex tachycardia these pt first as with AVNRT)
prone to A-fib and if conducted via accessory pathway irreg, broad complex may
result. without decremental conduction
Mahaim fibres atrio-fascicular, nodo-fascicular fibres entering ventricular
myocardium in RBB region.
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if not to fast you can see P waves which are negative in the inferior leads.
Atrial Fibrillation: Irregular, Narrow Irregular, narrow complex rhythm Common 5-10% of pt over 65yrs. 1. Prevent Thrombo-
No P waves Islands in atrial myocardium in differenct phases of de-/re-polarisation, leading to embolism-anticoagu-
Baseline appears irregular/untidy. numerous wavelets of re-entry 300-500/second. lation CHADS2
similar to treatment for 120-180 pm ventricular rate AV node filter Ventricular response seldom> 200pm unless access pathway 2. Control ventricular rate
aflutter above present. Random contract = Irregular pulse. (Rate/volume) Very rapid = pulse = beta blockers
High morbidity decr cardiac func. deficit. 3. Find treatable causes
Loss of atrial kick during diastolic filling of Thyrotoxicosis must rule out in new discovered AVF. 4. Regain sinus rhythm
ventricle Structural Heart disease. Rate.Rhythm control.
tachycardia-induced cardiomyopathy Ischaemic pulmonary artery area
Incr risk of Thrombo-embolic episodes. Hypertensive
ablated
Valve lesions
Cardiomyopathy leads to 80% cure but
Cor Pulmonale not really mortality
Alcohol intoxication benefit
Multifocal Atrial Irregular, Narrow QRS complexes preceded by P waves but vary in Caused by 3/more extopic atrial origins of rhythm present. See K&C P 723 table 13.12
tachyrhythmia (MAT) morphology. Obstructive airway disease. common Atrial tachy-arrhy
Ventricular Tachycardia Regular Broad Typical BBB often absent bizarre complex appearance. If in Doubt: Treat for VT
Distinguising VT from SVT w broad conduction on ECG can Initiate Electrical
be difficult. Cardioversion.
Observing AV dissociation (P waves and QRS complexes w Then start an anti-
no relation) = diagnostic. arrhythmic drug such:
May be diff to distinguish from supraventricular Amiodarone/lignocaine.
tachycardia w BBB or supra ventricular tachycardia in
presence of an accessory pathway w anterograde Three rules:
conduction. 1. Broad complex rhythm
Signs favouring VT: must always be
AV dissociation considered to be VT
Detecting P waves indep from Vent beats, fusion until proven otherwise
beats, capture beats 2. History of previous MI
QRS duration ? 140ms is very strong indicator
Bizarre QRS complex not displaying typical L/RBBB of VT
Electrical concordance (all complexes are either 3. If in doubt treat for
pos/neg through the chest leads) VT.
Northwest axis or largely differing from that of sinus
rhythm.

Ventricular Flutter. Regular Broad Complex Rate B/w 250-350 beats pm Uncommon. Very unstable rapidly progresses to ventricular fibrillation.

Non-sustained Ventricular 3/more consecutive beats of ventricular origin, but lasting less than 30 seconds. Refer to cardiologist to
Tachycardia Commonly observed in pt w significant struct heart disease and decreased LV consider prophylactic anti-
function. arrhythmic drug or
Incr risk for sudden death. Implantation of an
implantable defibrillator.
Irregular Broad complex VT is a regular broad complex Multifocal VT and
tachycardia. Most common cause for irreg broad complex tach = atrial fibrillation in the Torsades de pointes
presence of a BBB. Need to be excluded!
Torsades de point Irregular broad complex Polymorphic ventricular tachycardia ass w prolonged QT Prolonged QT Electrical cardioversion
tachycardia appearing to interval. (Drugs Quinidine, disopyramide, Sotalol, amiodarone, Tricuclic antridep Avoiding predisp drugs incl

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twist in tornado-like (amitriptyline) Pheothizines, Antipsychotics (holoperidol, olanzapine), Macrolides, anti-arrhythmics

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fashion around the iso- Quinolones, Methadone.) Correcting electrolyte
electric line. Poisons organophosphates. disturbances, in part, low Mg

Short QT syndrome
Accelerated Idioventricular
rhuthm
Ventricular Fibrillation
Premature atrial ectopic
beats
Premature nodal extopic
beats.
Prem ventricular ectopic
beats:
Escape rhythms:
Hypo kalaemia, -magnasaemia, -calcaemia Maintaining adequate HR
Bradycardia, mitral valve prolapse, acute MI, Diabetes, Prolonged fasting, CNS dis. through isoprenaline
Jervell-Lange-Nielsen, Romano-Ward syndromes infusion/cardiac pacing.
Short QT complex. Ventricular arrhytmias and sudden Heriditary. ICD best option.
death.
Intermittent broad complex and narrow complex rhythms. Enhanced automaticity of Ventricular pacemaker, leading to competition bw Pt mostly asymptomatic and
Broad complex rhythm shows typical AV dissociation w ventricular pacemaker and SA node. no anti-arrhythmic
independent P waves, fusion beats and capture beats. Typically after MI, when inherent ventr escape rhythm of 40 pm is accel to bw 60 treatment is indicated.
and 120 per minute, causing competition, leading to (ECG)
Irregular, rapid, shapeless electrical activity w an absence Simi to a-fib w very rapid, irrgular ventricular activation in random fashion. Inititation of advanced
of organised complexes. No mechanical activity of ventricles. cardiac life support and
Pt is pulseless and rapidly becomes unconscious. electrical defibrillation.
Regular sinus rhythm is sometimes interrupted by extra If occur w/in a day or wo
cardiac beats, premature extopic beats occ earlier than win MI, prophylaxis
normally expected. probably unnecessary.
Premature exopic beats must be distinguished from escape Implantable cardioverter
beats defib.w
Ectopic beats occur prematurely, whereas escape beats
are initiated following pause due to sinus node/AV nodal
dysfunction.
Premature, narrow WRS complex preceded by P wave of Atrial ectopic beats may precede atrial fib in later life.
which morphology diff from normal sinus P wave. Mainly benign rhythm not requiring treatment.
After a compensatory pause the normal sinus rhythm
proveeds.
ECG char sim to actral extopic beat except there is no
preceding P wave before extopic beat.
Premature, braod complex not preceded by a P wave Exclude structural heart
followed by a compensatory pause. disease as it carries a good
prognosis in absence of
When monitoring pt after MI certain ECG characteristics struct heart disease, but may
indicate high risk for developing VT/VF indicate high risk in presence
5< ventricular extopic beats per minute of ischaemic/struct disease.
Couplets/non-sustained VT Refer to cardiology.
Multifocal ventricular ectopic beats
R on T phenomenon, where V ectopic beat occ
on T wave of preceding QRS complex.
Every myocardial cell has capacity to depolarise thythmically and spontaneouly at
an inherent rate.
SA node 60-100
Rest of Atrium 60-80
Av 40-60 pm
Ventricle 20-40
Faster pacemaker contrls HR as all other pot pacemakers dep by faster
pacemaker befor it has opp to discharge.
If QRS complex delayed due to sinus node dysfunction/ AV conduction
abnormality one of slower potential pacemakers generates escape rhythms.
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WPWS: Pre-excitation Accessory pathway (Bundle of Kent) providing additional conn bw atria and WPWs pt develop Tachy-
Prone to tachyrhythmias ventricles. arrhythmias due to re-entry
Pre-excitation = shortening of PR interval as normal delay via accessory pathway.
of impulse in AV node is bypassed. Prone to AF as discussed
Pre-excited Ventricular tissue causeses slurred initial QRS under AVRT, creating
deflection delta wave. dangerous, irregular, broad
When normal electrical impulse coming through AV node complex tachycardia due to
reaches BB system delta wave fuses into normal antegrade conduction of AF
appearing QRS. via accessory pathway.
See AVRT.
Bradycardias and Heart Block:
HR <60 bpm.
Failure of impulse formation OR conduction
Sinus bradycardia Regular, narrow Each QRs complex preceded by a P wave. Divided into: ID and remove causes.
complex rhythm. Sinus arrhythmia may be present. Variation in ventricular Extrinsic: Temp pacing until sinus rate
rate with in-and expiration. Normal phenomenon. Drugs (Beta blockers, Ca blockers, digitalis anti-arrhythmic drugs) restored or perm pacing.
Hypothyroidism Chronic SSS = perm. Pacing +
Cholestatic jaundice drugs to manage tachy.
Raised intracranial pressure Acoid vasovagal stimulating
Neuro-cardiogenic syndromes elements.
Intrinsic:
Chronic degenerative changes (sick sinus syndrome)
Ischaemic H disease
Sick sinus syndrome Inappropriate sinus bradycardia (does not correlate w May cause symptoms due to extreme bradycardia/episodes of tachy- In symptomatic pt cardiac
exercise or atropine, sin-atrial block, sinus arrest and slow arrhythmias/ mainly from supraventricular origin. pacing may be required.
atrial fibrillation (in absence of Drug therapy) Also referred to as Bradycardia-tachycardia syndrome.
Chronic degenerative changes such as fibrosis of atrium and sinus node.
SA block/arrest Characterized by pause when no P wave is seen, followed
by escape beat.
Must be distinguished from higher degree AV block where
a pause follows an unconducted P wave.
AV block:
1st degree HB PR interval is prolonged by more than 200 miliseconds and Fit, healthy individuals No treatment indicated
remains constantly prolonged. Drugs (Beta blockers)
Rheumatic fever
Myocarditis
Ischaemic Heart disease.
2nd degree: Mobitz 1 PR interval is progressively lengthened until a beat is After MI tends to resolve spontaneously. Pt should be monitored
(Wenckebach dropped. pacing not required unless it
phenomenon) Cycle then repeated w normal PR interval progressively progresses to a higher degr
lengthening. of AV block.
Young healthy indiv this dose not freq progress to higher In elderly symp pt w struct
degrees of AV block. HD pacing necessary.
Mobitz 2: PR interval is constantly prolonged, but QRS complexes Often prog to 3rd degree
periodically dropped. heart block and pacemaker is
Usually every second/third/fourth beat (2nd degre block w indicated.
2:1/3:1/4:1 conduction)\
Usually QRS wide.
3rd degree Heart block ECG charac by regular bradycardia. Conduction bw atria and ventricles completely interrupted and an atrial rhythm See above.

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QRS complexes can be narrow if escape rhythm is from AV junction. and ventricular escape rhythm occur independently.

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But commonly ventricular in origin and thus broad complex.
RBBB QRS > 120ms Congenital
Tall, slurred R wave in V1, resulting in chracteristic rSR pattern. Cardiac or Pulmonary conditions. Alone does not alter electrical axis of the
Deep slurred S waves in V6 and SI heart.
Inverted T waves in V1-V3 Axis deviations signify RVH or co-existant fascicular block.
Tall late R wave in V1
LBBB Greater than 120ms Often ass w extensive left ventricular disease.
Pred neg QRS complex in septal region Most common causes: Table 13.10 p 720 K&C.
Deep S in V1
Tall late R wave in V6 and SI
Broad predominantly positiv, M shaped complex in V6 + high later
T wave inversion in V5-6 _ hight lateral

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 BERNHEIM effect

Heart Failure Results in complex interaction cont even after aetiology has been Aetiology:
Prognosis 50% 5 yr mortality for whole spectrum and 1 year for corrected: HAEFA
severe. diastolic failure can send you into acute flash pulmonary IHD
Apoptosis oedema.
older, females. HTNsives
DCM
When the heart fails in itsw func to maintain effective CO which meets Hypertrophy 50% of HF Systemic HPTN
often due to remodelling and fibrosis. due to hypertrophy and
the requirements of metabolising tissue (or can only do so when at an Fibrosis stiffness. poor relaxation and filling. tachycardia pushes over Cor pulm
increased filling pressure). In prac. HF is recog as clinical syndrome Exam:
Endothelial dysfunct + oxidaxitve stress
the edge.
RHD General -
charac by Congestion and inadequate organ perfusion. o Neuro-endocrinepresents SOB .LVH, small hypertrophied heart. Valve lesions Oedema
o Cytokines treat precipitants. (tachy, fluid overload ) Other COM Cardiac Cachexia
Distinguish bw: See notes for explanation. Altered gene expression. no real treatment for diastolic failure per se. Jaundice
Congenital HD
All of the above = remodelling. Peripheral cyanosis
Symptoms and Myocarditis
Acute vs chronic Fever
signs of HF along Pericardial
Subclinical vs overt Systolic vs diastolic failure:
with objective Other Cardiovascular system:
Forward vs backward General definition of HF implies systolic dysfunc/fail. Prim cardiac path
evidence - Primary etiology
Left vs right (eg HOCM), restrictive cardiomyopathy, ischaemic or cardiac Clinical picutre: - Raised JVP (N=4cm above
Systolic vs diastolic (Cardiomegaly, compensatory mech (hypertrophy, fibrosis in infarct), leads to inability sternal angle at 45 deg)
Low output vs high output. S3, Murmurs, of ventricle to relax w diastole consequent inpairment of ventr filling. Exertional dyspnoea - Cardiomegaly
Abnormal echo, Ejection fraction remains the same (HFPEF). (Will lead to dyspnoea, Orthopnoea
- Hepatojugular reflux
Pathophysiology: raised Natriuretic - S3
pulm oedema and RHF) PND - Pulsus alternans
peptide) HFPEF - when EF >50% Congestion: - Abnormal valsalva response
Result of primary cardiac defect See figure 4. P6 of notes. o Oedema
and compensatory mechanisms (Exceptions:Constrictive
o Liver discomfort
Subclinical vs overt HF. o GIT complaints
pericarditis, restrictive
1. Pump dysfunction cardiomyopathy, MS, Acute
Other (Fatigue, weka, nocturia, Heart
reduced cerebral func + CNS
Failure)
Stage Treatment
Prim response of failing heart due to impaired inotropic func is to symp)
A High risk (eg risk factor) Education
maintain CO by incr stroke volume acc to Frank-Starling principle. Sfx of treat
Control risk factor
(Massive incr preload) leading to congestive symptoms. Adjustment B Structural disease (LVH from ACE inhibitor
Hptn, no symptoms) Consider BBlockers See Clinical examination section in Talley and OConnor
needed on cellular and struct level (remodelling to incr stroke volume
C Struct disease w symp, ACE inhib Varies acc to spec aetiology, acuteness of onset, degree of disab,
leads to further decompensation)
previous and current Beta-Blocker for mortality reduction predominant pathophysiological disorder and therapy.
Aldosterone antagonist
2. Compensatory mech
Diuretics only symptomatic. aim for lowest See NYHA classification of risk factors.
Digitalis doses.weight monitoring useful. Dyspnoea: abnormal unpleasant awereness of breathing.
Type Cardiac Fluid Vasoconstriction D- Advanced/refractory Specialist management Exertional dyspnoa self-explanatory. Look for change in level at which
rentention Remember: Intervention
occurs.
(incr MAP= CO X SVR High output v low output HF. The following can cause red. Output:
preload) high output failure
Mechanisms Hypertrophy Act RAS Same as fluid Orthopnoea: Beware pt who habitually sleeps on more than one pillow.
AV fistula
(AS) Sympath retention Seek evidence of change in number of pillows. Not spec. (lung disease,
Pagets disease (bone disease w extensive AV fistulae in
Dilatation stim Allows blood ascites). Sometimes nocturnal cough only symptom.
(MI, DCM) ANP press to be bone)
Tachycardia system maintained Pregnancy PND: Acute onset. Not relieved immediately. takes at least 10
NYHA classification of functional impairment:
despite Decr CO. Thyrotoxicosis minutes

10
I - No limitation of normal physical activites
Disadvantages Incr heart Beyond Causes Anaemia Dyspnoea/orthopnoea Pulm venous/cap HPTN
II - Comfortable at rest, usual physical activities
wall tension optimal inadequate Beriberi
consider Caddiac re synchronization therapy III - Symptomatic when performing less than usual PND Interstitial oedema
Diastolic point on perfusion of vital

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1 lead in RA activities Pulm oedema Alveolar oedema
dysfunc starling organs (kidneys) 1 in RV
IV - Symptamatic at rest (includes orthopnoea and PND) Most die from Arrhythmia.
1in coronary sinus.
Arrhythmias curve, and activates
congestion RAS (forward 30% don't respond
occurs failure) ICDs for all pts with EFsbelow 35%.
Mech of dyspnoea: incr work of breathing stiff lungs, reduced ability to work, incr breathing drice (incr pCO2)

General: CV system: GIT Resp system

Oedema (ankle, sacral)
Cardiac cachexia
Peripheral cyanosis
Jaundice
Fever (Cut vasoconstric = heat
loss)
Further tests/comparisons:
Prim aetiology
Incr JVP (N= 4cm above steranl
angle at 45 deg)
Hepatojugular reflux
S3
Pulsus alternans
Abnormal valsalva response
Cardiomegaly (except in
constrictive pericarditis,
restrictive cardiomyopathy,
mitral stenosis and acute
heart failure.)
Tender hepatomegaly Basal crackles
Ascites Pleural effusion (bilateral or
right sided, only left if suspect
pulm embolism Right side
has greater surface area for
fluid to transudate into. Right
2X as likely as left and bilateral
far more likely than unilateral)

