OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY

Exam # 3 | Dr. Antonio Dans | October 10, 2012
OUTLINE
I.
Anatomic
Categories
of III.
Cardiovascular Disease
A.
Prototypes of Diseases
B.
Risk Factors
II.
Disorders
of
Conduction
System
A.
Early Beats
B.
Tachycardias
IV.
C.
Pauses
D. Bradycardias

E.
Dysrhythmias
Congenital Heart Diseaes
A.
Atrial Septal Defect
B.
Ventricular Septal Defect
C.
Patent Ductus Arteriosus
D. Transposition
of
the
Great Arteries
E.
Tetralogy of Fallot
Peripheral Vascular Diseases

I summarized all your lectures into 4 tables. Dr. Dans

I. ANATOMIC CATEGORIES OF CV DISEASE

A. PROTOTYPES OF DISEASES
Note: Sir tackled the anatomical diseases by layers, emphasizing prototype diseases to facilitate better understanding and easier
recall.
Table 1: Anatomic Categories of CV Diseases
Endocardial
Myocardia
Pericardia
Disease
l Disease
l Disease
Prototy
RHD (when
IHD (most
Constrictive
pe
chronic) because common;
Pericarditis
it affects the
rare:
(CP)(rare:
valves.
myocardial
pericardial
Other variation:
cardiomyopat
malignancy
IE (when acute)
hies due to
to
alcoholism
pericardium,
and
tamponade)
pregnancy)
*others: IDC,
RCM
Early
Easy Fatigue;
Angina
Pleuritic
Sympto
SOBOE
Chest Pain
ms
(shortness of
breath on
exertion) (MS)
Late
Worsening
Acute MI or
Edema
Sympto
SOBOE
Unstable
(failure to
ms
->RVF (edema/
Angina
fill), RVF,
anasarca)
Pectoris CHF
usually no
SOBOE unless
lesion is
exclusive at
the RV
Main
Vasodilate or
Rx (need
Surgery
Rx
decrease HR
statins even
(removal of
(MS); repair or
if cholesterol
the
replace valve
is normal;
pericardium
(AS)
ACE-I even if
which is a
BP is normal)
dispensable
PTC
layer)
Angiogram,
CABG
Preventi
Rheumatic Fever
Risk factor
TB Control
on
prophylaxis
control (HPN,
(penicillin
DM, smoking,
injections, esp
high
for high risk); IE
cholesterol,
Prophylaxis
obesity, lack
(undergo
of exercise,
surgery with
unhealthy
high possibility
diet, stress)
of bacteremia)

Review for differentiating etiologies of edema: Cardiac ascending; Renal descending; Hepatic stomach
(centrifugal)-> ascending then descending.

ENDOCARDIAL DIASEASE: RHEUMATIC HEART

DISEASE
Patient: G.G., 24/F, consulted for dyspnea
Shortness of breath on exertion (SOBOE)
Ascending edema
3-pillow orthopnea
Paroxysmal nocturnal dyspnea (PND)
Cardiac cachexia
Social and financial costs

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Notes:
Symptoms initially stopped her from sports, later
from climbing stairs, later from even going to
school
Highly intelligent. Quit school at 2nd year, although
she really wants to study.
Wants to become a nurse one day so she can help
her sibs through school
Deathly afraid of dying, so she doesnt work
Cant afford surgery (400 thou), and she cant
afford PTMC (350 thou) - even as a charity patient
Lost weight in the past year, partly from the
disease, partly from depression

She is literally dying before our eyes

Plain Radiography
Fig.1. Normal heart.
Heart shows no signs of
enlargement and observable
abnormalities in the aorta and
the pulmonary artery; with
unremarkable pulmonary
vascular markings

Fig. 2. Pathologic heart

common in mitral stenosis
(MS).
There is enlargement of the
heart, straightening of the left
border of the cardiac
silhouette and a rounded
apex. Apex forms right angle
with diaphragm, which is
indicative of RVH. (Note: A
cardiophrenic angle >90
forming a rounded apical edge
indicates RVH while an angle
>90 indicates LVH). Increased
vascular markings are also
observable. The LA is enlarged
while the LV is underloaded.

Electrocardiogram

Fig.3. ECG tracings of a normal heart. Normal sinus rhythm; neither hypertrophy nor axis deviation may be observed; no
ischemia nor infarction.

