4910: C13 Diseases of the Cardiovascular System Flashcards Preview

MD 4910 NCP I > 4910: C13 Diseases of the Cardiovascular System > Flashcards

Flashcards in 4910: C13 Diseases of the Cardiovascular System Deck (164)
Loading flashcards...
1
Q

What is the role of the cardiovascular system

A

To regulate blood flow to the tissues to deliver oxygen and nutrients & retrieve wastes from cell metabolism. Thermoregulation. Hormone transport, tissue defense and repair, gas exchange.

2
Q

What are the three tissue layers of the heart?

A

Epicardium - outer layer. Myocardium - middle layer, responsible for muscle contraction. Endocardium - inner layer.

3
Q

The right side of the heart is ?, and pumps blood to ?

A

Is comprised of the R atrium - which receives blood from the inferior and superior vena cava, and the R ventricle - which pumps deoxygenated blood to the lungs via the pulmonary arteries.

4
Q

The left side of the heart is the ?, and pumps blood to ?

A

Is comprised of the L atrium - which receives oxygenated blood from the lungs via the pulmonary veins, and the L ventricle - which pumps blood into systemic circulation via the aorta.

5
Q

left ventricular hypertrophy (LVH)

A

Enlargement of the left ventricle; most commonly related to hypertension and/or congestive heart failure.

6
Q

ejection fraction

A

The % of the LVEDV that is ejected in the systolic phase; in normal, apparently healthy adults, the typical ejection fraction is 50% to 60%; defined mathematically as stroke volume ÷ LVEDV

7
Q

diastolic blood pressure

A

pressure that occurs as ventricles relax (diastole phase of the cardiac cycle)

8
Q

stroke volume

A

The volume of blood that is ejected from the left ventricle with each systolic phase; defined mathematically as LVEDV - LVESV.

9
Q

systolic blood pressure

A

Pressure exerted when ejected from the ventricles (systole phase of the cardiac cycle)

10
Q

cardiac output

A

heart rate X stroke volume. V of blood ejected from the LV each minute.

11
Q

Which cranial nerve stimulates the SA node

A

The vegas nerve - parasympathetic

12
Q

The three layers of veins and arteries

A

Tunica externa - elastic, collagenous connective tissue. Tunica media - smooth muscle fibers. Tunica interna - endothelium.

13
Q

What is the devise used to measure BP

A

sphygmomanometer

14
Q

What three things affect cardiac output and peripheral vascular resistance?

A

The sympathetic nervous system (SNS), kidneys, RAAS.

15
Q

When BP falls ? is secreted by the ?, which acts to ?

A

norepinephrine, SNS, which increases BP through vasoconstriction.

16
Q

When BP falls the kidneys secret what hormone?

A

Renin

17
Q

How renin influences blood pressure?

A

Renin catalyzes the conversion of angiotensinogen to angiotensin I. Angiotensin I is converted to II in the lungs.

18
Q

Role of angiotensin II in BP

A

Is converted in the lungs. Causes adrenal cortex to release aldosterone which increases water reabsorption in the kidneys. Also, increases Na+ retention and vasoconstriction. Also increases thirst.

19
Q

Three reasons renin is released

A

renal hypotension, SNS stimulation, decreased Na+

20
Q

If peripheral resistance increases BP will

A

Increases

21
Q

If CO increases BP will

A

Increases

22
Q

Hypertension increases risk of?

A

MI, stroke, renal failure, accelerated atherosclerosis.

23
Q

Essential hypertension

A

No specific cause

24
Q

Secondary hypertension

A

Caused by other diseases

25
Q

Factors correlated with the onset of essential hyper tension?

A

Genetics, V of blood in vascular system, blood flow to kidneys, atherosclerosis, obesity, family hx, dietary factors, life style factors.

26
Q

Normal blood pressure

A

120/80 mmHg &

27
Q

Prehypertension

A

120-139 / 80-89 mmHg or

28
Q

Stage I hypertension

A

140-159 / 90-99 mmHg or

29
Q

Stage II hypertension

A

160-179 / 100-109 mmHg or

30
Q

Complications of HTN: target organ damage

A

Increased risk of TIA, heart disease, nephropathy, peripheral artery disease, retinopathy

31
Q

Pharmacological Interventions for HTN

A

Diuretics, ACE inhibitors, Angiotension II Receptor Blockers (ARB), Beta-adrenergic blocking Agents

32
Q

Diuretics

A

Primary action is to decrease blood V, which lowers BP.

33
Q

Three categories of diuretics?

