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ARCHIVED: Pathophysiology > Exam 2: Cardiac > Flashcards

Exam 2: Cardiac Flashcards

(127 cards)

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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
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 ```

ARCHIVED: Pathophysiology (18 decks)

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