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Pathophysiology > 24. Cardiac Disease and Shock > Flashcards

24. Cardiac Disease and Shock Flashcards

1
Q

volume of blood ejected by ventricle w/ each beat

A

stroke volume (SV)

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2
Q

volume in LV just before ejection

A

preload (aka EDV)

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3
Q

fraction of EDV ejected in each stroke volume (how much blood left the ventricle w/ each contraction)

A

ejection fraction

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4
Q

How to calculate EF

A

EF% = SV/EDV (usually about 55%)

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5
Q

total volume of blood ejected by ventricle per minute

A

cardiac output

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6
Q

How to calculate CO

A

CO = SV x HR (usually about 5 L/min)

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7
Q

Pressure required to eject blood (open aortic valve)

A

afterload

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8
Q

resistance to blood flow in systemic circulation

A

peripheral vascular resistance (PVR)

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9
Q

increased PVR increases what?

A

afterload -> more pressure to push blood out of heart if pressure is higher is system

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10
Q

Increased preload is a result of what?

A
  • hypervolemia - renal failure - regurgitation of cardiac valves
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11
Q

Increased afterload is a result of what?

A
  • hypertension - vasoconstriction
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12
Q

Explain how increased preload can lead to decreased SV and heart failure

A
  • increased preload -> stretching of myocardium -> decreased contractility -> decreased SV + increased ventricular end-diastolic pressure -> pressure backs into pulmonary and venous systems (pulmonary and peripheral edema)
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13
Q

lipoprotein responsable for delivery of cholesterol to the tissues

A

LDL

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14
Q

lipoprotein responsible for transport of excess cholesterol from the tissues to the liver

A

HDL

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15
Q

Optimal levels for total cholesterol, LDL, and HDL

A
  • total cholesterol: <200 mg/dL - LDL: <100 mg/dL - HDL: >60 mg/dL
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16
Q

condition characterized by thickening and hardening of the vessel wall

A

arteriosclerosis

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17
Q

form of arteriosclerosis that is caused by accumulation of lipid-laden macrophages within the arterial wall which leads to the formation of a lesion called a plaque

A

atherosclerosis

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18
Q

6 possible causes of endothelial injury

A
  • smoking - HTN - DM - increased LDL - decreased HDL - autoimmunity
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19
Q

Explain the pathophysiology of atherosclerosis

A
  • injury to endothelial cells in artery wall -> inflammation - inflammatory process summons macrophages and produces oxygen free radicals - LDL becomes oxidized (causes additional recruitment) - macrophages engulf oxidized LDL -> foam cells - accumulation of foam cells = fatty streak - fatty streak + collagen from injured vessel = fibrous plaque - plaques may occlude blood flow or rupture (rupture initiates clotting and thrombus formation -> ischemia -> infarction)
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20
Q

plaques that have ruptured are called what?

A

complicated plaques

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21
Q

What usually causes CAD?

A

atherosclerosis (plaque formation)

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22
Q

develops if flow or O2 content of coronary blood is insufficient to meet metabolic demands of myocardial cells

A

myocardial ischemia

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23
Q

plaques that are prone to rupture

A

unstable plaques

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24
Q

Explain how coronary occlusion leads to myocardial infarction

A
  • myocardial cells become ischemic in 10 seconds of occlusion - cells deprived of glucose needed for aerobic metabolism -> switch to anaerobic (lactic acid accumulation) - heart cells lose ability to contract -> CO decreases
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25
Q

How long can myocardial cells go without O2 before myocardial infarction

A

about 20 minutes

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26
Q

angina caused by gradual luminal narrowing and hardening of arterial walls; consistent type of pain

A

stable angina pectoris

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27
Q

clinical manifestation of stable angina pectoris

A
  • transient substernal chest pain (may be mistaken for indigestion) - pallor, diaphoresis, and dyspnea (may all be associated w/ pain)
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28
Q

common symptoms of stable angina pectoris seen in women

A
  • atypical chest pain - palpitations - sense of unease - severe fatigue
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29
Q

What relieves stable angina pectoris?