Fig. 4. ECG Tracings of the RHD patient. There is normal sinus rhythm and rate. There is an observable increase in the height of
the P-wave indicating the presence of RA overload. There is no axis deviation however the tall R waves in lead V1 indicate RV
hypertrophy.

2-D Echocardiography
Main Finding: Mitral valve stenosis (most common lesion in RHD)
The anterior leaflet elbows out before diastolic filling (manifests as the diastolic Opening Snap upon auscultation)
Observable blood sludging. Latrine of blood may be visible which is about to form a thrombus, blood swirls in the LA
causing LAE.
Table 2. Murmurs of Prototype Lesions of Endocardial Diseases
STENOSIS Failure to
INSUFFICIENCY
Open
Failure to close
MITRAL VALVE
Location
Apex

Apex

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Timing
Quality

Diastolic
LUB-DUB-Brrr
(Diastolic rumble);
opening snap because
of elbowing of MV

Systolic
ZHHHHH-DUB
(Holosystolic murmur)
*S2 disappears in
severe cases

Effect

Exertional dyspnea
(Hinihingal kapag
napagod)
Caused by the LVs
inability to fill, leading
to pulmonary
congestion
Reduce HR to prolong
diastolic filling time
Beta-blocker;
digitalis (fibrillation)

Easy fatigability
(Latang-lata)
Caused by poor
forward flow, due to
regurgitation

Treatment

AORTIC VALVE
Location
Base
Timing
Systolic
Quality
ssSSHHhh-DUB
(Systolic Ejection)
Diamond-shaped
murmur
Effect

Treatment

Easy fatigability
Caused by poor
forward flow.
If severe/longstanding, may cause
syncope.
No medical treatment
(worst lesion)
Surgery if severe
Vasodilators are
contraindicated; will
cause hypotension.
DONT inc HR, Px
might faint

Vasodilators

Base
Diastolic
LUB-dhuu
(Diastolic blow-softest
murmur)
High pitch
Easy fatigability
Caused by poor
forward flow

Vasodilators (Ca
Blockers; ACE
inhibitors)

*Main determinants: location and timing (phase of murmur)

Clinical Pearl: In the end, as the disease progresses, they all present with dyspnea, so its important to find out the
order the symptoms came about.

MYOCARDIAL DIASEASE: ISCHEMIC HEART

DISEASE
Patient: E.H., 70/M consulted for chest discomfort
Chest discomfort upon exertion, relieved by rest; tighten rather than pain
Quit work because of illness
Recent widower, lives alone, worries about his health
Walk-through phenomenon slowing down makes the chest pain go away
Just came back recently because he couldnt afford med
Stopped follow-up and his meds
Came back with acute MI
Developed heart failure and no needs more meds
Clinical Pearl: It is important to probe if pain is really felt during exertion. Px could misunderstand and report pain upon
exertion although pain was felt in the afternoon at rest after a particularly taxing day at work.
Plain Radiography

Fig.5. Left Ventricular Enlargement. Cardiac apex is infero-laterally displaced. Edge of cardiac border meets diaphragm in an
acute angle, indicative of LVE. Ration of cardiac shadow to thoracic diameter >0.5

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Electrocardiogram

Fig.6. ECG tracings of myocardial infarction. Note ST-depressions in the lateral wall (V4-V6)-ischemia; ST-elevations in (V1-V3)-MI

2-D Echocardiography
Findings: A heart contracting more weakly than a normal heart. LV is seen to be larger than normal (LV enlargement is
actually an adaptive Modification). Given the same % Ejection Fraction, a larger ventricular volume results to more
blood pumped.
Review of IHD Pathogenesis
1. Normal
2. Early Streak (early 20s)
3. Asymptomatic Plaque (30-40s)
4. Significant Obstruction (with pain) - angina
5. Acute thrombus formation (partial or complete obstruction)
6. Reorganization
7. Chronic Obstruction syndrome (heart failure symptoms, myocardial weakness)

Fig.7. IHD Pathogenesis

Notes:
In significant obstruction, there is stable
angina (pain during exertion)
In acute thrombus formation, acute MI may
occur
In reorganization, there is unstable angina
Common Sx
Angi
na

Chronic
recurrent mild
chest pain

Acut
e MI

Acute severe
chest pain

CHF

SOBOE,
orthopnea PND,
RVF

Table 3. Comparison of Common (Prototype) Syndromes:

