1

Cardiac Pathophysiology

Pericarditis
Often local manifestation of another
disease
May present as:
Acute pericarditis
Pericardial effusion
Constrictive pericarditis

Acute Pericarditis
Acute inflammation of the pericardium
Cause often unknown, but commonly
caused by infection, uremia, neoplasm,
myocardial infarction, surgery or trauma.
Membranes become inflamed and
roughened, and exudate may develop

$ymptoms:
$udden onset of severe chest pain that
becomes worse with respiratory
movements and with lying down.
Generally felt in the anterior chest, but
pain may radiate to the back.
May be confused initially with acute
myocardial infarction
Also report dysphagia, restlessness,
irritability, anxiety, weakness and malaise

$igns
Often present with low grade fever and
sinus tachycardia
Friction rub (sandpaper sound) may be
heard at cardiac apex and left sternal
border and is diagnostic for pericarditis
(but may be intermittent)
ECG changes reflect inflammatory
process through PR segment depression
and $% segment elevation.

%reatment
%reat symptoms
Look for underlying cause
f pericardial effusion develops, aspirate
excess fluid
Acute pericarditis is usually self-limiting,
but can progress to chronic constrictive
pericarditis

Pericardial effusion
Accumulation of fluid in the pericardial cavity
May be transudate
May be exudate
May be blood
Not clinically significant other than to indicate
underlying disorder, unless:
Pressure becomes sufficient to cause cardiac
compression cardiac tamponade

f development is slow, pericardium can

stretch
f develops quickly, even -1 ml of
fluid can cause problems
When pressure in pericardium = diastolic
pressure, get filling of right atrium,
filling of ventricles, cardiac output
circulatory collapse.
Outcome depends on how fast fluid
accumulates.
1
Clinical manifestations
!uIsus paradoxus B.P. higher during
expiration than inspiration by 1 mm Hg
Distant or muffled heart sounds
Dyspnea on exertion
Dull chest pain
Observable by x-ray or ultrasound
11
%reatment
Pericardiocentesis
%reat pain
$urgery if cause is aneurysm or trauma
1
Constrictive (chronic) pericarditis
Years ago, synonymous with %.B.
%oday, usually idiopathic, or associated
with radiation exposures, rheumatoid
arthritis, uremia, or coronary bypass graft
1
Fibrous scarring with occasional
calcification of pericardium
Causes parietal and visceral layers to
adhere
Pericardium becomes rigid, compressing
the heart C.O.
$tenosis of veins entering atria
Always develops gradually
Pathophysiology:
1
$ymptoms and $igns
Exercise intolerance
Dsypnea on exertion
Fatigue
Anorexia
1
Clinical manifestations
Weight loss
Edema and ascites
Distention of jugular vein (Kussmaul sign)
Enlargement of the liver and/or spleen
ECG shows inverted % wave and atrial
fibrillation
Can be seen on imaging
1
%reatment
Drugs and diet
Digitalis
Diuretics
$odium restriction
$urgery to remove restrictive pericardium
1
Cardiomyopathies
Disorders of the heart muscle
Most cases idiopathic
Many due to ischemic heart disease and
hypertension.
%hree categories:
Dilated ( formerly, congestive)
Hypertrophic
Restrictive
Heart loses effectiveness as a pump
1
Dilated cardiomyopathy
C.O.; thrombi Iormation ; contractility, and
mitral valve incompetence, arrhythmias Tx:
relieve symptoms oI heart Iailure, decrease
workload, and anticoagulants; transplants
1
Hypertrophic Cardiomyopathy
C.O. is normal, inflow resistance, and
mitral valve incompetence, arrhythmais
and sudden death.

Restrictive cardiomyopathy
Reduced diastolic compliance of the ventricle.
C.O. is normal or; formation of thrombi,
dilation of left atrium, and mitral valve
incompetence.
1
Disorders of the Endocardium:
Valvular dysfunction
Endocardial disorders damage heart
valves
Changes can lead to :
'aIvuIar Stenosis = too narrow
'aIvuIar Regurgitation = too leaky
(or insufficiency or incompetence)

Valves that are most often affected are the

mitral and aortic valves, but in .V. drug users
and in athletes that inject performance
enhancing drugs, > % involve only the
tricuspid valve.
Heart Murmur sound caused by turbulent
blood flow through damaged valves.

