Problem 4

Emergency Medicine
Carissa Cornelia Chundiawan
405140168 / 2017
Cardiac Arrest
Acute Coronary
Syndrome
 Acute Coronary Syndromes
• Pathogenesis of ACS

• disruption of atherosclerotic plaque + platelet

aggregation + formation of intracoronary
thrombus

• thrombus—impaired blood flow — imbalance

between myocardial O2 supply & demand

• 3 forms of ACS depends on degree of coronary

obstruction

• partially occlusive thrombus = unstable angina

• + myocardial necrosis = NSTEMI

• completely obstructed artery = STEMI (more

ischemia, more necrosis)
Pathology & Pathophysiology
• MI (STEMI/NSTEMI) — when myocardial ischemia is
sufficiently severe to cause myocyte necrosis

extent of necrosis within myocardial wall

span the entire thickness of myocardium and

transmural infarcts result from total, prolonged occlusion of
epicardial coronary aetery

involve the innermost layers of the myocardium

subendocardial subendocardium is the most susceptible bc:
infarcts -subject to the highest pressure from ventricle
-few collateral connection that supply it
 early changes in infarction
• cellular change
 late changes in infarction
• clearing of necrotic myocardium

• irreversibly injured myocytes do not regenerate, but

removed & replaced by fibrous tissue

• mø invade the inflamed myocardium — remove necrotic

tissue (yellow softening)

• deposition of collagen to form scar tissue

• scarring is complete by 7w after infarction

 functional alterations
• impaired contractility

• destruction of myocardial cells in infarction — impaired ventricular

contraction (systolic dysfx)

• CO is further compromised bc synchronous contraction of myocytes is

lost (hypokinetic, akinetic, dyskinetic regions)

• ACS — LV severely compromised by diastolic dysfx

• stunned myocardium

• tissue that demonstrate prolonged systolic dysfx after a discrete

episode of severe ischemia, despite restoration of adequate blood flow,
and gradually regains contractile force days to weeks later
• ischemic preconditioning

• brief ischemic insult — render that tissue more resistant to subsequent

episodes

• ventricular remodeling

• early post-MI period — infarct expansion

• the affected ventricles segment enlarges w/o additional myocyte necrosis

• remodelling of ventricle also involve dilation of the overworked noninfarcted

segment which are subjected to increased wall stress

• progressive enlargement — HF
 HISTORY AND ASSOCIATED SYMPTOMS

• main sx: chest discomfort (ask abt its severity, location, radiation,
quality)

• usually in substernal / left chest, with radiation to the arm, neck or

jaw.

• associated sx: N/V, diaphoresis, dyspnea, light-headedness,

syncope, palpitation

• precipitating factors: exercise, stress, cold environment

• angina: duration <10’. improves within 2-5’ after rest or NG

acute myocardial ischemia: more prolonged & severe chest
discomfort, little response to initial sublingual NG
• PHYSICAL EXAMINATION

• bradycardic rhythms — more common

with inferior wall MI. in the setting of acute
anterior wall infarction, bradycardia/new left sided hearfailure • rales (w/w.o S3 gallop
heart block is a poor prognostic sign

• BP can be normal, elevated or decreased

— extremes of BP: worse prognosis
•
jugular venous
• S3 — failing myocardium right sided heart failure
distention
• hepatojugular reflex
• peripheral edema
• new systolic murmur (+) — ominous
sign, bc it may signify papillary muscle
dysfx, flail leaflet of mitral valve with
resultant mitral regurgitation / VSD
- early invasive strategy recommended in pt w/ score >=3
(prior angiography should be done)
Cardiac Arrest
• Cardiac arrest — 4 rhythms

• shockable rhythms: pulseless ventricular tachycardia

(VT), ventricular fibrillation (VF),

• nonshockable rhythms: asystole, pulseless electrical

activity (PEA)
shockable rhythms
• high-quality CPR should be performed until
defibrillator is attached to the patient

• interruptions in chest compression should be

kept minimum

• rapid use of defibrillator

• if possible, use manual defib over an AED,

bc AED can result in prolonged interruptions
in chest compressions for rhythm analysis &
shock administration

