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Cardiac Pathology
Heart Failure, Ischemic
Heart Disease and more
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart II
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart Failure
• Ischemic Heart Disease
• Hypertensive Heart Disease
• Congenital Heart Disease
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart Failure
Heart failure
Definition
It is the pathophysiological process in which
the heart as a pump is unable to meet
the metabolic requirements of the tissue for
oxygen and substrates despite venous
return to the heart being normal or increased
Factors effecting
heart pump
effectiveness
Preload
• Preload can be defined as the initial
stretching of the cardiac myocytes prior to
contraction.
• Preload, therefore, is related to the sarcomere
length.
• Preload is also related to the volume of blood
in ventricles at the end of diastole
– Depends on venous return
– Depends on compliance
Afterload
• Force needed to eject blood into circulation
• Arterial B/P, pulmonary artery pressure
• Valvular disease increases afterload
Heart Failure
• End point of many heart diseases
• Common!
• 5 million affected each year
• 300,000 fatalities
• Heart can’t pump blood fast enough to meet
the needs of the body
– The heart can’t fill with enough blood or
– The heart doesn’t have enough force
Heart Failure
• System responds to failure by
• Releasing hormones (e.g., norepinephrine)
• Frank-Starling mechanism
• Hypertrophy
• Initially, this works
• Eventually, it doesn’t
• Myocytes degenerate
• Heart needs more oxygen
• Myocardium becomes vulnerable to ischemia
Heart Failure
• Heart failure develops over time
– Can affect right side of heart or both sides
• Right-side heart failure occurs if the heart
can't pump enough blood to the lungs to pick
up oxygen.
• Left-side heart failure occurs if the heart can't
pump enough blood to the rest of the body.
• Also known as Congestive Heart Failure
Heart Failure
(AKA-congestive heart failure)
• Pathophysiology
– Cardiac compensatory mechanisms
• Tachycardia
• Ventricular dilation-Starling’s law
• Myocardial hypertrophy
– Hypoxia leads to decreased contractility
R
L
cyanosis
pulmonary edema
hepatomegaly
Clinical
consequences
of left and
right heart
failure
peripheral edema
splenomegaly
ascites
Left Heart Failure
• Left ventricle fails; blood backs up in lungs
• Most Common Causes
• Ischemic heart disease (IHD)
• Systemic hypertension
• Mitral or aortic valve disease
• Primary heart diseases
• Heart changes
• LV hypertrophy, dilation
• LA may be enlarged too (risk of atrial fibrillation)
Left Heart Failure
• Dyspnea (shortness of breath)
• Orthopnea, paroxysmal nocturnal dyspnea
too
• Enlarged heart, increased heart rate, fine rales
at lung bases
• Later: mitral regurgitation, systolic murmur
• If atrium is big, “irregularly irregular”
heartbeat
Right Heart Failure
• Right-side heart failure may cause fluid to
build up in the feet, ankles, legs, liver,
abdomen, and the veins in the neck.
• Right-side and left-side heart failure also may
cause shortness of breath and fatigue
• Leading cause of heart failure is due to
diseases that damage the heart
– Diabetes
– High blood pressure
– Coronary heart disease
Right Heart Failure
• Right ventricle fails; blood backs up in body
• Most Common Causes
• Left heart failure
• Lung disease (“cor pulmonale”)
• Failure of the right side of the heart brought on by long-term
high blood pressure in the pulmonary arteries and right ventricle
of the heart
• Caused by long term hypoxia, ie. chronic bronchitis or obesity
• Some congenital heart diseases
• Heart changes
• Right ventricular hypertrophy, dilation
• Right atrial enlargement
Right Heart Failure
• Peripheral edema
• Big, congested liver (“nutmeg liver”)
• Big spleen
• Most chronic cases of heart failure are
bilateral
Cause
What is it?
How does it cause right
sided heart failure?
Left-sided heart failure
The left ventricle does not
pump blood efficiently, leading
to pressure building behind the
left side of the heart that
eventually causes the right side
of the heart to fail.