A

loop inhibitors (Lasix), potassium sparing (aldactone), thiazide diuretics (Lopressor)

34
Q

ACE Inhibitors

A

Angiotension converting enzyme inhibitors. Inhibit vaso constriction. Captopril

35
Q

Angiotension II Receptor Blockers (ARBs)

A

Cause vasodilation. Cozaar, Hyzaar Benicar, Micardis, Diovan

36
Q

Beta-adrenergic blocking agents

A

block beta-receptors in the heart to decrease HR and CO. propanolol, atenolol (tenormin), acebutolol

37
Q

a-Recptor antagonists

A

Block the vascular muscle that normally respond to sympathetic stimulation and thus will reduce stroke volume. Cardura, Minipress, Hytrin

38
Q

Ca Channel Blocking Agents

A

Ca antagonists. Major action is that by affecting the movement of Ca the blood vessels relax therefore ↓ vasoconstriction; also slows heart rate. ex. Cardizem, Verapimil

39
Q

Aldosterone Antagonist

A

Suppressor the actions of aldosterone. ex. Spironolactone, eplernone

40
Q

Direct renin inhibitors

A

By blocking renin, increases vaso dilation

41
Q

Lifestyle Modifications to treat BP

A

Maintain a healthy BMI, DASH diet, reduce Na+ intake, Aerobic physical activity, alcohol in moderation

42
Q

Nutrition therapy goals for treatment of HTN

A

wt reduction, assess dietary intake, meet DASH goals, tailor PA goals

43
Q

Which lifestyle modification has the greatest effect in regard to reducing systolic blood pressure?

A

wt loss

44
Q

The success of the DASH diet in helping to control BP results from which characteristic of the diet?

A

Increased intake of fruits, vegetables, and low-fat dairy.

45
Q

Which type of medications are the most effective in lowering LDL-C levels?

A

HMG-CoA reductase inhibitors.

46
Q

The regulation of MAP involves what three systems

A

The SNS, the RAAS, & renal function.

47
Q

Parasympathetic nervous system ? blood pressure?

A

Decreases HR via the vegas nerve and the SA and AV nodes. Acetylcholine is released

48
Q

The sympathetic nervous system ? BP?

A

Increases HR

49
Q

What neurotransmitter is released by the SNS to increase HR?

A

norepinephrine

50
Q

When there is a water deficit what hormone is released by the hypothalamus

A

Vasopressin is released. It acts to increase water reabsorption, increasing blood volume and thus BP.

51
Q

Role of angiotensin II in BP regulation?

A

Stimulated the adrenal cortex to release aldosterone, which causes an increase in reabsorption of Na+ and Cl-. Salt retention = water reabsorption as well and increased BP.

52
Q

Long term regulation of BP is regulated by?

A

Urine output, and thirst

53
Q

Short-term BP regulation is accomplished by?

A

The baroreceptor reflex, the autonomic nervous system, which increases CO and total peripheral resistance.

54
Q

Hypertension (HTN)

A

A chronic elevation in BP.

55
Q

HTN can lead to

A

HF, kidney failure, MI, stroke, and aneurysms. Also, vision problems, decreased ejection fraction, arrhythmias, sudden cardiac death.

56
Q

Primary HTN

A

aka essential HTN. Is idiopathic = 90% of all cases.

57
Q

Secondary HTN

A

Result of other disease including: renal disease, CVD, and endocrine or neurogenic disorders

58
Q

Standard aspects of the HTN nutrition intervention

A

DASH, wt loss, Na+, Alcohol, K+, Ca2+, Mg, PA, smoking cessation

59
Q

Benefits of wt loss and HTN

A

A 10% wt loss lowers BP

60
Q

JNC-7 recommendation for PA

A

30 minutes /day to reduce BP by 4-9mmHg.

61
Q

One teaspoon of table salt contains X sodium

A

2300mg

62
Q

Atherosclerosis

A

Thickening of the blood vessel walls specifically caused by the presence of plaque.

63
Q

Arteriosclerosis

A

General term for thickening of the blood vessel walls with a resulting loss of vascular elasticity and narrowed lumen.

64
Q

infarct

A

cellular necrosis due to lack of oxygen

65
Q

What caused increased dyslipidemia in hypothyroidism?

A

A lipogenic enzyme that down-regulates LDL receptors has decreased activity.

66
Q

apolipoprotein

A

The protein portion of the lipoprotein, allows for recognition of the lipoprotein.