Angina, Acute MI and CHF
Confirmati
Surgical
on
Intervention
(e.g. bypass) if:
Clinical
-Sx are severe
(stress test
-Stress test (with
to confirm if
triple vessel
mild or
disease)
severe)
-Angiogram
-Patients who
dont respond to
medical treatment
Enzymes (T,
Residual Sx Stress
CKMB), ECG,
test
pain
2-D Echo
Check for angina

Table 4. Medications for Angina, Acute MI and CHF

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012

Angina

Acute
MI

Medications

Sx

Beta
blockers>Nitrates>Calciu
m channel blockers
ASA
Statins
ACE/ARB
PCI> Fibrinolytic
LMWH (low molecular weight
heparin)

MR

Recu
r
-

+
+
+

+
+
+

+
+
+

+
+
+
+
+
+
-

+
+
+
+
+
-

AS+Clopidogrel
Statins
*BB
ACE/ARB
Nitrates (control acute pain)
CHF
ASA
+
+
Statins
+
+
BB
+
+
+
ACE
+
+
+
Digitalis
+
Diuretics
+
+
Heading: Sx (symptoms), recurrence of events, MR
(mortality)
*BB-use with caution. Studies show they may reduce
mortality by allowing receptors to regenerate. Relieve pain,
prevent re-infarction, lower mortality rate
Ex. ASA(aspirin) cannot relieve the symptoms of agina but is
used to prevent recurrence of events and mortality

PERICARDIAL DIASEASE: CONSTRICTIVE

PERICARDITIS
2D-Echocardiography
LVH; echo free space has constant diameter, indicating that it is thickened pericardium (vs. non-constant diameter if it
contains fluid)

B. RISK FACTORS
Sir did not discuss this.

THE BIG 9 (now 10) RISK FACTORS FOR CVD ND

CAD (with RR)
1. Smoking 4.79
6. Fruits and vegetables
0.70
2. Dyslipidemia 2.90 7. Alcohol 0.79
3. Hypertension 2.60 8. Exercise 0.72
4. Diabetes 2.40
9. Stress-free 0.77
5. Obesity 2.30
10. Education attainment &
Table 5. Risk Factors and Relative Risks for CV Diseases

Risk Factors

RR for Stroke

RR for CAD

Deaths in 2004

DM= 4.6%
4.0
2.4
4,148
Chol= 8.5%
1.8
2.9
5,730
Obes= 12/55 %
2.3
8,046
HPN
4.4
2.6
14,015
Smoking=35%
4.8
4.7
28,694
Smoking is most common RF in men and most common overall
Obesity is most common RF in women (55% F vs. 12% M)
Waist-Hip Ratio: better indicator of obesity than BMI because it is the ratio of adiposity to bone and not of weight to
height
Waist-between lowest rib and hip; measure of central adiposity, hardly any muscle and bone Hip-level of ASIS; bone
density Normal values: F </= 0.85 M </= 1.0
Psychosocial stress - 3 forms (Financial, work, home)
Absence of psychosocial stress: RR= 0.77 Social connectedness: RR=0.55 [FRIENDS!]

II. DISORDERS OF THE CONDUCTION

SYSTEM
Earl
y
Bea
t
SA
Nod
e

Ectopic
Rhythms

Tachy
cardia
s
Sinus
Tach

Pauses

Sinus
Pause
Sinus

Table 6. Disorders of the Conduction System

Brady
Dysrh
cardias
ythmi
as
Sinus
Brad

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Arrest
SA Exit
Block
Atri
a

PA
Cs
W

Atrial
Rhythm

AV
Nod
e

PN
Cs

Nodal
Rhythm

Ven
tricl
es
*AP
s

PV
Cs

Ventricul
ar
Rhythm

A
Tach
A Flut
A Fib
AVNR
T
AVRT,
SVT

2nd Deg
AVB-I
2nd Deg
AVB-II
(Mob I and
II)

V
Tach
V Fib

3rd Deg
AVB

1st
Deg
AVB

LBBB
RBBB
WPW
LGL

*AP- Accessory pathway

Disorders of impulse formation: abnormal automaticity are italicized, normal automaticity(sinus tachy, sinus brady)
Disorders of impulse conduction: Re-entry are color red, Blocks
Ventricular tachycardia can be both due to a block or a re-entry