Condition History/Examination: Xrays ECG and Echo Blood Tests Other special investigations:
Investigate for spec aetiology (MI vs Essential BNP> 400pg/ml HF likely Stress ECG
Emphysema) Often provide critically important Stress Echo
BNP incr in Cardiac dysp. info about underlying cause. Nuclear medicine (synch heart
Therapeutic: Cardiac relieved by scintigraphy, MIBI scans,
Diuretics cardiac MRI/ heart catheterization
Cardiac Dyspnoea Relieved by sitting up Cardiac enlargement BNP <100pg/ml Unlikely to be HF
Incr blood flow to upper lobes Hb u&e, troponin T/I and thyroid
Interstitial oedema (Kerley B lines) func NB to ID precipitant of
Alveolar oedema worsening HF. Anaemia marker of
Pulm Dyspnoea Relieved by coughing See Resp poor prognosis in HF= should always
be fully investigated.
Managing Heart failure: (Remember FCP: Is it Failure? Cause? Diet (maintain fluid balance, avoid becoming overweight, Thyrotoxicosis
Precipitant?) moderate salt restrict, alcohol mod. Normal fluid intake (except if
hyponatraemic.
1. Remove/treat primary cause. Multidisciplinary
2. Remove precipitants Immunize (Influenza and pneumocci) Antifailure therapy:
3. Anti-failure therapy
a. Block harmful mech Precipitants: A. Block harmful mech:
b. Reduce afterload a. RAS: ACE-I, aldosterone antag
c. Reduce preload Therapeutic errors b. Sympath system (Beta blockers)
d. Inotropic support o Inapp change in Rx B. Reduce acterload (Arterial vasodil, esp ACE-I)
o Neg inotropics (CCBs and anti-arrhythmics) C. Reduce preload: (Diuretic, venodilators- nitrates)
General: RAD MI o Sodium Excess D. Inotropic support
Secod Heart disease a. Digitalis
Rest Arrhythmias b. Sympathomimetic amines (IV in eps of Acute HF)
o Regular if not acute Systemic infect
o Strict bedrest if acute. Pulm embolism Initiate therapy:

11
Aspiration Renal failures
Of effusions, ascites, if Anaemia See attached algorithm

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large

Clinical groups:
Decomp chronic HF
Acute Pulm oedema
HPTNsive HF (Pulm
oedema w preserve
systolic func)
Cardiogenic shock
Islolated RHF
ACS +HF
Drugs used in Heart failure:
Acute Heart failure Resistant Heart failure
Goals of treat Therapeutic measures Exclude Precipitants Make sure there are no: If there are none:
(DMNR)
ID and treat cause Drugs (Diuretic, Non-compliant Surgically correctable IV therapy w diuretics,
Improve and correct: vasodilators, inotropic Sfx of Rx (Digitalis, Valve lesions vasodilators and inotropic
o Oxygenation support) dehydration, hypo- K,Na, Reversible Myocard Isch support.
o BP Non-invasive ventilation Cl) Pericardial Refer to cardiologist:
o Organperfusio (CPAP) Alchol abuse constrict/tamponade See therapies that can be
n Rhythm adaptations Excessive salt Large Pleural effusions given from there.
(Pace heart block, Rhythm disorders (sick
cardiovesion or anti- sinus) - Other drugs - amiodarone, warfarin, b
blockers
arrhythmics for Pulm emboli - Cardiac resynchornisation therapy (CRT) - in
tachydysrhythmias.) Pulm infect, UTI, IE pts w long PR interval and a LBBB
Mechanical support of Thyroid dysfunct, - Revascularisation for ischaemic heart
failure
cardiac func (Intra-aortic anaemia, kidney failure - Ultrafiltration for uncontrolled fluid overload.
balloon pump) - Implantable defibrillartor if episodes of
VT/VF or EF <35%
- Transplant in Suitable candidates - or LVAD
before then.

Drug and Example: Mechanism Side Effects and Contra-indications Pharmacokinetics

Diuretics
Loop diuretics (Furosemide, bumetanide)
Thiazide: Hydroclorothiazide, indapamide, metolazone
K+ sparing diuretics (sprinolactone, eplerenone)
Carbonic anhydrase inhibitors: Acetazolamide
Dangers of diuretic therapy:
Inhibit Na/K/2CL co-transport in ascending loop of At high doses, hypochloraemic metabolic alkalosis Bioavalability 60% (reduced in HF)
henle. develops
IV admin leads to venodilatation w decr preload. Toxic fx Ototoxic (NB slow infusion)
Haemodunamic fx dure to angiotensin II release w NB interaction = NSAIDS reduce effect!
subsequent arterial constriction and incr prostaglandin Hypo-K
release = venodilatation. Hypomagnasaemia
Inhib Na+Cl- reabsorption in distal convoluted tubule Undesirable metabolic profile: Ineffective if GFR is less than 30ml/min
Hypokalaemia
Hypomagnasaemia
Hyperlipidaemia
Glucose intolerance
Aldosterone antagonists Do not combine w K supplements and ACE inhib can Not potent, use in combo
Incr Na excretion and K retention cause hyperkalaemia.
Improves outcome through ingib of myocardial fibrosis Acidosis
Ingibit CA in prox con tubule (CA converts Water and HCO3- uria and hyperchloraemic metabolic acidosis. Used to counteract hypochloraemic alkalosis in diuretic
H2O to bicarbonate and a proton) Acidosis overuse.
Dehydration

Vasodilators
ACE (see other pharmacology summaries) (Captopril,
enalapril, perindopril, quinapril, ramipril)
ACE-I effect largely due to blocking RAAS, but also Guard against excessive hypotension at first dose (esp in Initiate at low doses
blockign the breakdown of bradykinin (beneficial for BP hypovolaemic pt) Quickly inc to optimal therapeutic dose
control, but can cause cough) Avoid combos w K sparing diuretics (spironolactone)
Can decr preload and afterload (and also eliminates Avoid in:
angiotensin stim of myocardium Severe aortic stenosis
Bilateral renal artery stenosis

12
Pt suff from intrinsic kidney disease w kidney
failure

Page
Hypotensive pt.
CI in pregnancy!
ARBs, Losartin, candesartan, valsartan Alt to ACE-I in pt w intolerance
Beta blockers: Carvedilol, metoprolol, bisoprolol, Mech unclear
nebivolol Decr energy req of myocard
Inhib sympath overactivity,(characteristic of HF)
Upreg of Beta receptors in myocard
start low, go slow.
increase every 4
days.
Inotropic support
Digitalis Inhib Na/K pump inc [Na], leads to incr in [Ca] via
Na/Ca exchanger incr Ca avail to contractile apparatus
positive inotropy.
Incr autmaticity of Pukinje fibres.
Decr conduction velocity in AV node (Via vagus_
Prolongs refractory period of AV node.
Shortens Refractory period.
Slows ventricular response to SVT
Diuresis, (inhib renal Na reabsorption
Incr vascular resistance (avoid acute IV bolus)
Sympathomimetic amines, eg dobutamine, dopamine, Positive inotropes via stim of myocard b2 receptors
noradrenaline. (mobilising Ca).
Vasodilatation (beta 2 recept stim.)
Also stims alpha receptors vasoconstriction
Dobutamine: Stims beta 1 >>>>alpha> beta 2
Therefore, net effect is: pos inotropic, very little effect
on peripheral vasc resistance (beta2 and alpha 1 effects
neutralise one another)
wirkup fkr a cause (ischaemia, haemachromatosis, SLE, HIV, peripartum
Dopamine:reverseit. Inotropic: also stims dopaminergic receptors at low doses.
Less coughing thatn ACE I but still CI in preg. Can be added to ACEI and BBlockers in resist pt.
CI in acute heart failure, diabetes, asthma, heart block. Initiate in a stable phase
nausea, diarrhoea, bronchospasm, dyspnea, cold Restore fluid balance in the oedematous pt before
extremities, exacerbation of Raynaud's syndrome, therapy.
bradycardia, hypotension, heart failure, heart block, Initiate at a very low dose and gradully incr daily
fatigue, dizziness, alopecia (hair loss), abnormal vision,
hallucinations, insomnia, nightmares, sexual
dysfunction, erectile dysfunction and/or alteration of
glucose and lipid metabolism. Mixed 1/-antagonist
therapy is also commonly associated with orthostatic
hypotension. Carvedilol therapy is commonly associated
with edema.[23]
Narrow Therapeutic dose. 1-2ng/ml (sometimes varying T1/2 = 36 hrs
levels can induce toxicity in diff pt. Steady state after 7 days w/out loading regimen
Pt w electrolyte disturbances, esp hypo-K very prone to Excretion=renal
digitalis toxicity. Bioavailability 67% (Cholestyramine decreases
Caution in eldery and decr renal func. absorbtion)
Symp of Toxicity: 23% protein bounded
GIT (Nausea, vomiting)
CNS(Headache, fatigue, confusion, cisual colour Dose: 0.25mg/day in avg pt w norm renal func. Stable at
percept, seotomata, halos around lights) 7 days.
CVS: All of rhythm dist in bood. Slow AV nodal Loading dose: IV
rhythms. Bigeminus, SVT
Treat: Check levels and electrolytes esp K. Stop
digitalis.
Bradycaredia pacemaker
Ventricular tachycardia
lignocaine/phenytoine
Specific antibodies Fab frag
Drug interactions (a few)
Decr absorption. Cholestyramine, antacids (give at diff
times)
Incr bioavailavility: Quinidine, amiodarone, verapamil
(decrease the does)
Downreg of B receptors Use in Cardiogenic shock
Tachycardia Acute HF
Haemodynamic fx as result of vasoconstriction/dilation Preioperatively and resistant chronic HF
Arrhythmias
Angina
Hypertension
Less tachycardia and haemodynamic fx than 2-10 microgram per kilogram per minute.
adrenalin/noradrenalin.
two chamber pacing Dosage: See notes

13
At high doses also acts as a pressor agnet (alpha receptor)
ACC class them.
Noradrenaline Vasopressor If bp cannot be maintained or in cases of ass septic
A - no sx, RX RISK factors Nor mor used in HF, since periph resist already elevated. ICDs (if EF <35%) shock NA can be used in combo w dobutamine.

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B - DYSFUNCTION of ventricle (eg. previous heart attack), asymptomatic Most die from arrhythmias
C - SOME SX .
d CRTD - crt and defibrillator!
II-
Hypertension treatment: HPT: At every visit: o Follow up dose titration or stepwise incr should be carried
Lifestyle modifications: out after 2 mths if BP remains unctrld.
2 BP readings take averages o Once a stable target BP has been achieved F/up every 3-
Weight reduction Mass 6mths.
Restriction of daily alchol and Na consump BMI o Drug dose should red if pt pres w symp of post hypotension,
Adherance to spec diet plan red fat intake incr intake of Waist circumference dizziness/ >20mmHg in SBP on standing.
fruits, vegetables, wholegrain foods
Physical exercise Some basic Physiology: See R&D p304. When to refer:
Smoking cessation.
o Renin Produced in Kidneys due to: I. Young pt (18-30)
Pt may already have major risk factors: o Incr renal perfusion pressure II. Pregnancy
o Incr GFR III. Uncontrolled BP despite 3 drugs (resistant)
Abdominal obesity o Incr B agonist and PGI2 IV. Any pt w severe target-organ damage and.or severe ass clin
Dyslipidaemia o Incr Sympath nerve act conditions
Type II DM o Decr Natriuretic peptide. V. Hypertensive urgency/emergency
Fam hist of early CV disease o Renin reacts w angiotensinogen to produce Angiontensin I
Smoking o A I reacts via ACE to form Angiotensin II Most pt w low/mod risk can be managed at prim care level and can be
o A II reacts w AT1 receptors to do the following seen every 6 months. Pt w high and very high added risk w numerous
Risk stratifications: 1. Vascular growth risk factors should be managed by physicians or med subspecialists
a. Hyperplasia/hypertrophy until BP cntrls.
1. BP Levels 2. Vasoconstriction:
2. Presence of 1-2 / >3 risk factors a. Direct
3. The presence of target organ damage/ DM b. Via incr noradrenaline release from sympath
4. Presence of other ass clin condi (HF, CHD, Stroke, TIA, PAD, nerves Managing severe HPT:
retinopathy) 3. Salt retention
a. Aldosterone secr Asympt Urgent Emergency
No symp w or w.out Symp: severe Acute & ongoing
Targets for BP lowering Treat: b. Tubular Na+ reabsorbtion.
signs of target organ headache, dyspnoea, damage
damage oedema encephalopathy and
Stage BP Level NB: HPTN can seldom be managed in isolation from other related ACS. Most pts SBP
All stages 140/90 chronic illnesses >220 and/or DBP >
In isolated Systolic hypertn dont 140 mmHG
lower DBP <65 Lifestyle mod, drug therapy and targets of management should be Outpt Inpt InpT ICU
High risk pt: <130/80 broadened to incl measures of other risk factors and co-morbidities. 2 drugs 2 drugs IV: Labetalol,
DM Ideally w/in 3months furosemide, sodium
Renal (Microalbuminuria, Incr CK) nitroprusside etc
Obesity, blood sugar and lipids along w BP contrl!
Congestive heart failure PO: LA nifedipine,
Severe HPT: DBP: >/= 110 and/or SBP >/ 180 captopril
Follow up 1 week Lower BP over 48- Lower BP over hours.
Investigations in HPT: 72h to diastolic of
o PT may be asymp w/wout target oragan damage and ass clin
100
cond.
Urine Dipsticks
o Keep p and let pt rest 1 hour
Microalbuminuria
o Repeat BP
Blood glucose
o If still raised start 2 drugs immediately.
Random total cholesterol
One drug must be low-dose thiazide diuretic. Other us a

14
o
Creatinine, Potassium, Resting ECG
dihydropuridine CCB
All the above in 1st visit then yearly if normal. Follow up <1week.

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o
o If nec escalate. if not ctrl w/in 2-4 wks = refer pt
Drug Mechanism Indications Contraindications SFX
Thiazide Diuretic Diuretic and vasodilator Step 1 in most treatment. Except Gout and Electrolyte distrurbances
diabetes. Hyperuricaemia
High doses: Glucose intolerance &
adverse lipid profile
ACEI and ARBS Blocks ACE or A receptor 1. Reduce effects of In DM II both ACE-Is and ARVs have red ARBs = High cost ACEI:
angiotensin Lower BP. microalbuminuria and delayed progg of o Incr K+
diabetic nephropathy o Hypotension
o Decr GFR
Hypertension o Angioedema
Cardiac failure o Chronic dryg cough.
Following MI Treat ACE I angioedema:
In ppl at risk of IHD Withdraw ACE-I
Diabetic Nephropathy Supportive treatment
Prog renal insufficiency C/S, anti-histamine, adrenalin
Calcium Channel Blockers - Blocks CC decr contractility of myocardium. Ankle oedema
Beta blockers: When used to treat HPT, BB do not reduce No longer used in steps 1-3 of HPT treat May induce new diabetes, esp when used
CV mortality or MI mortality CI in Diabetics w diuretics (thiazides)
May mask hypoglycaemia sympt.

15
Page
Kidney effective:

10-fold increase daily NaCl intake <1L ECFV

expansion, no BP changes

No NaCl diet ECFV contraction 1L over 3-

5days, no BP changes

Salt sensitivity

Black patients
Elderly
CKD

16
30% normotensive subjects (genetically determined)

Page
\ Summary - Pathogenesis

SVR:
o RAAS activation
o Sympathetic NS activation
o Hyperuricaemia
o Endothelial dysfunction
o Oxidative stress
o Abnormal baroreceptor response
o Obesity
Renal Hypothesis
o Barker-Brenner
o Lifton
o Goldblatt

Endothelium & oxidative stress

Summary Epidemiology

Overall prevalence increasing: 28.7%

Highest in black population

Patients aware of underlying diagnosis hypertension: 70%

17
BP controlled in only 1/3 (31%)

Page
Ischaemic HD (See Weich notes) Metabolic consequences of the Insulin Resistance Syndrome
Risk factors for coronary artery disease TG > 2.3 mmol/l
HDL < 1 mmol/l
Major Other LDL = N or slight but LDL small and dense
MAJOR Other PAI 1
Smoking Obesity Fibrinogen
Cholesterol Lack of exercise
Diabetes Age
Hypertension Male gender 20% of IHD patients have only 1 risk factor
Family history Menopause 80% of IHD have multiple risk factors
Multiple risk factors often linked
Modifiable Immutable Clustering of risk factors e.g. insulin resistance
Smoking Age syndrome
Diet Male sex Central obesity
Exercise Family history
Insulin resistance
Obesity of IHD
Hypertension Hypertension
Diabetes Dyslipidaemia
Dyslipidaemia
Estrogen deficiency

Unproven:
Hyperhomocysteinaemia
Infections (Mycoplasma,
Helicobacter)
Low anti-oxidant intake
Elevated CRP

Risk factor clustering

Impact of patient characteristics on risk of atherosclerosis

Age and Sex
Race
Sosioeconomic status
Lifestyle
Male > 45
Female > 55
Rare in SA blacks

18
Higher income group
Westernized lifestyle

Page
Just a brief reminder of what is considered strict risk factor control and Heparin STEMI: Reperfuse (TPA tissue plasminogen activator)
good glycaemic control: Nitrates UAP/NSTEMI:
LDL < 2.6 mmol/l CCB
TG < 2.3 mmol/l o Surgical Risk stratify
BP < 130/80 mm Hg PCI o High risk angiography
BMI < 25 kg/m2 CABG o Low risk: Medical
HbA1c < 7% Decrease demand: Anti platelet
(Fasting gluc. < 6.7 mmol/l) o Adapt activity Anti-coagulant
(Post prandial gluc. < 7,8 mmol/l) o Beta blockers Anti-ANginal
Beta-blockers
Atheromatous plaques: NB: Degree of obstruction not indicator of plaque rupture and vessel Nitrates
occlusion.
Stable: General:
o High lipid content In in healthy endothelium and stable atherosclerotic plaques =
o Thick, fibrous cap Significant protection.With SLAGS: Haemostasis: Arrest of blood loss after damge to a blood vessel
o Functional endothelium consists of platelet activation and adhesion to injury and coagulation of
o Little/no inflamm Smoking cessation blood (fibrin formation)
Vulnerable: Statins
o Inlamed endothelium Anti-hypertensives Thrombosis: Inappropriate activation of haemostasis: Arterial/Venous.
o Thin, fibrous cap Glucose control
Lifestyle modification Venous: Usually w stasis large component of fibrin and small platelet
No occlusion = Asymptomatic comp.
Incomplete Occlusion = Angina Pectoris Manage ACS: Arterial: Usually in presence of atherosclerosis with large platelet
Complete Occlusion = Acute coronary syndrome component.
1. Relieve symptoms
Symptomatic Coronary Artery Disease:
2. Prevent/limit MI
1. Stable Angina Pectoris
3. Improve prognosis
2. Acute Coronary Syndrome
a. Unstable Angina Pectoris
Remember: Individualize and Risk stratify! High risk = reperfuse
b. Myocardial infartion (Presence of Serum
low risk = medical tratment.
markers)
i. With ST elevation (STEMI)
Stages of MI:
ii. W/out ST elevation (NSTEMI)
Diagnosis: Inflammation
History Rupture
o Duration of pain >20 mins for STEMI Platelet Adhesion
o <2mins SAP + during exercise, relieved by rest Thrombosis
and/or nitrates. Spasm (not NB)
Symptoms Embolus
ECG
o Normal does not exclude ACS NB is infrastructure and Education to improve:
Myocardial Markers
Pain to Needle/Door to needle time.