Both types of valve disorders:

Cause increased cardiac work, and
increased volumes and pressures in the
chambers.
%his leads to chamber dilation and
hypertrophy.
Chamber dilation and myocardial
hypertrophy are compensatory
mechanisms to increase the pumping
capability of the heart.
Eventually, the heart fails from overwork

Aortic $tenosis
%hree common causes:
Rheumatic heart disease -Streptococcus
infection damage by bacteria and auto-
immune response
Congenital malformation
Degeneration resulting from calcification

Blood flow obstructed from LV into aorta during

systole
Causes increased work of LV
LV dilation & hypertrophy as
compensation
prolonged contractions as
compensation
Finally heart overwhelmed
increased pressures in LA, then lungs, then
right heart
Aortic $tenosis

Clinical manifestations
Develops gradually
Decreased stroke volume
Reduced systolic blood pressure
arrowed puIse pressure
Heart rate often slow and pulse faint
Crescendo-decrescendo heart murmur
Angina, dizziness, syncope, fatigue
Can lead to dysrhythmias, myocardial
infarction, and left heart failure

Mitral $tenosis
Most common of all valve disorders
Usually the result of rheumatic fever or bacterial
endocarditis
During healing the orifice narrows, the valves
become fibrous and fused, and chordae
tendineae become shortened
Get decreased flow from LA to LV during filling
Results in hypertrophy of LA

By causing LA to become pump:

Get increased pulmonary vascular
pressures; pressures increase through LA
into lung
W pulmonary congestion
W lung tissue changes to accommodate
increased pressures
W increased pressure in pulmonary artery
W increased pressure in right heart
W right heart failure

Clinical Manifestations
Atrial enlargement can be seen on x-ray
RumbIing decrescendo diastoIic
murmur, and accentuated first heart
sound
Dyspnea
%achycardia and risk of atrial fibrillation
Other signs and symptoms are of
pulmonary congestion and right heart
failure
1
Aortic Regurgitation
Caused by acute or chronic lesion of
rheumatic fever, bacterial endocarditits,
syphilis, hypertension, connective tissue
disorder (e.g.Marfan syndrome) or
atherosclerosis

Reflux of blood from aorta to LV during

ventricular relaxation.
Causes LV to pump more blood w/ each
contraction
W LV hypertrophy
LV takes on "globular shape
W increased pressures in LA, lung, right
heart

Clinical manifestations
idened puIse pressure
Prominent carotid pulsations and
throbbing peripheral pulses
Palpitations
Fatigue
Dyspnea
Angina
High-pitched or blowing heart sound
during diastole

Mitral Regurgitation
Causes: mitral valve prolapse, rheumatic
heart disease, infective endocarditis,
connective tissue disorders, and
cardiomyopathy
Permits backflow of blood from the LV
into the LA during ventricular systole
oud pansystoIic murmur that radiates
into the back and axilla

Causes blood to flow simultaneously to

aorta and back to LA.
Both LV and LA pump harder to move
same blood twice
LV hypertrophy and dilation as
compensation
Compensation works awhile, then see C.O.
heart failure
Also LA hypertrophy
W increased pressures through lungs
pressures in right heart right heart failure
Can see edema, shock

Clinical Manifestations
Weakness and fatigue
Dyspnea
Palpitations

Mitral Valve Prolapse

Cusps of valve billow upward into the LA
during ventricular systole
Mitral regurgitation can occur
Most common valve disorder in U.$.
$tudies suggest an autosomal dominant
inheritance pattern
Many cases completely asymptomatic
Regurgitant murmur or midsystoIic cIick

Clinical manifestations
Palpitations
%achycardia
Light-headedness, syncope, fatigue,
weakness
Chest tightness, hyperventilation
Anxiety, depression, panic attacks
Atypical chest pain

Once considered to be a psychiatric malady

May have an autonomic dysfunction in which
large quantities of catecholamines are
produced.
May be a normal variant
Can see:
chorda rupture
ventricular failure
systemic emboli and sudden death
actually associated with minimal morbidity and
mortality

Management
Echocardiography for diagnosis
Related to degree of regurgitation
Antibiotics before invasive procedures
blockers to relieve syncope, severe
chest pain, or palpitations
Avoid hypovolemia
$urgical repair
1
General %reatment for Valve
disorders
Antibiotics for $trep
Anti-inflammatories for autoimmune
disorder
Analgesics for pain
Restrict physical activity
Valve replacement surgery

Heart failure
Definition When heart as a pump is
insufficient to meet the metabolic
requirements of tissues.
Acute heart failure
% survival rate
Chronic heart failure
Most common cause is ischemic heart
disease

schemic Heart Disease

Coronary Artery Disease (CAD),
myocardial ischemia and myocardial
infarction are progression of conditions
that impair the pumping ability of the heart
by depriving it of oxygen and nutrients.

