PathoPhysiology Chapter 18

1. CHAPTER 18
ALTERATIONS IN CARDIAC
FUNCTION

2. • 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

3. 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

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CORONARY HEART DISEASE (CONT.)

5. CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE (CONT.)

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CORONARY HEART DISEASE (CONT.)
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

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CORONARY HEART DISEASE (CONT.)
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

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CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE
(CONT.)

11. CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE
(CONT.)
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

13. CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE
(CONT.)
Clinical Features and Management of
Coronary Syndromes
• Acute coronary syndrome (ACS) associated with
acute changes in plaque morphology and
thrombosis
• Unstable angina
• Myocardial infarction

15. CORONARY HEART DISEASE
(CONT.)
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

16. CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE
(CONT.)

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CORONARY HEART DISEASE
(CONT.)

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CORONARY HEART DISEASE
(CONT.)

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CORONARY HEART DISEASE
(CONT.)
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

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CORONARY HEART DISEASE
(CONT.)

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CORONARY HEART DISEASE
(CONT.)

23. 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 DiseaseCoronary Heart Disease (Cont.)(Cont.)

24. CORONARY HEART DISEASE
(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

25. 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

26. 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

27. ENDOCARDIAL AND
VALVULAR DISEASE (CONT.)
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

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ENDOCARDIAL AND
VALVULAR DISEASE (CONT.)

29. 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 andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

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

31. 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
Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

32. 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
Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

33. Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

34. 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
Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

35. Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

36. 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
Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

37. • Infective endocarditis
• Invasion and colonization of endocardial structures
by microorganisms with resulting inflammation—
vegetations
• Most common bacteria
• Streptococcus
• Staphylococcus
• Predisposing risk factors typically present
Endocardial andEndocardial and
Valvular DiseaseValvular Disease (Cont.)(Cont.)

38. 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

39. 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

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Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

41. Cardiomyopathy
• Classified by cause or functional impairment
• Primary: dysfunction of unknown cause
• Secondary: known cause
• Dilated
• Hypertrophic
• Restrictive
Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

42. 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
Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

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Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

44. 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
Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

45. 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
Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

46. Specific Cardiomyopathy
• Presumed known origin
• Present functionally as dilated, hypertrophic,
or restrictive disorders
Myocardial DiseasesMyocardial Diseases (Cont.)(Cont.)

47. PERICARDIAL DISEASES
• Typically sequelae of other disorders such as:
• Systemic infection
• Trauma
• Metabolic derangement
• Neoplasia

48. PERICARDIAL DISEASES (CONT.)
Pericardial Effusion
• Accumulation of noninflammatory fluid in the
pericardial sac
• Composition of usual fluids
• Serous
• Serosanguineous
• Chylous
• Blood

49. 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

50. 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

51. 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

52. 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

53. 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

54. 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

55. CONGENITAL HEART DISEASES
(CONT.)
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

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CONGENITAL HEART DISEASES
(CONT.)

57. 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 DiseasesCongenital Heart Diseases (Cont.)(Cont.)

58. 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
Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

59. 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
Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

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CONGENITAL HEART DISEASES
(CONT.)

61. 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
Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

62. Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

63. 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
Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

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PATENT DUCTUS ARTERIOSUS

65. CONGENITAL HEART DISEASES
Coarctation 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

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COARCTATION OF THE AORTA

67. CONGENITAL HEART DISEASES
Pulmonary 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

68. CONGENITAL HEART DISEASES
(CONT.)
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

69. CONGENITAL HEART DISEASES
(CONT.)
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

70. 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
Congenital Heart DiseasesCongenital Heart Diseases (Cont.)(Cont.)

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TETRALOGY OF FALLOT

72. CONGENITAL HEART DISEASES
Transposition 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

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TRANSPOSITION OF THE GREAT
ARTERIES

74. CONGENITAL HEART DISEASES
Truncus 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

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TRUNCUS ARTERIOSUS

76. CONGENITAL HEART DISEASES
Tricuspid 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