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Cardiac Pathologies > CARDIAC PATHOPHYSIOLOGY > Flashcards

CARDIAC PATHOPHYSIOLOGY Flashcards

1
Q

what type of edema you may see in CHF

A

May see PULMONARY &/or SYSTEMIC EDEMA

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2
Q

a highly cardiac specific enzyme that is released into the blood during an MI

A

troponin

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3
Q

Atherosclerotic Heart Disease a.k.a.

A

Coronary Artery Disease

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4
Q

in myocardial ischemia…

Increased myocardial oxygen demand caused by?
Decreased myocardial oxygen supply caused by?

A
  • Increased: exercise, mental stress, spontaneous fluctuations of HR or BP
  • Decreased: decreased coronary blood flow (need 70% occlusion)
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5
Q

arteriography

A
  • radiography of an artery, carried out after injection of a radio-opaque substance.
  • preparation for surgery of peripheral artery aneuyrysm
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6
Q

Restrictive CM (RCM):

characteristics and causes

A
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7
Q

Type B aortic aneurysm

A

a aortic aneurysm anywhere but the ascending aorta

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8
Q

LDL:HDL ratio levels

A
  • Provides a composite risk marker
  • < or = 3:1 ratio is ↓ risk
  • > or = 5:1 ratio is an ↑ risk
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9
Q

Pericarditis is commonly caused by

A

viral infection

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10
Q

MUSCULOSKELETAL Physiologic Consequences of CHF

A
  • Muscle wasting & possible skeletal muscle myopathies and osteoporosis are possible due to inactivity or other co-morbidities and to vasculature’s impaired ability to vasodilate; leads to sedentary lifestyle.
  • Inability in increase HR and SV
  • Diastolic dysfunction is exacerbated with exercise
  • EF correlates to exercise tolerance
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11
Q

normal LDL and HDL cholesterol levels

A
  • Low Density Lipoprotein = <100 desirable, more than 190 very high
  • High (healthy) Density Lipoprotein = >60 optimal, less than 40 low
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12
Q

📣

st wave elevation may be

A

transmural MI

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13
Q

Is there a difference between Coronary Heart Disease and Coronary Artery Disease?

A
  • Terms used interchangeably
  • CHD is actually caused by CAD
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14
Q

Surgical management of CHF

A
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15
Q

Transmural MI

A
  • full thickness
  • Q wave MI
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16
Q

Ventricular Remodeling in diastolic heart failure

A

hypertrophied heart

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17
Q

MI Classification:

(types of MI)

A
  • Subendocardial = partial thickness = NSTEMI = Non-Qwave MI
  • Transmural = full thickness = STEMI = Q wave MI
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18
Q

Pathogenic mechanism of plaque formation: the lipid hypothesis:

A

increased LDL in blood penetrates arterial wall → lipids accumulate in smooth muscle cells → hyperplasia of smooth muscle → endothelium tears and platelets aggregate → results in thrombus formation

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19
Q

‼️

Left ventricular hypertrophy results in ___________ dysfunction (impairs filling of
ventricles)

A

diastolic

Rapid ventricular emptying →may see high ejection fraction

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20
Q

Why is HDL cholesterol considered “good” cholesterol?

A

HDL cholesterol protects against CHD by taking LDLs out of the blood and keeping it from building up in arteries

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21
Q

Types of Aneurysms:
can be classified by shape and size and described as…

A
  • Saccular: Usually spherical in shape and involve only a portion of the vessel wall
  • Fusiform (“spindle-shaped”): often involve large portions of the ascending and transverse aortic arch, abdominal aorta, or less frequently the iliac arteries
  • Mycotic: caused by the growth of fungi or bacteria within the vascular wall, usually following impaction of a septic embolus
  • Dissecting: Resulting from hemorrhage that causes longitudinal splitting of the arterial wall, producing a tear in the intima and establishing communication with the lumen
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22
Q

HR protocol post MI

A

20-25 bpm of baseline (resting heart rate) in the first 6-8

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23
Q

Is felt as pulsatile mass on one or both sides of the thigh

A

may be femoral artery aneurysm

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24
Q

total cholesterol normal levels

A

less than 200 = desirable
more than 240 = high

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25
Q

endocarditis can cause ______ damage → CAN BE FATAL

A

valve

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26
Q

Pericarditis may progress to →

A

Pericardial effusion (excess fluid around the heart)