Blood backs up behind the left
ventricle into the left atrium, in
the lungs, and then eventually
into the right ventricle, which
also eventually fails, allowing
blood to then back up farther
into the extremities, the liver,
and the other organs.
Chronic lung disease
Includes emphysema,
pulmonary embolism, and other
causes of pulmonary
hypertension
High blood pressure in the
pulmonary arteries increases
the workload of the right
ventricle, eventually causing
the right ventricle to fail.
Coronary artery disease
Blockage of the arteries that
supply blood to your heart
CAD can cause left-sided heart
failure leading to right-sided
heart failure or can directly
cause right-sided heart failure
by blocking blood supply to the
right ventricle.
Pulmonic Stenosis
Narrowing of the pulmonic
valve that limits blood flow out
of the right ventricle
Increases the work of the right
ventricle; similar to chronic lung
disease
Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function
of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc.
pressure or volume overload as in Heart failure
American Heart Assn-Media files Animations
Hepatic blood flow
“Nutmeg” liver
Nutmeg
Symptoms
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart Failure
• Ischemic Heart Disease
• Hypertensive Heart Disease
• Congenital Heart Disease
Ischemic Heart Disease
• Myocardial perfusion can’t meet demand
• Usually caused by decreased coronary
artery blood flow (“coronary artery
disease”)
• Four syndromes:
• angina pectoris
• acute MI
• chronic IHD
• sudden cardiac death
• http://www.youtube.com/watch?v=2
2bDs8teiZA
Angina Pectoris
• Intermittent chest pain caused by
transient, reversible ischemia
• Typical (stable) angina
• pain on exertion
• fixed narrowing of coronary artery
• Prinzmetal (variant) angina
• pain at rest
• coronary artery spasm of unknown
etiology
• Unstable (pre-infarction) angina
• increasing pain with less exertion
• plaque disruption and thrombosis
Myocardial Infarction
• Necrosis of heart muscle caused by ischemia
• 1.5 million people have MIs each year
• Most due to acute coronary artery thrombosis
• sudden plaque disruption
• platelets adhere
• coagulation cascade activated
• thrombus occludes lumen within minutes
• irreversible injury/cell death in 20-40
minutes
• Prompt reperfusion can salvage myocardium
• https://www.youtube.com/watch?v=zeS0au8ij4
Morphologic Changes in Myocardial Infarction
Time
Gross changes
Microscopic changes
0-4h
None
None
4-12h
Mottling
Coagulation necrosis
12-24h Mottling
More coagulation necrosis;
neutrophils come in
1-7 d
Yellow infarct center
Neutrophils die, macrophages
come to eat dead cells
1-2 w
Yellow center, red borders Granulation tissue
2-8 w
Scar
Collagen
Acute Myocardial Infarction
MI: day 1, day 3, day 7
Myocardial Infarction
• Clinical features
• Severe, crushing chest pain ± radiation
• Not relieved by nitroglycerin, rest
• Sweating, nausea, dyspnea
• Sometimes no symptoms
• Laboratory evaluation
• Troponins increase within 2-4 hours
and remains elevated for a week.
• CK/MB increases within 2-4 hours,
returns to normal within 72 hours.