67
Q

Borderline high and High cholesterol numbers

A

200-239 mg/dL = borderline high. 240mg/dL and above = high cholesterol

68
Q

HDL Cholesterol Levels

A

< 40mg/dL = major risk factor. 40-59mg/dL Normal. HDL > 60 mg/dL = protective against CVD

69
Q

LDL Cholesterol Levels

A

LDL < 100 mg/dL = optimal. 100-129mg/dL = near optimal. 130-159mg/dL = borderline high. 160-189mg/dL = High. LDL > 190mg/dL = Very high.

70
Q

Triglyceride Levels

A

TG < 150 mg/dL = normal. 150-199mg/dL = borderline. 200-499 mg/dL = high. TG > 500 mg/dL = Very high.

71
Q

Nitric oxide (NO)

A

Is produced by endothelial cells and controls relaxation of smooth muscle in the arteries. In AS the action of NO is reduced. Low NO levels increase the inflammatory state.

72
Q

foam cells

A

Macrophage cells containing lipid; found within the fatty streaks in the development of AS.

73
Q

thrombus

A

blood clot

74
Q

Plaques are made up of?

A

Exterior is fibrous. Interior: connective tissue, lipids, macrophages smooth muscle cells, thrombus, Ca++.

75
Q

Currently accepted nutrition therapy for the prevention of AS

A

TLC as part of the ATP III.

76
Q

stearic acid

A

An 18-carbon saturated fatty acid found in beef.

77
Q

Effect of stearic acid on LDL

A

Has neither a positive nor negative effect on cholesterol and LDL levels.

78
Q

Trans-fats contribute to atherogenic process how?

A

Associated with an increased inflammatory response which may contribute to the atherogenic process.

79
Q

HMG CoA reductase

A

Enzyme of the rate limiting step in the synthesis of cholesterol. Target of Rx intervention.

80
Q

Folate and Vit B12 are required for the conversation of ? to ?

A

homocysteine to methionine

81
Q

ischemic heart disease (IHD)

A

Heart disease characterized by inadequate blood supply to the heart.

82
Q

hypertrophic cardiomyopathy

A

A genetic disorder causing abnormal thickening of the left ventricular wall.

83
Q

Acute coronary syndrome

A

Condition characterized by an episode of acute unstable angina

84
Q

Unstable angina

A

Occurs at rest. Chest pain caused by oxygen deficit to the heart.

85
Q

What four mechanisms can initiate an MI or angina in pt with IHD?

A

Sudden blockage of a coronary artery. Hemorrhage into an atherosclerotic plaque. Arterial spasm. Increase in Myocardial oxygen demand

86
Q

emboli

A

A blood clot that breaks from the cellular surface and freely moves through the circulation.

87
Q

ventricular fibrillation

A

Can cause heart to come to a stop. Uncontrolled contraction of the ventricle; often associated with MI.

88
Q

Pericarditis

A

Complication of MI. Infarcts of the epicardium may cause fluid accumulation in the pericardial sac.

89
Q

Cardiac rupture

A

Complication of MI. Leak develops due to transmural infarct and blood leaks into the pericardium.

90
Q

Cardiac tamponade

A

The heart can not expand in diastole to receive blood due to pressure from a cardiac rupture.

91
Q

ventricular aneurysm

A

It fills with blood during systole, and impacts ejection fraction. Leads to HF.

92
Q

Stable angina

A

Chest pain associated with increased oxygen demand such as occurs with physical exertion, or emotional stress.

93
Q

Cellular contents that are markers of MI

A

MB isoenzyme of creatine kinase (CK MB). Lactate dehydrogenase isoenzyme (LD I). Cardiac troponin I (cTnI). Cardiac troponin T (cTnT). myoglobin.

94
Q

Bedrest after an MI in indicated for how long?

A

The first 24-48 hours.

95
Q

Initial oral intake post MI

A

Clears. No caffeine. Decreases risk of aspiration, and arrhythmia.

96
Q

Peripheral Arterial Disease (PAD)

A

Occlusion of blood flow in non-coronary arteries, and in general refers to the lower extremities.

97
Q

Claudication

A

Pain in arms and legs due to inadequate blood flow to those muscles.

98
Q

Ankle Brachial Index (ABI)

A

A measure of peripheral vascular disease. Ratio of Doppler-recorded systolic blood pressures between upper and lower extremities.

99
Q

Claudication

A

A measure of peripheral vascular disease. Ratio of Doppler-recorded systolic blood pressures between upper and lower extremities. Used to diagnose PAD.

100
Q

Mean Arterial Pressure (MAP) is determined by?

A

A combination of CO and total peripheral resistance.

101
Q

Cardiac Output (CO) is influenced by?

A

Heart rate (HR), and stroke volume.

102
Q

Peripheral Resistance is influenced by?