Leading to → Cardiac Tamponade ***EMERGENCY***

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27
Q

Type A aortic aneurysm

A

aortic dissection in the ascending aorta

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28
Q

____________ is the most common type of heart
disease, killing more than 370,000 people annually

A

Coronary heart disease

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29
Q

nodular deposits of fatty material that line the walls of the artery (plaques), and the vessel walls may also lose their elasticity and become sclerotic

A

Atherosclerotic Heart Disease a.k.a. Coronary Artery Disease

(“Hardening of the Arteries”)

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30
Q

Transports fatty acids and lipids

A

Cholesterol

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31
Q

Are cardiac tumors common?

A

no, generally very rare and many are curable with surgery

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32
Q

Inferior wall MI:

A
  • RCA
  • SA node
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33
Q
  1. Malignant cardiac tumors are usually classified as…
  2. which one is the most common?
A
  1. usually classified as sarcomas
  2. Hemangiosarcomas (most common)
  • Rhabdomyosarcoma
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34
Q

The Newest and Preferred Marker enzyme for the diagnosis of MI?

A

troponin

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35
Q

Localized dilatation and weakening of the wall of a blood vessel

A

Aneurysms

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36
Q

normal triglycerides levels

A

<150 normal

>500 very high (high risk)

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37
Q

NUTRITIONAL physiologic Consequences of CHF

A

May see anorexia that can lead to malnutrition & cachexia

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38
Q

SYMPATHETIC NS (SNS) Compensation for CHF

A

Decreased CO sensed by baroreceptors → Leads to increased SNS activity → Release of norepinephrine → increases HR, SV, myocardial contractility AND ↑systemic resistance and BP due to peripheral vasoconstriction that stimulates the kidneys to increase renin release

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39
Q

Classic Symptom Of Ischemia

A

Angina Pectoris (Angina)
Described as “pressure” or “heaviness”

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40
Q

Syndrome where the heart is unable to pump enough output to meet the body’s metabolic demands

A

Congestive Heart Failure (CHF)

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41
Q

Occurs almost exclusively at rest due to coronary artery spasm

A

Prinzmetal’s Angina (Variant or Atypical Angina)

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42
Q

Diverse group of diseases involving primary disorder of the myocardial cells with ultimate cardiac dysfunction (involve the myocardium) in which contraction, relaxation, or both of cardiac muscle are impaired

A

Cardiomyopathy (CM)

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43
Q

Dilated cardiomyopathy results in:
Prognosis?

A
  • Decreased stroke volume
  • Impaired ability to increase cardiac output with exercise
  • Eventual development of left ventricular failure and right ventricular failure (less effective pump)
  • Prognosis is good WITHOUT clinical heart failure
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44
Q

in Left Sided/Ventricular Failure: CHF may also see

A

– Also may see increased LVEDP (pressure)
– Also LV dilatation may stretch mitral valve

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45
Q

Compensated vs Decompensated CHF

A

Compensated: Mild/moderate symptoms & degree of volume overload

Decompensation: baseline abnormalities become further deranged

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46
Q

Clinical Manifestations of CHF, right ventricular failure:

A
  • Dependent edema
  • Hepatomegaly
  • Ascites
  • Fatigue
  • Anorexia, nausea, bloating
  • Right sided S3 or S4
  • Accentuated P2 (heart sound—closure of pulmonic valve)
  • Pulmonary or Tricuspid valve murmurs
  • s/s: JVD, weight gain, RUQ (liver) pain, jaundice, cyanosis (nail bed), ↓urine output
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47
Q

The first symptom of hypertrophic CM my be

A

sudden collapse & possible death

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48
Q

Cardiac/Ventricular Remodeling

A
  • Pathologic and physiologic changes in size, shape, structure and physiology of the heart after injury to the myocardium.
  • Left ventricle may change from elliptical to spherical
  • Apoptosis—programmed death of cells, is more severe with CHF
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49
Q

