CARDIOVASCULAR DIAGNOSIS

OVERVIEW pressure and right ventricular end-diastolic pressure.

• best estimated from the right internal jugular vein,
which has the most direct channel into the right
atrium

CHEST WALL LOCATION

• POINT OF MAXIMAL IMPULSE: locates the left

border of the heart and is normally found in the 5th
intercostal space at or just medial to the left
midclavicular line

CARDIAC EXAMINATION
BLOOD PRESSURE
• rest for at least 5 minutes in a quiet setting with feet
on the floor
• choose a correctly sized cuff
• position the patient’s unclothed arm at heart level,
o resting on a table if the patient is seated
o supported at midchest level if supine or
standing.
(higher arm levels, the blood pres- sure recordings will
be lower; at lower levels, the blood pressure recordings
will be higher.)
• Make sure the bladder of the cuff is centered over
the brachial artery.
• SYSTOLE: ventricular contraction • Inflate the cuff approximately 30 mm Hg above the
o AORTIC VALVE open, MITRAL VALVE close pressure at which the brachial or radial pulse
• DIASTOLE: ventricular relaxation disappears
• S1: Closure of mitral valve • Listen to the Korotkoff sounds
• S2: Closure of aortic valve
• Jugular venous pressure ( JVP) reflects right atrial MEASURING JVP
pressure, which in turn equals central venous
• Assess from right internal jugular vein which is 30°. First inspect the neck for carotid pulsations,
directly in line with the superior vena cava and right often visible just medial to the SCM muscles.
atrium. • Thrills: vibrations
o Deep to SCM • Never palpate both carotid arteries at the same
o Difficult to see in <12 years old time. This may decrease blood flow to the brain and
• JVP vs. Carotid pulse induce syncope.
o JVP is inward, rarely palpable, pulsations • carotid pulse is small, thready, or weak in
change with position, pressure and falls in cardiogenic shock; the pulse is bounding in aortic
inspiration regurgitation
o Carotid pulse is outward, palpable, • pulsus alternans, the rhythm of the pulse remains
pulsations unaffected by changed position, regular, but the force of the arterial pulse alternates
pressure or inspiration because of alternating strong and weak ventricular
• JVP is usually contractions. Pulsus alternans almost always
measured in indicates severe left ventricular dysfunction. It is
vertical distance usually best felt by applying light pressure on the
above the sternal radial or femoral arteries.
angle (also called • Paradoxical Pulse. This is a greater than normal drop
the angle of Louis) in systolic blood pressure during inspiration. If the
• JVP measured pulse varies in amplitude with respiration or you
at >3 cm above the suspect cardiac tamponade (because of jugular
sternal angle, or >8 venous distention, dyspnea, tachycardia, muffled
cm above the right atrium, is considered elevated or heart tones, and hypotension),
abnormal.
1. Usual starting position is at 30 deg. INSPECTION & PALPATION
o If hypovolemic: JVP is low • Left lateral decubitus: patient
o Hypervolemic: JVP is high • Right side: physician
2. Use tangential lighting and examine both sides • Identify apical impulse, heaves, thrills,
of the neck. Identify the external jugular vein on • Apical impulse: brief early pulsation of the left
each side, then find the internal jugular venous ventricle
pulsations. o Palpation of the heart begins with the patient in
3. Identify the highest point of pulsation in the the supine position at 30° and can be enhanced
right jugular vein. by placing the patient in the left lateral
decubitus position.
o The normal LV impulse is <2 cm in diameter
and moves quickly away from the fingers; it is
better appreciated at end expiration, with the
heart closer to the anterior chest wall.

AUSCULTATION
• Stethoscope:
o Diaphragm: high-
pitched sounds: S1&2
o Bell: low-pitched
sounds: S3&4

CAROTID PULSE
• assess amplitude and contour, the patient should be HEART MURMURS
supine with the head of the bed elevated to about SYSTOLIC MURMURS
• fall between S1 & S2

2
• Midsystolic= functional murmurs: decrease in blood pressure, stroke volume, and the volume of
intensity with maneuvers that reduce left ventricular blood in the left ventricle all decline.
volume, such as standing, sitting up, and straining • With squatting, vascular and volume changes occur
during the Valsalva maneuver in the opposite direction.
These maneuvers help
(1) to identify a prolapsed mitral valve
(2) to distinguish hypertrophic cardiomyopathy from
aortic stenosis.
• Valsalva maneuver involves forcible exhalation
against a closed glottis after full inspiration, causing
increased intrathoracic pressure

DIASTOLIC MURMURS
• Between S2 & S1

ECG

CONFIGURATION OF MURMURS
• Crescendo: grows louder
• Decrescendo: grows softer
• Crescendo–decrescendo murmur: First rises in
intensity, then falls.
• Plateau: same intensity throughout.

