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Flashcards in Exam 4 -- Cardiovascular and PVD Deck (110):
1

What are some of the risk factors for heart failure?

Ischemic cardiomyopathy (#1 risk factor), age, smoking, alcohol abuse, obesity (lack of exercise, poor diet), DM, HTN, high-sensitivity C-reactive protein, dyslipidemia, poor dental health.

2

What are the most common causes of heart failure? What are some other causes?

Ischemic heart disease is most common, followed closely by dilated cardiomyopathy, then hypertension. It can also be caused by restrictive or hypertrophic cardiomyopathy, valvular heart disease, congenital heart disease, and high output states such as thyrotoxicosis and anemia.

3

Left ventricular systolic dysfunction (LVSD) is a type of heart failure in which the left heart blood ejection fails. What are the common causes of LVSD?

Ischemic heart disease (heart tissue has died, decreasing the ability of the heart to pump blood), hypertension (heart has a lot more pressure to push against), and valvular disease (the valve is either not opening all the way, requiring more force from the heart to get the blood out, or the valve doesn't close completely, allowing blood from aorta to come back into ventricle, requiring more force to get enough blood out to body).

4

Right ventricular systolic dysfunction (RVSD) is a type of heart failure in which the right heart blood ejection fails. What are the common causes of RVSD?

It most common occurs due to LVSD, but can also arise from pulmonary disease or tricuspid valve disease.

5

Diastolic heart failure is an issue with the heart filling with blood. What are the common causes of diastolic heart failure?

This commonly occurs due to decreased left ventricular wall compliance (the ventricle is either stiffer or thicker), and is more common in elderly hypertensive patients, or with cardiomyopathy (hypertrophic, infiltrative, or restrictive).

6

What are the two most common symptoms of heart failure?

Progressive breathlessness (dyspnea with ordinary exertion --> dyspnea at rest --> orthopnea (shortness of breath while lying down) --> paroxysmal nocturnal dyspnea (SOB during sleep that causes patient to wake up) and fatigue. Note that reduced renal perfusion --> increased blood volume is another common sign of heart failure.

7

What are some of the signs of heart failure?

Severe pulmonary edema (evidenced by pulmonary congestion and rale/rattles and nocturnal cough that may produce bloody sputum), tachycardia (due to lack of blood perfusion), anorexia, hepatomegaly, peripheral edema and cyanosis, cardiomegaly (either dilation or hypertrophy), and gallop rhythm (S3 and/or S4).

8

S1 and S2 are normal heart sounds associated with the closing of valves. Which valve closures cause S1? S2? Which sound is associated with the pulse?

S1 is caused by the mitral and tricuspid valves closing, S2 is caused by the aortic and pulmonary valves closing. S1 is the sound associated with the pulse.

9

Of S3 and S4 heart sounds, S3 can be normal in younger or pregnant patients, but is always considered pathologic over the age of 30-35. S4 is always pathologic.

Free card.

10

Which of the extra heart sounds (S3 and S4) is associated with an enlarged ventricle? A hypertrophied ventricle?

S3 = enlarged ventricle, S4 = hypertrophied ventricle

11

How would heart failure generally be diagnosed?

Chest X-ray, echocardiogram and/or catheterization for chamber, valvular, or blood flow abnormalities, possibly EKG.

12

What are the four stages of heart failure, according to the ACA/AHA? What determines each stage?

Stages A-D. Stage A = no structural disease or symptoms, but risk factors. Stage B = structural disease present, but no signs or symptoms. Stage C = current or past symptoms of heart failure (SOB). Stage D = patients with heart failure that is difficult to treat with just meds, need to consider transplantation.

13

What would be recommended as general therapy for a patient in any stage of HF?

Patient education, correct underlying risk factors, flu and pneumococcal vaccines, dietary salt restriction, get enough rest and avoid overexertion, but do get some exercise.

14

In addition to general therapies of heart failure, what would you include for a patient in stage B?