Response to MI
🚨

A
  • 24h: inflammatory response to necrosis
  • 2 - 4 days: visible necrosis, recovery begins
  • 4 - 10 days: Debris cleared → matrix laid down
  • 10 – 14 days: Formation of weak fibrotic scar

**The scar tissue is inelastic and is not able to contract and relax like healthy myocardial tissue

50
Q

Right Sided/Ventricular Failure: Cor Pulmonale

A

Prolonged pulm HTN → Increased right ventricle afterload → Anatomical changes to right ventricle (dilatation → possible hypertrophy) → Right ventricular end-diastolic pressure (EDP) increases → Reflects back up to right atrium and venous system

51
Q

Popliteal artery aneurysm use _______ to diagnose and measure diameter

A

ultrasound

52
Q

Hormones Involved in CHF

A
53
Q

what is the the most common cause of right CHF

A

left CHF

54
Q

most common bening cardiac tumor

A

myxoma

55
Q

Popliteal artery aneurysm Account for ____ of all peripheral artery aneurysms

A

~85%

56
Q

the release of Natriuretic peptides (brain NP, atrial NP, endothelial C type NP) may reflect or indicate

A

acute and chronic volume pressure overload

57
Q

what is the recommended LDL value for patients with DM or other CHD risk factors

A

less than 100

58
Q

Cardiac Enzymes release after MI:

A
  • Troponin (4-6 h): last several days
  • Creatine kinase (4-8h): released when cells die, last 2-3 days
  • Myoglobin (1-4 h): protein released with injury to the myocardium
59
Q

Hypertrophic CM (HCM) characterized by

A
  • Considerable increase in cardiac mass (hypertrophy)
  • No cavity dilatation
  • Normal or increased systolic function
  • May demonstrate left ventricular outflow obstruction
    (hypertrophic obstructive CM or IHSS)
60
Q

Types of angina:

A
  • Chronic stable angina: treat
  • Unstable angina: don’t treat
61
Q

Difference between ischemia and infarction

A
  • Ischemia: decrease in blood flow
  • Infarction: tissue death caused by ischemia
62
Q

Causes of dilated cardiomyopathy

A
  • Idiopathic (arises spontaneously or for which the cause is unknown)
  • Heart disease and uncontrolled HTN (most common)
  • Myocarditis
  • Infectious or non-infectious inflammatory process
  • Toxins (ex: ETOH, drugs, chemo)
  • Pregnancy
  • Metabolic disorder
  • Hereditary disease (ex: muscular dystrophy)
63
Q

Medical management of CHF

A
64
Q

Treatment of CHF

A
65
Q

Diagnosis of CHF:

A
66
Q

difference between chronic stable angina and unstable angina

A
  • Chronic Stable Angina: precipitated by exertion, emotional streess, heavy meals
  • Unstable Angina: symptoms of angina without the demands that usually generate it
67
Q

Treatment of Aneurysms

A

Surgical excision and grafting
– Endovascular (prefered) repair vs Open repair

68
Q

Causes of MI:

A

👉🏻 Whatever leads to severe vasoconstriction

  • Prolonged myocardial ischemia (atherosclerosis)
  • Prolonged vasospasm
  • Embolic occlusion
  • Cocaine
  • ➔ Leads to focal death of myocardial tissue in the area supplied by the involved coronary artery * Very often in the LV*
69
Q

In Right Sided/Ventricular Failure: Cor Pulmonale, may also see what?

A

May see jugular venous distension (JVD), liver engorgement, ascites, and peripheral edema

70
Q

when does troponin become elevated after an MI?

A

Elevated between 4-6 hours post MI
Peaks at 24 hours

71
Q

Non-Drug Management of CHF

A
72
Q

what is the recommended LDL value for patients with CHD or vessel disease?