A

rest and nitrates

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30
Q

chest pain attributable to to transient ischemia of myocardium that occurs unpredictably and often at rest; caused by vasospasm of one or more major coronary arteries with or without atherosclerosis

A

prinzmetal angina (varient angina)

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31
Q

myocardial ischemia that may not cause detectable symptoms

A

silent ischemia

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32
Q

2 things linked to silent ischemia

A

DM and chronic stress

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33
Q

angina that is increasing in severity or frequency, new-onset, or at rest; result of reversible myocardial ischemia and is a sign of impending infarction

A

unstable angina

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34
Q

results when there is prolonged ischemia causing irreversible damage to heart muscle

A

myocardial infarction (MI)

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35
Q

EKG changes during unstable angina

A

ST depression and T wave inversion

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36
Q

procedure whereby stenotic (narrowed) coronary vessels are dilated w/ a catheter

A

percutaneous coronary intervention (PCI)

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37
Q

persistent coronary occlusion leads to infarction of the myocardium closest to the endocardium

A

non-STEMI

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38
Q

EKG signs of non-STEMI

A

ST depression and T wave inversion without Q waves

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39
Q

continued coronary occlusion that leads to transmural infarction extending from endocardium to pericardium

A

STEMI

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40
Q

EKG signs of STEMI

A

marked elevations of ST segments

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41
Q

explain how acute mental stress can lead to MI or sudden cardiac death

A
  • stress -> ANS activity -> increased HR, BP and coronary constriction - atherosclerosis or poor LV function -> increased demand and decreased supply - leads to ischemia, plaque rupture, and thrombosis (from platelet activity) - may also cause electrical instability -> VFib/Vtach
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42
Q

temporary loss of contractile function that persists for hours to days after perfusion has been restored

A

myocardial stunning

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43
Q

describes tissue that is persistently ischemic and undergoes metabolic adaptation to prolong myocyte survival until perfusion is restored

A

hibernating myocardium

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44
Q

classic signs of myocardial infarction

A
  • heavy/crushing chest pain - pain may radiate to neck, jaw, back, shoulder, or left arm - N/V - diaphoresis
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45
Q

4 areas of damage caused by HTN

A
  • retina - renal disease - CAD/CHF - neurologic disease (stroke, dementia, encephalopathy)
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46
Q

HTN caused by an underlying disorder (ex. renal disease)

A

secondary HTN

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47
Q

What factors lead to HTN

A
  • genetics + environment - obesity, adipokines, insulin resistance - dysfunction of SNS, RAAS, and ANP/BNP - inflammation
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48
Q

How do the factors leading to HTN cause damage

A
  • vasoconstriction -> increased PVR - renal salt and H2O retention -> increased blood volume - increased PVR + increased volume -> sustained HTN and vascular remodeling
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49
Q

rapidly progressive HTN in which diastolic pressure is usually greater than 140 mmHg

A

hypertensive crisis (malignant HTN)

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50
Q

name 3 acute coronary syndromes (ACS)

A
  • unstable angina - non-STEMI - STEMI
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51
Q

when the heart is unable to generate adequate CO -> decreased perfusion of tissues or increased diastolic of LV filling pressure

A

heart failure

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52
Q

how is left heart failure/congestive heart failure categorized

A

whether there is reduced ejection fraction or persevered ejection fraction

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53
Q

ejection fraction <40% and an inability of the heart to generate adequate CO to perfuse tissues

A

heart failure w/ reduced ejection fraction (HFrEF) or systolic HF

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54
Q

3 major determinants of stroke volume

A
  • contractility - preload - afterload
55
Q

Explain how increased PVR can lead to heart failure

A
  • increased PVR -> increased afterload (increased resistance to ventricular ejection) - increased workload in LV - increased RAAS and SNS - hypertrophy - increased myocyte demand for O2 (reactive ischemia) - ventricular remodeling - decreased contractility (decreased CO and perfusion of tissues)
56
Q

RAAS and SNS release what neurohormones that play a role in ventricular remodeling?

