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ARCHIVED: Pathophysiology > Exam 2: Cardiac > Flashcards

Exam 2: Cardiac Flashcards

1
Q

Myocardial ischemia is characterized by:

A

Metabolic O2 demand that exceeds supply

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2
Q

Most common cause of myocardial ischemia:

A

Narrowing of coronary arteries d/t atherosclerosis

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3
Q

Secondary causes of myocardial ischemia:

A 
HTN or tachycardia (severe)
Coronary vasospasm
Hypotension (severe)
Hypoxia
Anemia
Aortic insufficiency/stenosis (severe)
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4
Q

Mortality rate of myocardial infarction:

A

1/3rd

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5
Q

Incidence of myocardial ischemia in surgical patients:

A

5-10% (estimated)

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6
Q

Major risk factors for myocardial ischemia:

A 
Age (75+)
Male
↑LDL
Diabetes
Hypertension
Smoking
\+ family hx
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7
Q

Minor risk factors for myocardial ischemia:

A 
Obesity
CV disease
PVD
Menopause
Use of estrogen BCPs
Sedentary lifestyle
High stress/type A personality
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8
Q

Describe how atherosclerosis leads to myocardial damage:

A

Plaque partially obstructs blood flow

Unstable plaque ruptures/thromboses

Transient ischemia leads to unstable angina; sustained ischemia leads to myocardial infarction/inflammation/necrosis

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9
Q

Effects of sustained ischemia on myocytes:

A

Stunned/hibernating myocytes

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10
Q

Effects of myocardial infarction/inflammation on myocytes:

A

Myocardial remodeling

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11
Q

Characteristics of plaques prone to rupture:

A

Lipid rich core

Thin, fibrous cap

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12
Q

Factors that lead to plaque rupture:

A

Shear forces
Inflammation
Apoptosis
Macrophage enzymes

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13
Q

Results of plaque rupture:

A

Inflammation and cytokine release, platelet activation, thrombin production

Thrombus forms over lesion; vasoconstriction of vessel

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14
Q

Results of thrombus formation d/t atherosclerotic plaque rupture:

A

Acute decrease in coronary blood flow

Unstable angina or myocardial infarction

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15
Q

Cells that infiltrate atherosclerotic plaques:

A

T cells and macrophages

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16
Q

Six characteristics of rupture-prone plaques:

A
  1. T cells in the shoulder region
  2. Macrophages clustered around T cells
  3. Thin, fibrous cap
  4. Lipid rich core
  5. Newly formed capillaries within the wall
  6. Lymphocyte/mast cell infiltration
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17
Q

More significant to plaque: size or instability?

A

Instability

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18
Q

Substances that degrade the collagen plaque cap:

A

Metalloproteinases

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19
Q

Mechanical stress on plaques maximal at this point:

A

Junction of fibrous cap and plaque-free vessel wall

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20
Q

Physiologic responses to stress (4):

A

↑ catecholamines, HR, BP
↓ plasma volume
↑ coronary constriction
↑ platelet activity

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21
Q

Cardiac changes due to physiologic responses to stress (3):

A

↑ electrical instability
↑ demand
↓ supply

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22
Q

Pathologic effects of stress on cardiac function (4):

A

VF/VT
Ischemia
Plaque rupture
Coronary thrombosis

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23
Q

Surgical stressors that can impact cardiac function:

A

Pain
Anxiety
Hypovolemia

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24
Q

Describe stable angina:

A

No change in precipitating factors for 60+ days

No change in frequency, duration of pain

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25
Q

Describe unstable angina:

A

Caused by less than normal activity
Prolonged duration
Increasing frequency

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26
Q

Unstable angina signals:

A

Impending MI

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27
Q

Physiological changes associated with stable angina:

A

Fixed narrowing: 75% or greater
O2 demand close to normal at baseline
Relieved by rest, reducing demand, or NTG

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28
Q

Physiological changes associated with unstable angina:

A

Acute plaque changes
Partial thrombosis
Crescendo-ing intensity
↑ frequency, duration, etc

Can cause infarction!

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29
Q

Describe Prinzmetal angina:

A

Occurs at rest
Coronary spasm
In plaque area or normal vessel
Can be associated with other vasospastic diseases (Reynaud’s)

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30
Q

Define infarction:

A

Necrosis caused by ischemia

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31
Q

Where and when does infarction occur?