19
Relieve symptoms:
Increase supply: Or Door/pain to balloon time.
Medication:

Page
o
Aspirin
Drug Mechanism Indication CI SFX How to use:
Aspirine Irriversible inhibitor of COX Reduces CV events when used in Bleeding
COX leads to Platelet aggregation stable angina Nephrotoxic (rare)
Lasts for entire lifespan of platelet Hepatotoxic
(8-10 days) Asthma (Drives up LT prod)
COX 1 protects Gastric mucosa and Gastric ulceration (Inhib protective
leads to Platelet aggregation PG)
COX 2 causes pain/inflamm,
regulates renal flow, produces
prostacyclin.
HMG CO-A inhibitors (Statins) HMG- CoA is converted to See Hyperlipidaemia notes
mevalonate by reductase (rate- Major= myopathy and incr serum
limiting step in cholesterol synth) transaminases.
Statins are comp inhibo f HMG Co-A
Decr hepatic cholesterol = Upreg of
LDL receptors
LDL scavenged from periph circ.
Decr mortalitiy
Beta-Blockers: Multifactorial: Exact unclear. Asthma VOST: Principle:
Initial fall in HR and CO Uncontrolled Heart Failure Vertigo Start w low dose,
Lower mycoard energy Heart Block Orthostatic Hypotension uptitrate, monitor
expend Diabetes (esp Type I) Sexual dysfunction Add to existing ACE-I &
Prolonged diastolic filling Tachycardia diuretic when stable =
Incr myocardial blood Bradycardia not NYHC III/IV
flow Never stop abruptly (risk
Blockade of renal B- Heart Block Ischaemia/infarct
receptros, decr renin Peripheral arterial spasm, Proven Benefit only for
Decr sympth tone CNS by Difficult diabetic contrl Carvedilol, metoprolo,
inhibiting prejunctional Bronchospasm bisoprolol
receptors on neurons Heart Failure If stable on Bclocker and
and decr NA release. Tiredness deteriorates Dont stop
Claudication. BB! (Incr mortality
CCB: Alternative to BB See ACE-I Improves survival if given after
Hypertension notes MI, esp if there is myocard dysfunc.
Nitrates: Exogenous source of vasodilatory Symptomatic relief of Use w caution in pt who have used Headaches Discard 60 days after opening
nitric oxide produce coronary angina/prevention of angina Sildeafil (viagra) in last 24-48 hrs Hypotension/Syncope Keep in original container (not in
vasodilation. Tolerance (Prevent w nitrate free plastic)
Venodilatro and therefore decr interval/eccentric dosing)
preload and LV EDP = less wall stress Tachycardia Pt should be sitting
As dose incr, afterload is also Bradycardia Take one every five mins till pain
reduced by arteriolar dilatation. stops of 4-5 tables have been taken
Can be given as sublingual spray

To prevent:
Isosorvide dinitrate/mononitrate
Patch can be used but promotes
resistance.

20
Page
Approach to Chest pain ST elevation: NB: Angina = ECG

DDX: o Saddle shaped = Pericarditis Know Chest anatomy

o Straight probably MI
1. Skin (herpes zoster) DDx acc to anatomy.
2. Chest wall (costochondritis,trauma) GORD:
3. Heart (Angina, pericarditis, mitral valve prolapse Divide chest pain into diff catergories.
4. Aorta (dissection Most common DDx for angina
5. Lung (PE, Pneumonia, Pneumothorax,pleuritis) caused by oesophageal spasm, iritaion of mucosa Always remember who gets non-ischemic typer pain although isch
6. Oesophagus (GORD, Spasm) Pain>night,at rest present.
Relieved by nitrates if spasm.
Types of Pain: Trial of antacid/proton pump inhib
Special tests = gastroscopy.
1. Ischeamic (angina)
a. Crushing, pressing, retrosternal pain radiating to Is it Ischaemic?
nexk, should and arm (usually left)
b. Comse on w exercise, better w rest or nitrates Type
c. Ass dyspnoea, sweating, nausea Onset
2. Pleuritic Known w ischaemic heart Disease
a. Shard, stabbing pain, worse w coughing, Any major risk factors:
breathing, change in position (lung/pericarditis) o DM
3. Other: GORD, Dissection o HPT
o Hypercholestrolaemia
Aortic Dissection: o Smoking
o Fam hist of ischaemic HD
Look for fx of dissection o Chronic renal failure.
check symmetry of pulses
BP in each arm Non-Ischaemic Chest pain w ischaemia (no typical chest pain or atypical
special investigations: chest pain w ischaemia): DEW
o CXR
o Echo Diabetics (autonomic neuropathy)
o Trans-oesophageal echocardiography The Elderly
Treatment Bp control and URGENT surgery Women (higher pain threshold)

Pericarditis: How manage ischaemic chest pain:

o Inflamm of pericardium O2
o Pain may be positional/pleuritic Aspirin
o Incvest Nitrate sublingual
o ECG ECG
Saddle ST Cardiac enzymes (4-6) hours after pain at peak
PR depression in all but aVR
Echo

21
o
o Treat:
Address cause

Page
o
o Anti-inflamm
 Atheromatous plaques can be subdivided into 3 categories: IHD is on a spectrum:
Stable plaques - with no inflammation - no increased risk of IHD
Inflamed plaques - which are inflamed and eroding their fibrin caps. - Asymptomatic
Compliated/unstable plaques - which greatly increase risk of ACS - Thin fibrous cap - Stable Angina pectoris
which is eroded and exposes atheroma to circulation. - ACS: UAP, NSTEMI, STEMI, SUD
Pathogenesis of IHD: SAP: - Heart failure Stress ECG:
1. Coronary Artery Obstruction: (Remember TASTES-CA)
a. Trauma Cond charact by asttacks of chaest pains resulting from myocard isch. CI to Stress ECG:
b. Atheroma Is it angina? Following on increase demand and/or insuff delivery of ox blood.
c. Spasm Is it stable? relieved before damage. AMI (wait at least 4 weeks)
Can i fix precipitants? UAP
d. Thrombus
e. Embolus Nature: (SOCRATES) Untreated and life threat rhythm distrub. (VT)
Always:
f. Syphilis - Rx risk factors Inability to ecercise
g. Congenital - Rx ischaemia Site: Retrosternal Acute viral infect. (FEVER!)
h. Arteritis Onset: Sudden Incompensated HF
2. Reduced Supply of Ox Blood: (CHAC)
Risk stratify: Character: Burning pressing, choking Obstructive heart lesions, (Critical aorta stenosis HOCM)
- 1. Risk Fx Incontrolled HBP
a. Cyanotic cond. Radiation: To left arm, mandible and/or throat.
- 2. Complications
b. Hypotension Alleviated by rest, NO High greade AV block
- 3. ECG
c. Anaemia -4. Stress ECG Time: Never longer than 20mins. Relative CI:
d. Carboxyhaemoglobinaemia Exacerbated: Exercise, emotions, large meal, drug therapy o Digitalis,
3. Increased Oxygen Demand (HHAT) Increased risk? lpse, incr. BP, Cold, Early morning, Heart failure, rhythm o Betal blockers
- Angiography +/- LBBB
a. Hypertrophic Cardiomyopathy distrb, dreams. o
- Revascularization.
b. Hypertension Severity: Merely discomfort (Except in DEW) o Electrolyte imbalance
c. Aortic Stenosis Low risk?
d. Thyrotoxicosis SeeBeta
- Medical Rx (Aspirin, Nitrates - sx, DDx in Approach to chest pain. Terminate Exercise if:
4. Cardiac Syndrome X blockers, CCB if BB CI)
Clin exam: Mostly none. Poss signs of risk factors: Xanthelasma, Target HR reached.
a. Typical angina, Pos stress -EXG,
No symptom control?
normal cornoary
- Consider cantomas, hypertension, tobacco signs, Fold on ear. Maybe 3 heart rd 3 Things in the ST: Angina
arteries (maybe spasm, small blood vessels
sound. - 2mm or more ST Diagnostic ST segment changes.
desease, or abnormal pain impulse. segment elevation in a Excessive tiredness ,acute dyspoea, unwillingness to
non-Q-wave leads
Types of IHD: Classification of Angina: continue.
- ST depression
pesisting more than 5 Rhythm distrub.
1. Symptom free Ischaemia Class 1: No angina with normal activities appears w
minutes into rest phase. Poor prognostic signs
2. SAP prolonged work, exercise. - o >/= 2mm horizontal,m down sloping ST seg
3. ACS Class 2: Slight impair daily act. With more strenuous exer. depression.
2 things about the Inadequate incr/red in BP
a. UAP Class 3: Profound impair of mornal daily acti. 1 flight stairs, o
exercise:
b. NSTEMI street block. o Inability to cont w phase 1 of Bruce protocol
- Inadequate
c. STEMI Class 4: Angina at rest. incr/reducation in BP o Cont >30seconds VT
d. Sudden Cardiac death. - Inability to continue o Ex induced ST seg elevation in a non-Q-wave lead
Special investigation: with phase 1 of bruce (not AVR)
Symptom free ISchaemia protocol o ST dep persis > 5mins into rest phase.
ECG: Poor test, reveals only 3% of pt w isch HD, only value compare.
1 other:
Typical ECG, no sympt. Holter Req. Diagnosis: Varying degrees of ST segment elevation, depression as well
30 seconds VT
Radioisotope scintigram shows myocard. Isch during ECG Possible signs: Deep eqyal sided T wave inversion as ST incline. BAYES theorem: Greater possibility of clinical diagnosis of
changes. Horizontal ST segments w sharp ST-T transition. IHD, greater diagnostic importance of small ECG changes during
Maybe abnormal pain perception Horizontal ST depression w sharp ST-T transition. exercise. Usually pos:
Majority of these pt. Have atheromatous coronary art LBBB

22
involve. + sometimes aexperience typical angina. Abnormal high peaked T wave. 1mm/more horizonta/downwart sloping ST segm
Diffuse flat T-wave. depression.
Routine treat red. Freq.

Page
Development of LBBB pattern.
No proof treat. Improves prognosis.
In IHD poss high pt slight upward inclined ST acceptable.
NOT: Upward inclined ST seg elevation, J point depression, no STEMI Rhythm disturbances (VT,VF and 3rd degree AV block) Treat
depression relative to PR interval. as nec. Tachyrhythmiacs (AT and AF) must be immediately
Following rupture and thrombus formation, red cells rich thrombus corrected. Ectopic beats a danger signs indicate imminent
Correct Diagnosis in (40% w 1 vessel disease, 60% w 2, 80% w 3) may form (red thrombus) = complete obstruction. No blod supp = VFib:
False Pos in females, hypertension, digitalis. necrosis. Not nec to experience angina. May be first signs of IGD. o More than 5 ectopics at a time
Prcess of infarct van be completely revesed if blood supp can be re- o R on T
Prognosis: instated w/in period not exceeding 20 mins W/in 90 mins major o Multifocal
Good- if pt can complete phase 4 of BRUCE. portion of myocardium may still be saved. Therafter damage incr o 2 or more repeats
Poor:: rapidly and after 6hrs reperfusion little value. Infarct finally complete Pericarditis: 2 kinds w mostly post-MI high dose
Poor prog signs bw 12-24 hrs. Clear demarcation, limit to coronary artery supp. aspirine
o o Haemorrhagic (Treat w NSAIDS)
high dose brufen
o Persist ST seg depression o Dressler Syndrome: Cause is auto-imune react
o ST seg elevation over area of earlier infarct. Diagnosis: See Table. against damaged myopericardium. Usually app
Stress MIBI: Correct in 95% of PT w ischaemic HD. 10-14 days after acute infarction.
Stress Echo: Similar sens/spec to MIBI Thrombolysis CI: o Resents anew w chest pains that can be mistaken
Coronary Angiography: Results indicate path/anatomy of coronary for re-infarction. Can repeat recurrently after
arteries as opp to ischaemia in tests discussed above. (Not nec =) >12 hrs after pain commnce.
several months. Treat by NSAID and cortisone
Acute Coronary Syndromes: Uncontrolled Hptn may even be needed.
UAP No clear signs of new infarct on ECG (<1mm ST seg elevation Papillary muscle dysfunc.
NSTEMI in 2 or more consec recording or no new LBBB pattern) o Ischaemia
STEMI Older than 75yrs o Infarction
Sudden Cardiac Death Bleeding tendencies o Rupture
NSTEMI and UAP: Active peptic ulcers o Teating of chordae
Usually from rupture of small atheromatous plaque, platelet Recent surgery o Heals by fibrosis
aggregation, formation of platelet rich white thrombus (not leading to Revent Suscitation Embolism: DVT and Mural thrombosis
full occlusion.) Can evolve if full obstruct by thrombus. Receiver streptokinase 5 days 9mnths previously. Remodelling of ventricle. Aggravated by Cortisone, NSAIDS,
Presentation: (See table) treated w ACE-I
Exclusions: Risks: Rupture
Prinzmetal;s angina (vessel spasm, during rest, mostly w Signs of effective Thrombolysis: o Rupture of septal infarct w estab of VSD.
associated atheroma at spasm site.) Bleeding ST segments decrease by 50% - on ECG o Papillary muscle rupture cangive rise to
o Usually pain incr and last longer. Reperfusion arrhythmia 90mins after Admin fulminating HF and demands immediate surgery.
o Elevated ST during pain. Reperfusion damage Reperfusion arrthythmia - Idioventricular o Free wall rupt. In late hosp phase. More common
o Treat w vasoldilators (Never Betablockers) Allergic reactions. on pt w cortisone. Sudden collapse w ECG cont
rhythm
Insufficient Medication, depletion, termination normally on monitor = not treatable.
Complications: HARPPERRA
then move to a cardiac care centre
Imitators: Aneurism:
o Infect w fever.
Uncontrolled HF Heart Failure: below 3 hours the biggest
o acute and late benefit! Infarct sybtypes:
o Disturb of rhythm w tachy complications o Manage w killip classification (only applicable in
o Incr exercise/activity HF following MI) see below RVH: Decrease BP, inferior infarct Move V4-6 to right side of chest. IV
o Incr emotional stress Angina: Angiography w revascularization urgent if: fluids needed. NB: CI Diuretic!
o Anaemia (Hb>10g/dl) o Stuttering first phase infarct
o Hyperthyroidism o Angina experienced in after-acute phase, before Sudden Death:
Uncontrollable hypertension dismissal

23
o
o Casoconstriction (Cocaine, amphetamine, LSD) o Angina,positive Stress ECG in 6 months after Causes: VT/VF, asystole, Electro-mechanical dyssociatione.
o Withdrawal of Nitrates/Beta-blockers dismissal.

