PathoPhysiology Chapter 18

CHAPTER 18

ALTERATIONS IN CARDIAC FUNCTION

• CHD is characterized by insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries (CADs)

• Sequelae of CHD include:• Angina pectoris• Myocardial infarction• Dysrhythmias• Heart failure• Sudden cardiac death

Coronary Heart DiseaseCoronary Heart Disease

CORONARY HEART DISEASE (CONT.)

Etiology of Coronary Heart Disease• Known risk factors• Atherosclerosis causes narrowing of the

arterial lumen that can lead to cardiac ischemia through:• Thrombus formation• Coronary vasospasm• Endothelial cell dysfunction

Elsevier items and derived items © 2010, 2005 by Saunders, an imprint of Elsevier Inc.



Mechanisms of Coronary Atherosclerosis• Lipids are transported via apoproteins• Lipoproteins associated with a greater risk

of atherosclerosis• High-density lipoproteins transport

cholesterol from peripheral tissue back to the liver, clearing atheromatous plaque





Mechanisms of Coronary Atherosclerosis• Atherosclerotic plaque formation initiated by

injury to coronary artery endothelium• Endothelium becomes permeable and recruits

leukocytes• LDL insudation occurs with oxidation by

endothelial cells and macrophages• Oxidized lipids are damaging to endothelial and

smooth muscle cells, and stimulate recruitment of macrophages into the vessel



Mechanisms of Coronary Atherosclerosis• Macrophages engulf the lipids; foam cells release

inflammatory mediators and growth factors, attracting more leukocytes and stimulate smooth muscle proliferation

• Excess lipid and debris accumulate within vessel wall and coalesce into lipid core



Mechanisms of Coronary Atherosclerosis• Vulnerable plaques may rupture or become

eroded, which stimulates clot formation on the plaque

• Vulnerable plaques have:• Large lipid core• Thin cap• High shear stress




Pathophysiology of Ischemia• Ischemia occurs when oxygen supply is

insufficient to meet metabolic demands• Critical factors in meeting cellular demands

for oxygen include:• Rate of coronary perfusion• Myocardial workload



Pathophysiology of Ischemia• Coronary perfusion can be altered by:

• Large, stable atherosclerotic plaque• Acute platelet aggregation and thrombosis• Vasospasm• Failure of autoregulation by the microcirculation• Poor perfusion pressure


Clinical Features and Management of Coronary Syndromes

• Chronic syndromes with slow progression due to chronic obstruction from stable atherosclerotic plaques• Stable angina pectoris• Ischemic cardiomyopathy



Clinical Features and Management of Coronary Syndromes • Acute coronary syndrome (ACS) associated with

acute changes in plaque morphology and thrombosis• Unstable angina• Myocardial infarction


Angina Pectoris• Chest pain associated with intermittent

myocardial ischemia• May result in inefficient cardiac pumping

with resultant pulmonary congestion and shortness of breath

• Three patterns of angina pectoris• Stable or typical angina• Prinzmetal or variant angina• Unstable or crescendo angina


Acute Coronary Syndrome• Chest pain usually more severe and lasts

longer than typical angina• Plaque rupture with acute thrombus

development• Unstable angina—occlusion is partial• MI—occlusion is complete• ECG and biomarkers used for diagnosis









Acute Coronary Syndrome• MI leads to drop in CO, triggering compensatory

responses including sympathetic activation• Sympathetic nervous system activation leads to

increased myocardial workload by increasing:• Heart rate• Contractility• Blood pressure





Sudden Cardiac Death• Unexpected death from cardiac causes

within 1 hour of symptom onset• Use of external defibrillators and CPR has

increased survival• Lethal dysrhythmia (such as ventricular

fibrillation) is usually the primary cause

Coronary Heart Disease Coronary Heart Disease (Cont.)(Cont.)


Chronic Ischemic Cardiomyopathy• Heart failure develops insidiously due to

progressive ischemic myocardial damage• Typically have history of angina or MI• More common in older adults

ENDOCARDIAL AND VALVULAR DISEASE

• Endocardial and valvular structures may be damaged by:• Inflammation and scarring• Calcification• Congenital malformations

• Cause altered hemodynamics of the heart and increase myocardial workload

ENDOCARDIAL AND VALVULAR DISEASE (CONT.)

• Stenosis: failure of the valve to open completely results in extra pressure work for the heart

• Regurgitation: inability of a valve to close completely results in extra volume work for the heart


Mitral Stenosis• Blood flow from the left atrium to the left

ventricle is impaired during ventricular diastole

• Increased pressure of the left atrium leads to atrial chamber enlargement and hypertrophy

• Can lead to chronic pulmonary hypertension, right ventricular hypertrophy, and right-sided heart failure

• Low-pitched, rumbling diastolic murmur



Mitral Regurgitation• Backflow of blood from the left ventricle to

the left atrium during ventricular systole• Left atrium and ventricle dilate and

hypertrophy due to extra volume• May lead to left-sided heart failure• High-pitched, pansystolic, blowing murmur

Endocardial and Endocardial and Valvular Disease Valvular Disease (Cont.)(Cont.)