MURMUR GRADES

PREPARATION
• Skin:
o Skin oils reduce adhesion of electrode and
hinder
o penetration of electrode gel
o Dead, dried skin cells do not conduct well
MANEUVERS
o Rubbing skin with a gauze pad can reduce skin
• standing up, venous return to the heart decreases,
oil and remove some of dead skin cells
as does peripheral vascular resistance. Arterial

3
• Artifacts:
o Patient, cable Movement
o Electromagnetic interference
• If you have artifacts in:
o Leads I or II, check the patient’s RA
o Leads I or III, check the patient’s LA
o Leads II or III, check the patient’s LL

CHEST PLACEMENT

• The small P wave of atrial depolarization (duration

up to 80 milliseconds; PR interval 120 to 200
milliseconds)
• The larger QRS complex of ventricular
depolarization (up to 100 milliseconds), consisting
of one or more of the following:
o the Q wave, a downward deflection from septal
depolarization V1: fourth intercostal space to right of sternum(red lead)
o the R wave, an upward deflection from V2: fourth intercostal space to left of sternum(yellow
ventricular depolarization lead)
o the S wave, a downward deflection following an V3: directly between leads V2 and V4(green lead)
R wave V4: fifth intercostal space at left midclavicular line(put
• T wave of ventricular repolarization, or recovery this first before putting V3)
(duration relates to QRS) V5: level with V4 at left anterior axillary line
INDICATIONS: V6: level with V5 at left midaxillary line
• Determine cardiac rate, rhythm, MI, Conduction
disturbance
• Aid in diagnosis of IHD, pericarditis, electrolyte
abnormalities & pacemaker malfunction

ECG PAPER
• 1 small box= 0.1mV, 0.04s
o 1 large box (horizontal) =5 small
squares=0.2 s
o 1 large box (vertical) =5 small squares=0.5 s
o For MI with posterior involvement:
• X-axis=time • V8 – Tip of the scapula
• Y-axis= amplitude • V7 – posterior axillary line
• V9 – in between the vertebra and V8
LEAD PLACEMENTS
LIMB PLACEMENT CONTIGUOUS LEADS

4
High lateral wall – supplied by left circumflex artery
Septal and anterior wall – supplied by left anterior
descending artery
Inferior wall – supplied by right coronary artery

ECG INTERPRETATION
• Heart rate:
o 1500/small boxes
o 300/big boxes
o Check R-R interval
o Normal: 60-100
• Rhythm
• Axis
• Check for hypertrophy, ischemia, infarction

NORMAL SINUS RHYTHM

VI – negative to positive (upright deflection) • SA Node
VII – negative to positive (upright deflection) o Dominant pacemaker with an intrinsic rate
VIII – negative to positive (upright deflection) of 60 - 100 beats/minute
aVF – center going downwards (upright deflection) • AV Node
aVL – center going to the left (upright deflection) o Back-up pacemaker with an intrinsic rate of
aVR – center going to the right (the only 40 - 60 beats/minute
downwarddeflection) • Ventricular cells
o Back-up pacemaker with an intrinsic rate of
20- 45 bpm
CALCULATE FOR RATE
• 1500/ # OF SMALL SQUARES= bpm
• Atrial rate: start with P wave
• Ventricular rate: start with R wave
• For regular rate:

5
 Count the # small squares in R and subtract the
# small squares in S in Lead aVF and plot

o Bradycardic – more than 5 big squares in

between two QRS complexes
o Normal – 3-5 big squares
o Tachycardic – less than 3 big squares
• For irregular rate:
o 3 seconds strip=15 big boxes
§ Rate /min = Number of complexes x 20
o 6 seconds strip=30 boxes
§ Rate/min = number or complexes x 10

SINUS RHYTHM
SIMPLE WAY:
• There is the presence of a P wave , followed by a
QRS complex at a regular rate followed by T wave
with normal intervals and duration of segments
• A T wave should not be prolonged if you fulfill that,
that is a normal sinus rhythm.