A
  • angiotensin II (aldosterone and vasoconstriction) - aldosterone (retain Na and H2O) - catecholamines (increased HR and BP) - cytokines (inflammation)
57
Q

symptoms of left heart failure (CHF)

A
  • paroxysmal nocturnal dyspnea - cough (w/ frothy/pink-tinged sputum) - orthopnea - exertion dyspnea - fatigue - decreased urine output - edema
58
Q

Exam findings of left heart failure (CHF)

A
  • cyanosis - inspiratory crackles - pleural effusions - HTN or hypotension
59
Q

What serum level will be elevated in left heart failure (CHF)

A

serum B-type natriuretic peptide (BNP)

60
Q

pulmonary congestion despite a normal stroke volume and CO; results from increased LVEDP which reflects back into pulmonary and venous system

A

heart failure w/ preserved ejection fraction (HFpEF) or diastolic heart failure

61
Q

inability of the RV to provide adequate blood flow into pulmonary circulation; usually due to preceding left heart failure

A

right heart failure

62
Q

clinical manifestations of right heart failure

A
  • fatigue - distended jugular veins - ascities - edema - anorexia and GI distress
63
Q

inability of the heart to adequately supply body w/ blood-borne nutrients despite adequate blood volume and normal or elevated myocardial contractility

A

high-output failure

64
Q

condition of excess fluid in the lungs

A

pulmonary edema

65
Q

valve orfice is constricted and narrowed so blood cannot flow forward and the workload of the cardiac chamber proximal to the diseased valve increases

A

valvular stenosis

66
Q

valve leaflets (cusps) fail to shut completely -> allow blood to flow backwards into previous chamber (increases volume heart must pump and workload)

A

valvular regurgitation (insufficiency/incompetence)

67
Q

most common valvular abnormality

A

aortic stenosis

68
Q

3 causes of aortic stenosis

A
  • congenital bicuspid valve degeneration - changes w/ aging - rheumatic heart disease
69
Q

cardiovascular and pulmonary outcomes of aortic stenosis

A
  • LV hypertrophy -> left heart failure - pulmonary edema
70
Q

impairs blood flow of blood from LA to LV; leads to LA hypertrophy and right heart failure

A

mitral stenosis

71
Q

most common form of rheumatic heart disease

A

mitral stenosis

72
Q

results from inability of aortic valve leaflets to close properly during diastole; leads to LV hypertrophy and left heart failure

A

aortic regurgitation

73
Q

causes of aortic regurgitation

A
  • infective endocarditis - connective tissues diseases (Marfan syndrome) - dilation of aortic root from HTN or aging
74
Q

permits back flow of blood into LA from LV; leads to LA hypertrophy and left heart failure

A

mitral regurgitation

75
Q

causes of mitral regurgitation

A
  • MVP - rheumatic heart disease - infective endocarditis - MI - connective tissues diseases (Marfan syndrome) - dilated cardiomyopathy
76
Q

permits back flow from RV to RA; usually due to functional problem with the valve (congenital)

A

tricuspid regurgitation

77
Q

valvular abnormalities that cause systolic murmur

A
  • aortic stenosis - mitral regurgitation (heard throughout) - tricuspid regurgitation (heard throughout)
78
Q

valvular abnormalities that cause diastolic murmur

A
  • mitral stenosis - aortic regurgitation
79
Q

when one or both cusps of mitral valve billow upward into LA during systole

A

mitral valve prolapse (MVP)

80
Q

painful, red, raised lesions found on the hands and feet. They are associated with a number of conditions, including infective endocarditis, and are caused by immune complex deposition

A

Osler’s nodes

81
Q

non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis

A

Janeway lesions

82
Q

systemic, inflammatory disease caused by delayed exaggerated response to infection by group A B-hemolytic streptococcus (pharyngeal infection only)

A

rheumatic fever

83
Q

antibodies directed against M proteins of streptococci cross-react w/ tissues of heart

A

rheumatic heart disease (RHD)

84
Q

symptoms of rheumatic fever

A
  • fever - lymphadenopathy - N/V and ABD pain - arthralgia - epistaxis - tachycardia
85
Q

general term used to describe infection and inflammation of the endocardium (especially valves)