Mitral Valve Prolapse• Displacement of the mitral valve leaflets

into the left atrium during ventricular systole

• Typically asymptomatic• Complications may include infective

endocarditis, sudden cardiac death, cerebral embolic events, and progression to mitral regurgitation

• Midsystolic click or systolic murmur


Aortic Stenosis• Predominant cause is age-related calcium

deposits on the aortic cusps• Results in obstruction of aortic outflow from

the left ventricle into the aorta during systole

• May result in ischemia and left-sided HF• Crescendo-decrescendo murmur during

ventricular systole with prominent S4



Aortic Regurgitation• Incompetent aortic valve allows blood to

leak back from the aorta into the left ventricle during diastole

• Leads to left ventricle hypertrophy and dilation with eventual left-sided HF

• High-pitched blowing murmur during ventricular diastole



Diseases of the Endocardium• Rheumatic heart disease

• Acute inflammatory disease that follows infection with group A β-hemolytic streptococci

• Antibodies against the streptococcal antigens damage connective tissue in joints, heart, and skin

• Occurs mainly in children


• Infective endocarditis• Invasion and colonization of endocardial

structures by microorganisms with resulting inflammation—vegetations

• Most common bacteria• Streptococcus• Staphylococcus

• Predisposing risk factors typically present


MYOCARDIAL DISEASES• Myocarditis: inflammatory disorder of the

heart muscle characterized by necrosis and degeneration of myocytes

• Cardiomyopathy may be genetic or acquired and is noninflammatory

MYOCARDIAL DISEASES (CONT.)Myocarditis• Causes include microbial agents, immune-

mediated diseases, physical agents• Viral etiology most common• Characterized by left ventricular

dysfunction and general dilation of all four chambers


Myocardial Diseases Myocardial Diseases (Cont.)(Cont.)

Cardiomyopathy• Classified by cause or functional

impairment• Primary: dysfunction of unknown cause• Secondary: known cause• Dilated• Hypertrophic• Restrictive


Dilated Cardiomyopathy• Cardiac failure associated with dilation of

one or both ventricular chambers• May be related to:

• Alcohol toxicity• Pregnancy• Postviral myocarditis• Genetic abnormality

• Slow progression of biventricular heart failure with low ejection fraction




Hypertrophic Cardiomyopathy• Thickened, hyperkinetic ventricular muscle

mass• Septum may be affected, leading to

idiopathic hypertrophic subaortic stenosis• Genetic abnormality• Clinical course is variable, typically slow

progression


Restrictive Cardiomyopathy• Rarest form of cardiomyopathy• Stiff, fibrotic ventricle with impaired

diastolic filling• Most commonly associated with

amyloidosis• Decreased cardiac output and left-sided

heart failure can result


Specific Cardiomyopathy• Presumed known origin• Present functionally as dilated,

hypertrophic, or restrictive disorders


PERICARDIAL DISEASES• Typically sequelae of other disorders such

as:• Systemic infection• Trauma• Metabolic derangement• Neoplasia

PERICARDIAL DISEASES (CONT.)Pericardial Effusion• Accumulation of noninflammatory fluid in

the pericardial sac• Composition of usual fluids

• Serous• Serosanguineous• Chylous• Blood

PERICARDIAL DISEASES (CONT.)Cardiac Tamponade• When fluid accumulation in the pericardial

sac is large/sudden it can lead to external compression of the heart chambers such that filling is impaired

• Symptoms include:• Reduced stroke volume• Compensatory increases in heart rate

PERICARDIAL DISEASES (CONT.)Pericarditis• Acute or chronic inflammation of the

pericardium• Categories:

• Idiopathic• Infectious• Immune-inflammatory• Neoplastic• Radiation induced

Early postcardiac sxEarly postcardiac sx HemopericardiumHemopericardium TraumaTrauma CongenitalCongenital MiscellaneousMiscellaneous

PERICARDIAL DISEASES (CONT.)Acute Pericarditis• Most cases idiopathic and presumed viral• Uncomplicated form resolves spontaneously• Complicated forms involve pericardial

effusion, or persistent/recurrent inflammation

• Typically presents as chest pain

PERICARDIAL DISEASES (CONT.)Chronic Pericarditis• Two principal forms:

• Adhesive mediastinopericarditis— pericardial sac is destroyed and the external aspect of the heart adheres to surrounding mediastinal structures

• Constrictive pericarditis—pericardial sac becomes dense, nonelastic, fibrous, and scarred

CONGENITAL HEART DISEASES• Abnormality of the heart that is present

from birth• Different congenital heart anomalies result

in two primary pathologic processes:• Shunting of blood through abnormal pathways in

the heart or great vessels• Obstruction to blood flow because of abnormal

narrowing

CONGENITAL HEART DISEASES (CONT.)