A. PREMATURE BEATS
PREMATURE VENTRICULAR CONTRACTIONS
(PVCs)
Wide, bizarre QRS complex, with the absence of preceding P wave
Trigeminy VPC follows 2 sinus beats
Bigeminy VPC follows ever sinus beat
Couplet VPCs occur successively

PREMATURE ATRIAL CONTRACTIONS (PACs)

Abnormally shaped P wave because the beat initiates outside the SA node

PREMATURE NODAL CONTRACTIONS (PNCs)

Occurs when AV node fires before receiving the signal from SA node
Absent P wave, wimpy QRS complex and normal T wave

What is this?

Premature atrial contraction. P wave is hidden in the abnormal T-wave.

B. TACHYCARDIAS
SINUS TACHYCARDIA
RR interval is less than 3 big squares
Presence of P waves indicates presence of sinus rhythm
QRS is not widened

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012

ATRIAL TACHYCARDIA
P waves come one after the other
Very regular rhythm with rates from 140-220 bpm

ATRIAL FLUTTER
Caused by a reentrant rhythm in either left of right atrium
Differences in the refractory periods of the different sections in the atrial tissue create electrical activity that moves in
a localized self-perpetuating loop
Presence of classic saw-tooth appearance
Atrial rate usually between 250-350 bpm
Ventricular rate is half of atrial rate

ATRIAL FIBRILLATION
Most common cardiac arrhythmia involving both atria of the heart
Uncoordinated, irregular rhythm with poorly defined P wavs
Associated with irregular ventricular rhythm
P waves replace irregular baselines

SUPRAVENTRICULAR TACHYCARDIA (AVNRT)

Conventionally refers to AV Nodal Reentrant Tachycardia

Rapid rhythm of the heart in the accessory pathway
P wav is present after each QRS complex
Retrograde P wave may be absent, buried in the QRS complex or may appear as distortions of the terminal and/or
initial parts of the QRS complexes

VENTRICULAR TACHYCARDIA
Tachycardia with wide QRS complexes
Every beat is a PVC
May lead to ventricular fibrillation
Potentially life threatening

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
VENTRICULAR FIBRILLATION
Polymorphic QRS complexes due to very rapid rate
Uncoordinated, haphazard ventricular contractions
LIFE THREATENING = RESUSCITATE STAT!

C. PAUSES
SINUS PAUSE
Presence of pause before the next PQRST wave
Length of pause is not a multiple of the prior RR interval

SA EXIT BLOCK
Length of pause is exactly the same measure of the previous PQRST wave: actual skipping
Distance between the start and the end of the pause in in exact multiples of the prior interval

2ND DEGREE AV BLOCK (MOBITZ TYPE I,

WENKEBACH)
Exaggerated PR prolongation followed by a drop beat that has no QRS component
Reflects the failure of atrial impulses to reach the ventricles
PR interval is not constant
Considered as a benign condition
(A TIRED AV node!!)

2ND DEGREE AV BLOCK (MOBITZ TYPE II)

Absence of PR prolongation
The drop beat occurs unexpectedly
PR interval is constant
Malignant; needs prompt intervention
(A LAZY AV node!!)

D. BRADYCARDIAS
SINUS BRADYCARDIA
RR interval is greater than 5 big squares
P waves are present

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
3RD DEGREE AV BLOCK
No atrial impulse propagates to the ventricles
SA node controls the atrium, AV node controls the ventricles
QRS occurs independent of the P wave

E. DYSRHYTHMIAS
1ST DEGREE AV BLOCK
Prolonged AV conduction with wide QRS complex
Marked PR interval prolongation (>0.20 seconds)

BUNDLE BRANCH BLOCK

QRS complex duration is greater than 120 ms
RBBB causes prolongation of the last part of the QRS complex
o May shift the hearts electrical axis slightly to the right
LBBB widens the entire WRS complex (image below)
o Shifts the hearts electrical axis to the left most of the time

WOLFF-PARKINSON-WHITE SYNDROME
Shortened PR interval
Presence of Delta waves: slurred QRS upstroke
Wide QRS complex with initial decrease in depth of upstroke