AXIS DETERMINATION
• Which leads to check?
o Lead I (+0°)
o Lead aVF (+90°)

CHECK PQRST
• P wave Abnormalities
o Atrial Abnormalities
LEFT ATRIAL ABNORMALITIES
LEAD 1: • Prolonged P wave duration to >120 msec in lead II
Count the # small squares in R and subtract the • Prominent notching of P wave usually most obvious
#small squares in S in Lead I and plot inlead II, with interval between notches of >40 msec
(Pmitrale)
• Ratio between duration of P wave in lead II and
LEAD aVF:
durationof PR segment >1.6

6
• Increased duration and depth of terminal-negative
portion of P wave in lead V1 (P terminal force) so that
area subtended by it >0.04 mm-sec
• Leftward shift of mean P wave axis is between -30
and -45 degrees

o Conduction Abnormalities
§ Bundle Branch Blocks: leads to check:
RIGHT ATRIAL ABNORMALITIES • Lead V1 or V2
• Peaked P waves with amplitudes in lead II to >0.25 • Lead V5 or V6
Mv(P pulmonale) § Fascicular Blocks
• Prominent initial positivity in lead V1 or V2 >0.15 mV • No RIGH FASCICULAR BLOCK
• Increased area under initial positive portion of P o Leads to check: Lead V1, Lead V6, aVL/aVR
wave inlead V1 to >0.06 mm-sec • QRS-ST Abnormalities
• Rightward shift of mean P wave axis to >+75
degrees

• T wave abnormalities:
o Leads to check: Lead II and Lead V1 o Ischemic changes
• QRS Abnormalities o Electrolyte abnormalities (Potassium)
o Chamber Enlargement (LVH, RVH)

7
• Count the number of small boxes x 0.04 secs

OTHER ABNORMALITIES
PR INTERVAL:
FIRST DEGREE AV BLOCK
• PR interval is >0.20 seconds
SECOND DEGREE AV BLOCK SINUS BRADYCARDIA
Mobitz type 1 (Wenckebach) <60bpm
• Progressive lengthening of PR interval with Can be physiological in athletes (40-60) or during sleep
intermittent dropped beats Pathological causes:
• Check from the start of the P up to the start of the Q. • Hypothyroidism, anorexia, inferior wall MI, &
At first, you have a normal PR and then it prolongs Cushing reflex due to increased ICP (triad of
and you have another P and do not have the QRS bradycardia, HTN, irregular respiratory pattern)
complex.
• This is called the dropped beat.

SINUS TACHYCARDIA
>100 bpm

Mobitz type 2
ATRIAL FIBRILLATION
• Fixed PR interval with intermittent dropped beats.
• No organized atrial depolarization, so no normal P
• There is fixed PR interval. Either its prolonged or not
waves(impulses are not originating from the sinus
normally its fixed and you’ll see a P wave not
node).
followed by a QRS and then another P wave and a
• Atrial activity is chaotic
dropped beat.

ATRIAL FLUTTER
• No P waves. Instead flutter waves (note “sawtooth”
pattern) are formed at a rate of 250 - 350 bpm.
THIRD DEGREE AV BLOCK
• Complete AV block
• atrial rate is independent from the ventricular rate.
o Atrial>ventricular PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
• The heart rate suddenly speeds up, often triggered
OSBORN WAVE by aPAC (not seen here) and the P waves are lost.