Page
ACS With blood transfusion does
badly
Condition: Symptoms
Stable Angina Pectoris
Stable angina pectoris is NOT ACS
UAP
Approach to Non-ST elevation ACS
- Admission (History, Exam, ECG,
Cardiac markers)
Management:
Site: Retrosternal Reduce Precipitating Factors
Onset: Sudden Control Risk Factors
Character: Burning pressing, choking (Exercise, Hypertension control, Lipid Control, Diabetes control)
Radiation: To left arm, mandible and/or throat. Medication:
Alleviated by rest, NO Nitrates
Beta-Blocking Agents
Time: Never longer than 20mins.
Exacerbated: Exercise, emotions, large meal, drug therapy lpse, incr. BP, Cold, CCB (if BB CI)
Early morning, Heart failure, rhythm distrb, dreams. Salicylates
Severity: Merely discomfort (Except in DEW) Coronary angiography with PTCA or surgery, if indicates:
Unacceptable degree of angina despite full med therapy
History Poor prognositc signs w stress ECG
Stress ECG
This is not specific for SAP Minor indications:
Stress ECG 1mm/more horizonta/downwart sloping ST segm depression. o Uncertain diagnosis
Development of LBBB pattern. o Presumed unnecessary insurance loading
In IHD poss high pt slight upward inclined ST acceptable. o Non-spec ECG changes (for pilots license)
Poor prognosis
o >/= 2mm horizontal,m down sloping ST seg depression.
o Inadequate incr/red in BP
o Inability to cont w phase 1 of Bruce protocol
o Cont >30seconds VT
o Ex induced ST seg elevation in a non-Q-wave lead (not AVR)
o ST dep persis > 5mins into rest phase.
Thrombolysis in Myocardial infarction
Crescendo angina- Reduced threshold w incr greq, duration and/or severit of angina 1.
Admission in an intensive care coronary unit (if ICU not abail)
attacks. At least to Class II or more. (Days rather than weeks) Medication: 2. Anti-platelet
Prolonged Angina (>20mins ) during rest. a. Salicylates LMW, (no monitoring) Anti-coagulant
New presentation of angina of at least CCS Class III b. Heparin unfractionated - protamine reversible. needs monitoring
Aim for HR below 70bpm. depends on Anti-anginal (Beta blockers,
lmw heparin. 1mg/kg x2 daily
Post- infarction angina c. Beta blockershaemodynamics.usually 25mg atenolol nitrates - hypotension, nolife
Normal ECG, normal cardiac Enzymes. d. Clopidogrel (if avail)9-12 months clopidogrel benefit, tolerance)
e. Nitroglycerin 75mg daily
Risk stratifying NSTEMI/UAP f. Glycoprotein IIb/IIIa receptor antagonists add statins (high dose 20-40mg
Haemodynamically unstable g. Long-working CCB (if BB CI) statins), ACE I
Dangerous arrthythmias - ventricular rhythms 3. Risk Stratify with TIMI score (1/2 = conservative treatment): Remember STEAKS 3/65
Persistent chest pain a. >65 Revascularization -
- Immediate cath lab! b. 3/more risk factors for CAD
- Ballooning, Stenting, CABG

- Medication (increase supply, decrease c. CA stenosis of 50% or more (established CAD) 10-14% of people will react with scar tissue
ci to stress ecg If not complicated: d. ST seg change of > 0.5 mm formation to stenting - so if they didn't have
demand) - Wellens' sign e. 2/more episodes of angina in past 24hrs.
Angian before, they would have it now.

- Risk stratify - Dynamic ECG Changes f. Incr levels of cardiac markers CABG better if:
- TIMI of 5 or high GRACE score
- Angiography? In SA - All NSTEACS g. Salicylates used during preceding 7days - 3 vessels disease
- Troponin positive - 2 vessels with Prox LAD
4. Coronary angiography with view to to revascularization procedure: - Mainstem disease
will be Angiographed - These also require angiography/cath lab!
a. ASAP in High risk (TIMI>5)
(use leg veins and graft them to Aorta or use Left
b. Dynamic ECG changes
If none of the above: Internal mammary artery from Left Subclav -
c. Hemodynamic ECG chnages lasts longer)
repewt Troponin within 6-8
d. If cont angina attacks take place after 48 hrs of full med thrapy in hospital.
(depends on sensitivity of assay used)
e. Low risk pt on grounds of Angiography with view to Revascularize:

24
Low risk - do Stress ECG TIMI 6 or more
i. Poor resp to treat Dynamic ECG changes
ii. Poor prog signs w stress ECG Wellens' Sign Haemodynamic Instability
NSTEMI Same as above Same as Above

Page
Electrical instability (repeat VT)
Killip Class for Heart failure: If continued angina attacks after >48
Prolonged angina with normal ECG, but raised Cardiac enzymes 1 - No symptoms hours of Rx in Hosp
Previous CABG
2 - Bibasal crackles +/- S3 gallop Recent PCI
3 - crackles more than 50% of lungs Lower risk pts on grounds of poor
4 - Cardiogenic shock prognostic signs with Stress ECG
 Prodromal (tiredness, UAP) symptoms. Immediate:
20-60% of infaction does not present w symp (DEW!) o Salicylates (300mg)
Severe angina of long duration (2-12 hrs) o Morphine ( 10mg in 10ml wates. Titrate by IV infusion until level of pain tolerance
STEMI Characteristic anxious facial expression w ass cold sweats, dizziness, nausea reached. Try to do it within 30 minutes!
and sypnoea o Nitroglycerin
Before 3 hours - PCI and
Pulse useuall rapid and reg. Ectopic beats may be present. o Admit highest level of nursing care available (intensive if poss) Thrombolysis - Outcome is
Pulse rate normalises as pain and anxiousness dissipate. Contain infarct size (Increase OX supp to myocard) same.
Blood press usually normal. (can rise w anxiousness. In massive infarct can o Thrombolysis: Streptokinase (55% success) or TPA (75%, but expensive) After 3 hours (and beore 12
hours) - PCI better!
drop to under 90mmHg) o Ox mask: Unclear if it has a value.GIving it if patient does not have low sats, causes peripheral vasoconstriction.
Ausculation= 4th heart sound (reduced left ventricular compliance) Papillary o Nitroglycerin and increases afterload on LV.
muscle invole holosystolic mitral regurgitation murmur may be heard. o Correct hypotension by IV fluids. (if <90mmHg, consider dobutamine)
70% of deaths outside hosp. Cardiogenic shock and VF main cause of death in o Correct anaemia should Hb drop below 10g/dl)
acute phase. Contain infarct sizee reduce Ox consump:
Side room tests: Fever, raised white cell count, raised erythrocyte sedimentation rate may o Bed rest, small meals, sedation, avoid constipation
be found after one day. o Nitroglycerin IV
ECG: o Beta blocking agents. First dose myst be admin immediately and IV, then Oral. (Check CI
1-hrs: Angle bw ST and T wave straightens out. T wave incr in height and peaks. before. Treat complication)
ST seg deviates toward T wave peak. Prevent complications: Admit to ICU or equiv. ECG monitoring/trained nursing staff. IV infusion for
1-2 days: Typical infarction pattern established by ST seg that elevates emergencies.
convexly, T wave becomes inverted and path Q wave appears. Rehabilitation:
1-2 weeks: St seg returns to base line. o Pt must not develop cardiac neurosis
1-2 months T waves return to normal upright. Path Q waves are permanent. o Boost confidence on admission. Treat family as well.
Localize infarct (see ECG notes) o Creae positive atmosphere by early mobilize (bed rest in a chair)
Serum Enzymes: o Provide info on episode, risk factors and road ahead.
Troponin T most sensitive.AST and LDH not used. CK non-spec. (Do MB fraction, o Inform relative on later problems and danger of overpretection.
Myoglobin) Troponin T highly spec cardiac muscle protein released into blood streat w o Watch out for signs of stress or depression and treat actively.
myocardial damage. Used as an early diagnostic indicator in ACS or diag of AMI. False Trop o Mobilize progressively (if no comp) till pt can walk 200m/climb 1 flight of stairs before
positive renal failure, sepsis. discharge.
Heart Scintigram 3-6 days after infarct. o Give clear instructions at discharge on meds, cont exercise programme, risk
management and follow-ups.
o Let pt join a controlled ex group approx 1 month after episode.
Long term treat
o Salicylates for life
o B blocking agents for life.
o ACI if large area of infarcted myocard for life.
o Strict risk factor management for life!
Suddent Death 25% of cases no hist of IHD and sudden death first manifest of IHD. Implantable cardio-defibrillator. (Expensive)
More common in males
Resus success in well-trained units 25-30%
Cause: Prob a small thrombus or Transient episode of ischaemia.

HIV related . proximal LAD

occlusion

25 Page
Lipid lowering Therapy:
Aims:
Idepenpednt isk factors for CVD:
o Elevated LDL cholesterol (LDL-C)
o Decreased HDL cholesterol (HDL-C)
o Increased Triglyceride leves.
Lowering LDL-C is primary goal of treatment of
hyperlipidaemia.
Aim to reduce LDL-C level by at least 30% from baseline.
Target LDL should be based on Pt risk for developing CHD
In established CHD/CHD equivalent eg.:
o Peripheral vascular disease
o Caroid artery stenosis
o Abdominal aneurysm
Drug name and structure Mechanism
Statins: Structurally statins are sim to HMG-cA and
HMG- CoA reducatse inhibitors: occupy the active binding site on enzyme.
(3-hydroxy-3-methylglutaryl coenzyme A_ This competitive inhibition leads to decr
HMG CoA reductase catalyze conversion prod of chol.
of substrate HMG-CoA to mevalonate. Thus less intracellular chol upreg of LDL
This reaction is early and rate-limiting step receptors and reducion in LDL-C levels -
in synthesis of cholesterol. increased clearance by LDL receptor.
(Cholesterol and Triglyceride lowering)
Statins also reduce releace of lupoproteins
from liver into circulation.
At high doses - statins decr triglyceride
lbls.
Bile acid sequesterants: Large polymers that bind negatively charged bile
(Cholesterol lowering) acids and bile salts in small intestine
Interrupts enterohepatic circulation of bile acids,
causing increased conversion of cholesterol into
bile in liver.
Resulting decreased hepatocyte cholesterol
promotes increase in LDL receptors:
Thus incr clearance of LDL from circ.
Reduce LDL-C w a corresponding decr in total
cholesterol (about 20%)
HDL-C level may incr modest (as much as 10%)
Can incr Cholesterol synth
Adding HMG-CoA reductase inhib (Statin)
ameliorates this effect, leading to substantial
LDL-C reductions when BAS+Statins
o Pt who have calc 10yr risk greater than 20% o Hypertension
For all aboveL LDL-C goal should be o Current cig smoking
<100mg.dl (2.5mmol) o Low HDL-C
o Very high risk defined as established vascular o HDL-greater than 60mg/dL count neg risk facor
disease w any additional conditions incl multiple remove one risk facor from otal number.
risk factors (eg diabetes), severe and poorly o P w 2/more risk factors cat further 10 yr risk w
controlled risk factors: (cig smoking), metabolic Framingham score.
syndrome (high triglyceride, low HDL-C) and acute Pt w no or one risk factor:
coronary syndromes. o LDL-C level less than 160mg/dL should be goal.
American Diabees ass recomm a trgt LDL-C lvl <70mg/dL in
diabetic pt w CVD. To convert mg/dL of HDL or LDL chol to mmol/L = divide by 39.
Risk factors include:
o Age To convert mg/dl of triglycerides to mmol/l divide by 89.
o Gender
o Fam history of prem CHD
Indications Side effects Contra-indications
Most efective drugs to lower LDL-C Most common: Pregnant womenn
Used in hyperlidiaemia where LDL-C is Abdominal pain Nursing mothers
elevated. Constipation Pt w significant hepatic dysfuntion.
Efective in familial hypercholesterolaemia Flatulence
and combined hyperlipidaemia. Nausea
Also used to lower LDL-C in sec prevention. Diarrhoea
Less effective homozygous LDL receptor Headache
deficiency Fatigue
LDL-C lowering seen w/in 1-2 weeks after Muscle complaints
start of therapy and is stable in about 4-6
wks.
Statins decr rise of triglyc lels that can occ Large polymers neither absorbed nor Pt who have bowel obstruction or total biliary
w BAS metabolized by intestine hence very safe. obstruction.
BAS most useful when elevated LDL-C level Canby used in women of childbearing age Sever constipation
is major lipid abnormality. not using Contraception. As monoherapy in pt who have high triglyceride
Can be combined w statins/nicacin to Common side fx: levels.
achieve greater LDLC reductions in PT who GI disturbances. Pt w normal baseline triglyceride experience
have severe LDL-C elevations Constipations minimal trig incr but those who have baseline
Nausea trig levels higher than 200mg/dL may incre
Can be used alone for initial therapy in pt substantial elevation
Bloating
at low risk or pt who cannot tolerate statins Abdominal pain
at any dose. Flatulence
Aggravation of haemorrhoids.
Cholestyramine/colestipol can affect the
26
absorption of oher oral drugs.
Page
Nicotinic Acid: Independent of viamin action. Flushing (Use aspirine)
Chol + trig lowering Nicotinamide not effective.
First choice in US but use limited by sfx.
Action is decr of hepatic VLDF output w
subsequent drop in IDL & LDL.
Pronouned incr in HDL.
Also decre Lipoprotein A levels.
Effective dose 2-8g/day
Ezetimibe Inhib cholesterol absorption from brush Can be useful in pt intolerant of statins
border of small intestine. (as monotherapy of combo.)
Inhibition of absorption of cholesterol in
intertine much from biliary cholesterol
leads to decr hepatric cholesterol and incr
clearance of LD-C from Plasma and
consequent reduction of plasma LDL-C
Produces recttion of approx 14-25% in LDL-
C
W statins = additive fx.

Fibrates Reduces plasma trig levels by 25% to 40% Mixed dyslipidaemia ie raised serum trigs GI upset Avoid in renal failure and alcoholics.
and also red. postprandial triglyceride as well as cholesterol provided this is not
levels. caused by excessive alcohol.
Reduce circulating VLDL, hence triglyceride Resistant dyslipidaemia can be comb w
w a modest reduction in LDL and approx other lipid lowering drugs. (may incr risk
10-15% incr in HDL. of rhabdomyolysis)
Agonists of peroxisomal proliferator
activated receptor (PPAR) alpha. that
induce expression of genes needed for beta
oxidative degradation of fatty acids in
tissue.
This action inc induction of Lipoprotein
lipase (LpL) thus incr hydrolysis of trig in
chulomicrons and VLDL particles liberate
free fatty acid for storage in fat or for
metabolism in muscle.
Omega 3 fish oils Main fx lowering TG by reducing VLDL Sever Hypertriglyceridaemia w fibrates. GI upset
synth in liver. In combo w statins in mixed
hyperlipidaemia.

27
Page
 Combo Therapies:
To be used if mono inadequte
Fam hypercholesterolaemia may req substantial LDL-C reductions not be achieved w monother.
Can be diff to achieve LDL-C of <70mm/dL w mono
W max statin dose: Incr risk of side fx
Can combine statins w ezetimibe and bile acid-binding resins.
Statin +BAS BAS +Niacin: Statin + Ezetimibe: Niacin +Statin Statin + Fibrate: Statin/Resin/Niacin BAS+ Ezetimibe:
Statin/Ezetimibe/
Niacin
Cholesteryramine . Useful in Pt Prod additional trig red of 7% to 13% and This combo decr LDL=C and trig levels & Used in PT w combined trig and cholesterol Three medications can . Also used in pt who
can interfere w unable to use increase in HDL-C level of 1-5% raises HDL-C level more than statin alone. elevations be useful in High risk do not tolerate a
absorption of statins Disadvantage: Lack of clinical outcomes Proven regression of atherosclerosis by Problem: pt who have Incr LDL-C statin at any dose or
statins: data for ezetimibe and statin Ezetimibe coronary angiography. Incidence of myopathy incl in order to max LDL for whom statins are
Both drugs decr combos. Also decr incidence of CVE in High risk pt. rhabdomyolysis incr w this reduction. May be nec CI.
CHD events Problems: combo. in pt w Familial
Flushing Fibrates interfere hypercholesterolaemia
Hyperglycemia glucoronidation of statins w a
Elevation of uric acid resultant higher serum levels or
Myopathy statins.
Hepatotoxicity CI: Renal insuff and CHF
Avoid niacin in gout + liver
disease.

