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Pathophysiology > Case studies 11, 12, 15 (heart attack, failure, and disease) > Flashcards

Case studies 11, 12, 15 (heart attack, failure, and disease) Flashcards

1
Q

Heart failure

A
  • No longer able to pump adequate amount of blood
  • The ventricles fail to maintain cardiac output to adequately perfuse the tissues
    (chronic and acute)
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2
Q

forward heart failure

A

reduced blood flow to tissues → reduced renal blood flow → activates renin-angiotensin-aldosterone mechanism → salt and water retention to increase blood volume and venous pressure → edema

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3
Q

backward heart failure

A

blood “back ups” in veins draining to the heart → increased venous pressure, congestion, edema

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4
Q

congestive heart failure etiology

A 
Any type of heart disease that cause
- myocardial weakness
- restrictions to pumping
- increased after load
(AKA EVERYTHING)
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5
Q

left side heart failure

A
  • Left ventricle is failing
  • Blood backs up in pulmonary circulation
  • Pulmonary congestion and more pronounced respiratory difficulties occur
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6
Q

right side heart failure

A
  • Right ventricle is failing
  • Blood backs up in systemic circulation
  • Liver and spleen enlarge and peripheral edema is more prominent
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7
Q

Pulmonary edema

A
  • Fluid accumulation in the lungs
  • Caused by left-sided heart failure
  • Causes an increase in blood hydrostatic pressure in the pulmonary capillaries
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8
Q

Pleural effusion

A
  • Excess accumulation of fluid in the pleural space

- Eventually the same processes will lead to fluid leaking into the pleural space and causing the effusions

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9
Q

Pitting edema

A

Swelling in which a persistent depression is left when pressure is applied

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10
Q

Hepatomegaly

A
  • Systemic venous congestion impairs the drainage of blood from the liver into the inferior vena cava
  • Blood vessels in the liver become congested with blood
  • the liver enlarges
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11
Q

Natriuretic Peptides in Heart Failure

A
  • Peptides are released from stretched cardiac muscle
  • Results from overdistention or elevated pressure in cardiac chambers
  • promote urinary loss of salt and water, counteracting the effects of the renin-angiotensin-aldosterone system
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12
Q

Type B natriuretic peptide (BNP)

A
  • released from ventricles is more significant physiologically than atrial peptide
  • Measurement helpsdistinguish dyspnea due to heart failure (high BNP) from dyspnea caused by pulmonary disease (no significant BNP elevation)
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13
Q

Benign Prostatic Hyperplasia

A

The prostate enlarges and, because it surrounds the urethra, it causes constriction of the urethra and obstructs the outflow of urine

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14
Q

Acute myocardial infarction (MI)

A

Necrosis of myocardial tissue caused by the development of severe ischemia

Precipitating event often involves the disruption of an atheromatous plaque

often involves muscles of the LV and septum

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15
Q

Transmural infarct

A

full-thickness infarct from endocardium to epicardium, usually from clot in major coronary artery

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16
Q

Subendocardial infarct

A

only part of wall undergoes necrosis

17
Q

cardiac arrest may result from

A
  1. Arrhythmia

2. Asystole

18
Q

acute MI classical symptoms

A 
- Severe chest pain
often radiating to left shoulder, arm, or jaw
- Diaphoresis 
- Shortness of breath/Breathlessness
- Anxiety
- Nausea and vomiting
- Lightheadedness, dizziness, fatigue 
- Signs of falling cardiac output
19
Q

who is most likely to experience atypical MI symptoms

A

women
elderly
people with diabetes

20
Q

myoglobin

A
  • A heme containing protein found in cardiac and skeletal muscle
  • It is released early from damaged cardiac cells
  • Increase within 2-4 hrs of injury
  • Peak within 6-12 hrs
  • Return to baseline 24-36 hrs
21
Q

creatine kinase

A

enzyme in muscle and brain

22
Q

CKMB

A
  • Isoenzyme of CK found mainly in cardiac muscle
  • Increase within 3-12 hrs of injury
  • Peak within 24 hrs
  • Return to baseline 24-72 hrs
23
Q

troponin

A
  • Muscle protein complex
  • Consists of 3 subunits
    Troponin T and I each have a subtype specific to cardiac muscle
  • Increase within 3-13 hrs of injury
  • Peak within 24-48 hrs
  • Return to baseline 5-14 days
24
Q

MI early treatment

A 
MONA
oxygen
aspirin
morphine
nitroglycerine
25
Q

cause of coronary heart disease

A

arteriosclerosis of coronary arteries
(Narrowing of arteries from lipid deposits (neutral fat and cholesterol) by diffusion from bloodstream –> Atherosclerosis)

26
Q

pathogenesis of coronary heart disease

A
  • Initial endothelial injury
  • Cholesterol and lipids accumulate in cytoplasm of these cells producing unstable plaques
  • Cholesterol precipitates as crystals, causing cell necrosis
  • Cholesterol crystals, debris, enzymes leak out of damaged cells –> secondary fibrosis, calcification, degenerative changes in arterial wall
27
Q

Atheroma or atheromatous plaque

A
  • Irregular mass of yellow, mushy debris encroaching on lumen of artery and extending into muscular and elastic tissues of arterial wall
  • rough and ulcerated at the surface
28
Q

stable plaques

A

Are less likely to rupture, but cause permanent narrowing of vessel

29
Q

coronary heart disease major risk factors

A

Elevated blood lipids
High blood pressure
Cigarette smoking
Diabetes

30
Q

cholesterol

A

synthesized in body and from diet

High levels associated with premature atherosclerosis and increased CVD risk; transported by lipoproteins

31
Q

LDLs

A

carry cholesterol to tissues for utilization

BAD

32
Q

HDLs

A

carry cholesterol not used by the tissues back to the liver for metabolism or excretion in bile
GOOD, protective

33
Q

Angina pectoris

A

Chest pain from temporary reduction in blood flow to cardiac muscles despite increased oxygen demand

34
Q

Classic or Stable angina

A

midsternal pressure or discomfort on exertion, subsides with rest or intake of nitroglycerine

35
Q

Unstable angina

A

pain lasts longer, occurs more frequently with less exertion, and is less completely relieved by nitroglycerine

36
Q

Prinzmetal’s angina (Variant angina)

A

pain at rest rather than exertion, caused by coronary artery spasm; does not respond to nitroglycerine

37
Q

why does myocardial ischemia develop

A

increased oxygen demand

decreased oxygen supply

38
Q

Nitroglycerine

A
  • Relaxes vascular smooth muscle

- Decreases cardiac preload and afterload**

Pathophysiology (3 decks)

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