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Flashcards in Exam 2: Cardiac Deck (127):
1

Myocardial ischemia is characterized by:

Metabolic O2 demand that exceeds supply

2

Most common cause of myocardial ischemia:

Narrowing of coronary arteries d/t atherosclerosis

3

Secondary causes of myocardial ischemia:

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

4

Mortality rate of myocardial infarction:

1/3rd

5

Incidence of myocardial ischemia in surgical patients:

5-10% (estimated)

6

Major risk factors for myocardial ischemia:

Age (75+)
Male
↑LDL
Diabetes
Hypertension
Smoking
+ family hx

7

Minor risk factors for myocardial ischemia:

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

8

Describe how atherosclerosis leads to myocardial damage:

Plaque partially obstructs blood flow

Unstable plaque ruptures/thromboses

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

9

Effects of sustained ischemia on myocytes:

Stunned/hibernating myocytes

10

Effects of myocardial infarction/inflammation on myocytes:

Myocardial remodeling

11

Characteristics of plaques prone to rupture:

Lipid rich core
Thin, fibrous cap

12

Factors that lead to plaque rupture:

Shear forces
Inflammation
Apoptosis
Macrophage enzymes

13

Results of plaque rupture:

Inflammation and cytokine release, platelet activation, thrombin production

Thrombus forms over lesion; vasoconstriction of vessel

14

Results of thrombus formation d/t atherosclerotic plaque rupture:

Acute decrease in coronary blood flow

Unstable angina or myocardial infarction

15

Cells that infiltrate atherosclerotic plaques:

T cells and macrophages

16

Six characteristics of rupture-prone plaques:

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

17

More significant to plaque: size or instability?

Instability

18

Substances that degrade the collagen plaque cap:

Metalloproteinases

19

Mechanical stress on plaques maximal at this point:

Junction of fibrous cap and plaque-free vessel wall

20

Physiologic responses to stress (4):

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

21

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

↑ electrical instability
↑ demand
↓ supply

22

Pathologic effects of stress on cardiac function (4):

VF/VT
Ischemia
Plaque rupture
Coronary thrombosis

23

Surgical stressors that can impact cardiac function:

Pain
Anxiety
Hypovolemia

24

Describe stable angina:

No change in precipitating factors for 60+ days
No change in frequency, duration of pain

25

Describe unstable angina:

Caused by less than normal activity
Prolonged duration
Increasing frequency

26

Unstable angina signals:

Impending MI

27

Physiological changes associated with stable angina:

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

28

Physiological changes associated with unstable angina:

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

Can cause infarction!

29

Describe Prinzmetal angina:

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

30

Define infarction:

Necrosis caused by ischemia

31

Where and when does infarction occur?

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

32

Size of infarction depends on:

Proximity of lesion
Collateral circulation

33

Complications of myocardial infarction:

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

34

Describe rupture of myocardial infarct:

Occurs day 4-7
Followed by tamponade and death

35

Sequelae of mural thrombi:

Stroke

36

Timing of post-MI pericarditis:

Day 2-4

37

Most common site for ventricular aneurysm:

Anteroapical region

38

Incidence of cardiogenic shock post-MI:

10%

39

Leads which look at LV:

II, V5

40

Define vascular hypertension:

Diastolic > 90mmHg
Systolic > 140mmHg

41

Incidence of HTN:

25%
↑ in black pts

42

HTN is a primary risk factor in:

CAD
CVA
Cardiac hypertrophy
Renal failure
Aortic dissection

43

Causes of HTN:

90-95% idiopathic
5-10% secondary to renal disease

44

Causes of secondary HTN:

Renal
Endocrine
Cardiovascular
Neurologic

45

BP = ? x ?

BP = CO x PVR

46

CO factors that ↑ BP:

Blood volume
Contracility

47

PVR factors that ↑ BP:

Constrictors/dilators in bloodstream
Neural influences
Local factors

48

Genetic risk factors for HTN:

Polygenic and heterogenous

Polymorphisms at several different gene loci

49

Environmental risk factors for HTN:

Stress
Obesity
Smoking
Salt consumption
Sedentary lifestyle

50

Renal theory of HTN:

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

Vasoconstriction d/t autoregulation leads to ↑ BP

51

Vasoconstriction/hypertrophy theory states that ↑ PVR caused by:

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

52

Causes of secondary HTN:

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

53

Define hypertensive crisis:

Sudden increase in DBP to > 130mmHg

54

HTN crisis is caused by:

Activation of RAAS

55

Tx for HTN crisis:

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

Usual cause of mitral stenosis:

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

57

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

25mmHg

58

Left atrial enlargement predisposes the heart to:

Atrial fibrillation
Stasis of blood/formation of thrombi

59

Symptoms of mitral stenosis:

Dyspnea on exertion when CO ↑
Severe stenosis - CHF

60

Pathway from mitral stenosis to LV failure:

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

Usual cause of isolated aortic stenosis:

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

62

Usual cause of aortic stenosis associated with mitral stenosis:

Rheumatic fever

63

Measurements associated with hemodynamically significant aortic stenosis:

Transvalvular gradient > 50mmHg
Orifice area < 1cm2

64

Triad of symptoms associated with aortic stenosis:

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

65

How does aortic stenosis cause syncope?

↓ SV and flow to brain

66

What determines compensation for aortic stenosis?