A

less than 70

73
Q

when does myocardial recovery begin s/p MI

A

2 - 4 days s/p MI

74
Q

symptoms of angina

A
  • Pain, pressure and heaviness over the heart (precordial), in the shoulder, arm, throat or jaw
  • DOE (dyspnea on exertion)
  • Fatigue
  • Weakness
  • Syncope
75
Q

Occurs when myocardial oxygen demand is greater than the supply

A

Myocardial Ischemia

76
Q

The earliest detectable atherosclerotic lesion is known as

A

the fatty streak (lipid foam cells)

Fatty streak → fibrous plaque

77
Q

Diagnosis of MI, at Least 2/3 of the following symptoms must be present

A
  • Anginal Symptoms: Chest pressure, heaviness, pain, arm, jaw
    • DOE
    • Fatigue
    • Syncope
    • Belching
  • EKG Changes
  • Rise of Cardiac Enzymes
78
Q

Dilated cardiomyopathy characterized by:

A
  • Increased cardiac mass
  • Dilatation of all 4 cardiac chambers
    • With little or no wall thickening
  • Systolic dysfunction
79
Q

Cholesterol comes from 2 sources:

A
  • 75% our bodies
  • 25% from food sources (animal products only)
80
Q

Chronic Stable Angina is relieved with

A

nitroglycerin (NTG)

(vasodilation)

81
Q

Peripheral Artery Aneurysms occur almost exclusively in

A

men

82
Q

Athero =
Sclerosis =

A
  • gruel, soft deposit
  • hardening
83
Q

Systolic Heart Function Failure:

A
  • Increased preload → lead to pump failure
  • Increased afterload → leads to pump failure
  • Decreased contractility of the myocardium → leads to pump failure; most common.
  • Changes in rate of contraction (chronotropic) → (to slow or too fast) lead to pump failure.
84
Q

3 main categories of cardiomyopathy

A
  • Dilated Cardiomyopathy (DCM)
  • Hypertrophic Cardiomyopathy
  • Restrictive Cardiomyopathy
85
Q

PANCREATIC physiologic Consequences of CHF

A

Possible impaired insulin secretion & subsequent glucose tolerance – May also be another source of a myocardial depressant factor

86
Q

Pathogenic mechanism of plaque formation: chronic endothelial injury

A

Injury of the interior of the cell wall by macrophages causes platelets, monocytes, lipids & smooth muscle cells to migrate and aggregate from the media to the intima where they form a fibrous cap → platelets form clots & release proteins with tough fibers further hardening the artery → Can block blood flow or break off and throw a clot.

87
Q

Inflammation of endocardium (usually due to microbial infection)

A

Endocarditis

88
Q

Silent Myocardial Infarction

A
  • No symptoms of angina
  • Can occur in any patient but more common in those with DM and ETOH (alcohol) abuse
    – Peripheral neuropathies may contribute to this
  • Must be ruled in by EKG changes and Cardiac Enzymes
89
Q

Clinical Manifestations of CHF, left ventricular failure:

A
  • Progressive Dyspnea (exertion→rest)
  • Dyspnea & orthopnea PND (paroxysmal nocturnal dyspnea)
  • Fatigue/weakness
  • Pulmonary rales
  • S1 heart gallop, S3
  • Enlarged heart
  • Functional MR, TR
  • s/s: pulmonary edema, pallor, cyanosis, diaphoresis, tachypnea, anxiety, agitation, s/s of cerebral hypoxia
90
Q

How is myocardial ischemia diagnosed?

A
  • by exercise stress test
  • arrhythmias and T wave inversion on an EKG → later becoming ST elevation
91
Q

NEUROCHEMICAL Physiologic Consequences of CHF:

A

Increased sympathetic stimulation desensitizes heart to β1-adrenergic receptor stimulation → decreases heart’s inotropic effect (strength of the contraction)

92
Q

Ventricular Remodeling in systolic heart failure

A

dialated heart

93
Q

Types of thoracic aneurysms:

A
  • Infrarenal (90%): May be symptomatic/asymptomatic.
    • Symptoms: chronic mid-abdominal &/or low back pain
  • Thoracic: Usually asymptomatic.
    • May also be due to Marfan’s syndrome
94
Q

Counter-regulatory Hormones in CHF

A
95
Q

HEMATOLOGIC Physiologic Consequences of CHF

A

Possible anemia and hemostatic abnormalities

96
Q

cardiac disease count for 1 in every ___ deaths

A

4

97
Q

CARDIAVASCULAR Physiologic Consequences of CHF:

A

Decreased myocardial performance → try to increase venous return w/peripheral vascular constriction → increased peripheral vascular resistance (sympathetic ns contributes to this)

98
Q

📣

What are the systems involved in compensating CHF?