A

infective endocarditis

86
Q

Risk factors for introduction of bacteria into endocardium

A
  • dental, GU, or cardiac procedures - skin, wound, lung, or GU infections - indwelling catheters - injection drug use
87
Q

signs and symptoms of infective endocarditis once vegetation forms

A
  • fever, night sweats, malaise, weight loss - heart murmurs and failure - embolization of vegetation -> abscesses, petechiae, splinter hemorrhages, Osler nodules, and Janeway lesions, right-side emboli = PE; left-side emboli = stroke
88
Q

acute inflammation and rubbing together of layers of the pericardium

A

acute pericarditis

89
Q

symptoms of acute pericarditis

A

sharp stabbing chest pain behind the sternum in left chest

90
Q

constriction of the pericardium which results in decreased pump power

A

chronic/constrictive pericarditis

91
Q

compression of the heart due to fluid accumulation within the pericardium

A

pericardial effusion

92
Q

cardiovascular system fails to perfuse tissues adequately -> widespread impairment of cellular metabolism

A

shock

93
Q

What is missing from cells in all types of shock? What is a common finding in all types of shock?

A
  • oxygen (either not receiving or not able to use it) - decreased CO
94
Q

Describe the effects of impaired O2 delivery and use in shock

A
  • no O2 -> anaerobic metabolism -> decrease ATP and increase lactic acid - increased lactic acid -> metabolic acidosis - decrease ATP -> decrease Na/K pump -> increased intracellular volume (cellular edema) -> decreased circulatory volume - cellular edema -> lysosomal enzymes -> inflammation and activation of clotting cascade
95
Q

Describe the effects of impaired glucose delivery and use in shock

A
  • increased serum cortisol, thyroid hormone, and catecholamines -> increased lipolysis, gluconeogenesis, and glycogenolysis - lypolysis = increased serum triglycerides - glycogenolysis = decreased energy stores - gluconeogenesis = proteins used for fuel, decrease albumin and increased urea and ammonia formation - muscle wasting and build up of metabolic products
96
Q

How does the body compensate for shock

A
  • decrease CO and tissue perfusion -> SNS activation - increased BP, HR, and contractility - RAAS activation (retain Na and H2O to increase preload) - vasoconstriction and activation of ADH -> increase preload - increased volume and CO -> restoration of perfusion
97
Q

4 types of shock

A
  • hypovolemic - cardiogenic - distributive - obstructive
98
Q

decreased CO and evidence tissue hypoxia in the presence of adequate intravascular volume (heart cannot contract effectively; fluid volume not affected)

A

cardiogenic shock

99
Q

causes of cariogenic shock

A

direct pump failure - MI, cardiac arrest - ventricular dysrhythmia

100
Q

signs and symptoms of cariogenic shock

A
  • confusion - tachycardia - hypotension - tachypnea - venous and pulmonary edema - oliguria (urine output < 30mL/hour) - dusky skin color; skin cold and clammy
101
Q

caused by loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, DI, emesis, diarrhea, or diuresis) in large amounts

A

hypovolemic shock

102
Q

signs and symptoms of hypovolemic shock

A
  • hypotension - tachypnea - tachycardia (weak pulse) - hypoxia - decreased/absent urine - thirst, agitation, anxiety, confusion - skeletal muscle weakness - cold, clammy, cyanotic skin
103
Q

shock due to decreased vascular volume or tone -> vasodilation w/ pooling causes decrease preload, SV, and CO

A

distributive shock

104
Q

3 types of distributive shock

A
  • neurogenic shock - anaphylactic shock - septic shock
105
Q

result of widespread and massive vasodilation due to parasympathetic overstimulation and sympathetic understimulation