VENTRICULAR TACHYCARDIA

8
• Impulse is originating in the ventricles (no P waves, CLINICAL FEATURES
wideQRS). • may be completely asymptomatic and manifest as
an ECG anomaly such as sinus bradycardia; sinus
arrest and exit block; or alternating supraventricular
tachycardia, usually atrial fibrillation, and
bradycardia.
VENTRICULAR FIBRILLATION
• develop supraven- tricular tachycardia, usually atrial
• No discernable P wave and QRS, completely
fibrillation or atrial flutter.
abnormal

ECG FINDINGS
• sinus bradycardia, sinus pauses, sinus arrest, sinus
exit block, tachycardia (in SSS), and chronotropic
STEMI incompetence.
• sinus rate of <40 beats/min in the awake state in the
absence of physical conditioning generally is
considered abnormal
• Type I second-degree SA block results from
progressive prolongation of SA node conduction
with intermittent failure of the impulses originating
in the sinus node to conduct to the surrounding
atrial tissue.
DISORDERS OF RHYTHM • Second-degree SA block appears on the ECG as an
DISORDERS OF SA NODE intermit- tent absence of P waves
ETIOLOGY: • Complete or third-degree SA block results in no P
waves on the ECG.
• Tachycardia-bradycardia syndrome is manifest as
alternating sinus bradycardia and atrial
tachyarrhythmia

TREATMENT
• Pacemaker
• Pharmacologic tx:
o Isoproterenol or atropine administered IV may
increase the sinus rate acutely
o Digitalis

DISORDERS OF AV NODE
ETIOLOGY:
AV node is subendocardial structure originating in the
transitional zone, which is composed of aggregates of
cells in the posterior-inferior right atrium.

9
 • Temporary or permanent artificial pacing is the most
reliable treatment for patients with symptomatic AV
conduction system disease.
• Correction of electrolyte derangements and
ischemia, inhibition of excessive vagal tone, and
withholding of drugs with AV nodal blocking
properties may increase the heart rate.
• Adjunctive pharmacologic treatment with atropine
or isoproterenol may be useful if the block is in the
AV node

ECG FINDINGS
• Slow conduction
• First-degree AV block (PR interval >200 ms) is a
slowing of conduc- tion through the AV junction (Fi.
The site of delay is typically in the AV node but may
be in the atria, bundle of His, or His-Purkinje system.
A wide QRS is suggestive of delay in the distal
conduction system, whereas a narrow QRS suggests
delay in the AV node proper or, less commonly, in
the bundle of His.
• second-degree AV block there is an intermittent
failure of electrical impulse conduction from atrium
to ventricle.
o Second-degree AV block is subclassified as
Mobitz type I (Wenckebach) or Mobitz type II.

TREATMENT

10
 SUPRAVENTRICULAR TACHYARRHYTHMIAS
Supraventricular tachyarrhythmias originate from or are
dependent on conduction through the atrium or
atrioventricular (AV) node to the ventricles. Most
produce narrow QRS-complex tachycardia (QRS
duration <120 ms) characteristic of ventricular activation
over the Purkinje system.

CLINICAL PRESENTATION
• CEHST PAIN, PALPITATIONS, DYSPNEA, SYNCOPE,
DIMINished exertional capacity

EVALUATION

11
 ATRIAL FIBRILLATION
• characterized by disorganized, rapid, and irregular
atrial activation with loss of atrial contraction and
with an irregular ventricular rate that is determined
by AV nodal conduction
• Risk factors:
o Age
o Underlying cardiac disease
o DM
o Obesity
Next step for tx: ADENOSINE- blocked by theophylline o Sleep apnea
and caffeine • occasionally associated with an acute precipitating
factor such as hyperthyroidism, acute alcohol
intoxication, or an acute illness such as myocardial
infarction or pulmonary embolism.
• Paroxysmal AF is defined by episodes that start
spontane- ously and stop within 7 days of onset.
Paroxysmal AF is often initiated by small reentrant or
rapidly firing foci in sleeves of atrial muscle that
extend into the pulmonary veins (PV). Catheter
ablation that isolates these foci usually abolishes
paroxysmal
• Persistent AF has a longer duration, exceeding 7
days and will continue unless cardioversion is
performed
o long- standing persistent AF (>1 year),
significant fibrosis is usually present and it is
difficult to restore and maintain sinus rhythm.
Some patients progress over years from
paroxysmal to persistent
CLINICAL FEATURES
• Rapid rates may cause hemodynamic collapse or
heart failure exacerbation
• Exercise intolerance and easy fatigability
• Syncope due to pauses when AF terminates to sinus
rhythm
• Depressed ventricular function with car-
diomyopathy may develop in response to chronic
tachycardia (rates persistently faster than 100–110
bpm)