28
Page
Vavlular Disease:
Disease Aetiology Haemodynamics Symptoms Signs ECG Treatment
CXR
Echo
Mitral Stenosis Vitually all from RHD from prev RF. Normal area 4-6cm2 Dispnoea Mitral facies (pinched red ECG: P mitrale Penicillin prophyl until at least
Min 2 yrs to develop. Often long >2 mild Orthopnoea cheeks) RVH 35yrs for RF
latent period. 1-2 Moderate PND Normal heart size Prophylaxis for IE
Congenital rare <1% <1 Severe Tiredness Tapping apex beat CXR: If dyspnoea bw 2-4 consider
Degenerative Palpitations RV heave Normal heart size w PA (enlarged RA w valvuloplasty/otomy/replace
Diverse: Flow diastolic time Cough Loud P2 lateral.
Rheum arthritis MS: Incr gradient Haemoptysis Graham steale Murmur Larger LA: Wide carina, double shadow, Presurgery:
SLE Incr LA press Angina TI prominence on lateral. (Barium swallow) Consider diuretics for
Carcinoid Incr Pulm venous Emboli Mitralization of heart shadow: Straight left dyspnoea
Mucopolisaccharidosis prss. Hoarseness Murmur: heart border. Control HR esp w AF BB
LVEDP= Normal Mitral area Prominent pulm Artery Digoxin also used if AF.
LVED volume Norm in Diastolic Prom L A auricle
85% and lower in rest. Rumbel Calcification of Mitral valve Anticlot:
Low pitch Kerley B lines In presence of AF
Pre-systolic accentuation W large LA
Better w exercise, on left Ech: Sensitive. Acc in dt of valve area and Histroy of prev
side w bell. gradient. Provides info on cond of entire embolus
mitral valve and thus det correct therapy. Pt older than 40 yrs

Mitral incompetence Annulus Volume overload in LA Tiredness Pulse: Nromal or small ECG: P mitrale Penicillin for RF 35yrs
Valves pressures remain Dyspnoea LV enlargement (dilation and LVH/RVH IE prophylaxis
Chordae normal for long. W Palpitations hypertrophy) Sometimes AF If haemodynamically severe,
Papillary muscles chronic MI volume Cough/Haemoptysis LV func decrease, incr of
RHD still most common overload develops w Emboli Soft K1 CXR: Enlarge LV symptoms, consider valve
Other dilattastion of LV K3 LAE replacement.
Degenerative Lowerd effective Murmur: Calcification of Mitral
IHD (papillary mus) forward CO. Mitral area HVS symp Decr preload, vasodilators
IE Spreads to axilla Lower Preload, diuretics
Congenital (Primum ASD) Systolic Echo: Sens: Det degree, sens. Digoxin in AF to contrl
Trauma Holosystolic speed.
Blowing Anticlot- AF/ prev history.
More MS More MI
Loud K1 Soft K1
OK K3
Short K2-OK interval No OK
Prominent diastolic murmur Prominent systolic murmur
No LV enlarge Large LV

29
Page
Tricuspid Stenosis Always RHD If Gradienst >5cm Hg Low CO tiredness Great a wave Sensitive Echo If haemodynamic bad w symptoms
5% of RHD cases Area< 2cm2, , remember incr w ,weight loss No signs of pulm hyptension consider valvotomy, replace.
Sometimes:atrial myxoma inspiration Oedema Murmur:
Carcinoid syndrome Ascites Diastolic
Constrictive pericarditis Hepatomegaly Rumbel
Apsent of MS, LPS/4ICS
orthopnoea, PND, Incr w inspiration
hemoptysis
Tricuspid 2 degree pulm hypert PHT Well tolerated: If 2 degree: ECHo diff bw 1st and 2nd degree. Treat cause
incompetence: 1degre: RF Later develop AF, Pressures. Usually well-tolerated.
Cong Ebsteins anomaly tiredness and right Large CV Sometimes anuloplasty during a
IE- mostly IV drugs sided stuwing RK enlarge different valve surgery.
Carcinoid syndrome Enlarge pulsating liver SOMETIMES valvuloplasty (tissue)
IHS papillay musc dysfunc
Atrial myxoma Murmur:
Holosystolic
LPS, 4ICS
Incr w inspiration

Aortic Stenosis Supravalvular Valve area decr Initially asymp Plateu pulse ECG: LVH w systolic overloading. Asymptomatic:
Remeber 3s Subvalvular Gradient over aortic valve Late: LVH (heaving apex beat Large LA Little space for meds: (Digoxin,
Valvular Outflow obstruct Angina 5yr survive Thrills (nexk, chest) Ass w degen in conduction in 5%: diuretics)
o RHD Incr afterload Syncope 3yrs Ausculattion AV block Avoid vasodilators.
o Bicuspid Hypertrophy Dyspnoea 2yrs Ejection systolic murmur LAHB Prophylaxis
o Senile Fixated SV rough, late peak , If AS severe avoid strenuous
degen spreads to neck. CXR: exercise.
Often normal: Follow up often.
Abnormalities:
Enlarge LV Surgery
Caclcification If sympt
Post stenotic dilatation of aorta If valve area <0.7cm2
Seldom meaningful if in adult w/out If gradient >70mmHg
caclification If LV begins to decompensate.
Echo:
Very NB for diagnosis and for follo-up Valvuloplasty:
of gradient incr. High mortality, morbidity and aorta
valve replacement is preferred.
In pt over 50yrs and/or if angina
present. Consider concurrent
coronary artery lesions and thus
angiogrpahy to determine and plan
AVR and bypass.

30
Page
Aortic incompetence: Valve sails: Compensate w incr in LVED Long asymptomatic Hyperdynamic circ = waterhammer ECG Asymptomatic
RHD cross section. phase tolerate ex pulse fast rising and falling legs. LVH w diastolic overload, No treat = only prohylaxis and
IE LVH Cor bovinum well. LV dilatation SI, aVL and V4-6 look for prom Q waves counciling
Con (Bicusp, Incr compliance, LVEDP not Later deve incr De Musset Sign and upwards displaced ST segments Consider vasodilator
Supracrystal VSD) rise. exercise Corrigans sign (pulsation in jugular and large peaked T waves.
Rheamatoid Acc to Laplace law dilatation intolerance: notch. Later ST depression, LBBB Symptomatic:
arthritis, SLE incr wall tension, Sypnoea, Pistol shots If AI from Aortitis (syphilis) = long PR For LV dysfunction:
Aortic Root: hypertrophy, incr CO orthopnoea, PND Duroziez sign interval. Preload: Diuretics
Syphilis W exercise vasodilatation and Sometimes Quincke sign Afterload: Vasodilators (ACE-I of
Systemic medial tachycardia, decr in diastolic nocturnal angina. Auscultation: CXR: calcium antagonists)
necrosis backflow thus well tolerated. Palpitations Diastolic murmur LV dilatation Inotropes, digoxin
(marfans) Decressendo Dilatation of proximal aorta Severe AI follow up 6monthly to
Sero negative W acute aortic incomp (IE, Bette rif pt sits forward on det surgery at optimal time.
arthritis dissection/trauma) experation Echo
Hypertension No time to compensate. Heart Spreads left of sternum (if right, Very NB in the diagnosis and follow Surgery:
Osteogenesis not dilated and not more consider aneurism.) up of Incomp and LV dilatation. Valve replacement.
imperfecta compliant LVEDP incr. Not K2 soft or absent
well tolerated. Mitral area sometimes Austin
Flint murmur (fluttering of Ant
Mitral valve sail differentiate
from MS: Loud K1, OK=MI present)

Pulmonary stenosis: Common: Second most Mostly Short a wave Valvuloplasty in adult if
common congenital among asymptomatic RV heaving Symptomatic
adults When Gradient Efection systolic murmur.
Maybe aquired lesions (RHD, >80mmHg: Max 3nd ICS LPS
Carcinoid) Dyspnoe P2 late
a Click (if valve stenosis)
Syncope
Angina
Pulmonary Secondary to Hypertension Mostly If secondary Signs of PHT Well tolerated no spec therapy.
Incompetence: (Eg. Graham Steele Murmur asymptomatic
in MS) Murmur:
Primary Early diastolic
RHD In pulm area
IE (IV drug users) Spread along sternum
Carcinoid Not ass w breathing (in
Caculoplasty comp w other right
sided murmurs)

31
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Heart valve surgery

Mitral stenosis

Indications for surgery

Symptomatic patient with a mitral valve area less than 1.5

cm

Valve not suitable for balloon valvuloplasty

Thrombus in left atrium

Flow dynamics:

32
Page
Warfarin

Oral anticoagulant

Vitamin K antagonist

Inhibits vitamin K dependant clotting factors (II, VII,IX,X)

Prolongs prothrombin time and INR

33
Normal INR is 1

Page
Dosage of Warfarin varies between patients
 Therapeutic INR aims for 2 to 4 Mitral valve incompetence

Regular INR monitoring is very important for patients on Indications for surgery
Warfarin therapy
Symptomatic patient (decreased exercise
tolerance,dyspnea, PND, orthopnea)

Asymptomatic patient with signs of left ventricular

decompensation (left ventricular dilatation)

Repair or replace?

Mitral valve repair

Annuloplasty

Resection of prolapsing posterior leaflet segment

Aortic valve incompentence

Indication for surgery

Symptomatic patient (decreased exercise

tolerance,dyspnea, PND, orthopnea)

Asymptomatic patient with signs of left ventricular

decompensation (left ventricular dilatation)

34
Page
Aortic valve stenosis

Indications for surgery

Symptomatic patients (syncope, angina left

heart failure) Surgical Compx:
Mortality (2-5%)
Aortic valve gradient > 50mm Hg
Stroke (2-5%)
Bleeding
Cardiac complications
Poor ventricular function
Valve dysfunction
Transcatheter aortic valve implantation (TAVI)
Arrhythmias
Lung complications
Atelectasis
Indications Pneumonia
Patients with severe aortic stenosis who are Infection
too high risk for conventional surgery Lung
Urinary tract
Currently very expensive (R200 000 per Wound

35
valve)

Page
 Native valve Infective Endocarditis o Rickettsiae
Acute Infection Coxiella burnetti (Q-fever)
Normal valves Fungi
Infective Endocarditis
o o
o Destruction of valves and rapidly fatal if Candida spp.
Definition untreated Aspergillus spp.
Infective Endocarditis is an infection of the endocardium or o Acutely ill patient with/without metastatic foci Histoplasmosis
vascular endothelium. o Organisms:
Commonly runs an insidious course and caused by bacteria - Staphylococcus aureus Prosthetic Valve Endocarditis
subacute bacterial endocarditis (SBE). Streptococcus pneumoniae,
Early Onset (< 60 days post operative)
May cause a fulminant (acute) infection Streptococcus pyogenes
Surgical contamination
May be caused by other organisms (Fungi, Rickettsiae, etc) Neisseria gonorrhoea
Organisms:
=> Preferred terminology: Infective endocarditis Others
o Staphylococcus
Classification Subacute Infection
epidermidis > S. aureus
According to cultured organism: o Abnormal valves
o Gram negative bacilli
Example: Viridans streptococcal endocarditis Rheumatic heart disease (MI, AI)
o Fungi
According to clinical presentation: Congenital heart disease (PDA, VSD,
o Native valve infective endocarditis etc)
Late Onset (> 60 days post operative)
Acute - Fulminating (destructive) Mitral valve prolapse
Transient bacteraemia
process, normal valves Degenerative heart disease (Calcified
Slow incubation
Subacute - Insidious nature, abnormal AS)
Organisms:
valves o Disease of young adults in SA, male
o As for early onset PVE
o Prosthetic valve endocarditis predominance
o Other common organisms
o Infective endocarditis in IV drug users o Insidious illness, initially subacute onset
(As above)
o Non infective endocarditis o Eventually also fatal if untreated
Viridans
o Organisms:
streptococci
Viridans Streptococci
Enterococci, etc
Enterococci
Others
Infective Endocarditis associated with IV Drug abuse:
Etiology:
Patient profile:
o Streptococci
Right sided endocarditis (TV)
Alpha haemolytic (Viridans Group)
Beta Haemolytic: Group D: Septic pulmonary emboli
Enterococci Most often young males
Beta Haemolytic: Group D: Non-
Enterococci Etiology:
Beta Haemolytic: Group A, B (Multiple) organisms found on skin:
o Staphylococci Staph aureus
Staphylococcus aureus Gram negatives (Pseudomonas)
Staphylococcus epidermidis Fungi
o HACEK
Slow growing, fastidious group of Non-Infective Endocarditis:
SLE (Libman-Sacks endocarditis)

36
organisms
o Other Bacteria Rheumatic fever (valvulitis)
S. pneumoniae, Neisseria gonorrhoea, Marantic endocarditis (Paraneoplastic)

Page
Gram Negative bacilli, etc, etc. Antiphospholipid syndromes
 Systemic signs and complications: Echocardiography
Embolic / Vascular phenomena: o Transthoracic Echo (TTE)
o Clubbing Vegetations
o Infarction: > 2 cm size
Heart visible
Stroke 80% of native
Kidney valve
Spleen, etc endocarditis
o Mycotic aneurysms visible
o Janeway lesions 50% of
Clinical Features: Haemorrhages:
o prosthetic valve
o Worsening heart failure From mycotic aneurysms endocarditis
o Fever Conjunctival visible
o Weight loss haemorrhages Underlying valvular disease
o Night sweats Splinter haemorrhages Cardiac (LV) function
o Malaise Immunological phenomena: o Transesophageal Echo (TEE)
o Arthralgia & myalgia o Glomerulonephritis (Low Suboptimal quality TTE
o Other non specific complaints complement) Prosthetic valve
o Acute complications: Splenomegaly
o Others:
Stroke Oslers nodes
o o ESR and CRP raised
Other embolism Roths spots
o o C3 (C4) low
Rupture mycotic aneurysm Reactive arthritis
o o Raised circulating immune complexes
o Toxically ill (septicaemia)
o FBC: Normocytic anaemia, modestly
Special Investigations: raised WCC
Specific cardiac signs: Blood cultures o CXR: Cardiac size, cardiac failure,
Valvular lesions (Mostly valvular incompetence) o IMPORTANT emboli, etc.
o Worsening existing pathology 3 X 10 ml (from different sites)
o o ECG: AF, conduction defects (heart
o New lesions BEFORE starting antibiotics block)
Cardiac failure o Culture negative endocarditis
o Worsening of (20%):
Complications Diagnosis of IE incorrect
o Progressive valvular incompetence Exposure to antibiotics
o Severe cardiac failure before collecting
o Perivalvular spread: specimens
Conduction defects Inaccessible bacteria -
Abscesses related to age of
Fistulas vegetation
Fastidious organisms
(HACEK)
Specialised culture
techniques (Rickettsiae,

37
Chlamydiae, etc)
-Require serology / PCR (Bartonella)

Page
Diagnosis:
Positive culture from intracardiac abscess,
vegetation or embolism, OR
Positive histological confirmation of vegetation
or abscess, OR
Modified Duke Criteria for Infective Endocarditis:
2 major, OR
1 major and 3 minor, OR
5 minor criteria
Major:
2 or more positive blood cultures of
typical organism, known to cause IE or
accepted serology criteria for i.e.
Coxiella burnetti (PCR?)
1 of Evidence of endocardial
involvement:
o Echo showing endocarditis
OR
o New valvular regurgitation
OR
o Abscess OR
o (Partial) dehiscence of
prosthetic valve
Minor:
Predisposing cardiac disease or IV
drug abuse
Fever > 38C
Vascular phenomena
Immunological phenomena
Microbiological evidence, not
satisfying major criteria (above)
Echocardiographic evidence, not
satisfying major criteria (above)
Treatment:
Supportive:
o Treat cardiac failure
(Acute valve replacement)
Antimicrobials:
o Bactericidal antibiotics
o Sufficient (high) doses
o Sufficient (long duration) time
o Preferably Directed according to
blood cultures (antibiotic sensitivity)!
Empirical Antibiotic Choices:
Subacute infection:
Cover: Streptococcal and enterococcal
Penicillin and Gentamycin for 4-6
weeks
Staphylococcal etiology also considered:
Cover: Above, and add Staphylococcal
cover
Penicillin, Cloxacillin and Gentamycin
If Methicillin resistance expected:
Replace Cloxacillin with Vancomycin
Prosthetic valve endocarditis:
Cover: Add for Methicillin resistant
Staphylococci
Vancomycin, Gentamycin , Rifampicin
for 6 weeks
Directed antibiotic therapy:
With positive cultures and sensitivities
Directed therapy may lead to better
outcome, less toxicity
Generally use empirical guidelines for
specific organism
Surgical valve replacement:
Progressive (severe) cardiac failure
Untreatable Infection:
o Fungal endocarditis
o Relapse or poor response (blood
cultures remain positive)
o Cultures remain negative with
persistent fever
Complications:
o Paravalvular extension (abscess)
o Dehiscence of prosthetic valve
o Annular abscess
o Rupture of sinus of Vasalva
o Repeated emboli
Most cases need to be considered for elective valve replacement
following treatment
Prognosis:
Local (TBH) mortality rate of 35%
Factors associated with poor prognosis:
o Non streptococcal or culture negative
disease
o Bacterial resistance
o Heart failure
o Aortic valve involvement
o Prosthetic valve endocarditis
o Older age
o Valve ring or myocardial abscess
38
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Prophylaxis of Infective Endocarditis:
Evidence based data limited, re: benefit of prophylaxis for IE
Examples:
Risk of daily activity (chewing food or brushing teeth) causing IE
probably much greater than that of a dental procedure. More benefit
to improve oral hygiene!
Benefit of prophylaxis in GIT or GUT procedures even less established
than for dental procedures
USA (AHA) Guidelines:
Combine patient risk of developing IE and risk of procedure causing
IE:
High risk patients:
Prosthetic valves
Previous endocarditis
Complex (congenital) cyanotic heart disease
Surgically constructed systemic-pulmonary
shunts
Moderate risk patients:
Other congenital cardiac lesions, excluding
secundum ASD
Rheumatic valvular disease
Hypertrophic cardiomyopathy
Mitral valve prolapse with regurgitation
Patients not requiring prophylaxis:
Patients with surgically repaired secundum atrial
septal defect, ventricular septal defect, or patent
ductus arteriosus who are more than 6 months
post-operative and have no murmur.
Patients who have undergone coronary artery
bypass grafting (CABG)
Patients with mitral valve prolapse but no
regurgitation
Patients with functional murmurs or who have
had rheumatic fever but have no valvular
dysfunction
Patients with pacemakers
Dental procedures known to cause bleeding
(dentogingival manipulation) - but not fillings
or adjustment of braces
Tonsillectomy or adenoidectomy (but not
tympanostomy)
Surgical operations that involve intestinal or
respiratory mucosal incisions
Rigid, but not flexible, bronchoscopy
Oesophageal dilation, or sclerotherapy for
oesophageal varices
Biliary tract surgery, or ERCP in the presence of
obstruction
Cystoscopy, urethral dilatation or prostatic
surgery.
Urethral catheterisation in a patient with a
urinary tract infection
Incision and drainage of infected tissue
Vaginal delivery in the presence of suspected
infection such as with prolonged rupture of
membranes or manipulative vaginal deliveries
Low Risk Procedures:
(Consider prophylaxis only if high risk patient)
Shedding of primary teeth
Endotracheal intubation
Cardiac catheterisation
Endoscopy with or without gastrointestinal
biopsy
Urinary catheterisation in the absence of
infection
If infection is not suspected:
o caesarean section or vaginal
hysterectomy
o dilatation and curettage
o uncomplicated vaginal delivery
o therapeutic abortion
o sterilisation procedures, or
o insertion / removal of intrauterine
devices.
Specific prophylaxis:
Dental, oral , respiratory tract or oesophageal
o Clindamycin 600mg (20mg/kg) PO or
1st generation Cephalosporin or
Azithromycin/Clarithromycin if
Penicillin allergic
GIT and GUT procedures (Benefit uncertain / not
generally recommended):
o High risk patient:
Ampicillin 2g (50mg/kg),
AND
Gentamycin 1.5 mg/kg
30 min before procedure IV (IM) and followed by
Ampicillin/Amoxicillin 1g
(25 mg/kg)
6 hours later
Penicillin allergy: Vancomycin and Gentamycin before procedure
o Moderate risk patient:
Amoxicillin/Ampicillin only
before procedure
Penicillin allergy:
Vancomycin before
procedure
Infective Endocarditis Prophylaxis (Situation in 2011 - NICE):
No clear evidence re: efficacy of procedure in preventing IE:
Bacteremia following invasive dental procedures equal to that of tooth
brushing
Prophylactic antibiotics may decrease bacteremia during and following
a procedure, but do not completely prevent bacteremia.
Low but important risk re: side effects (allergy, anaphylaxis) of
prophylactic antibiotics
Financial cost of antibiotics and the procedure vs. limited (no)
established benefit
BUT:
High mortality and morbidity of condition in our setting
Although no benefit demonstrated, also no clear lack of efficacy shown
THUS:
Probably to continue prophylaxis for time being, keeping relevant
risks / costs in mind. This topic should be reviewed regularly.
Dr H W Prozesky
Division of Infectious Diseases