ACE inhibitor or ARB (these both lower systemic vascular resistance and venous pressure, and decrease level of circulating catecholamines). In some patients you might also add a beta blocker to allow the heart to fill up more and thus contract with more force (Frank-Starling).

15

In addition to general therapies of heart failure, what would you include for a patient in stage C?

Stage B therapy (ACEi or ARB, and a beta-blocker), diuretics (thiazide first then loop if needed), aldosterone antagonists (decreases fibrosis), cardiac glycoside to increase contractility in some patients (digoxin).

16

In addition to general therapies of heart failure, what would you include for a patient in stage D?

Inotropes to increase the strength of contraction (beta agonists such as dobutamine; dopamine has been used); biventricular pacemaker if patient has a conduction defect or is not responding to therapy; implantable defibrillator; parachute device if infarction has induced left ventricle dilation; left ventricular assist device to pump blood while waiting for transplant; transplant.

17

Atherosclerosis is a very common cause of death in the US. It is the most common cause of heart disease (ischemic heart disease and myocardial infarction); it can also cause stroke and possibly increase the risk of dementia.

Free card.

18

Atherosclerosis involves damage to the endothelium. What sort of trauma might cause endothelial damage?

Elevated shear stress (especially at bifurcations and curved areas, and with high BP), biochemical abnormalities (such as high LDL, which inhibits the release of NO thus resulting in vasoconstriction, which increases damage from shear stress; also in diabetes, the AGEs can damage the endothelium), inflammation (increased platelet adhesion), smoking (toxic damage to BVs), advanced age.

19

Briefly outline atheroma formation.

Vessel walls become more permeable to LDL, which is then oxidized (which inhibits NO). Macrophages eat up the LDL (and are then called foam cells, which progress to form fatty streaks). Growth factors are released by platelets and the macrophages to cause migration and proliferation of smooth muscle cells, which then develop a fibrous cap.

20

Of the two types of vascular remodeling (positive and negative), which decreases lumen size?

Negative.

21

Of the two types of vascular remodeling (positive and negative), which is more commonly associated with unstable lesions, and why?

Positive; this is due to a softer core and a less developed cap.

22

Of the two types of vascular remodeling (positive and negative), which is associated with stable angina?

Negative.

23

Of the two types of vascular remodeling (positive and negative), which is more stable, and why?

Negative; its cap is more stable. These types of atherolmas are less likely to rupture.

24

Of the two types of vascular remodeling (positive and negative), which preserves lumen size?

Positive.

25

Of the two types of vascular remodeling (positive and negative), which is more likely to cause acute coronary syndrome?

Positive.

26

What are the three factors that can contribute to plaque vulnerability (and hence potential disruption)?

"Shoulder" of plaque (junction between plaque and less diseased vessel) is where the cap is thinnest and most prone to disruption; macrophage activity (proteolytic enzymes that weaken the cap); cap fatigue (with repetitive stress from pressure, shear stress, stretch from the heart beat).

27

There are two mechanisms of thrombosis due to atherosclerosis. Briefly describe them. Which is usually more serious?

Supericial endothelium breaks down, and platelets adhere to the underlying collagen, and a thrombus forms. The other form is a deep endothelial fissure tears the atheroma cap. Blood then enters the plaque and starts to form a large thrombus. The deep thrombus is usually the more serious.

28

What is the first symptom of atherosclerosis?

The first symptom (intermittent claudication) is on exertion due to the reduced oxygen supply for the greater demand.

29

What are some of the symptoms of advanced atherosclerosis?

PVD, MI, kidney disease, aneurysm, angina, sudden death, stroke.

30

What are some diagonistic imaging techniques that can be used for atherosclerosis?

Ultrasound, OCT, CT, MRI, angiography.

31

What sort of laboratory testing can be done for atherosclerosis?

Fasting total cholesterol (want total ~50 mg/dL, want LDL <150 mg/dL). Serum highly sensitive C-reactive protein (hs-CRP) can also be done for patients who have a 10 year CHD risk of 10% or more.

32

What is C-reactive protein? What is an average CRP value?