12
TREATMENT
• Symptomatic
• New-onset AF that produces severe hypotension,
pulmonary edema, or angina should be electrically
cardioverted starting with a QRS synchronous shock
of 200 J, ideally after sedation or anesthe- sia is
achieved.
• Administration of intravenous ibutilide lowers the
energy requirement for atrial defibrillation and may
be useful if AF terminates and reinitiates, but should
not be used in patients with a prolonged QT interval
or severe LV dysfunction because of a significant risk
of torsades de Pointes
• If the duration of AF is unclear or is known to be >48
h, anticoagulation must be commenced before
cardioversion
o major source of thromboembolism and stroke
in AF is formation of thrombus in the left atrial
appendage where flow is relatively stagnant,
although thrombus occasionally forms in other
locations as well
• Acute rate control can be achieved with beta
blockers and/or the calcium channel blockers VENTRICULAR ARRHYTHMIAS
verapamil and diltiazem. Digoxin may be added, • Ventricular arrhythmias originate from a focus of
particularly in heart failure patients, if negative myocardial or Purkinje cells capable of automaticity,
inotropic and other adverse effects of beta blockers or triggered automaticity, or from reentry through
and calcium channel blockers limit their use areas of scar or a diseased Purkinje system.
• For patients who remain in AF chronically, the goal • QRS complex during ventricular arrhythmias will be
of rate control is to alleviate and prevent wide, typically >0.12 s.
deterioration of ventricular function from excessive • Types:
rates. o Premature ventricular beats (also referred to as
o β-Adrenergic blockers and calcium channel a premature ventricular contraction or PVC) are
blockers are often used in combination. single ventricular beats that fall earlier than the
Digoxin is added selectively next anticipated supraventricular beat
o Exertion-related symptoms are often an o Ventricular tachycardia (VT) is three or more
indication of inadequate rate control.. The consecutive beats at a rate faster than 100
initial goal is a resting heart rate of <80 beats/min.
beats/min that increases to <100 beats/min § VT that terminates spontaneously within
with light exertion, such as walking. 30 s is designated non-sustained
• If adequate rate control in AF is difficult to achieve o Monomorphic VT has the same QRS complex
o Consider pacemaker or catheter ablation of AV from beat to beat, indi- cating that the
junction activation sequence is the same from beat to
beat, and that each beat likely originates from
the same source
o Very rapid monomorphic VT has a sinusoidal
appearance, also called ventricular flutter,
because it is not possible to distinguish the
QRS complex from the T wave .
o slow sinusoidal VTs have a wide QRS indicative
of slowed ventricular conduction
o Hyperkalemia, toxicity from excessive effects of
drugs that block sodium channels (e.g.,

13
 flecainide, propafenone, or tricyclic o Bradyarrhythmias and negative inotrophic
antidepressants) and severe global myocardial effects are the major cardiac adverse effects.
ischemia are causes. • Calcium channel blocker such as verapamil &
o Polymorphic VT has a continually changing diltiazem
QRS morphology indicating a changing o risk of pro-arrhythmia is low, but they have
ventricular activation sequence negative inotropic and vasodilatory effects that
o Ventricular fibrillation (VF) has continuous can aggravate hypotension.
irregular activation with no discrete QRS • sodium channel blockade include mexiletine, qui-
complexes nidine, disopyramide, flecainide, and propafenone
CLINICAL FEATURES: • Sotalol and dofetilide block the delayed rectifier
• palpitations, dizziness, exercise intolerance, potassium channel IKr, thereby prolong- ing action
episodes of lightheadedness, syncope or sudden potential duration (QT interval) and the cardiac
cardiac arrest leading to sudden death refractory period, known as the Class III
• Syncope is a concerning symptom, that can be due antiarrhythmic drug effect. Sotalol also has non-
to an episode of VT that produces severe selective beta-adrenergic blocking activity
hypotension, which often indicates that there is a • Amiodarone blocks multiple cardiac ionic currents
risk for cardiac arrest and sudden death with and has sympatholytic activity. It is the most effective
arrhythmia recurrence. Although benign processes, antiarrhythmic drug for suppressing ventricular
such as reflex mediated neuro- cardiogenic arrhythmias. It is administered intravenously for life-
(vasovagal) syncope and orthostatic hypotension, threatening arrhythmias.
are the most common causes • Implantable Cardioverter Defibrillators (ICD)
• Catheter ablation
o patients with recurrent ventricular arrhythmias
associated with poor cardiac function
o endocardium: via femoral artery
o subepicardium: pericardial
puncture/pericardiocentesis
• surgery