A

Within 20-30 mins of ischemia
Subendocardial regions
Reaches full size in 3-6 hrs

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32
Q

Size of infarction depends on:

A

Proximity of lesion

Collateral circulation

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33
Q

Complications of myocardial infarction:

A 
Papillary muscle dysfunction & valvular disease
Rupture of infarct
Mural thrombi
Acute pericarditis
Ventricular aneurysm
Arrythmias
LV failure & pulmonary edema
Cardiogenic shock
Rupture of wall/septum/papillary muscle
Thromboembolism
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34
Q

Describe rupture of myocardial infarct:

A

Occurs day 4-7

Followed by tamponade and death

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35
Q

Sequelae of mural thrombi:

A

Stroke

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36
Q

Timing of post-MI pericarditis:

A

Day 2-4

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37
Q

Most common site for ventricular aneurysm:

A

Anteroapical region

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38
Q

Incidence of cardiogenic shock post-MI:

A

10%

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39
Q

Leads which look at LV:

A

II, V5

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40
Q

Define vascular hypertension:

A

Diastolic > 90mmHg

Systolic > 140mmHg

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41
Q

Incidence of HTN:

A

25%

↑ in black pts

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42
Q

HTN is a primary risk factor in:

A 
CAD
CVA
Cardiac hypertrophy
Renal failure
Aortic dissection
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43
Q

Causes of HTN:

A

90-95% idiopathic

5-10% secondary to renal disease

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44
Q

Causes of secondary HTN:

A

Renal
Endocrine
Cardiovascular
Neurologic

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45
Q

BP = ? x ?

A

BP = CO x PVR

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46
Q

CO factors that ↑ BP:

A

Blood volume

Contracility

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47
Q

PVR factors that ↑ BP:

A

Constrictors/dilators in bloodstream
Neural influences
Local factors

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48
Q

Genetic risk factors for HTN:

A

Polygenic and heterogenous

Polymorphisms at several different gene loci

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49
Q

Environmental risk factors for HTN:

A 
Stress
Obesity
Smoking
Salt consumption
Sedentary lifestyle
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50
Q

Renal theory of HTN:

A

↓ renal excretion of Na+ leads to ↑ fluid volume/CO

Vasoconstriction d/t autoregulation leads to ↑ BP

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51
Q

Vasoconstriction/hypertrophy theory states that ↑ PVR caused by:

A
  1. Factors that induce vasoconstriction (neurogenic, vasoconstrictive agent release, genetic Na+/Ca++ transport defect)
  2. Stimuli that induce structural ∆s
52
Q

Causes of secondary HTN:

A 
OCPs (older)
Renal parenchymal disease
Renin-secreting tumors
Aldosteronism
Cushing's
Pheochromocytoma
53
Q

Define hypertensive crisis:

A

Sudden increase in DBP to > 130mmHg

54
Q

HTN crisis is caused by:

A

Activation of RAAS

55
Q

Tx for HTN crisis:

A

Fast but controlled ↓ in BP with NTP, 0.5-1 μg/kg/min
Monitor UOP, A-line
Bring DBP ↓ to 100-110 over several minutes to hours

56
Q

Usual cause of mitral stenosis:

A

Fusion of mitral valve leaflets at commissures d/t rheumatic fever

57
Q

Mitral valve area < 1 cm2 requires a mean left atrial pressure of:

58
Q

Left atrial enlargement predisposes the heart to:

A

Atrial fibrillation

Stasis of blood/formation of thrombi

59
Q

Symptoms of mitral stenosis:

A

Dyspnea on exertion when CO ↑

Severe stenosis - CHF

60
Q

Pathway from mitral stenosis to LV failure:

A 
Mitral stenosis
↓ LA emptying
↑ LA preload
↓ force of LA contraction
↓ delivery of blood to LV
↓ LV output + ↓ O2 supply from pulmonary edema
LV failure
61
Q

Usual cause of isolated aortic stenosis:

A

Progressive calcification/stenosis of congenitally abnormal valve (bicuspid instead of tricuspid)

62
Q

Usual cause of aortic stenosis associated with mitral stenosis:

A

Rheumatic fever

63
Q

Measurements associated with hemodynamically significant aortic stenosis:

A

Transvalvular gradient > 50mmHg

Orifice area < 1cm2

64
Q

Triad of symptoms associated with aortic stenosis:

A

Angina pectoris (often without ischemic heart disease)
Dyspnea on exertion
Syncope

65
Q

How does aortic stenosis cause syncope?