It is an indicator of inflammation; average value is about 2 mg/L

33

How is atheroscleroma managed?

Lifestyle modifications (lose weight, modify diet, increase physical activity), drugs, possibly surgery.

34

There are a few different classes of drugs used for the treatment of atheroscleroma. Which class(es) help decrease inflammation?

Aspirin, perhaps statins

35

There are a few different classes of drugs used for the treatment of atheroscleroma. Which class(es) help harden the cap of the lesion?

Statins

36

There are a few different classes of drugs used for the treatment of atheroscleroma. Which class(es) help lower LDL?

Statins, bile acid binders, niacin

37

There are a few different classes of drugs used for the treatment of atheroscleroma. Which class(es) help lower TGs and increase HDL?

Fibrates and niacin

38

Drugs used for the treatment of atheroscleroma may have an impact on the patient's ocular health. What ocular implications do statins have?

They increase retinal blood circulation, may decrease diabetic neuropathy and retinopathy. (Note: antibiotics like erythromycin and clarithromycin interfere with the breakdown of statins, prolonging their effect.)

39

Drugs used for the treatment of atheroscleroma may have an impact on the patient's ocular health. What ocular implications do bile acid binders have?

They could interfere with the absorption of other drugs (beta blockers, tetracycline, oral contraceptives, etc.)

40

Drugs used for the treatment of atheroscleroma may have an impact on the patient's ocular health. What ocular implications do fibrates have?

May protect against diabetic neuropathy and retinopathy

41

Drugs used for the treatment of atheroscleroma may have an impact on the patient's ocular health. What ocular implications does niacin have?

Can cause macular edema and toxic amblyopia

42

Ischemic heart disease (IHD) is also known as coronary artery disease (CAD) and coronary heart disease (CHD). What is the major cause of ischemic heart disease?

Coronary atherosclerosis

43

Although prevalence of ischemic heart disease is equal between genders, which gender is less likely to survive a myocardial infarction, and what pathophysiology of this gender might help account for this difference in survival?

Women; they have smaller coronary arteries (even correcting for body size). Due to this smaller size, women may be affected more by the decrease in NO caused by oxidized LDL. For unknown reasons, women also tend to experience positive remodeling, which is more prone to cause coronary problems.

44

What diagnostic testing may be done for a women who is suspected of having IHD?

Intravascular ultrasonography, stress echocardiography and stress thallium, and ACh challenge test for endothelial function.

45

Briefly outline the ACh challenge test (diagnostic tool for IHC, especially in women).

ACh by itself causes vasoconstriction in the coronary arteries, but it also causes a release of NO. The end result is vasodilation, since the vasodilative effect of NO is greater than the vasoconstrictive effect of ACh. In a patient with IHD, NO release is impaired so administration of ACh will cause vasoconstriction instead of the expected vasodilation.

46

Stable (typical) angina is the result of what type of remodeling in the coronary arteries?

Negative.

47

Stable angina is usually provoked by exercise or emotional stress and usually doesn't last very long. What relieves stable angina?

Rest, or sublingual nitroglycerin (NTG).

48

Prinzmetal's (variant) angina is caused by vasospasm and is more common in which gender?

Women.

49

When does prinzmetal's angina tend to occur?

Night or early morning.

50

What relieves prinzmetal's angina?

Nitroglycerin

51

If angina is not relieved by 2-3 NTG tablets given five minutes apart, this indicates a medical emergency.

Free card.

52

What medications can be used in the management of angina?

Aspirin, nitrates (vasodilation), beta blockers (reduce oxygen demand), calcium channel blockers (prevents vasospasm, also induced vasodilation), Ranolazine can be used if the angina persists.

53

Surgical management of angina can be considered when medications aren't working. Percutaneous coronary intervention (PCI) is one of the procedures discussed in class. Briefly outline this surgery. When might PCI be preferred over CABG (the other procedure)?