Embryologic Development• Heart defects commonly associated with

these abnormalities:• Development of atrial septum• Development of the ventricular septum• Division of the main outflow tract (truncus

arteriosus) into the pulmonic and aortic arteries• Development of the valves


Etiology and Incidence of Congenital Heart Disease• Congenital heart disease is the most

common heart disorder in children• Overall incidence is 0.8% of all live births• May be attributed to

• Maternal rubella during first trimester of pregnancy

• Exposure to cardiac teratogens• Genetic influences



Pathophysiology of Congenital Heart Disease• Result in two primary pathologies

• Shunt: abnormal path of blood flow through the heart or great vessels

• Obstruction: interference with blood flow leading to increased workload of affected chamber

Congenital Heart Diseases Congenital Heart Diseases (Cont.)(Cont.)

Acyanotic Congenital Defects• Disorders that result in left-to-right shunting

of blood or obstruction to flow are generally acyanotic

• These disorders include:• Atrial septal defect• Ventricular septal defect• Patent ductus arteriosus• Coarctation of the aorta• Pulmonary and aortic stenosis or atresia


Atrial Septal Defect• Majority of atrial septal defects occur at the

location of the foramen ovale• Long-term increase in pulmonary blood flow

may eventually lead to pulmonary hypertension, right ventricular hypertrophy, and reversal to a right-to-left shunt




Ventricular Septal Defect• Most common congenital cardiac anomaly• Typically located in the membranous

septum, near the bundle of His• Increase in pulmonary blood flow can result

in pulmonary hypertension, right ventricular hypertrophy, and reversal of the shunt



Patent Ductus Arteriosus• Conditions that cause low blood oxygen

tension may contribute to continued patency

• No clinical significance in early life• Continued patency identified by harsh,

grinding systolic murmur or thrill• Results in pulmonary hypertension, and can

lead to right-sided heart failure



PATENT DUCTUS ARTERIOSUS

CONGENITAL HEART DISEASESCoarctation of the Aorta• Narrowing or stricture of the aorta that

impedes blood flow• Commonly located just before or after the

ductus arteriosus• Preductal coarctation usually more severe

and associated with other anomalies• Usually accompanied by systolic murmurs

and ventricular hypertrophy


COARCTATION OF THE AORTA

CONGENITAL HEART DISEASESPulmonary Stenosis or Atresia• Pulmonary atresia—blood must enter the

lungs by traveling through a septal opening and a patent ductus arteriosus

• Pulmonary stenosis—usually due to abnormal fusion of the valvular cusps and can lead to right ventricular hypertrophy


Aortic Stenosis or Atresia• Aortic atresias are not compatible with

survival• Aortic stenosis may involve the valvular

cusps or the subvalvular fibrous ring and results in high left ventricular afterload with left ventricular hypertrophy


Cyanotic Congenital Defects• Disorders that result in right-to-left shunting

of blood result in cyanosis• These disorders include

• Tetralogy of Fallot• Transposition of the great arteries• Truncus arteriosus• Tricuspid atresia

Tetralogy of Fallot• Four defining features

• Ventricular septal defect• Aorta positioned above the ventricular septal

opening• Pulmonary stenosis that obstructs right ventricular

outflow• Right ventricular hypertrophy



TETRALOGY OF FALLOT

CONGENITAL HEART DISEASESTransposition of the Great Arteries• Aorta arises from the right ventricle and the

pulmonary artery arises from the left ventricle

• Results in two separate, noncommunicating circulations

• Incompatible with life unless mixing of blood occurs through other defects


TRANSPOSITION OF THE GREAT ARTERIES

CONGENITAL HEART DISEASESTruncus Arteriosus• Failure of the pulmonary artery and aorta to

separate; results in formation of one large vessel that receives blood from both the right and left ventricles

• Results in systemic cyanosis• High pulmonary blood flow may cause

pulmonary hypertension and right ventricular hypertrophy


TRUNCUS ARTERIOSUS

CONGENITAL HEART DISEASESTricuspid Atresia• Usually associated with underdevelopment

of the right ventricle and an atrial septal defect

• Allows blood to bypass right ventricle• A patent ductus arteriosus is required to

perfuse lungs• Cyanosis present at birth, mortality high

Date post:	15-Apr-2017
Category:	Education
Upload:	theslaps
View:	322 times
Download:	3 times

PathoPhysiology Chapter 18

Education