39
Department of Medicine
Procedures for which endocarditis prophylaxis should be given, procedures:
hwp@sun.ac.za
include: o Amoxicillin 2g (50mg/kg) PO 1h
March 2011

Page
(All patients, excluding low risk patients, not requiring prophylaxis - before procedure
above )
 Acute pericarditis: PR-segment depression (look in
inferior leads and in V4)
Pericarditis and myocarditis Inflammation of the pericardium
Pericardial disease: Intense substernal chest pain Occasionally tall, peaked T waves
o Acute pericarditis o Often pleuritic quality
o Pericardial effusion and tamponade Stabbing With or without sinus tachycardia
o Constrictive pericarditis Worse with inspiration
Myocarditis Positional component Later (chronic/convalescent phase)
Beskryf die kliniese beeld van akute perikarditis o Decreases sometimes when sitting foreward
ST segments normalise and T wave inversion develops
Beskryf die kliniese beeld van perikardiale effusie o Increases sometimes by lying on back.
Beskryf die kliniese beeld en diagnose van tamponade Sometimes spreads to shoulder and/or neck
Noem die mees algemene oorsake van perikardiale Can be VERY atypical
effusie
Bespreek die diagnose van tuberkuleuse perikarditis Etioloy:
Bespreek die behandeling van tuberkuleuse
perikarditis Viraal, Maligniteite
b.v. Coxsackie virus (limfoom, mamma,
Bespreek die hantering van n pasiente met
Miokardiale infarksie brongus )
tamponade (20% van pasinte Bakterile infeksie
Bespreek die kliniese beeld van miokarditis akuut) (S.aureus, S.
Rumatiekkoors pneumoniae)
`n 28 Jarige man presenteer by jou met borskaspyn. Hy beskryf die pyn (pankarditis) Uremie
as `n steekpyn wat vererger as hy diep inasem of gaan le en dit TB (nie tipies akuut (indikasie vir dialise)
verbeter as vooroor sit. Hy voel ook grieperig vir die afgelope 4 dae. Hy nie) Bindweefselsiektes
Dressler sindroom (SLE, RA)
rook 5 sigarette per dag maar het geen ander risikofaktore vir
(Imuun gemedieer 10 Trauma
aterosklerose nie. -14 dae na MI) Idiopaties Chest X Ray : Cardiothoracic ratio enlarged only if
dressler syndrome associated pericardial effusion
Watter diagnose/diff. diagnose vermoed jy? Clinical Picture

Hoe sal jy te werk gaan om jou diagnose te probeer
bevestig?
Watter behandeling gaan jy voorskryf?
1. Chest Pain (characteristic features noted above)
Cardiac Enzymes normal unless associated myocarditis or
2. Fever and constitutional symptoms : misdiagnosis of MI
recent viral illness ( I have had the flu recently Doc)

TB pericarditis (Chronic Weight loss, night sweats etc.) ECHO Can be normal, can show pericardial effusion

3. Pericardial rub on cardiac auscultation

SPECIAL INVESTIGATIONS Specific Tests: to look for an etiology

ECG is NB:

40
In the first week (Acute phase) (Please note: Pericarditis is essentially a clinical and ECG
diagnosis)

Page
Saddle shaped ST elevation in most
leads
Treatment of pericarditis o Pulsus paradoxus specific for tamponade. Thinking about TAMPONADE
Special investigations: o Behind which cardiac chamber does pericardial
Treat the underlying cause as appropriate (E.g. TB) o CXR: fluid never collect? Why?
Large globular heart o Which cardiac chamber is compressed first in
Analgesia typically with High dose Asprin or other NSAIDS Enlarged SVC TAMPONADE? Why?
(Majority of viral etiology is self limiting and requires Seldom pulmonary venous o Where in the cardiac cycle will compression of
temporary pain relief only) engorgement this chamber first manifest? Why?
o ECG: o How do you practically assess for pulses
Colchicine (useful in recurrent idiopathic effusions)
Small QRS complexes paradoxus?
Inverted T waves or non-specific T Special investigations
Oral steroids e.g. prednisone rarely needed
wave changes, Tests to look for a specific cause: Consider clinical scenario
Electrical alternans (Often done on aspirated pericardial fluid or pleural fluid if an
Sometimes AF associated pleural effusion is present)
Pericardial effusion: o ECHO: Blood tests:
Most sensitive and specific General inflammation e.g. WBC, ESR, CRP,
Fluid in the pericardial space o Renal function e.g. Urea and Creatinine
hypothyroidism causes
Usual follows on pericarditis Thyroid function: TSH and T4
effusions
o First dry, fibrinous inflammatory reaction Collagen vascular screen incl. ANF and RF
o Later forming a pericardial effusion Pericardial /pleural fluid :
A potential life threatening complication of a large and fast Chemistry and cell count
accumulating effusion is cardiac tamponade - - Transudate vs Exudate
o Tamponade: - Lymphocytosis vs. Neutrophillia
Clinical diagnosis Staining - Gram stain for bacterial infection and Auramine
Must know it stain for acid fast bacillae (TB)
If the pericardium cant stretch - ADA (Adenosine deaminase level) usefull in
further, the fluid in the pericardium diagnosing TB if lymphocytic effusion), ANF, RA
leads to compression of the heart. etc.
The heart cant fill and the patients - Culture then stain and look for bacteria/TB
haemodynamic status is threatened - Cytology to look for malignancy
Fall in BP Pericardial / pleural Biopsy : Histology for granuloma etc
Tachycardia and microbiology.
Pulsus paradoxus (fall in systolic BP
in >10mmHg)
Raised JVP in the presence of a
pericardial effusion
Pericardial effusion clinical picture:
o Mainly det by:
Amount of fluid
Speed of accumulation
o Absent apex beat
o Soft heart sounds (with or without pericardial

41
rub)
o Cardiac dullness may be enlarged

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o Raised JVP
o JVP raised during inspiration = Kussmauls sign
Evaluation of TB pericardial effusion 3. Constrictive Pericarditis What makes constriction different?
Typical patient
Large effusion with evidence of chronicity on echo Definition: 1. Cardiac filling is very rapid and limited to the first
Evidence of TB elsewhere e.g. Pulmonary TB half of diastole.
Fluid analysis: (Pleural or pericardial) Thickened and non compliant pericardium covers the heart
and restricts ventricular filling 2. Maximal cardiac volume is limited and fixed.
o Blood stained or straw coloured
o Exudate: Know Criteria Note: There is no increased pericardial pressure and thus no
compression of the heart. 3. End diastolic pressure equalization occurs in all
o Lymphocytic predominance
chambers (The single cardiac pressure
o High Adenosine Deaminase (ADA)
What does Constriction look like? chamber)
o Microscopy: Acid fast basillae on auramine
Depends largely on Chronicity.
staining - low yield (Culture if stain
Thick peel - becomes adhesive and non compliant 4. Thick pericardial peel isolates intra-cardiac
negative)
Calcified pressures from intra-thoracic pressures
o Biopsy of pericardium or pleura
Adherent
o Caseating granulomas 5. The myocardium is typically normal
Spicules growing into myocardium
o AFBs on Auramine stain (else culture)
Peel stage Chisel Stage
Note: These features combined with the dynamics of breathing
Leading Causes ?
produce the 2 defining physiological characteristics of constriction nl:
3rd World
Treatment: Post TB
Dissociation of intra-thoracic and intra-cardiac
Post TB
pressures
Diagnosis of clinical tamponade Post TB
3rd World and 1st World
Enhanced ventricular interaction
Urgent pericardiosentesis through catheter Idiopathic
U/S guided if possible Previous Pericarditis of any cause Constriction physiology:
Mx of specific disease (eg TB 6 months as for pulmonary 1st World
TB) Previous cardiac surgery The respiratory pump mechanism
Pain relief Previous Radiotherapy
Pericardial window surgery if it is a recurring problem.
Constriction physiology:

42
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The respiratory pump in action
Dissociation of intrathoracic and intracardiac pressures in pericardial
Why does your BP not drop significantly during inspiration?
constriction

The cardiac cavities are also intrathoracic

Left is normal, right is severe AR

Enhanced ventricular interaction

This mainly affects the rate of RV vs. LV filling during respiration.

Ventricular interdependence
During inspiration intra-cardiac pressures fall in concert with intra-
thoracic pressures.

The normal association between intra thoracic and intra cardiac

pressures maintains the normal respiratory flow gradients into the left
and right heart during respiration. (Almost)

This determines the reciprocal nature of RV and LV final filling volumes

(Driven by the different filling rates from pressure dissociation and
septal shift)

43
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Is septal shift only a bystander?
Clinical Picture: Think Right Heart Failure
NB: You Need a high index of suspicion
Easily missed:
1. Insidious onset, Slowly progressive, Remote causative event
2. Varied presentation - can be non specific incl.
- Unexplained RHF
- RHF >> LHF
- Diastolic Dysfunction
- Low CO Symptoms Often non sp.
Mimics other conditions RHF of any cause
Chronic liver disease (JVP NB)
Abdominal malignancy (JVP NB)
Any cause of effort intolerance
Why easily missed: Insidious onset and slowly progressive with
causative event often remote to patients presentation
Varied presentation often Clinical Examination
mimicking other conditions or with initially subtle symptoms and signs
A) Reduced RV compliance + High Filling Pressures
Presentation: Unexplained HF
Elevated JVP
Right heart failure >> Left heart failure
Predominant Right Heart failure
Beware
branding pt with HF with Normal EF or Diastolic Heart Failure without Kussmauls sign (20%)
considering constriction This is the one form of diastolic HF with a
very specific form of treatment B) Rapid, Early ventricular filling
Low output Prominent Y descent in JVP waveform
symptoms: The runner running out of steam
Pericardial knock
Prev AVR now tired , effort intolerance
Diastolic Apex beat
Mimics : Any cause of right heart failure
C) Dissociation of Intra-Thoracic and Intra-Cardiac pressures
Chronic liver disease (JVP NB)
Pulsus Paradoxus (20%)
Abdominal malignancy (JVP NB)
Clinical picture thus dominated by:
Any cause of effort intolerance
Evidence of severe systemic venous congestion
Raised JVP
Clinical History Risk Factors NB:
Hepatomegaly
NB: Search for risk factors a good history is vital:
Ascites
1. Previous TB
Peripheral Oedema (Can be absent)
2. Previous cardiac surgery or cardiac intervention e.g. pacing
Little evidence of Pulmonary Venous congestion
3. Previous mediastinal irradiation
Little dyspnoea
( h/o Lymphoma?)
No orthopnoea
4. Previous pericarditis, MI, renal failure etc.
No crackles in the chest
5. Often idiopathic
Diagnosis is based on demonstration of:
NB: If you dont think about it and you dont ask
44
1. Abnormal and thickened pericardium
about it youre unlikely to diagnose it
Page
2. Demonstration of constriction physiology
Special investigations: o Ventricular arrhythmia or
Heart block (AVB I, II, III)
Myocarditis:
o
Chest Exrays o ST and T wave abn
Inflammation of myocardium Echocardiography:
Small heart and calcification on lateral xray Usually immune mediated o Dilated poor functioning heart
Definitive etiology usually not determinable o Regional areas of weak myocardial contraction
Echo thickened pericardium sometimes seen (proves constriction
May lead to dilated cardiomyopathy o Exclude other causes
physiology
Endomyocardial biopsy and histology:
Etiology: o Sometimes done if a specific etiology is
CT and MR thickened and calcified pericardium well demonstrated
suspected (eg. Sarcoidosis, giant cell myocarditis)
Infective: Inflammatory cell infiltrate consists of
Heart cathetirzation - Invasive haemodynamic studies to prove
o Bacterial lymphocytes and macrophages must be
physiology.
Part of Acute rheumatic fever shown+/- fibrosis
Diphtheria Viral studies contribute little
Chlamydiae ASOT, ANF, RF can help sometimes
Constriction physiology is demonstrated using: Rickettsia, coxiella Cardiac enzume (Trop T and I, as well as CKMB may be incr)
o Virusses
1. Clinical examination HIV Treatment:
Influenza
2. Echocardiography Coxsackie virus Bed rest in acute phase
Rubella, polio, adeno, echo Rx for HF and arrhythmia as indicated (ACE-I, Bblocker,
3. Cardiac catheterization o Protoxoa aldosterone blocker, loop diuretic)
Chagas (tyrpanosoma cruzii Rx of etiologic agents (eg, ARVs)
Treatment of Constriction Toxoplasma gondii Coricosteroids as indicated for sarcoidosis and SLE with
Non-infective myocarditis)
Surgical stripping of the pericardium o Adriamicine (anthracycline)
o ELad
Remember: anything from peel to chisel
o SLE

Can be very high risk surgery

Clinical picture:

Only option for cure

Heart failute and/or arrhythmia associated with recent
febrile illness
During or after febrile illness
Predictors of surgical outcome (Why NB to diagnose early) Sometimes follows a resp illness
Part of systemic illness
1. Age Soft heart sounds with S3 and tachycardia
Sometimes associated pericardial rub (So-called myo-
2. NYHA class pericarditis increased cardiac enzymes sometimes help)

3. Previous Irradiation Special investigations:

45
4. Chronicity post op ventricular ballooning CXR Cardiomegaly with or without signs of LV failure
ECG:

Page
o Sinus tahcy or
Non - atherosclerotic Aortic disease
OUTCOMES

Briefly describe in terms of anatomic and physiological

principles the mechanisms involved in producing Aortic
pathology

Broadly classify Aortic disease

Discuss the clinical presentation of Aortic disease

Name 5 imaging modalities used in the diagnosis of Aortic

disease and at least one strength and one limitation of each
modality

Pathology: Aortic aneurysm

Describe the clinical characteristics of :

Dilatation of all 3 layers of the aorta

a. Fibrillinopathies

In atherosclerotic disease the athermatous lesions lead to

b. Takayasus arteritis
weakening of the media; in vasculitic disease it is due to
c. Syphilitic Aortitis inflammation; in connective tissue disease it is due to loss of
supportive tissue.
d. Giant cell artheritis
Damage of the supportive media leads to focal or general
Give a general scheme for the management of Thoracic aortic wall thinning and weakening
Aortic aneurysms
La Place : W = P x D/2h

(W= wall tension, P=pressure, D=diameter

h=wall thickness)

Thin (h), weakened areas will increase wall tension locally

and tend to dilate (D) the aorta.

This dilatation (D) will further increase wall tension (W)

Hypertension (P) also increases wall tension , accelerating

aneurysm formation. (High BP is a Bad co morbid condition
treat aggressively)

Spectrum of Aortic disease :Aneurysm, Dissection,

46

Intramural haematoma, Rupture, Scarring with stricture
formation, Side branches

Page
Imaging Modalities MR Angio

CXR

Transthoracic Echo (TTE)

Transoesophageal Echo (TOE)

CT Angiography

MR Angiography

Conventional Angiography (Invasive)

A Classification

Or tranoesophageal.CT Angio

Age at presentation is important Any previous aortic

surgery?