A

↓ SV and flow to brain

66
Q

What determines compensation for aortic stenosis?

A

Timing: chronic AS better tolerated than acute stenosis

67
Q

Effects of aortic stenosis on LV:

A

Hypertrophy & dilation

Poor pumping ability

68
Q

Pathway of early atrial stenosis:

A 
Atrial stenosis obstructs LV ejection
↑ pressure in LV
↑ LV mass (hypertrophy)
LV compliance ↓ but contractility remains
↑ preload, atrial kick
Normal stroke volume
69
Q

Pathway of late atrial stenosis:

A 
Atrial stenosis obstructs LV ejection
↑ pressure in LV
↑ LV mass (hypertrophy)
Fibrosis and ↓ contractility
LV dilation
↓ stroke volume
70
Q

Common cause of mitral regurgitation:

A

Rheumatic fever (associated with mitral stenosis)

71
Q

Principle pathologic change produced by mitral regurgitation:

A

LA volume overload d/t retrograde flow from LV during systole

72
Q

Mitral regurgitation responsible for ____ wave on PAOP waveform:

A

V wave

Size of wave correlates to magnitude of regurgitant flow

73
Q

Ultimate pathological result of mitral regurgitation:

A

Tricuspid regurgitation

74
Q

Acute causes of aortic regurgitation:

A

Infective endocarditis
Trauma
Dissection of thoracic aneurysm

75
Q

Chronic causes of aortic regurgitation:

A

Prior rheumatic fever

Persistent systemic hypertension

76
Q

Changes in heart function with aortic regurgitation:

A

Regurgitation of part of LV stroke volume from aorta back into ventricle
↓ SV
LV dilation

77
Q

First organ affected by aortic regurgitation:

A

Kidneys; RAAS and SNS activation makes s/s worse

78
Q

Three types of cardiomyopathies:

A

Dilated
Hypertrophic
Restrictive

79
Q

Two forms of dilated cardiomyopathy:

A

Inflammatory

Non-inflammatory

80
Q

Early s/s of inflammatory myocarditis:

A

Fatigue
Dyspnea
Palpitations

81
Q

Typical cause of inflammatory myocarditis:

82
Q

Late s/s of inflammatory myocarditis:

A

CHF
Pulsus alternans
Tachycardia
Pulmonary edema

83
Q

Prognosis of inflammatory myocarditis:

A

Usually complete recovery with long-term abx

84
Q

Causes (5) of non-inflammatory cardiomyopathy:

A 
Toxicity (ETOH)
Idiopathic process
Degenerative process
Infiltrative process (resolved infection)
Post-MI necrosis/remodeling
85
Q

Manifestation of non-inflammatory cardiomyopathy:

86
Q

Characteristics (3) of cardiomyopathy-induced heart failure:

A

Elevated filling pressures
Failure of contractile strength
Inverse relationship between arterial impedance and stroke volume

87
Q

Describe how dilated cardiomyopathy leads to heart failure:

A

↓ contractility leads to dilation of the ventricle (to ↑ contractility from stretch on muscle fibers - Frank Starling)
Increased ventricular radius = increased cardiac work and O2 consumption
Cardiac output falls
↑ SNS outflow (renal trigger) in order to ↑ HR/SVR
Stroke volume falls

88
Q

“Forward failure” presents with:

A

Fatigue
Hypotension
Oliguria d/t ↓ renal blood flow

89
Q

“Backward failure” presents with:

A 
Elevated filling pressures required by heart
Mitral regurgitation (from dilation of ventricle)
90
Q

Left sided failure presents with:

A

Orthopnea
Pulmonary edema
Paroxysmal nocturnal dyspnea

91
Q

Right sided failure presents with:

A

Hepatomegaly
JVD
Peripheral edema

92
Q

Other names for hypertrophic cardiomyopathy:

A

Idiopathic hypertrophic subaortic stenosis**
Asymmetrical septal hypertrophy
Hypertrophic obstructive cardiomyopathy
Muscular subaortic stenosis

93
Q

Type of genetic trait that causes hypertrophic cardiomyopathy:

A

Autosomal dominant

94
Q

Main defect in hypertrophic cardiomyopathy:

A

Increase in density of Ca++ channels in contractile elements of heart

95
Q

Presenting symptom of hypertrophic cardiomyopathy for 50% of patients:

A

Sudden death or cardiac arrest in 3rd/4th decade

↑ HR during athletic activity means ♥︎ goes into SVT/Vtach

96
Q

S/s of hypertrophic cardiomyopathy:

