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Pathophysiology > Unit 2 - Cardiovascular System Part 1 > Flashcards

Unit 2 - Cardiovascular System Part 1 Flashcards

1
Q

s/s cardiovascular disease

A 
pain 
palpitations 
dyspnea 
fatigue
syncope 
cough
cyanosis 
peripheral edema 
claudication
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2
Q

pain

A
  • classical angina (chest pain of cardiac origin) often presents as substernal chest pain
  • (pressure, tightness, squeezing, heaviness)
  • ischemia is the underlying problem, angina is how it presents
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3
Q

angina and MI symptoms

A

may produce similar symptoms but MI tend to be more severe

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4
Q

palpitations

A

may indicate underlying heart disease that is resulting in an abnormal heart rhythm (arrhythmia)

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5
Q

dyspnea

A

shortness of breath

may be due to:

  • cardiac disease
  • pulmonary disease
  • deconditioning
  • other (anxiety, obesity, neuromuscular)
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6
Q

syncope

A

loss of consciousness due to decreased BP and inadequate cardiac output

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7
Q

fatigue

A

major symptom of angina/MI especially in women

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8
Q

cough

A

possible indicator of left sided heart failure with resulting back up into the lungs
“pulmonary congestion”

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9
Q

peripheral edema

A

occurs commonly in the presence of heart failure, LE first

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10
Q

claudication

A

“leg pain”
may occur as a result of severe atherosclerotic disease affecting the arteries that supply the LEs

“peripheral vascular disease” (PVD)

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11
Q

age associated changes

A
  • Reduced # of cardiac myocytes (electrical conduction)
  • cardiac fibrosis (heart hardening)
  • dec calcium transport across the membrane
  • dec capillary density
  • dec responsiveness to beta-adrenergic stimulation
  • dec autonomic reflex control of HR
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12
Q

additional age associated changes in cardiovascular system

A

Thickening of the left ventricular wall (“especially in the face of underlying HTN”).
Stiffening/calcification of the ventricles, valves, and arteries
Increased likelihood of clinically significant atherosclerotic heart disease
Note: Age is a non-modifiable risk factor for heart disease.

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13
Q

functional changes in cardiovascular system with aging

A

Decrease in maximal HR (MHR = “approx.” 220 – age)
Decrease in cardiac output (Q) (HR X SV = Q)
Decrease in VO2 max (“aerobic fitness”)
Increase in the incidence of arrhythmia’s

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14
Q

gender differences and the cardiovascular system

A
  • Increased incidence of Mitral Valve Prolapse (MVP) in females
  • Increase in LV mass with aging (remains constant in men)
  • Increased risk of dangerous arrhythmias
  • Decreased responsiveness to anticoagulants and thrombolytics, but a higher incidence of bleeding.

RISK OF CAD RISES POST MENOPAUSE

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15
Q

CAD in women

A

CAD is the leading cause of death in both men and women in the U.S.
Risk of CAD rises sharply with menopause
Historically women have not been treated as aggressively as men (“hysterical chest pain”)
Hormonal Influence
Estrogen appears to be “cardio-protective”
Increased HDL levels
Reduces clotting risks
Both estrogen and estradiol have a dilating effect on blood vessels (helps maintain normal BP and blood flow)
Note: Hormone Replacement Therapy has not been shown to provide “cardio-protective” benefits. This remains a controversial subject

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16
Q

oral contraceptives and cardiovascular risk

A

Oral contraceptives may increase the risk of blood clots and subsequent MI/stroke. This is especially true in women over 35 who are smokers!!

17
Q

“response to injury”

A
  • this is the most widely accepted theory explaining the pathogenesis of atherosclerotic disease, including CAD and cerebrovascular disease (CVD).
18
Q

response to injury theory

A

Damage to endothelial lining occurs (potential causes - HTN, smoking, high levels of lipids in the blood)
Platelets and monocytes adhere to injured area
Platelets release PDGF, promoting infiltration of smooth muscle cells from media to intima
Plaque composed of smooth muscle cells, connective tissue, and cellular debris forms
Lipids (LDL’s) deposited in the plaque

19
Q

risk factors for CAD - non modifiable

A

Age (83% of deaths from CAD occur in individuals > 65 y/o)
Gender (males are at greater risk, especially when compared to pre-menopausal women)
Genetics (a family history of premature heart disease is associated with elevated risk)

20
Q

risk factors for CAD - modifiable

A

HTN (SBP > 130 or DBP > 80 mmHg)*
Cholesterol (Total chol. > 200 mg/dl)
Smoking (There is no safe amount)
Inactivity (Increases risk for many chronic disease conditions including heart disease)
Obesity (BMI > 30 kg/m2)
Diabetes (fasting glucose level > 126 mg/dl)
Stress (“Can you say Type A?”)