Look for risk factors for atherosclerotic disease

Look at the company it keeps associated lesions/signs

If all else fails remember non atherosclerotic disease

47
associated with Marfans and Bicuspid Aortic valve

Page
NB: Clinical presentation of Thoracic Aortic disease (think Aneurysm, Offer surgery in time ( know your cut-offs) Connective tissue disorders
Dissection, Aortitis)
Appropriate Antibiotics for infective conditions Marfan syndrome

Appropriate anti inflammatory / steroid therapy for Most important fibrillinopathy

Pain Dissection, AMI (dissection flap and aortitis affecting
coronary ostia)
( Beware chest pain that radiates through to the back,
Sometimes described as tearing.)
Haemodynamic collapse Aortic rupture, Tamponade,
acute severe AR
Altered consciousness - Syncope / TIA / Embolism / Stroke
syndrome
inflammatory conditions
Autosomal dominant 75%, Sporadic 25%
Anticipate and treat complications
Prevalence 1:5000
Mutation of the fibrillin gene, Chromosome 15
Multisystem involvement - esp. Musculosceletal, Ocular,
Cardiovascular systems
Diagnose with Ghent Nosology/Criteria

Peripheral /mesenteric arterial occlusion painful white leg, Think abnormal supporting tissue and tissue overgrowth
abdo pain
Dominant negative vs. haploinsufficiency
Mediastinal compression syndrome Cough, Stridor,
Haemoptysis - (A Bad Element vs. Not enough of the good stuff)

- Hoarseness Born BAD vs. Becomes BAD

- Dysphagia Structural problem vs. Regulatory

Pulsating mass

Aortic regurgitation

Differential pulses

Incidentally CXR, Echo, CT, MRI

General Treatment scheme

Lifestyle Advice Pregnancy, Activity / Sport

Endocarditis prophylaxis

Aggressive BP control

48
Beta blockade ( Dp/dt )

Monitor Aortic diameter

Page
Clinical presentation

Musculosceletal: Long limbs, Arachnodactyly, Lax ligaments

resulting in premature osteoarthritis (OA), kyphoscoliosis,
pectus, pes planus, High arched palate etc.

Ocular: Lens dislocation, myopia

Cardiovascular: Aortic Aneurysm, Aortic dissection, Aortic

regurgitation, Mitral valve prolapse

Scin and Soft tissue: Femoral and inguinal hernias, striae

atrophicae

Lungs: Emphysema and spontaneous pneumothorax

Dura mater: Dural ectasia

49
Page
Spot the sign, spot the problem and make the diagnosis! Takayasus arteritis

Rare
Arch of aorta is usually affected
Pulseless disease
Unknown aetiology, possibly associated with TB
Young females more prone
During active (vasculitic) phase it presents like influenza-like
illness sometimes associated with claudication ( activity
related limb pain ) or carotid bruits
Hypertension or cardiac failure
Strokes
Diagnosis of Takayasus arteritis
Active phase vs. Burnt out phase
Usually high erythrocyte sedimentation rate (ESR) and C-
Please dont learn the Ghent Criteria off by heart reactive protein (CRP) during active phase
Angiography demonstrates arterial narrowing and/or
This just to show multisystem nature of disease and so you dilatation
have the criteria on file Especially branches of aorta
In children it classically affects renal arteries (causing
Ghent criteria improves the specificity of diagnosis hypertension)
Exclusion of other causes
It includes genetics and Family History in criteria
Treatment:
Acute phase: oral corticosteroids (Prednisone) plus / minus
Marfan Major vs. Minor different dissection risk
oral methotrexate (steroid sparing)
Control of BP may be difficult
Management
Angioplasty with or without endovascular stent
See general scheme
Vascular bypass grafts
Prophylactic Aortic root replacement:
Diameter at level of Sinus of valsalva:
> 5cm - generally
> 4.5 cm family history of aortic rupture <5cm
- growing rapidly (>1cm per year)
> 4cm planning to become pregnant
Prognosis:
Prognosis determined by Aortic pathology
Pregnancy NB: 10% Dissection risk if Aortic diameter > 4cm
Survival: Mean age of death in 1970s 32yrs in 2007
- 72 yrs
The future:
Anti TGF drugs
Anti MMP drugs

50
ACE I, ARB's (ARBIItype1)

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Syphilitic aortitis Treatment of syphilitic aortitis
Endarteritis obliterans of vasa vasorum Treat with long acting penicillin (benzathine penicillin)
Causes necrosis of media and destruction of elastic tissue 2.4 mil units intramuscularly (imi) once weekly for 3 weeks
Usually asymptomatic If allergic to penicillin, treat with doxycycline 100 mg orally
Rarely symptomatic aneurysm formation of ascending aorta twice daily (bd) for 4 weeks
which may result in aortic regurgitation (AR)
Can cause coronary ostial stenosis with angina pectoris Systemic disease, seronegative arthritis and aortitis
Reiters syndrome
Psoriatic arthritis
Ankylosing spondylitis
Inflammatory bowel disease
Bechets syndrome

Syphilitic aneurysm

Coronary Ostial Disease

Giant cell arteritis or

temporal arteritis

Age > 50yr

In association with PMR (polymyalgia rheumatica)
Involvement of temporal artery invariable
Can have associated Aortitis and coronary arteritis
Temporal headache/tenderness common
Diagnosis of syphilitic aortitis
High ESR / CRP (ESR>100mm/hr)
On chest radiograph (CXR):
Temporal artery biopsy NB: skip lesions
Linear calcification in ascending aorta

51
Treat with oral steroids
Serological:
Symptomatic relief
Positive RPR and FTA-Abs tests
Prevention of blindness and strokes

Page

Echocardiography:
Dilated aorta and aortic regurgitation

CARDIOMYOPATHY AND TUMOURS
OF THE HEART
Most cases of cardiac failure can be attributed to ischaemic heart
disease, hypertension, valvular disorders, congenital defects or lung
disease. Only when these have been excluded are unusual causes
considered. The term cardiomyopathy is often loosely applied to these
disorders but strictly this term should be restricted to disorders of
completely unknown cause or clinical association.
In practice terms like alcoholic cardiomyopathy and amyloid
cardiomyopathy are used to describe systemic diseases with cardiac
involvement.
UNUSUAL DISORDERS OF KNOWN CAUSE OR ASSOCIATION
Multisystem diseases
Cardiac changes are often present in association with multisystem
disease.
Sarcoidosis and rheumatoid disease granulomatous heart lesions
which can cause conduction abnormalities. Amyloidosis glassy
macroscopic appearance can cause cardiac failure.
Acromegaly cardiac hypertrophy heart failure usual cause of death.
Alcoholism
Cardiac failure is not uncommon in chronic alcoholism. In some cases
it can be attributed to other disorders such as coronary artery disease
or hypertension. Sometimes no specific cause is determined and
alcoholic cardiomyopathy is diagnosed, morphologically similar to
congestive (dilated) cardiomyopathy. There is still some uncertainty
about the role of the heavy alcohol consumption.
Pregnancy
Substantial circulatory changes occur in pregnancy, most notably an
increase in circulating blood volumes. Cardiac failure may become
apparent for the first time during pregnancy, especially in patients with
valvular disorders. Hypertension is one of the main signs of pre-
eclampsia but, while cardiac failure and pulmonary oedema can
develop, the disease is not primarily cardiac.
Puerperal cardiomyopathy occurs in the last months of pregnancy, or
within 6 months of delivery. There is no history of previous heart
disease and clinical outcome is variable. In some cases, cardiac failure
resolves completely, although recurrence in subsequent pregnancies is
likely.
Iatrogenic disease
Cytotoxic drugs and radiotherapy can cause cardiac damage.
Radiotherapy causes patchy interstitial fibrosis and pericarditis while
drugs like doxorubicin can produce cardiac muscle necrosis.
IDIOPATHIC CARDIOMYOPATHIES
Congestive (dilated) cardiomyopathy
In Europe and North America the incidence of this disorder is 2 8
cases per 100,000 per year. The median age at presentation is 50
years. Typically the coronary arteries are normal but the ventricles are
dilated and hypertrophied.
Mural thrombi may be present and there may be histological evidence
of interstitial fibrosis and hypertrophy of muscle fibres. Current
studies are demonstrating an increasing range of mutation in the
cardiac muscle of these patients. Some cases of viral myocarditis
appear to progress to dilated cardiomyopathy. As already mentioned,
chronic alcoholic heart disease shows a similar morphologic pattern.
Prognosis is poor 50% to 60% survive two years. Young patients with
dilated cardiomyopathy are considered for heart transplantation.
The main cause of heart failure is reduced systolic contraction.
Hypertrophic (obstructive) cardiomyopathy
The chief morphological feature is massive left ventricular hypertrophy,
usually most marked in the interventricular septum close to the aortic
outflow tract. Patients present with a variety of signs and symptoms of
which atrial fibrillation, ventricular arrhythmias and sudden death are
the most important.
52
Many cases are familial and chromosomal abnormalities can be
identified in up to 50% of patients. Mutations have been studied in
detail on chromosome 14 which codes for the beta chain of cardiac
muscle myosin.
Different genetic abnormalities have been shown in patients with
hypertrophic cardiomyopathy. In the future, it is possible that the
different forms of cardiomyopathy will be classified according to
genetic abnormality.
Other cardiomyopathies
Endomyocardial fibrosis
This is a form of myocardial disease found chiefly in Uganda and Sudan.
The cause is unknown. There is marked fibrosis of the inner parts of
the myocardium and mural thrombi are common. In some patients
there is a prominent persistent peripheral blood eosinophilia. This
type is sometimes placed in a group called restrictive
cardiomyopathies.
Puerperal cardiomyopathy - described together with pregnancy.
TUMOURS OF THE HEART AND PERICARDIUM
Primary tumours of the heart and pericardium are extremely rare
although metastases especially from lung cancer are relatively
common.
Myxoma
This is the most frequent primary tumour and usually occurs in the left
atrium where it arises as a polypoid or peduculated tumour from the
endocardium.
50% of the lesions cause mitral valve symptoms. The tumours are
friable and can fragment and embolise. Myxomas are most common in
adults.
The tumours arise from undifferentiated connective tissue cells in the
subendocardial layers of the heart.
52
Other tumours include lipomas, rhabdomyomas, rhabdomyosarcomas
and angiosarcomas.
Page
The commonest primary pericardial tumour is a mesothelioma and
mesotheliomas of the pleura can also infiltrate the pericardium.
Cardiomyopathies
Amyloidosis heart
(Disease of heart muscle)
Hemochromatosis

Sarcoidosis Special invest

Storage diseases X-R chest . large heart , signs of heart failure
Definition: EKG: No typical picture
Diseases where myocardium is primarily affected and not the FUNCTIONAL VS. STRUCTURAL & FUNCTIONALABNORMALITIES LVH to LBBB, low voltage and T-wave flattening
consequence of hypertension, congenital, valve, coronary or
Some diseases of heart muscle does not en/or reversal
pericardial abnormalities have recognizable anatomic / pathologic Echocardiography: ventricle enlargement,

Unknown association (primary) abnormalities diminished ejection fraction (EF), absence of

Known association (secondary) = ONLY FUNCTIONAL valve disease , absence of pericardial disease
Heart catheterization: ventricle enlargement,
KNOWN ASSOCIATION poor emptying, low EF, Normal coronary

Inflammatory Morphologically: blood flow & coronary arteries
o Infective Dilated cardiomyopathy (DCM) Other: Normal 02 extraction , raised enddiastolic
o Auto-immune
Hypertrophic cardiomyopathy (HCM) pressures. Normal or decreased stroke volume

Infiltrations
Restrictive cardiomyopathy and/or cardiac turnover

Medicines/ Toxic substances
Right ventricular cardiomyopathy (alt: arrhythmogenic Biopsy: Insensitive / not specific

Physical right ventricular dysplasia / cardiomyopathy [RVD, ARVC]) Other investigations : MRI, Radioisotope

pregnancy
Other

Metabolic DCM management :

Nutritional Conduction system disease Rx factors worsening heart failure +
deficiencies Progressive familial heart block type I and consequences; Not enough knowledge for

Neuromuscular II (PFHBI & PFHBII) Rx of cause; As for heart failure in general.
NB: ACE-INHIBITORS!

Genetic and/or Aneurism cardiomyopathy
Cardiac repolarization syndromes DCM complications
familial
Lang QT Syndrome (LQTS)/ Brugada Ventricular and atrial rhythm disturbances
syndrome (NB atrial fibrillation [AF])
INFECTIVE CAUSES
Systemic and pulmonary embolism

Viruses: mostly Coxsackie B all causes of myocarditis

Ricketsiae DCM:
Dilated cardiomyopathy (congestive) Peripartum cardiomyopathy

Bacterial: toxin of diphtheria, Trypanosoma
Peri-partum cardiomyopathy late in pregnancy or short after birth; same
Cruzi in South America
Familial cardiomyopathy geographic spread as DCM in Africa

Protozoa: Toxoplasma
Clinical + special investigation as for DCM

Fungi Recovers but tendency to re-occur with
Medication/ Toxins DCM Symptoms, Clinical signs & diagnosis
Clinical: exercise intolerance, dispnea, edema, subsequent pregnancies

Alcohol
chest pain

Chemotherapy
signs : small to full pulse (+/- atrial

Anabolic steroids
fibrillation), blood pressure normal or low ,
Neuromuskulr
large heart (cardiomegaly) +/- LVH, Gallop

Muscular dystrophy
(K3), signs of heart failure, murmur of mitral

53

Myotonic dystrophy
incompetence, arrhythmias

limb-girdle dystrophy
diagnosis: consider specific causes of , and

Page

Other
associations with, heart failure and a large
Infiltrations & Metabolic diseases

53
Important occasional reversible HOCM: echocardiography: Specific but less sensitive than EKG.
associations Clinical definition:hypertrophy of ventricular muscle in a non-dilated Thickened wall (hypertrophy).

Alcohol heart with absence of a cause such as hypertension or aorta stenosis Hemodynamic characteristics, vb., SAM or
o typical DCM intraventricular gradient
o Holiday heart (arrhythmia -> AF) HOCM Pathology and molecular defect: Heart catheterization: confirm normal coronary arteries

Chronic tachycardia Important characteristic: Ultra structural disorganization / cellular Biopsy: not sensitive and not specific

Other disorganization Genetic diagnosis: May help to determine risk of sudden
o Thyroid disease , nutritional, low magnesium, Other characteristics death
o hypocalcaemia, selenium shortage, Cocaine, myocyte hypertrophy as well as fibrosis present. Other : Radioisotope, CT/MRI
o anabolic steroids hypertrophy of any part of the ventricle; most
common septum. Mx and Rx:
Molecular defect: for symptoms
disease of the sarcomere in most cases. Most Asymptomatic none
common Myosin-heavy chain, Troponin T, Myosin Symptomatic
binding protein C. Medical B-blocker, Ca-antagonist Verapamil
Epidemiology: Interventional: Surgical myomectomy or decrease in muscle
Occurence : 1/500 mass by therapeutics infarction via catheter (percutane),
Most common cause of sudden death of pacemaker , heart transplant
young athletes for prognosis
Often develop in late puberty low dose Amiodarone, Disopyramide
Mostly familial ( > 70%); autosomal Implanted defibrillator (ICD)
dominant inheritance
Sx and Signs:
Presentation : most often asymptomatic, chest pain ,
dispnea, tiredness, syncope, sudden death (SD)
o Family history of young unexpected deaths
Signs : Ventricular hypertrophy. Apical mid to late systolic
ejection murmur (occasional)
softer with squatting. louder with
standing
Diagnosis: not affected by valsalva
Murmur: consider HCM, aorta
stenosis, sclerosis, functional murmur
Conside possibility of HCM in all 1st
degree relatives even if no symptoms
or signs are present
Special investigation of paramount
importance for prognostic management
and genetic advice
HCM Dx with special investigations:
X-R chest : little use

54

EKG: sensitive investigation, but non specific.
occasional ST-T changes , LVH or Q- wave +/- left

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atrial enlargement

54
Resctrictive Cardiomyopathy Right ventricular cardiomyopathy (RVC)
Endomyocardial fibrosis Right Ventricle Dysplasia (RVD)
o Tropics & sub-tropic Africa
Replacement of parts of right ventricle by
Eosinophilic endo-myocardial disease fat- and connective tissue
o May be part of the hiper-eosinophilsyndrome
Association with cell-adhesion molecules
Endocardial fibroelastosis
Sporadic or familial

Ventricular arrhythmias common
RCM Simptome, Clinical signs & diagnosis
Important cause of sudden death in young
heart failure, mostly right sided persons in Northern Italy
diagnosis
Rx: Anti-arrhythmic drugs, ablation, ICD
Differentiate from constrictive pericarditis,
Infiltrations
RCM special investigations
X-R chest , EKG, echocardiography, Heart
catheterisation, CT/MRI
Biopsie: diagnosis of infiltrate

RCM management & treatment

Medical unsatisfactory
Surgical

RCM Komplikasies
Embolism
Arrythmias

55
Page
55

ATHEROSCLEROSIS
Chief source Underwood 4rd edition 2004 pages 278 285 5th Edition Buergers disease
2009 : 272 - 278
Introduction: Cardiovascular diseases are the leading cause of death in
most Western societies. The diseases are also frequent in South Africa.
In England ischaemic heart disease accounts for 27% and
cerebrovascular disorders 13% of all deaths.
Unknown causes specific clinical features
Scleroderma
Cranial (giant cell) arteritis
Pulseless (Takayasus) disease
porridge) Its frequency has increased dramatically during the last 50
Veins
ATHEROSCLEROSIS
Atherosclerosis is a degenerative disease of large and medium sized
arteries, characterized by lipid deposition, fibrosis and chronic
inflammation. (Atheroma is derived from the Greek word for gruel,
years. In some countries such as the USA it appears to have peaked
and is now declining. In a country like South Africa, it is already very
common in some population groups and is currently increasing in
others.
AETIOLOGY