Myocardial Infarction
• Complications
• Contractile dysfunction
• Arrhythmias
• Rupture of muscle
• Chronic progressive heart failure
• Prognosis
• Depends on remaining function and
perfusion
• Overall 1 year mortality: 30%
• 3-4% mortality per year thereafter
Rupture of papillary muscle after MI
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart Failure
• Congenital Heart Disease
• Ischemic Heart Disease
• Hypertensive Heart Disease
Hypertensive Heart Disease
• Can affect either L or R ventricle
• Cor pulmonale is RV enlargement due to
pulmonary hypertension caused by
primary lung disorders
• Result: myocyte hypertrophy
• Reasons for heart failure in hypertension
are poorly understood
Left ventricular hypertrophy (L) and cor pulmonale (R)
Drugs
• Chronotropic
– Alters heart rate
• Ionotropic
– Alters myocardial contractility
– Digitalis is a positive ionotropic drug
• Diuretics
– Loop – reduces sodium reabsorption
– Thiazide – increases sodium loss , water loss
• ACE Inhibitors
• Nitrates
– Induces NO release by vessels = vasodilation
Cardiac Pathology Outline
• Blood Vessels
• Heart I
• Heart Failure
• Ischemic Heart Disease
• Hypertensive Heart Disease
• Congenital Heart Disease
Congenital Heart Disease
• Abnormalities of heart/great vessels present
from birth
• Faulty embryogenesis, weeks 3-8
• Broad spectrum of severity
• Cause unknown in 90% of cases
Congenital Heart Disease
• Left-to-right shunts
• atrial septal defects
• ventricular septal defects
• Patent ductus arteriosus
• Right-to-left shunts
• tetralogy of fallot
• transposition of the great
arteries
• Obstructions
• aortic coarctation
Atrial Septal Defects
• Initially, left-to-right shunt (asymptomatic)
• Eventually, pulmonary vessels may become
constricted (“pulmonary hypertension”),
leading to right-to-left shunt
(“Eisenmenger syndrome”)
• Surgical repair prevents irreversible
pulmonary changes and heart failure
Ventricular Septal Defects
• Most common congenital cardiac anomaly
• Most close spontaneously in childhood
• Small VSD: asymptomatic
• Large VSD: big left-to-right shunt, may
become right-to-left
Patent Ductus Arteriosus
• Ductus: allows flow from PA to aorta
• Closes spontaneously by day 1-2 of life
• Small PDA: asymptomatic
• Large PDA: shunt becomes right-to-left
PDA
Tetralogy of Fallot
• Most common cause of cyanotic
congenital heart disease
• Four features:
• VSD- ventricular septal defect
• obstruction to RV outflow tract
• overriding aorta
• RV hypertrophy
• Cyanosis, erythrocytosis, clubbing of
fingertips, paradoxical emboli
• http://www.cincinnatichildrens.org/health
/t/tof/
Clubbing of fingertips
Normal (L) and clubbed (R) fingertips
Transposition of Great Arteries
• Aorta arises from R ventricle; pulmonary
artery arises from L ventricle
• Outcome: separation of systemic and
pulmonary circulations
• Incompatible with life unless there is a big
shunt (VSD)
• http://www.cincinnatichildrens.org/health
/t/transposition/
Aortic Coarctation
• Coarctation = narrowing
“Infantile” (preductal) and “adult”
(postductal) forms
• Cyanosis and/or low blood pressure in
lower extremities
• Severity depends on degree of coarctation
•
Coarctation of the aorta
The End
Essential functions of the heart are secured
by integration of electrical and mechanical
functions of the heart
Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)
- changes of the heart rate
- changes of stroke volume
• Control of HR:
- autonomic nervous system
- hormonal (humoral) control
• Control of SV: - preload
- contractility
- afterload
Adaptive mechanisms of the heart to increased load
• Frank
- Starling mechanism
• Ventricular
hypertrophy
– increased mass of contractile elements  strength
of contraction
• Increased
sympathetic adrenergic activity
– increased HR, increased contractility
• Increased
activity of R–A–A system
Causes leading to changes of number and size of
cardiomyocytes
Heart Failure
Etiology and Pathophysiology
• Systolic failure- most common cause
– Hallmark finding: in *Decrease in left ventricular ejection
fraction (EF)
• Due to
– Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)
Heart Failure
Etiology and Pathophysiology
• Diastolic failure
– Impaired ability of ventricles to relax and fill
during diastole > decreased stroke volume and CO
– Diagnosis based on presence of pulmonary
congestion, pulmonary hypertension, ventricular
hypertrophy
Heart Failure
Etiology and Pathophysiology
• Mixed systolic and diastolic failure
– Seen in disease states such as dilated
cardiomyopathy (DCM)
– High pulmonary pressures
• Biventricular failure (both ventricles may be
dilated and have poor filling and emptying
capacity)
Heart Failure
Etiology and Pathophysiology
• Primary risk factors
– Coronary artery disease (CAD)
– Advancing age
• Contributing risk factors
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–
–
–
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Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent
Valvular heart disease
Hypervolemia