A

neurogenic/vasogenic shock

106
Q

results from widespread hypersensitivity reaction known as anaphylaxis

A

anaphylactic shock

107
Q

signs and symptoms of anaphylactic shock

A
  • vasodilation and increase capillary permeability (due to histamine) -> hypovolemia - decreased contractility and dysrhythmia - bronchial edema and pulmonary obstruction - widespread hypoxia
108
Q

toxins and endotoxins related into blood cause systemic inflammatory response syndrome (SIRS); metabolism becomes anaerobic due to decreased MAP, clot formation in capillaries, and poor cellular uptake of O2

A

septic shock

109
Q

signs of sepsis

A
  • bacteremia + SIRS - SIRS: fever, tachycardia, tachypnea, leukocytosis
110
Q

septic shock is related to what clotting abnormality

A

DIC

111
Q

shock due to fluid shift from blood to interstitial space

A

capillary leak

112
Q

shock due to indirect pump failure (cardiac tamponade, or PE); cardiac function decreases by non-cardiac factors (total body fluid not affected)

A

obstructive shock

113
Q

signs of cardiac tamponade

A
  • JVD - paradoxical pulse - decrease CO - muffled heart sounds
114
Q

signs of PE

A
  • sudden onset dyspnea and pleuritic chest pain - apprehension/restlessness/ feeling of impending doom - cough/hemoptysis - tachypnea and decreased O2 - diaphoresis and low grade fever
115
Q

progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury

A

multiple organ dysfunction syndrome (MODS)

116
Q

most common cause of MODS

A

septic shock

117
Q

Explain pathogenesis of MODS

A
  • injury/sepsis/trauma -> neuroendocrine response and release of inflammatory mediators - activation of complement, coagulation, and kinin systems (massive systemic inflammatory response) - hypermetabolism - vasodilation and selective vasoconstriction -> maldistribution of blood flow -> hypoperfusion and decreased CO - hypermetabolism and hypo perfusion -> increased O2 demand -> tissue hypoxia/metabolic failure -> acidosis - organ dysfunction
118
Q

what is induced by extremely severe tissue ischemia or by a pathogen

A

cytokine storm

119
Q

describe 4 parts of cytokine storm

A
  • endothelium activated (vasodilates and express adhesion molecules) - monocytes activated (release cytokines) - WBC obstructed capillaries - DIC
120
Q

autoimmune condition characterized by formation of thrombi filled w/ inflammatory and immune cells; strongly associated w/ smoking

A

Buergers disease

121
Q

characterized by attacks of vasospasm in the small arteries and arterioles of the fingers

A

Raynaud phenomenon

122
Q

triggers of attacks in Raynaud phenomenon

A
  • cold temperatures - emotional stress - smoking (vasoconstriction)
123
Q

atherosclerotic disease that perfuses the limbs (especially LEs)

A

peripheral vascular disease (PVD)

124
Q

pain w/ ambulation due to gradually increasing obstruction of arterial blood flow to the legs by atherosclerosis in the iliofemoral vessels; seen in arterial PVD

A

intermittent claudication

125
Q

3 factors that promote venous thrombosis (triad of Virchow)

A
  • venous stasis (immobility, age, CHF) - venous endothelial damage (trauma, IV meds) - hypercoagulable states (inherited disorders, pregnancy, malignancy, OCP, or HRT)
126
Q

inadequate venous return over a long period

A

chronic venous insufficiency (CVI)

127
Q

A wound on the leg or ankle caused by abnormal or damaged veins; copious serous exudates, brown/tawny skin color

A

venous stasis ulcer

128
Q

due to a blood clot just below the surface of the skin

A

superficial venous phlebitis

129
Q

vein in which blood has pooled, producing distended, tortuous and palpable vessels; typically involve saphenous veins

A

varicose vein

130
Q

test specific for myocardial muscle damage

A

troponin

131
Q

sudden onset of thrombus or embolus preventing blood flow distal to the clot

A

acute arterial occlusion

132
Q

6 Ps of acute arterial occlusion

A
  • Pain - Paresthesias - Paralysis - Pallor - Pulselessness - Perishingly cold/Poikilothermia
133
Q

caused by hypercoagulability, injury to a vein, and venous stasis

A

deep vein thrombosis (DVT)

Pathophysiology (20 decks)

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