• CPR is always immediately resumed for 5

cycles between each shock
 defibrillation & shock
• biphasic: electrical current travels from one paddle to other paddle and then Synchronization avoids the
back in other direction. delivery of a LOW ENERGY
shock during cardiac
• requires less energy to restore normal heart rhythm, reduce skin burns & repolarization (t-wave). If the
cellular dmg to heart shock occurs on the t-wave
(during repolarization), there is
• biphasic defib with VF or pulseless VT — start with 120-200J, increase the a high likelihood that the shock
dosing in stepwise fashion as needed (120 J > 200 J > 300 J > 360J) can precipitate VF (Ventricular
Fibrillation).
• synchronized & unsynchronized cardioversion if the patient is stable, QRS-t
complex (+), use (LOW
• synchronized cardioversion: LOW ENERGY SHOCK uses a sensor to ENERGY) synchronized
deliver electricity that is synchronized with peak of QRS complex cardioversion. If the patient is
indication — unstable AF, atrial flutter, atrial tachycardia, pulseless / unstable and the
defibrillator will not synchronize,
• unsynchronized cardioversion (defibrillation): HIGH ENERGY SHOCK. use (HIGH ENERGY)
shock may fall randomly anywhere within the cardiac cycle (QRS complex) unsynchronized cardioversion
indication — no coordinated intrinsic electrical actv (pulseless VT/VF) (defibrillation).
 Vasopressors
• produces vasoconstriction & rise in BP.

• for VF/pulseless VT — epinephrine

• important bc help increase blood flow to brain & heart

rhythm check should be performed every 5 cycles of CPR.
limit rhythm check to <10s to minimize interruption
pulse check — when rhythm check reveals a change in rhythm that
is organized & could be generating a pulse

• antiarrhythmic drugs: amiodarone, lidocaine, magnesium

 Asystole
• no discernible electrical activity on ECG monitor (flat line)

• confirm that a “flat line” is truly asystole

• common cause of isoelectric line that is not asystole:

1. loose / disconnected leads
2. loss of power to the ECG monitor
3. low signal gain on ECG monitor

• asystole —result of prolonged illness / cardiac arrest,

prognosis is very poor
H’s and T’s of ACLS
 Vasopressors

• epinephrine

• for asystole, epinephrine can be given ASAP but its

administration shoild not delay initiation or continuation of
CPR.

• after initial dose, epinephrine is given every 3-5 minutes

 Pulseless Electrical Activity
(PEA)

• organized rhythm w/o palpable pulse, and is the

most common rhythm present after defibrillation

• PEA — poor outcomes

• positive outcome of an attempted resuscitation

depends on 2 actions: 1. providing effective CPR,
2. identification & correction of the cause of PEA

• medications used in PEA: epinephrine

Tachycardia
Supraventricular Arrhythmias
• sinus tachycardia: SA node discharge rate >100
bpm (100-180 bpm) with normal P waves & QRS
complexes

• bc increased symphatetic / decreased vagal tone.

• appropriate response to exercise, but can result

from pathologic cond: fever, hypoxemia,
hyperthyroidism, hypovolemia, anemia
• atrial premature beats:

• from automaticity / reentry in atrial focus outside SA node,

exacerbated by sympathetic stimulation

• ECG: earlier-than-expected P wave w/ abnormal shape

QRS comples usually normal bc ventricular conduction is not
impaired

• premature P wave that is not followed by QRS complex —

blocked APB

• abnormally wide QRS complex — APB with aberrant

conduction
• atrial flutter

• rapid, regular atrial activity (180-350 bpm)

• these fast impulses reach AV node during its refractory period and do not conduct to
ventricles, resulting in slower ventricular rate, often an even fraction of the atrial rate

• if atrial rate is 300 bpm, ventricular rate is 150 bpm (2:1 block)