A
  1. Autonomic Nervous system: ↑vasocontriction
  2. Renin-Angiotensin-Aldosterone system: ↑vasocontriction, ↑water retention
  3. Natiuretic peptide counter-regulatory system: ↑vasodilation, ↓filling pressures, improved myocardial relaxation, ↑ water excretion, suppression of AS and ANS activity
99
Q

EKG Changes with MI

A
  • Peaked T Waves
  • ST Elevation (transmural)
  • Q Wave Present
  • T Wave Inversion
100
Q

Sign of aneurysm:

A

pulsating swelling that produces blowing murmur on auscultation

101
Q

In a multi-center study of 515 women who had an acute myocardial infarction (MI), the most frequently reported symptoms were:

A
  • unusual fatigue,
  • sleep disturbances
  • shortness of breath,
  • indigestion and anxiety
102
Q

Symptoms of Prinzmetal’s Angina

A
  • Often severe chest pain, awakening patient from sleep
  • Often spasm responds to NTG (though not always)
103
Q

types of aneurisms

A
  • True aneurysm (3 layes involved)
  • False or Pseudo-aneurysm: blood leaking confined by sourrounding tissues
104
Q

Pressure in pulmonary vasculature where see pulmonary edema develop is ~___ mmHg

A

25

105
Q

myocardial infarction

A

COMPLETE interruption of blood supply to an area of the myocardium

106
Q

How are cardiac enzymes used in the diagnosis of MI/

A

Cardiac muscle cells become necrotic resulting in the diffusion of several cardiac markers into the blood

  • Troponin
  • Creatine kinase
  • Myoglobin
107
Q

Lateral wall MI:

A

Left Circumflex Artery

108
Q

2 types of peripheral artery aneurysm in men:

A
  • Popliteal artery aneurysm
  • Femoral artery aneurysm
109
Q

Decreased SV and CO (decreased EF) → Increased LVEDV → Decreased LV compliance → Increased left atrial dilatation → Increased pressure in pulmonary vessels → Transudation of fluid from pulmonary capillaries

A

Left Sided/Ventricular Failure: CHF

110
Q

CHF may result from:

A

Any structural/functional cardiac disorder that impairs the filling or pumping ability of the ventricles

111
Q

PULMONARY Physiologic Consequences of CHF:

A

Develop pulmonary edema due to increased filling pressures

112
Q

Anterior Wall MI:

A
  • Left Coronary Artery
  • More severe effect: L ventricle
113
Q

New York Heart Association of CHF

A
114
Q

RENAL Physiologic Consequences of CHF

A

Due to decreased CO → decreased renal blood flow & glomerular filtration rate → sodium & fluid retention

{Heart failure also associated with increased circulating levels of arginine vasopressin (vasoconstrictor & inhibitor of water excretion)}

115
Q

📣

ST wave depression may be

A

Subendocardial MI

116
Q

HEPATIC physiologic Consequences of CHF

A

Possible cardiac cirrhosis due to hypoperfusion due to decreased CO or hepatic venous congestion

117
Q

Subendocardial MI

A
  • partial thickness
  • Non Qwave MI
  • May not have as significant EKG changes, but pt symptomatic and lab values indicate injury
118
Q

“Build-up of plaque in the heart’s arteries that can cause a heart attack.”

A

Coronary Heart Disease (CHD)

119
Q

Left Sided/Ventricular Failure aka

A

CHF

120
Q

tissue zones of infarction: which area is recoverable?

A
  • Zone of Infarct: cell death
  • Zone of Injury: not cell death
  • Zone of Ischemia: recoverable area
121
Q

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM Compensation for CHF

A
  • systems that maintain BP when we have low volume in our bodies
  • increases venous and atrial tone
  • triggers the release of norepinephrine
  • The release of RENIN (by the ANS) in the system → Angiotensin II: Powerful vasoconstrictor → Initially restores BP but can ultimately lead to decreased CO, renal perfusion, Contributes to remodeling and promotes the release of aldosterone (Acts on the kidneys increase resorption of water)
122
Q

Is myocardial ischemia reversible?

A

yes, usually with rest

Cardiac Pathologies (13 decks)

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