Normal arterial structure The exact cause of atherosclerosis is not known. One of the features of
atherosclerosis is the wide variation in the severity and distribution of
Intima single layer endothelium lesions between individuals, even within the same population groups.
Many factors increase the risk of an individual to develop severe or
Internal elastic lamina premature atheroma, but some people with clinical disease have not
clear risk factors. There is thus not a clear simple aetiology.
Media In the aorta elastic tissue is prominent, in medium sized Risk factors
arteries, smooth muscle predominates eg coronary arteries. A. Constitutional
Age atherosclerosis worse with increasing age
Adventitia outermost layer, connective tissue. Small blood vessels, Gender less severe in females before the menopause
the vasa vasorum, supply much of the media. FAMILIAL PREDISPOSITION
B. Major acquired risk factors
The intima and innermost media are supplied from the lumen of the Hypertension
vessel. Raised LDL cholesterol levels
Diabetes mellitus
A CLASSIFICATION OF DISEASES OF ARTERIES AND OTHER BLOOD Cigarette smoking
VESSELS C. Minor risk factors

Age related changes arteriosclerosis Obesity

Sedentary life style
ATHEROSCLEROSIS The commonest and most important vascular Low social economic status
disease Low birth weight
Stress
Cystic medial necrosis aortic dissection Oral contraceptives
Syphilitic aortitis Hyperuricaemia
Hypertensive changes High carbohydrate intake
Diabetic vascular disease Hyperhomocysteinaemia
Immunological vascular diseases immune complexes Chlamydia pneumoniae

Henoch Schnlein purpura

Polyarteritis nodosa
Wegeners granulomatosis
Systemic lupus erythematosus
MORPHOLOGY
Spectrum of atherosclerotic lesions: The more advanced atherosclerotic plaque is a mixture of
macrophages, lymphocytes and smooth muscle cells, usually capped
Fatty streak with a layer of fibrous tissue. (Fig 13.6) Growth factors, particularly
Fibrolipid plaque PDGF (platelet derived growth factor), stimulate the proliferation of
Complicated atherosclerotic lesion intimal smooth muscle cells which also produce collagen, elastin and
mucopolysaccharide. PDGF is secreted by a large number of cells of
Fatty streaks linear elevations composed of lipid filled histiocytes connective tissue origin, by macrophages and by endothelium. Even
ost obvious in the thoracic aorta and coronary arteries, have been trivial endothelial damage can lead to platelet aggregation and PDGF
identified in all populations groups that have been studied in detail. secretion with smooth muscle proliferation.
Fibrin and platelets are important constituents of early lesions.
Early atheromatous lesions are associated with monoclonal
proliferations of smooth muscle cells. This suggests that atheromatous
lesions are like small benign neoplasms. The mechanism of this is
uncertain.
SUMMARY ATHEROSCLEROSIS

It is likely that, in patients predisposed to atherosclerosis by genetic or
environmental factors, they progress to fibrolipid plaques and
complicated lesions.
Fatty streaks and fibrolipid plaques have little clinical significance.
Complicated lesions complications include
Endothelial erosion with thrombus formation
Plaque rupture or fissuring
Aneurysm formation, especially in the aorta
Embolism of atherosclerotic debris or overlying thrombus
Rupture of the endothelial lining with exposure of the collagen is a
stimulus for thrombus formation. It is also a way for blood to enter the
plaque. These sorts of mechanisms are usually responsible for
myocardial infarcts.
Lipids and apolipoproteins
Lipids are poorly soluble and are transported in the blood as
lipoproteins. The protein components of lipoproteins are termed
apolipoproteins. An increased level of low density lipoprotein (LDL)
cholesterol or reduced levels of high density lipoprotein are common
abnormalities which predispose to atherosclerosis.
LDL cholesterol levels are influenced by both genetic and
environmental factors. In studies of large populations, LDL
cholesterol can be closely correlated with the death rate from coronary
heart disease.
Patients with a total or partial lack of cell membrane receptors for LDL,
show clearly raised levels of LDL cholesterol and a raised incidence of
coronary artery atherosclerosis.
Affects large and medium sized arteries
Lesions comprise fatty streaks, fibrolipid plaques and
complicated lesions the last named is most associated
with clinical disease.
Risk factors include A Constitutional such as increased age
and male gender, B- Major acquired risk factors
hypertension, smoking, diabetes and hypercholesterolaemia
and C- Minor risk factors.
Associated with raised levels of LDL cholesterol and
reduced levels of HDL-cholesterol
Major cause of organ ischaemia (eg myocardial infarction)

PATHOGENESIS Inflammation and disordered immunity are also important but no

proof exists yet for a specific causative organism. Some of the
Inflammation, infection and abnormal immunity evidence includes the following:

It is difficult to follow the development of atherosclerosis in individual
patients. Therefore, much of the information comes from post
mortem studies as well as from animals which develop atherosclerosis
either spontaneously or on high fat or cholesterol diets.
Early in the disease lipid filled macrophages are found in the
subendothelial areas of arteries. They reach there, via gaps between
Atheromatous plaques contain inflammatory cells including
macrophages and T lymphocytes. Cytokines and growth factors are
found in atheromas. Elevated inflammatory markers such as C reactive
protein are found. Antibodies to Chlamydia pneumonia and other
organisms have been found.
OTHER PATHOGENETIC FACTORS

57
the endothelial cells or because of focal loss of endothelial cells. Some
of the molecular mechanisms which make it possible for macrophages In England, it has recently been shown that low birth weight babies,

Page
to bind to endothelium are similar to those of acute inflammation, but later show increased risk for fatal coronary artery disease, compared to
are not all known. normal birth weight babies.

57

BIOCHEMICAL MARKERS OF HEART
DISEASE
Outcomes:
After completing this session, you should be able to do the following:
1. Discuss the markers of myocardial damage. Differentiate
between specific and non-specific markers and their
subfractions.
2. Discuss, with the aid of a diagram and tables, the period of
time after a myocardial infarction and the appearance of
markers of myocardial damage.
3. Discuss C reactive protein (CRP) and its role in heart disease.
4. Discuss the chemical analysis of pericardial fluid.
5. Discuss the values of an adenosine deaminase (ADA)
determination in the diagnostic process in a patient with a
pericardial effusion.
Introduction
According to the World Health Organization (WHO), 17 million people
die of coronary vascular disease per year worldwide. According to the
American Heart Association (AHA), 700,000 Americans have a new
myocardial infarction (MI) and 500,000 have a recurrent MI per year.
Acute Coronary Syndrome (ACS)
ACS is a constellation of clinical symptoms due to myocardial
ischaemia. The basic lesion is atherosclerotic coronary artery disease
with erosion or rupture of the atherosclerotic plaque. The highly
procoagulant interior of the plaque is exposed to platelets and other
clotting factors in the blood stream. This leads to formation of an
intracoronary thrombus. If this thrombus is partially obstructive/
transiently occlusive, the patient presents with unstable angina (UA) or
non-ST elevated MI (NSTEMI). If this thrombus is totally occlusive, the
patient presents with an ST-elevated MI (STEMI).
Traditional Diagnosis of MI
Infarction is defined as the process by which necrosis (cell or tissue TRADITIONAL BIOMARKERS OF MI:
death) results from ischaemia (loss of blood supply).
1. CREATINE KINASE (CK)
There are many causes of myocardial ischaemia: Highest concentration found in skeletal muscle, myocardium and brain.
The most common cause is due to coronary atherosclerosis CK consists of two subunits of which there are two types - M and B.
with rupture of unstable plaque
Coronary vasospasm where arterial wall constricts in an Isoenzymes
abnormal and prolonged fashion due to hypersensitivity to MM: most abundant and found in skeletal and heart
normal vasoconstrictor signals muscle
Less common causes: severe anaemia and hypotension BB: the predominant form in brain
MB: found in cardiac muscle (minor amount also in
According to the World Health Organization (WHO) an MI is diagnosed skeletal muscle)
if 2 of the following criteria are satisfied (1978):
1. Chest Discomfort >20 minutes Causes of increased total CK
2. ECG changes with ST Elevation Heart: myocardial infarction
3. Elevated Cardiac enzymes Skeletal muscle: Trauma
The cardiac enzymes referred to were CK and CK-MB. At this stage, CK- IM injections
MB was the benchmark marker, although it is not totally specific for Muscular dystrophies
the myocardium. Rhabdomyolysis
Redefinition of MI Clinical use
CK-MB is used in the diagnosis of myocardial infarction. A value of
With the development of more specific cardiac biomarkers, the more than 3 % is indicative of myocardial infarction. The MB-fraction is
troponins, in 1999 the European College of Cardiology (ECC) and used to determine if the raised CK is of cardiac origin. CK-MB is a more
American College of Cardiology (ACC) convened a consensus specific indicator of cardiac muscle damage than total CK, and can be
conference to re-examine the definition of MI. detected in the serum within 4 hours after the onset of chest pain.
They stated that a persistent (not short term) increase of the Troponin 2. LACTATE DEHYDROGENASE (LD)
concentration (caused by oxygen deficiency) above the 99th percentile
of a normal healthy heart indicates myocardial necrosis (dying heart Ubiquitous. Highest concentrations found in heart, skeletal muscle,
muscle cells) and is interpreted as a MI. The troponins shouldnt be liver, kidney and erythrocytes. There are five isoenzymes in serum
measurable with an imprecision of worse than 10%. They recommend (LD1-5).
the use of troponin as the preferred biomarker, as it has nearly
absolute cardiac tissue specificity. Causes of high plasma LD activities
Artefact:
Cardiac Markers o Haemolysis
o Delayed separation of plasma from erythrocytes
When myocardial cells die, they release their contents into the Pathologic:
circulation. The traditional enzymes released in the circulation and Heart e.g. myocardial infarction
o
used to diagnose MI are described below. o Liver e.g. cell necrosis as in viral hepatitis
60
o Haematological malignancies
Clinical use
Page
Evaluation of possible myocardial infarction or haemolysis
This is a relative non-specific cardiac biomarker
60
 Differences between TnI and TnT
3. ASPARTATE AMINOTRANSFERASE (AST) Enzyme Initial Mean time to Time to
(marker) elevation peak return to Troponin T Troponin I
Causes of high plasma AST activity after MI elevations baseline Molecular 37 kDa 22.5 kDa
Artefact: Myoglobin 1 hr 4 hrs 12 hrs Weight
o Haemolysis Nature of Structural Catalytic
o Old specimen NEW MI BIOMARKERS TROPONINS protein
Physiological: Kinetics of Biphasic Only a single peak
o Increased in neonates Cardiac troponins are specific markers of MI and UA. The troponins are release
Pathological: regulatory proteins on contractile proteins of all myofibrils. They Duration of Up to 14 days 5-7 days
o Heart: myocardial infarction consist of a complex of 3 subunits: TnC, TnI and TnT elevation
o Liver: cell necrosis caused by viral hepatitis Number of 1 Several
They are localized primarily in myofibrils (94-97%), with a small amount assays
This is a relative non-specific cardiac biomarker. In myocardial found in the cytoplasm (3-6%). They are released into the circulation Ontogeny May be expressed Only ever expressed in
infarction the cardiac enzymes, CK, AST and LD are elevated. with myocardial cell injury. Cardiac troponins also play a vital role in in skeletal muscle in myocardium
the diagnosis and risk stratification of ACS. Troponin positivity below utero and in
Enzyme Initial Mean time to Time to return the cut-off for the diagnosis of MI suggests that these patients are at a diseased skeletal
(marker) elevation peak to baseline greater risk of future cardiac adverse events. muscle
after MI elevations
CK 3 6 hrs 12 24 hrs 3 4 days Troponin Isoforms: Cardiac Markers: Approximate levels vs. Time of Onset Post MI
AST 6 8 hrs 24 48 hrs 5 7 days
LD 6 12 hrs 24 48 hrs 8 12 days TnI:
Found in cardiac muscle + slow-and
MYOGLOBIN fast twitch skeletal muscle
Each encoded by distinct gene
Myoglobin is an oxygen-binding protein of cardiac and skeletal muscle. Unique amino acid sequence 40%
The proteins low MW and cytoplasmic location accounts for its early dissimilarity between isoforms
appearance in the circulation after myocardial injury. cTnI has 31 additional aa that lends
cardio-specificity
Increases in myoglobin may also occur after skeletal muscle injury; MW 24,000 Daltons
therefore it is a non-specific cardiac biomarker and is unable to
determine the tissue of origin. It is useful as an early screening test TnC:
(high sensitivity). It is a negative predictor of myocardial injury in an 2 isoforms, but cardiac isoform
emergency department setting. identical to slow-twitch muscle
isoform, therefore not of use as a
It is used as a rule out test - if negative 4 hours after onset of chest cardiac biomarker
pain, MI is highly unlikely, and an early discharge can be considered. If TnT:
positive, and if the clinical picture or ECG supports the diagnosis of MI, Cardiac-specific isoform also identified
this is an indication to start thrombolytic therapy, which must
commence within 4 hours.

61
It is not very helpful in the absence of convincing clinical evidence,

Page
since a positive result may be due to cardiac or skeletal muscle damage
and requires additional diagnostic tests.
61
ALGORITHM OF INVESTIGATION FOR SUSPECTED MI
Clinical picture and ECG typical of MI:
o Diagnostic tests: none needed
o Therapeutic tests: myoglobin (if thrombolytic
therapy considered)
o Prognostic tests: CK and CK-MB; Troponin T or I
Clinical picture and ECG not typical, therefore diagnosis uncertain:
o Diagnostic tests depending on time since
chest pain
OTHER CARDIAC MARKERS OF IMPORTANCE
Adenosine deaminase (ADA)
1. B-type natriuretic peptide (BNP):
ADA is a polymorphic enzyme involved in purine metabolism, catalyzing
BNP, an atrial natriuretic peptide, act as a dual natriuretic system in the deamination of adenosine and deoxyadenosine to inosine and
regulating blood pressure and fluid balance. The heart releases BNP in deoxyinosine respectively.
response to ventricle volume expansion and pressure overload. BNP is
a new diagnostic tool for the diagnosis of heart failure in patients It is found in most human cells, but its activity is greatest in lymphoid
presenting with dyspnoea of unknown origin. tissues, especially T-lymphocytes. ADA plays a role in the
differentiation of lymphoid cells and the maturation of monocytes to
2. Ischaemia-modified albumin (IMA) macrophages.

< 4 hrs Myoglobin Serum

- If negative before 4 hrs, albumin
repeat after is altered when exposed to free radicals produced in
4 hrs
ischaemic
- If negative after 4 hours, tissues. This leads to altered binding of albumin to cobalt
MI excluded ADA is useful for the diagnosis of a suspected tuberculous pericardial
- Positivity at any timeand is the
is not basis ofofthe
diagnostic MIanalytical test used to determine the quantity of effusion:
4 24 hrs CK and CK-MB IMA. IMA increases within minutes of an ischaemic event, is raised for
Preferably by mass determination > 50 with lymphocytosis: TB or malignancy.
Troponin T or I Preferable, if available 2-4 hours and detectable for up to 6 hours after the event. > 50 with neutrophylia: Infective (empyema)
> 24 hrs Troponin I PERICARDIAL EFFUSIONS:

C-REACTIVE PROTEIN (CRP): A pericardial effusion is an abnormal collection of fluid in the Dr AE Zemlin
pericardial space. It is traditionally classified as transudates and Division of Chemical Pathology
CRP is a sensitive marker of systemic inflammation and is usually exudates since it can help with diagnosis in respect of
present in the sera of acutely ill individuals. It is a substance that is able pathophysiological mechanism, differential diagnosis and whether
to bind the C-polysaccharide on the cell wall of Streptococcus further invasive investigations are necessary.
pneumoniae (first described in 1930). In the presence of calcium, CRP
binds not only polysaccharides present in many bacteria, fungi and Laboratory differentiation between transudate and exudate
protozoal parasites, but also phosphorylcholine, phosphatidylcholines
such as lecithin, and polyanions such as nucleic acids. In the absence of 1. Lights criteria: one or more of the following
calcium, it binds polycations, such as histones. Once complexed, CRP a) Pericardial fluid / Serum (P/S) Protein Ratio 0.5
activates the classic complement pathway - it thus initiates b) P/S Lactate dehydrogenase (LDH) 0.6
opsonization, phagocytosis and lysis of organisms such as viruses and c) Pericardial fluid LDH 200 U/L
bacteria.
2. Serum-effusion Albumin Gradient
CRP is one of the most sensitive acute phase proteins. Its levels are Gradient = Serum Albumin Pericardial Fluid Albumin
increased in MI, stress, trauma, infection, inflammation, surgery and 12 g/L is suggestive of an exudate.
neoplasms. Low circulating levels of CRP have been found to be an > 12 g/L is suggestive of a transudate
independent risk factor for cardiovascular disease. A sensitive CRP
assay with a lower limit of detection (high sensitive CRP) is used to 3. Pericardial fluid cholesterol concentration
measure CRP for risk stratification. Higher levels are associated with an Pericardial fluid Cholesterol 1.55 is suggestive of an exudate.
increased risk for MI and stroke. The increased risk is also associated Pericardial fluid Cholesterol < 1.55 suggestive of a transudate.

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for those who are older, smoke, have symptomatic angina, or have had
previous MIs. Screening with a sensitive CRP method plays a role in 1. P/S Bilirubin Ratio

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cardiovascular risk prediction. P/S Bilirubin ratio 0.6 is suggestive of an exudate.
P/S Bilirubin ratio < 0.6 is suggestive of a transudate
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