21
Q

emerging risk factors - c reactive protein and homocysteine

A

C-reactive Protein – marker for inflammation (nl = < 10 mg /L). Elevated levels are associated with an increased risk of MI.
Homocysteine – AA formed as body metabolizes methionine (“another AA”). Elevated levels seem to be associated with increased risk of CAD. B vitamins can help moderate homocysteine levels???? Recent studies have cast doubt on homocysteine as a CAD risk factor and thus remains somewhat controversial.

22
Q

emerging risk factors - lpa and metabolic syndrome

A

Lp(a) – a sub-type of LDL cholesterol associated with increased risk of clotting, atherosclerosis and myocardial infarction (MI)
“Metabolic Syndrome” – cluster of risk factors in a single individual (Three or more of the following)
Waist > 35” in women, > 40” in men
Triglyceride levels > 150 mg/dl
HDL < 50 mg/dl in women, < 40 mg/dl in men
BP > 130/85 mmHg
Blood sugar > 100 mg/dl

23
Q

“Acute Coronary Syndrome”

A 
– sudden reduction of blood flow to the heart muscle.
Unstable angina
Myocardial Infarction (MI)
STEMI “ST segment elevation MI”
NSTEM “Non-ST segment elevation MI”
24
Q

classification of angina

A

Stable- predictably induced with a given level of exertion (same RPP). Treat with rest and/or medications
Unstable- may or may not be brought on by exertion. Characterized by increasing frequency, duration, and intensity of ischemia, and/or a reduced “ischemic threshold”. – NOTE: “Physical activity is contraindicated with unstable angina”
Prinzmetal/ Variant- caused by coronary spasm. Anginal episodes may be cyclical, often occurring at the same time each day. Often occurs in the presence of underlying CAD. Treated with calcium channel blockers
Asymptomatic “Silent Ischemia”- up to 70% of ischemic episodes. Common in people with diabetes

25
Q

angina pectoris - Factors that precipitate:

A

Stress
Exposure to Cold
Physical Exertion/Exercise

26
Q

Dx of myocardial ischemia

A

Patient Hx: symptoms, risk factors, family hx
Patient Exam: HR, BP, auscultation - S3 or S4 audible?
Clinical Tests: EKG, GXT, Radionuclide imaging, Echocardiography, Cardiac catheterization

27
Q

perfusion scan

A

Provides information on blood perfusion throughout the myocardium (“heart muscle”).
Perfusion scanning is commonly included as part of a diagnostic “Graded Exercise Test” (GXT).
Rest images are compared to images taken immediately after stress (“exercise”) to look for evidence of reversible ischemia.

28
Q

cardiac catherization

A

(“coronary angiography”) – invasive procedure that allows visualization of the coronary arteries and identification of obstructive lesions.

29
Q

tx of myocardial ischemia/CVD

A

Rest
Medication
Percutaneous Transluminal Coronary Angioplasty (PTCA) (“angioplasty”)
Coronary Artery Bypass Graft (CABG)
Cardiac Rehab!! “this would only occur after the individual’s cardiac condition is stable”

30
Q

coronary artery bypass graft (CABG) - commonly used bypass vessels:

A
  • internal mammary
  • radial artery
  • saphenous vein
31
Q

cyanosis

A

blue coloration of the skin and mucous membranes due to the presence of deoxygenated hemoglobin in blood vessels near the skin surface

32
Q

cyanosis occurs when

A

the oxygen saturation of arterial blood falls below 85-90%, as may happen when blood pools in the lungs as a result of heart failure

33
Q

hypoxia

A

oxygen deficiency, leads to blue discoloration of lips etc

34
Q

atherosclerosis

A

a response to injury that causes a blockage

cause: something scratching arterial wall

high blood pressure bc it is pumping harder
plaques can come off and cause strokes

35
Q

congestive heart failure: atherosclerotic disease

A

over time, pump gets weak and cannot push blood out

Pathophysiology (27 decks)

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