Coronary Artery Disease

Any vascular disorder that narrows or
occludes the coronary arteries.
Most common cause is atherosclerosis

%he arteries that supply the heart are the first

branches off the aorta
Coronary artery disease decreases the blood
flow to the cardiac muscle.
Persistent ischemia or complete occlusion
leads to hypoxia.
Hypoxia can cause tissue death or infarction,
which is a "heart attack, which accounts for
about one third of all deaths in U.$.

Risk Factors
Hyperlipidemia
Hypertension
Diabetes mellitus
Genetic predisposition
Cigarette smoking
Obesity
$edentary life-style
Heavy alcohol consumption
Higher risk for males than premenopausal
women

Myocardial schemia
Myocardial cell metabolic demands not met
%ime frame of coronary blockage:
1 seconds following coronary block
Decreased strength of contractions
Abnormal hemodynamics
$ee a shift in metabolism, so within minutes:
Anaerobic metabolism takes over
Get build-up of lactic acid, which is toxic within
the cell
Electrolyte imbalances
Loss of contractibility

minutes after blockage

Myocytes are still viable, so
f blood flow is restored, and increased
aerobic metabolism, and cell repair,
ncreased contractility
About - minutes after blockage, if no
relief
Cardiac infarct & cell death

Clinical Manifestations
May hear extra, rapid heart sounds
ECG changes:
% wave inversion
$% segment depression

Chest Pain
First symptom of those suffering myocardial
ischemia.
Called angina pectoris (angina "pain)
Feeling of heaviness, pressure
Moderate to severe
n substernal area
Often mistaken for indigestion
May radiate to neck, jaw, left arm/ shoulder
1
Due to :
Accumulation of lactic acid in myocytes or
$tretching of myocytes
%hree types of angina pectoris:
$table, unstable and Prinzmetal

$table angina pectoris

Caused by chronic coronary obstruction
Recurrent predictable chest pain
Gradual narrowing and hardening of
vessels so that they cannot dilate in
response to increased demand of physical
exertion or emotional stress
Lasts approx. - minutes
Relieved by rest and nitrates

Prinzmetal angia pectoris

(Variant angina)
Caused by abnormal vasospasm of
normal vessels (1%) or near
atherosclerotic narrowing (%)
Occurs unpredictably and almost
exclusively at rest.
Often occurs at night during REM sleep
May result from hyperactivity of
sympathetic nervous system, increased
calcium flux in muscle or impaired
production of prostaglandin

Unstable Angina pectoris

Lasts more than minutes at rest, or
rapid worsening of a pre-existing angina
May indicate a progression to M..

$ilent schemia
%otally asymptomatic
May be due abnormality in innervation
Or due to lower level of inflammatory
cytokines

%reatment
Pharmacologically manipulate blood
pressure, heart rate, and contractility to
decrease oxygen demands
Nitrates dilate peripheral blood
vessels and
Decrease oxygen demand
ncrease oxygen supply
Relieve coronary spasm

blockers:
Block sympathetic input, so
Decrease heart rate, so
Decrease oxygen demand
Digitalis
ncreases the force of contraction
Calcium channel blockers
Antiplatelet agents (aspirin, etc.)

$urgical treatment
Angioplasty mechanical opening of
vessels
Revascularization bypass
Replace or shut around occluded
vessels

Myocardial infarction
Necrosis of cardiac myocytes
rreversible
Commonly affects left ventricle
Follows after more than minutes of
ischemia

$tructural, functional changes

Decreased contractility
Decreased LV compliance
Decreased stroke volume
Dysrhythmias
nflammatory response is severe
$carring results
$trong, but stiff; can't contract like healthy
cells
1
Clinical manifestations
$udden, severe chest pain
$imilar to pain with ischemia, but stronger
Not relieved by nitrates
Radiates to neck, jaw, shoulder, left arm
ndigestion, nausea, vomiting
Fatigue, weakness, anxiety, restlessness
and feelings of impending doom.
Abnormal heart sounds possible ($,$)

Blood test show several markers:

Leukocytosis
ncreased blood sugar
ncreased plasma enzymes
Creatine kinase
Lactic dehydrogenase
Aspartate aminotransferase (A$% or
$GO%)
Cardiac-specific troponin

ECG changes
Pronounced, persisting Q waves
$% elevation
% wave inversion

%reatment
First hours crucial
Hospitalization, bed rest
ECG monitoring for arrhythmias
Pain relief (morphine, nitroglycerin)
%hrombolytics to break down clots
Administer oxygen
Revascularization interventions: by-pass
grafts, stents or balloon angioplasty