LOWN-GANONG-LEVINE SYNDROME

Similar characteristics with WPW

Absence of Delta waves

III. CONGENITAL HEART DISEASE

Can be grouped largely into cyanotic and acyanotic presentations
ACYANOTIC
Shunts: PDA, VSD, ASD
Stenosis: PS, TS, AS, MS, Coarctation of the Aorta
CYANOTIC
Eisenmengerization (presents later in life)
Complex anomalies (present at birth): TGA, TOF, TAPVR

A. ATRIAL SEPTAL DEFECT

Certain insults (e.g. atherosclerosis) -> Pulmonary congestion/hypertension -> RV Overload -> RVH ->
Eisenmengerization complex

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Absence of murmur due to low interatrial pressure differences
Pulmonary congestion and increased pulmonary flow results in
P2 (fixed splitting)
Shunting occurs in diastole

(1) systolic ejection murmur and (2) delayed and loud

B. VENTRICULAR SEPTAL DEFECT

Initial RL shunt
All shunted blood goes back to LV, resulting in LVH
Loud holosystolic murmur (the smaller the VSD, the more turbulent the movement, the louder the murmur)
Predisposes patient to atherosclerosis and pulmonary HPN
Shunting occurs in systole

C. PATENT DUCTUS ARTERIOSUS

Initial LR shunt
Shunting occurs first in diastole then systole
Continuous machinery-like murmur, due to gradient present in both systole and diastole
LV overload
Classic pulmonary hypertension presentation
May present with cyanosis, usually in legs
If shunt is before the subclavian artery -> diffused cyanosis
If after subclavian artery > differential cyanosis, only on the toes

D. TRANSPOSITION OF THE GREAT

ARTERIES

Fatal unless septal defect is present to provide the necessary mixing of oxygenated and deoxygenated blood

E. TETRALOGY OF FALLOT

Comprised of VSD, Aortic Overriding, PS and RVH

RL shunt

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012
Aorta sits on top of the defect and automatically collects blood from the R chamber

IV. PERIPHERAL VASCULAR DISEASES

Table 5. Summary for Peripheral Vascular Diseases

ARTERIA
L

ACUTE
Arterial Embolism

CHRONIC
Chronic Arterial
Occlusion
Atherosclerosis
Chronic Pain*
Aspirin, clopidogrel

Cardio-embolism
Acute Pain
Heparin then
warfarin**
VENOUS
Deep Vein
Chronic Venous
Thrombosis
Insufficiency
In-Situ embolism
Varicose Veins
Acute Swelling
Chronic Swelling
Heparin then
Compression
warfarin**
Stockings
* A.K.A Intermittent Claudication; ** Taken for 6mo if uncomplicated
If taking acute PVD meds, check for prothrombin time (PT) monthly

SAMPLE CASES
Case 1
63/M with bilateral leg edema
5 years PTA;
excellent exercise capacity;
(-) exertional dyspnea or
chronic cough;
(+) edema and
hyperpigmentation of legs
Dx: Chronic venous
insufficiency
Tx: Compression stockings

Case 2
58/F with painful toe 3 hours
PTA;
(+) occasional palpitations, no
other Sx;
(+) irregularly irregular HR
(+) gangrenous toe
Dx: Acute arterial
embolism
Tx: Anticoagulants

Case 3
53/F with severe back pain
after a
vehicular accident 1 week
PTA;
Underwent spinal surgery 3
days ago
was doing well until today;
Developed sudden right lower
extremity pain and swelling
Dx: Deep vein thrombosis
Tx: Anticoagulants

Case 4
53/F with calf pain during her
morning walks since almost a
year ago;
pain used to occur after 30
minutes of walking and
whould be relieved by rest; in
the past month, pain has
been bothering the patient
after just 10 minutes; pain
has been occurring more
frequently
Dx: Chronic artertial
occlusion -> intermittent
claudication
Tx: Antiplatelets

CLASSROOM LEARNING
Books, Read, Memorize,
Few Years, IQ, Boring

THE MOST IMPORTANT TABLE AMONG TABLES

CLINICAL LEARNING
Peoples Lives, Empathize,
Remember, Lifelong, EQ, Fun

END OF TRANSCRIPTION

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UPCM 2016: XVI, Walang

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OS 213: Circulation and Respiration

LEC 36: CVS COURSE SUMMARY
Exam # 3 | Dr. Antonio Dans | October 10, 2012

Leandro Baldemor, Anne Curtis, Kristina Aquino

UPCM 2016: XVI, Walang

Kapantay!

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