A stent is put in place to open the clogged artery. Glycoprotein IIB/IIIA inhibitors are put in palce to inhibit platelet aggregation during the procedure. Overall, this is a simpler and less invasive procedure, preferred when the disease is single-vessel and relatively straight-forward.

54

Surgical management of angina can be considered when medications aren't working. Coronary-artery bypass grafting (CABG) is one of the procedures discussed in class. Briefly outline this surgery. When might CABG be preferred over PCI (the other procedure)?

Transplanted vessel (internal thoracic arteries, usually) are used to bypass the area of blockage. CABG would be preferred when the disease is complex, involving more than one vessel.

55

Acute coronary syndrome (ACS) is a term that encompasses which conditions?

Unstable angina, non-ST-elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI)

56

You can use enzyme tests and EKG to differentiate between unstable angina, NSTEMI, and STEMI. What would these tests show in a patient with unstable angina?

No enzyme increase (troponin, etc), and no ST elevation.

57

You can use enzyme tests and EKG to differentiate between unstable angina, NSTEMI, and STEMI. What would these tests show in a patient with NSTEMI?

Enzymes (troponin, etc) would be elevated, but there would be no ST elevation.

58

You can use enzyme tests and EKG to differentiate between unstable angina, NSTEMI, and STEMI. What would these tests show in a patient with STEMI?

Enzymes (troponin, etc) would be elevated; there would also be an ST elevation.

59

Which is more severe, NSTEMI or STEMI?

STEMI is more severe, and involves total inclusion of a coronary artery. (NSTEMI only partially occludes.)

60

What are some of the signs and symptoms of myocardial infarction?

Sudden onset of pericardial pain that may radiate to left arm and jaw (usually in the morning), pain lasts more than 30 minutes and is not relieved with NTG; nausea, diaphoresis, dyspnea; apprehension, hypotension and tachycardia.

61

What immediate therapy should be done for a patient with a myocardial infarction?

Morphine for pain, oxygen, NTG, aspirin (chewed), lidocaine (for arryhthmias); glycoprotein IIB/IIIA inhibitors and PCI if possible. If STEMI, can induce thrombolysis with alteplase within 3 hours (can also give concurrent low molecular weight heparins to enhance this activity). Hypoxia can be induced to minimize brain damage.

62

What adjunct therapy can be used for a patient with a myocardial infarction?

Beta-blockers (for arrhythmias and to reduce reinfarction risk), ACEi to reduce fibrosis, statins to stabilize plaques, anticoagulants (heparin), possibly antiplatelets (aspirin and clopidogrel or prasugrel)

63

What are some of the potential complications of myocardial infarction?

Acute arrhythmias and conduction defects (potentially life-threatening), heart failure (if more than 30% of heart tissue infarcted), chamber wall defects (ventricular septal defect/thinning, ventricular aneurysm, cardiac rupture)

64

What are some of the causes of aortic stenosis? Which cause is the most common?

Senile calcific stenosis (most common; an inflammatory process causes the valve to be too stiff); congenital stenosis/bicuspid aortic valve (defect causes aortic valve to only have two leaflets rather than three as is normal; calcification then occurs prematurely by the 4th or 5th decade; more common in men); rheumatic heart disease (not common in industrialized nations since it follows an untreated strep pharyngitis).

65

What is the heart's response to aortic stenosis?

The left ventricle undergoes hypertrophy in order to push against the increased pressure; this can lead to relative ischemia with angina and left ventricle failure.

66

What are the signs of aortic stenosis?

Carotid pulse is small volume/slow-rising (since blood has a hard time getting past the stenotic valve); systolic ejection murmur (due to turbulence as blood passes the stenotic valve); soft S2 sound (since aortic valve is contributing less to the sound); S4 development (due to hypertrophy)

67

The symptoms of aortic stenosis don't occur until the condition is moderately severe. They include angina (in 35-55% of patients, 50% of whom die in 5 years if the valve is not replaced), syncope with exercise (2-3 year survival if the valve is not replaced), and heart failure (50% of patients die within 1-2 years if the condition is not corrected.

Free card.