• vagal maneuver decrease AV nodal conduction —increase degree of block,

temporarily slowing ventricular rate

• caused by reentry over a large anatomically fixed circuit

• large parts of atrium are depolarized — sinusoidal / ‘sawtooth’ appearance

• rate <100 bpm, patient may be asymptomatic

• atrial fibrillation
• dangerous, because:
• chaotic rhythm with an atrial rate so fast (350- 1. rapid ventricular rate — compromise CO
600 discharges/min) — hypoTN, pulmonary congestion
2. blood stasis in atria — increase risk of
• distinct P waves are not discernible on ECG thrombus formation, particularly in left atrial
appendage
• average ventricular rate in untreated VF — 140
to 160 bpm
• treatment:
• mechanism: multiple wandering reentrant circuits
1. ventricular rate control
within atria, and rhythm repetitively shifts 2. restore sinus rhythms
between fibrillation atrial flutter 3. assessment the need for anticoagulation
to prevent thromboembolism
• often associated w/ right / left atrial enlargement
• AV nodal reentrant tachycardia (AVNRT)
• AV node consist of compact portion and several arterial
extensions

• arterial extension constitute two or more potential pathways for

conduction through the AV node

• slow- and fast-conducting pathways.

• under normal conditions, only the fast pathway impulse makes its
way forward to the ventricles

• transient unidirectional block in fast pathway (APB encountering

refractory tissue) and relatively slow conduction through the other
pathway

• ECG: regular tachycardia, normal width QRS complex. P wave not

apparent. when it is visible, they are superimposed on terminal
portion of QRS complex and inverted in limb leads II, III and aVF bc
caudocranial direction of atrial activation

• treatment Valsava maneuver, carotid sinus massage.

pharmacologic: iv adenosine — impairs AV nodal conduction and
aborts reentrant rhythm; CCB; betablockers
• ventricular pre-excitation syndrome / Wolf-Parkinson-
White [WPW] syndrome

• atrial impulses can pass in anterograde direction to the

ventricles through AV node and the accessory pathway

• conduction via accessory pathway is usually faster than

AV node, the ventricles are stimulated earlier than by
normal conduction over the AV node
 Ventricular Arrhythmias
• ventricular premature beats

• when ectopic ventricular focus fires an action potential

• ECG: widened QRS complex bc impulse travels from its ectopic site through the
ventricles via slow cell-to-cell connection than His-Purkinje system

• can also occur in repeating pattern — bigeminy / trigeminy

• not dangerous by itself

• treatment: reassurance, sx control: betablockers

• ventricular tachycardia

• series of ≥3 VPB

• categories:
- sustained VT: persist for >30secs, severe sx ( syncope / requires termination by cardioversion or adm of
antiarrhythmic drug)
- nonsutained VT: self terminating

• in pt w/ structural heart disease (MI, HF, ventricular hypertrophy)

• ECG: wide QRS complex (>0.12s), occur at a rate of 100-200 bpm and sometimes faster

• based on QRS morphology

- monomorphic VT: every QRS complex appears the same, rate is regular
- polymorphic VT: QRS complexed change in shape, rate varies from beat to beat — caused by TDP, AMI.

• sx: sustained VT: low CO — syncope; pulmonary edema; progress to cardiac arrest
if sustained VT is relatively slow (<130 bpm) — well tolerated, only cause palpitation
• management of VT

• acute tx: electrical cardioversion, iv antiarrhythmic drugs (amiodarone, procainamide,

lidocaine)

• after sinus rhythm restored — evaluate for underlying structural heart disease

• VT in absence of underlying structural heart disease — idiopathic VT (non-life threatening)

• B blockers, CCB, catheter ablation

 Torsades de Pointes
• polymorphic VT that presents as varying
amplitudes of QRS
• produced by early afterdepolarizations
(triggered activity), particularly in pt whoo
have a prolonged QT inverval
• prolonged QT interval bc electrolyte
disturbance (hypoK, hypoMg)
• persistent bradycardia
• drugs that block cardiac K currents (class
III drugs [sotalol, ibutilide, dofetilide], some
class I drugs [quinidine, procainamide,
disopyramide])
• sx: light-headedness/syncope. can
degenerate to VF
• tx: correct underlying metab abN
iv magnesium — suppress
repeated episodes
shortening QT interval — iv beta-
adrenergic stimulating agents
(isoproterenol) or artificial
pacemaker

• erythromycin, phenothiazines, haloperidol,

methadone
 Ventricular Fibrillation

• bc disordered, rapid stimulation of ventricle with no

coordinated conta