A

Arteriolar radius, and blood viscosity

103
Q

Heart rate is controlled by what two mechanisms?

A

Parasympathetic activity ↓. Sympathetic activity and epinephrine

104
Q

Stroke Volume is influenced by?

A

Sympathetic activity and epinephrine. Venous return.

105
Q

Venous return is influenced by?

A

Sympathetic activity and epinephrine. Blood volume. Respiratory activity. Skeletal muscle activity. Cardiac-suction effect.

106
Q

Blood Volume is influenced by?

A

Salt and water balance. Passive bulk-flow fluid shifts between vascular and interstitial fluid compartment.

107
Q

Arteriolar radium is influenced by?

A

Skeletal muscle via local metabolic control. Extrinsic vasoconstrictor control: sympathetic activity and epinephrin, vasopressin and angiotensin II.

108
Q

Blood Viscosity is directly related to?

A

Number of RBCs.

109
Q

Hypertension (HTN)

A

Condition of chronically elevated blood pressure.

110
Q

Diagnostic Criteria for HTN

A

Access risk factors, target organ damage. Find IDable causes. Hx and physical exam. ECG

111
Q

Lab for diagnostic criteria for JNC-7 for HTN

A

Lipid profile. Glucose. Urinalysis. Hematocrit. K+. Creatinine. Ca+.

112
Q

Risk factors for CVD

A

Obesity. HTN. Smoking. DM. Dyslipidemia. Age >55men, >65women. Microalbuminuria GFR <60 mL/min. Family history.

113
Q

Identifiable causes of HTN

A

Sleep apnea. Drug induced. Chronic kidney disease. Primary aldosteronism. Renovascular disease. Cushing’s /steroid use. Thyroid disease. Pheochromocytoma.

114
Q

Diuretics

A

Primary action is to decrease blood volume and therefore lower BP. Are categorized as loop diuretics (Lasix); potassium sparing (aldactone) or thiazide diuretics (Lopressor). Are the 1st line HTN treatment drugs.

115
Q

Ace Inhibitors

A

Angiotensin-converting enzyme inhibitors. Inhibit vasoconstriction. (Captopril)

116
Q

Angiotensin II Receptor Blockers (ARBs)

A

Cause vasodilation (Cozaar, Hyzaar, Benicar, Micardis, Diovan). 2nd line drugs

117
Q

Beta-adrenergic blocking agents

A

beta-blockers. Block B-receptors in the heart to decrease HR and CO. (propanolol, atenolol, acebutolol.

118
Q

a-Receptor antagonists

A

Block vascular muscle that normally respond to sympathetic stimulation and thus will reduce stroke volume. (Cardura, Minipress, Hytrin)

119
Q

Calcium channel blocking agents

A

Slow HR. By affecting movement of Ca, blood vessels relax and vasoconstriction is reduced. (Ca antagonists)

120
Q

Aldosterone antagonist

A

Suppress the actions of aldosterone - prevent Na reabsorption. (Spironolactone)

121
Q

Direct renin inhibitors

A

Block renin which increases vasodilation

122
Q

What is the general Nutrition Therapy for HTN?

A

wt reduction. Access dietary intake. Meet DASH dietary goals. Tailor exercise goals.

123
Q

Cardiovascular Disease (CVD)

A

Involves impeded blood flow to the network of vessels surrounding and serving the heart.

124
Q

The major cause of CVD is?

A

Atherosclerosis - structural and compositional changes in the inner wall of the arteries.

125
Q

CVD is manifested in the clinical endpoints of?

A

MI and sudden death.

126
Q

atheroma

A

or plaques consisting of lipids, platelets, fibrin, and cell debris.

127
Q

Pathophysiology of Arteriosclerosis

A

Plaques develop in response to local injury of the endothelium.

128
Q

The initial lesions in arteriosclerosis are?

A

called fatty streaks & occur in response to penetration of the arterial endothelium by cholesterol containing particles.

129
Q

Decreased density = ? lipid content

A

higher.

130
Q

Drug treatment of angina?

A

Vasodilators such as nitroglycerin or isordil for acute attacks. For treatment of chronic use B-blockers to decrease O2 demand by the heart.

131
Q

HMG CoA Reductase Inhibitors (Statins)

A

Inhibits HNG CoA reductase which catalyzes the rate limiting step for cholesterol. Reduces LDL and raises HDL

132
Q

Therapeutic benefits of Statin drugs

A

Reduce major coronary events, and CVD mortality. Reduce coronary procedures, reduce stroke

133
Q

Nicotinic Acid

A

Decreases lipolysis in adipose tissue.