68

True or false: almost all cases of mitral stenosis are secondary to rheumatic heart disease and are experienced by middle-aged men.

False; almost all cases are indeed secondary to rheumatic heart disease, but most of the patients are pregnant women.

69

Briefly outline the pathophysiology of mitral stenosis.

Left ventricle filling is impeded by the stenotic valve, so the backed-up pressure in the left atria causes pulmonary congestion. Right ventricle can fail due to the increased demand.

70

What are the signs and symptoms of mitral stenosis?

Progressively severe dyspnea (exertion, orthopnea, paroxysmal nocturnal dyspnea), hemoptysis (bloody cough from rupture of small bronchial veins), atrial enlargement potentially leading to fibrillations and vegetations that form due to stagnant blood. Hoarseness can also occur if the left atrium impinges on laryngeal nerve. Diastolic murmur is also possible.

71

What are some causes of aortic regurgitation?

Idiopathic, rheumatic heart disease, collagen vascular disease (lupus, scleroderma, Marfan's).

72

Briefly outline the pathophysiology of aortic regurgitation.

Part of the ventricular volume is regurgitated during diastole. This means a greater stroke volume is needed to compensate for the regurgitated amount. This can lead to LV dysfunction, and does lead to decreased diastolic pressure and increased pulse pressure.

73

What are some of the signs and symptoms of aortic regurgitation?

Palpitations, LV failure (and resulting progressive dyspnea), syncope, angina, increased LV size, Quincke's sign (capillary pulsation in nail beds) and De Musset's sign (head bobbing with heartbeat.

74

What are some causes of mitral regurgitation?

Mitral valve prolapse (due to redundant chordae tendinae), rheumatic heart disease, coronary artery disease (can damage papillary muscles), ventricular enlargement.

75

What are the signs and symptoms of mitral regurgitation?

Systolic murmur, S3 heart sound, left and eventually right heart failure (and resulting progressive dyspnea), palpitations, atrial fibrillation, systemic embolization.

76

How are valvular dysfunctions diagnosed?

Echocardiography, ECG, catheterization, chest radiography.

77

What medical therapy can be used for valvular dysfunction?

Diuretics (decrease volume), digoxin (increase contractility and decrease arrhythmias), anticoagulant (warfarin, decrease risk of embolism), vasodilators (decrease outflow resistance).

78

In terms of surgical treatment for valvular disorders, mitraclip can be used for mitral regurgitation, and commissurotomy and balloon valvuloplasty can be used for mitral stenosis. Vavlvular replacement can also be useful: homograft or allograft for people less than 55 years, mechanical valve for people 55-75, and heterograft for people over 75.

Free card.

79

Infective endocarditis is infection of the endocardial surface and valves. What are some of the common causes?

Staph aureus is the most common overall cause, and the most common bacterial cause; Candida albicans is the most common fungal cause.

80

Infective endocarditis has two types of presentations: acute and subacute. What are the symptoms of the acute presentation?

Fever and a new or changed heart mumur

81

Infective endocarditis has two types of presentations: acute and subacute. What are the symptoms of the subacute presentation?

Malaise, murmurs, cardiac failure, splinter hemorrhages of the conjunctiva, and Roth spots

82

True or false: Roth spots in and of themselves are diagnostic of infective endocarditis.

False.

83

How is infective endocarditis diagnosed?

Blood culture (at least three draws, seprated by 12 hours), echocardiography showing valve dysfunction or abscess. The following can support a diagnosis: fever, elevated CRP, emboli, hemorrhage, Janeway lesions (little red nontender macular lesions on palms of hands and soles of feet)

84

How would you treat infective endocarditis?

IV antibiotics and hospital care; surgery may be necessary if there is extensive valvular damage.

85

Dilated cardiomyopathy is impaired contraction in the absence of pressure overload. What factors might contribute to this condition?

Most commonly it is idiopathyic, but viral myocarditis and alcohol abuse can contribute as well.