A

Dyspnea, angina, syncope starting in 2nd/3rd decades

97
Q

Arrhythmia seen with hypertrophic cardiomyopathy:

A

75% ventricular dysrhythmias
25% SVT
5-10% atrial fibrillation

98
Q

Annual mortality for hypertrophic cardiomyopathy (overall and post-op):

A

3-8% overall

1-3% post-op

99
Q

Portion of the heart that enlarges in hypertrophic cardiomyopathy:

A

Interventricular septum, typically in top portion below aortic valve

100
Q

Pathophysiology of hypertrophic cardiomyopathy:

A

Diastolic dysfunction: cannot fully relax; atrial contribution may be 70% of SV; ↓ SV

Rapid LV ejection d/t overcontractility (80% during early systole!)

Subaortic pressure gradient

101
Q

Factors that improve systolic function in hypertrophic cardiomyopathy:

A

Volume loading
Vasoconstriction
Myocardial depression

All factors that impair contractility!

102
Q

Valvular disease seen in hypertrophic cardiomyopathy:

A

Mitral regurgitation

103
Q

Medical management of hypertrophic cardiomyopathy:

A

Beta blockers

CCBs

104
Q

Means by which beta blockers help in hypertrophic cardiomyopathy:

A

Blunts the SNS mediation of subaortic stenosis

Decreases tachyarrythmias

105
Q

Means by which CCBs help in hypertrophic cardiomyopathy:

A

Improves diastolic relaxation

106
Q

Surgical management of hypertrophic cardiomyopathy:

A

Myomectomy

107
Q

Echo findings in hypertrophic cardiomyopathy:

A

Thickened interventricular septum (apex thicker than base)
Poor septal motion
Anterior displacement of mitral valve

108
Q

Three left-to-right shunt defects:

109
Q

Cyanosis seen with L to R shunts:

A

Possible tardive cyanosis, but not seen from outset

110
Q

Most common heart defect dx’ed in adulthood:

111
Q

Development of ASD:

A

At 4-6 weeks of development

Foramen ovale does not close properly

112
Q

Clinical features of ASD:

A 
Eventual pulmonary HTN
Can reverse into R to L shunt (cyanosis, CHF)
Mitral insufficiency (sometimes)
113
Q

Most common heart defect dx’ed at birth:

114
Q

Development of VSD:

A

Malformation of ventricular septum at 4-8 weeks development

Can close spontaneously in childhood

115
Q

Clinical features of VSD:

A

Pulmonary HTN
CHF
Infective endocarditis from blood stasis

116
Q

PDA closes at birth due to:

A

↑ O2 level
↓ pulm resistance
↓ prostaglandins (PGE2)

117
Q

Two R to L shunts:

A

Tetralogy of Fallot

Transposition of great vessels

118
Q

Cyanosis seen with R to L shunts:

A

True cyanosis at birth

119
Q

Most common cause of cyanotic congenital heart disease:

A

Tetralogy of Fallot

120
Q

Four components of tetralogy of Fallot:

A
  1. VSD
  2. Dextraposed (R-shifted) aortic root overriding the VSD
  3. RV outflow obstruction (narrowing of pulmonary trunk)
  4. RV hypertrophy
121
Q

Clinical signs of tetralogy of Fallot:

A

↓ blood flow to lungs

↑ blood flow to aorta

122
Q

Manifestations of unrepaired tetralogy of Fallot:

A 
Erythrocytosis
↑ blood viscosity
Digital clubbing
Infective endocarditis
Systemic emboli
Brain abscesses
123
Q

Transposition of the great vessels must be associated with _____ for extrauterine life:

A

ASD, VSD, PDA - L to R shunts

124
Q

Clinical feature of transposition of the great vessels:

125
Q

Preductal vs. postductal coarctation of the aorta & relative incidence:

A

Where the narrowing is in relation to the ductus arteriosis

Postductal more common

126
Q

S/s and treatment of preductal coarctation of the aorta:

A

Dx in infants
Weak femoral pulses
Cyanosis of lower extremities
CHF

Must be surgically corrected for survival

127
Q

S/s of postductal coarctation of the aorta:

A 
Dx in older children, young adults
Collaterals developed
↓ renal perfusion
RAAS activation
↑ pressure in upper extremities, ↓ pressure in lowers
Intermittent claudication

ARCHIVED: Pathophysiology (18 decks)

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