134
Q

Fibric Acids

A

Decrease synthesis of fatty acids and cholesterol. Increases biliary excretion of cholesterol.

135
Q

Signs and symptoms of MI

A

pallor, diaphoresis, nausea, dyspnea. Hypotension, low grade fever

136
Q

Pathophysiology of L-sided HF

A

The ventricle weakens and cannot fully empty which causes a further decrease in CO. Blood V is increases. Blood backs up into the pulmonary circulation resulting in pulmonary congestion.

137
Q

Damage if L-ventricle from MI that leads to HF?

A

The left ventricle undergoes remodeling post MI to compensate for loss of contractility. Results in L-ventricle hypertrophy &/or dilation.

138
Q

Pathophysiology of R-sided HF

A

When the R-ventricle cannot maintain output blood backs-up into systemic circulation. Blood V is increased which leads to edema and possibly tachycardia

139
Q

Symptoms associated with R-sided HF.

A

R-ventricle cannot empty. CO is decreased. Decreased BV stimulated the RAAS. Blood backs up into circulation. Increased venous pressure causes edema in extremities and cavity, and distended neck veins and cerebral edema. Headache. Flushed face.

140
Q

Signs and symptoms of generalized hypoxia

A

Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance.

141
Q

Compensation symptoms in HF

A

pallor, tachycardia

142
Q

Gi symptoms in HF

A

Epigastric fullness (early satiety). Anorexia. Cachexia. Ascites / hepatomegaly.

143
Q

Symptoms of L-sided HF

A

Orthopnea. SOB. cough. hemoptysis

144
Q

Nutrition Therapy for HF

A

Reduced sodium intake. Fluid restriction. Correction of nutrient deficiencies. Nutritional rehabilitation - assure adequate kcal and PRO to prevent cardia cachexia

145
Q

Common Na+ restrictions for HF

A

2,000mg. 1500mg. 500mg

146
Q

Diuretics may lead to the loss of what nutrients?

A

All water soluble nutrients

147
Q

beriberi

A

Thiamin deficiency. Common in HF. 200mg/day for 6 weeks

148
Q

Carnitine

A

Supplement for HF to increase energy. A substance needed for the normal metabolism of fat for energy; it is mostly found in beef and lamb but can be synthesized endogenously from the AAs L-lysie & L-methionine. It shuttles fatty acids into B-oxidation.

149
Q

L-arginine

A

Supplement prescribed for HF. It is a precursor to NO, and increases vasodilation.

150
Q

Benefits of Cardiac Rehab in HF

A

Improves vasodilation and oxidation to muscles. Decreased cardiac workload. Increases exercise tolerance and so quality of life.

151
Q

Major solid organ transplants done in the US

A

Liver, kidney, heart, pancreas, lung, small bowel

152
Q

How are organ recipients matched to donors

A

Geographic location, blood type, body size, & in some instances human leukocyte antigen (HLA)

153
Q

Why is HLA matching important in organ transplant?

A

Improves changes of successful transplant. Promotes engraftment. Reduces the risk of graft vs host disease (GVHD).

154
Q

Engraftment

A

When the new cells (of an organ transplant) start to grow and make new blood cells.

155
Q

Graft-vs-Host Disease

A

Occurs when the immune cells from the donated marrow or cord blood (the graft) attack the recipients body (the host).

156
Q

In order to receive a transplant an recipient must meet what criteria?

A

The recipient must meet medical and psychosocial criteria determined by each transplant center.

157
Q

UNOS

A

United Organ Sharing Network.

158
Q

Four common reasons for heart transplant?

A

Cardiomyopathy. Ischemic heart disease (IHD). Congenital /valvular heart disease. Hypertensive heart disease

159
Q

What measure is used to evaluate potential heart transplant pt & their long term risk?

A

VO2. A VO2 > 14mL/min/kg is considered “too well” for transplant.

160
Q

Brain death

A

is necessary for any cadaveric organ donation. This is defined as absent cerebral function and brainstem reflexes with apnea during hypercapnea in the absence of any central nervous system depression.

161
Q

hypercapnea

A

A condition marked by an unusually high concentration of CO2 in the blood as a result of hypoventilation.

162
Q

Heart donors can not older than?

A

55 years old

163
Q

What are the goals of pharmacotherapy in heart transplant?

A

Prevent complications. Reduce morbidity. Reduce rejection.

164
Q

What equations are used for mechanically ventilated pt?

A

Ireton-Jones. Also, a version for critically ill pt spontaneously breathing. This equation can also be used for the morbidly obese.