86

The manifestations of dilated cardiomyopathy are similar to those of heart failure, and the prognosis is not good (35% die within 5 years, and 70% die within 10 years).

Free card.

87

How would you treat dilated cardiomyopathy?

Remove offending agent, if any, restrict salt intake, give high dose fish oil (omega-3), meds (diuretics, vasodilators, beta-blockers, digitalis), possible surgery (piece of dacron to strengthen the dilated ventricle, or cardiac transplant)

88

True or false: the hypertrophy of hypertrophic cardiomyopathy usually occurs mainly in the septum.

True.

89

True or false: hypertrophic myopathy generally occurs in an older patient who often has a strong family history of the condition.

False; the patient is most often a young adult, but they do indeed often have a strong family history.

90

What are the clinical manifestations of hypertrophic cardiomyopathy?

Exertional dyspnea, angina at rest, syncope after exercise. Sudden cardiac death is possible after exercise.

91

What medical therapy is used for patients with hypertrophic cardiomyopathy?

Beta-blockers. Digitalis can be used in the end stage after dilation has occurred.

92

What surgical options are available for a patient with hypertrophic cardiomyopathy?

Myomectomy (reduces septal thickness), pacemaker and defibrillator, intentional septal infarction, cardiac transplant.

93

What are some causes of acute pericarditis?

Viral infection, lupus, infectious endocarditis, cancer, radiation, drugs. Can occur after a MI

94

What are the clinical features of acute pericarditis?

Left chest pain on deep breath, friction rub during systole and diastole (sounds like a washing machine).

95

How would you treat acute pericarditis?

Treat the underlying disorder, use meds (NSAIDs, steroids, colchicine)

96

Pericardial effusion involves increased production of serous fluid. What is a common cause of pericardial effusion?

Inflammation of acute pericarditis

97

Pericardial effusion does not normally involve any additional symptoms to the pericardium, but the heart sounds do become soft.

Free card.

98

What is the therapy for pericardial effusion?

Treat the pericarditis, may need to aspirate the fluid.

99

What is cardiac tamponade?

A life-threatening condition in which rapid accumulation of fluid from pericarditis compresses the heart and inhibits cardiac filling.

100

What are the clinical features of cardiac tamponade?

Decreased systolic pressure with deep breath, shock.

101

What is the treatment for cardiac tamponade?

Pericardiocentesis (remove fluid from pericardium)

102

Constrictive pericarditis is when the pericardium becomes thickened in response to previous inflammation. What are the features of this condition?

Dyapnea on exertion, orthopnea, edema, ascites, hepatic tenderness with jaundice

103

What is the treatment for constrictive pericarditis?

Pericardiectomy (removal of pericardium); symptoms may persist for up to 6 weeks

104

Lower limb ischemia is a type of peripheral vascular disease that involves the arteries. It can be caused by atherosclerosis, thrombosis, or embolism. What are some of the presenting symptoms?

Pain and limping while walking, pallor, paralysis, pulselessness, hair loss

105

Patients with lower limb ischemia have an increased risk of heart failure, diabetic foot disease and Raynaud disease.

Free card.

106

What therapy should you advise for a patient with lower limb ischemia?

Patient education (avoid trauma, foot and toe hygiene, stop smoking, be careful with exercise), treat any underlying HTN and diabetes, anticoagulants (aspirin, clopidogrel), angioplasty with stent, or bypass surgery

107

Varicose veins are a form of peripheral vascular disease. These veins (superficial veins in lower extremeties) appear dilated and tortuous. Patients will experience pain with periods of standing.

Free card.

108

What causes varicose veins?

Inherited defects of the valves or vein walls. Increased venous pressure from prolonged standing or lifting can also play a role.

109

Apart from surgery, what can be done for varicose veins?

Wear support stockings, elevate legs, and limit activities of long standing.

110

What surgical options are available for a patient with varicose veins?

Sclerotherapy and compression (closes down the veins), removal of varicosity, endovenous laser therapy (causes scarring), radiofrequency ablation (same effect as laser therapy, but with heat)