DISORDERS OF THE HEART

HEART FAILURE
• complex clinical syndrome that results from
structural or functional impairment of ventricular
filling or ejection of blood, which in turn leads to the
cardinal clinical symptoms of dyspnea and fatigue
and signs of HF, namely edema and rales.
• Increased risk in aging, M>F
• now broadly categorized into HF with a reduced EF
(HFrEF; formerly systolic failure) or HF with a pre-
served EF (HRpEF; formerly diastolic failure).
ETIOLOGY
• Coronary Artery Disease: predominant cause
• Rheumatic heart disease remains a major cause of
HF in Africa and Asia, especially in the young.
Hypertension is an important cause of HF in the
African and African-American populations. Chagas’

TREATMENT:
• Antiarrhythmic drugs; bradyarrhythmia is a concern
• Beta blockers: first choice of therapy for most
ventricular arrhythmias

14
 disease is still a major cause of HF in South America.

MECHANISMS OF HF
HF W/ REDUCED EJECTION FRACTION
• myocyte hypertrophy
• alterations in the contractile properties of the myo-
cyte
• progressive loss of myocytes through necrosis,
apoptosis, and autophagic cell death
• β-adrenergic desensitization
• abnormal myocardial energetics and metabolism
• reorganization of the extracellular matrix with
dissolution of the organized structural collagen
PATHOGENESIS weave surrounding myocytes and subsequent
• damages the heart muscle, with a resultant loss of replacement by an interstitial collagen matrix that
functioning cardiac myocytes does not provide structural support to the myocytes.
• disrupts the ability of the myocardium to generate
force, thereby pre- venting the heart from LV REMODELING
contracting normally. • Wall thinning > dilation > wall stress
• COMPENSATORY MECHANISMS IN LV • hypoperfusion of the subendocardium, with
DYSFUNCTION: resultant worsening of LV function
o RAAS • increased oxidative stress, with the resultant
o Increased contractility activation of families of genes that are sensitive to
free radical generation (e.g., TNF and interleukin
1β)
• sustained expression of stretch activation of
hypertrophic signaling pathways.

CLINICAL FEATURES
Symptoms:
• fatigue
• SOB
• Orthopnea, which is defined as dyspnea occurring
in the recumbent position, is usually a later
manifestation of HF. Relieved by sitting in an upright
position
• PAROXYSMAL NOCTURNAL DYSPNEA (PND) :
acute episodes of severe shortness of breath and
coughing that generally occur at night and awaken

15
 the patient from sleep, usually 1–3 h after the patient COR PULMONALE
retires. PND may manifest as coughing or wheezing • Pulmonary heart disease
• Cheyne-stokes respiration: AKA periodic • altered RV structure and/or function in the context
respiration or cyclic respiration. It low cardiac output of chronic lung disease and is triggered by the
caused by an increased sensitivity of the respiratory presence of pulmonary hypertension.
center to arterial Pco2 and a lengthy circulatory Etiology
time. These changes in the arterial blood gas
content stimulate the respiratory center, resulting in
hyperventilation and hypocapnia, followed by
recurrence of apnea.
• Acute pulmonary edema
• Anorexia, nausea, and early satiety associated with
abdominal pain and fullness are common
complaints and may be related to edema of the
bowel wall and/or a congested liver.
• Cerebral symptoms such as confusion,
disorientation, and sleep and mood disturbances
• Nocturia