Timing: chronic AS better tolerated than acute stenosis

67

Effects of aortic stenosis on LV:

Hypertrophy & dilation
Poor pumping ability

68

Pathway of early atrial stenosis:

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

69

Pathway of late atrial stenosis:

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

70

Common cause of mitral regurgitation:

Rheumatic fever (associated with mitral stenosis)

71

Principle pathologic change produced by mitral regurgitation:

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

72

Mitral regurgitation responsible for ____ wave on PAOP waveform:

V wave

Size of wave correlates to magnitude of regurgitant flow

73

Ultimate pathological result of mitral regurgitation:

Tricuspid regurgitation

74

Acute causes of aortic regurgitation:

Infective endocarditis
Trauma
Dissection of thoracic aneurysm

75

Chronic causes of aortic regurgitation:

Prior rheumatic fever
Persistent systemic hypertension

76

Changes in heart function with aortic regurgitation:

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

77

First organ affected by aortic regurgitation:

Kidneys; RAAS and SNS activation makes s/s worse

78

Three types of cardiomyopathies:

Dilated
Hypertrophic
Restrictive

79

Two forms of dilated cardiomyopathy:

Inflammatory
Non-inflammatory

80

Early s/s of inflammatory myocarditis:

Fatigue
Dyspnea
Palpitations

81

Typical cause of inflammatory myocarditis:

Infection

82

Late s/s of inflammatory myocarditis:

CHF
Pulsus alternans
Tachycardia
Pulmonary edema

83

Prognosis of inflammatory myocarditis:

Usually complete recovery with long-term abx

84

Causes (5) of non-inflammatory cardiomyopathy:

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

85

Manifestation of non-inflammatory cardiomyopathy:

CHF

86

Characteristics (3) of cardiomyopathy-induced heart failure:

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

87

Describe how dilated cardiomyopathy leads to heart failure:

↓ 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

"Forward failure" presents with:

Fatigue
Hypotension
Oliguria d/t ↓ renal blood flow

89

"Backward failure" presents with:

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

90

Left sided failure presents with:

Orthopnea
Pulmonary edema
Paroxysmal nocturnal dyspnea

91

Right sided failure presents with:

Hepatomegaly
JVD
Peripheral edema

92

Other names for hypertrophic cardiomyopathy:

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

93

Type of genetic trait that causes hypertrophic cardiomyopathy:

Autosomal dominant

94

Main defect in hypertrophic cardiomyopathy:

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

95

Presenting symptom of hypertrophic cardiomyopathy for 50% of patients:

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

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

96

S/s of hypertrophic cardiomyopathy:

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

97

Arrhythmia seen with hypertrophic cardiomyopathy:

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

98

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

3-8% overall
1-3% post-op

99

Portion of the heart that enlarges in hypertrophic cardiomyopathy:

Interventricular septum, typically in top portion below aortic valve

100

Pathophysiology of hypertrophic cardiomyopathy:

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

Factors that improve systolic function in hypertrophic cardiomyopathy:

Volume loading
Vasoconstriction
Myocardial depression

All factors that impair contractility!

102

Valvular disease seen in hypertrophic cardiomyopathy:

Mitral regurgitation

103

Medical management of hypertrophic cardiomyopathy:

Beta blockers
CCBs

104

Means by which beta blockers help in hypertrophic cardiomyopathy:

Blunts the SNS mediation of subaortic stenosis
Decreases tachyarrythmias

105

Means by which CCBs help in hypertrophic cardiomyopathy:

Improves diastolic relaxation

106

Surgical management of hypertrophic cardiomyopathy:

Myomectomy

107

Echo findings in hypertrophic cardiomyopathy:

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

108

Three left-to-right shunt defects:

ASD
VSD
PDA

109

Cyanosis seen with L to R shunts:

Possible tardive cyanosis, but not seen from outset

110

Most common heart defect dx'ed in adulthood:

ASD

111

Development of ASD:

At 4-6 weeks of development
Foramen ovale does not close properly

112

Clinical features of ASD:

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

113

Most common heart defect dx'ed at birth:

VSD

114

Development of VSD:

Malformation of ventricular septum at 4-8 weeks development
Can close spontaneously in childhood

115

Clinical features of VSD:

Pulmonary HTN
CHF
Infective endocarditis from blood stasis

116

PDA closes at birth due to:

↑ O2 level
↓ pulm resistance
↓ prostaglandins (PGE2)

117

Two R to L shunts:

Tetralogy of Fallot
Transposition of great vessels

118

Cyanosis seen with R to L shunts:

True cyanosis at birth

119

Most common cause of cyanotic congenital heart disease:

Tetralogy of Fallot

120

Four components of tetralogy of Fallot:

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

121

Clinical signs of tetralogy of Fallot:

↓ blood flow to lungs
↑ blood flow to aorta

122

Manifestations of unrepaired tetralogy of Fallot:

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

123

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

ASD, VSD, PDA - L to R shunts

124

Clinical feature of transposition of the great vessels:

Cyanosis

125

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

Where the narrowing is in relation to the ductus arteriosis

Postductal more common

126

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

Dx in infants
Weak femoral pulses
Cyanosis of lower extremities
CHF

Must be surgically corrected for survival

127

S/s of postductal coarctation of the aorta:

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