Signs:
• Severe HF: labored breathing
• Mild HF: DOB when lying flat
• cool peripheral extremities and cyanosis of the lips
and nail beds is also caused by excessive adrenergic
activity.
• Jugular veins @ 45 deg. Normal: <8cm
• Pulmonary crackles (rales or crepitations) result
from the transudation of fluid from the intravascular
space into the alveoli
• Pleural effusions result from the elevation of pleural
capillary pressure and the resulting transudation of
fluid into the pleural cavities. Since the pleural veins
drain into both the systemic and the pulmonary
veins, pleural effusions occur most commonly with
biventricular failure. If unilateral: right pleural space Pathophysiology
• S3: volume overload • pulmonary hypertension and increased RV afterload
• Sustained pmi sufficient to alter RV structure
• Hepatomegaly • Acute cor pulmonale occurs after a sudden and
• Peripheral edema: predominantly in ankles and severe stimulus (e.g., massive pulmonary embolus),
pretibial region. Sacral and scrotum in bedridden with RV dilatation and failure but no RV hypertrophy
patients • Chronic cor pulmonale, however, evolves slowly
• Weight loss and with compensatory RV hypertrophy that lowers
wall tension and preserves RV function
Clinical features
DIAGNOSIS
• Dyspnea
• Routine lab test
• Elevated jugular venous pressures with promi- nent
• ECG
v waves indicative of tricuspid regurgitation,
• Chest X-Ray
hepatomegaly, pul- satile liver, ascites, and
• 2D Echocardiogram
especially lower-extremity edema
• Biomarkers: b-type BNP & NT-proBNP
• Cyanosis: late finding
• Exercise testing: to assess need for cardiac
Management
transplantation in patients with advanced HF.
o Peak O2 uptake:<14ml/kg= poor prognosis

16
 CARDIOMYOPATHY

• Fish oil
• Enhanced External Counterpulsation
• Exercise
• CABG

17
 forming the shape of the narrow-necked jar
(takotsubo) used in Japan to trap octopuses

DILATED CARDIOMYOPATHY
• enlarged left ventricle with reduced systolic function
• When myocardial injury is acquired, some myocytes
may die initially, whereas others survive only to have
later programmed cell death (apoptosis), and
remaining myocytes hypertrophy in response to
increased wall stress.
Myocarditis
• Cause: infective & noninfective causes, toxic,
metabolic, inherited metabolic pathway defects
o HIV, RNA virus (enteroviruses, coxsackie virus,
echovirus, and poliovirus. Influenza), DNA virus
(adenovirus, vaccinia (small- pox vaccine), and
the herpesviruses (varicella zoster,
cytomegalovirus, Epstein-Barr virus, and
human herpesvirus 6)
o Chagas’ dse: T. cruzi
o Spirochetal myocarditis: Borrelia burgdorferi
o Granulomatous myocarditis: most common for
noninfective
o Peripartum cardiomyopathy (PPCM) develops
during the last trimester or within the first 6
months after pregnancy
o Toxic: alcohol, chemotx (Doxorubicin,
Traztuzumab), cocaine, amphetamines,
o Takotsubo Cardiomyopathy: The apical
ballooning syndrome, or stress-induced
cardiomyopathy, occurs typically in older
women after sudden intense emotional or
physical stress. The ventricle shows global
ventricular dilation with basal contraction,

18
• Dallas Criteria: lymphocytic infiltrate with evidence
of myocyte necrosis and are negative in 80–90% of
patients with clinical myocarditis.
• Patients with recent or ongoing viral syndromes
have been classified into three levels of myocarditis
diagnosis.
o Possible subclinical acute myocarditis is
diagnosed when a typical viral syndrome
occurs without cardiac symptoms, but with
elevated biomarkers of cardiac injury, ECG
suggestive of acute injury, reduced left
ventricular ejection fraction or regional wall
motion abnormality.
o Probable acute myocarditis: w/ cardiac
symptoms
o Definite myocarditis is diagnosed when there is
histologic or immunohistologic evidence of
inflammation on endomyocardial biopsy and
does not require any other laboratory or clinical
criteria.
RESTRICTIVE CARDIOMYOPATHY
• abnormal diastolic function, often with mildly
decreased contractility and ejection fraction (usually
>30–50%).

HYPERTROPHIC CARDIOMYOPATHY

19
• left ventricular hypertrophy that develops in the
absence of causative hemodynamic factors, such as
hypertension, aortic valve disease, or systemic
infiltrative or storage diseases

CARDIAC TRANSPLANTATION

Clinical Features:
• Dyspnea
• Angina pectoris
• Exertional syncope
• Thrill on carotid arteries
• Early systolic ejection
• murmur of AS is characteristically an ejection (mid)
systolic murmur that commences shortly after the
S1, increases in intensity to reach a peak toward the
middle of ejection, and ends just before aortic valve
closure. It is characteristically low-pitched, rough
and rasping in character, and loudest at the base of
the heart, most commonly in the second right
intercostal space.
Management:

VALVULAR DISEASES
AORTIC STENOSIS
• In adults is due to degenerative calcification
• Rheumatic disease AORTIC REGURGITATION
• caused by primary valve disease, aortic root disease
or their combination.
• Total stroke volume ejected is increased

20
Clinical Features myxoma, and infective endocarditis with large
• Water-hammer pulse, collapses suddenly as arterial vegetations.
pressure falls rapidly during late systole and diastole • Normally, the mitral valve orifice is 4–6 cm2.
(Corrigan’s pulse), and capillary pulsations, an Clinical features:
alternate flushing and paling of the skin at the root • Dyspnea
of the nail while pressure is applied to the tip of the • Hemoptysis: results from rupture of pulmonary-
nail (Quincke’s pulse), are characteristic of chronic bronchial venous connections secondary to
severe AR. pulmonary venous hypertension.
• booming “pistol-shot” sound can be heard over the • Recurrent pulmonary emboli
femoral arteries (Traube’s sign), and a to-and-fro • Pulmonary infections
murmur (Duroziez’s sign) is audible if the femoral • murmur is usually louder during i tion and
artery is lightly compressed with a stethoscope. diminishes during forced expiration (Carvallo’s sign)
• Severe AR: aortic valve closure is absent on • Graham Steell murmur of PR, a high-pitched,
auscultation diastolic, decrescendo blowing murmur along the
• murmur of chronic AR is typically a high-pitched, left sternal border, results from dilation of the
blowing, decrescendo diastolic murmur, heard best pulmonary valve ring and occurs in patients with
in the third intercostal space along the left sternal mitral valve disease and severe pulmonary
border hypertension.
o Austin Flint murmur, a soft, low-pitched, MITRAL REGURGITATION
rumbling mid-to-late diastolic murmur. Etiology:
o However, when the murmur is louder along the
right sternal border, it suggests that the AR is
caused by aneurysmal dilation of the aortic root
Management

MITRAL STENOSIS
• Rheumatic fever is the leading cause of mitral PERICARDIAL DISEASES
stenosis (MS) Normal pericardium: double-layered; contains 15-20 ml
o iffuse thickening of the valve leaflets with ultrafiltrate of plasma
formation of fibrous tissue ACUTE PERICARDITIS
• Other less common etiologies of obstruction to left Diagnostic features
ventricular inflow include congenital mitral valve • Chest pain
stenosis, cor triatriatum, mitral annular calcification • Pericardial friction rub
with extension onto the leaflets, systemic lupus • ECG findings
erythematosus, rheumatoid arthritis, left atrial o Stage 1: ST segment elevation
o Stage 2: ST segemnts return to normal

21
 o Stage 3: T waves become inverted • colchicine (0.5 mg qd [<70 kg] or 0.5 mg bid [>70
o Stage 4: ECG returns to normal kg]), should be administered for 3 months.
• Pericardial effusion Colchicine enhances the response to NSAIDs and
also aids in reducing the risk of recurrent
pericarditis. (CI in hepatic/ renal dysfunction)
• Glucocorticoids (e.g., prednisone 1 mg/kg per day)
usually suppress the clinical manifestations of acute
pericarditis in patients who have failed therapy with
or do not tolerate NSAIDs and colchicine. (Should
only be given 2-4 days)
Cardiac tamponade
• Beck’s triad
o Hypotension
o soft or absent heart sounds
o jugular venous distention with a prominent
x (early systolic) descent but an absent y
(early diastolic) descent.
• Quantity of fluid needed to produce cardiac
tamponade is 200 ml.
• Paradoxical pulse: greater than normal (10 mmHg)
inspiratory decline in systolic arterial pressure
• Treatment: pericardiocentesis

Myocardial Infarction
Deep venous thormbosis & pulmonary
thromboembolism

Diagnosis: Echocardiography
Treatment:
• Bed rest
• anti-inflammatory treatment with aspirin (2–4 g/d),
with nonsteroidal anti-inflammatory drugs (NSAIDs),
such as ibuprofen (600–800 mg tid) or indomethacin
(25–50 mg tid), and should be administered along
with gastric protection (e.g., omeprazole 20 mg/d).

22