4910: C13 Diseases of the Cardiovascular System 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
Factors correlated with the onset of essential hyper tension?
Genetics, V of blood in vascular system, blood flow to kidneys, atherosclerosis, obesity, family hx, dietary factors, life style factors.
26
Normal blood pressure
120/80 mmHg &
27
Prehypertension
120-139 / 80-89 mmHg or
28
Stage I hypertension
140-159 / 90-99 mmHg or
29
Stage II hypertension
160-179 / 100-109 mmHg or
30
Complications of HTN: target organ damage
Increased risk of TIA, heart disease, nephropathy, peripheral artery disease, retinopathy
31
Pharmacological Interventions for HTN
Diuretics, ACE inhibitors, Angiotension II Receptor Blockers (ARB), Beta-adrenergic blocking Agents
32
Diuretics
Primary action is to decrease blood V, which lowers BP.
33
Three categories of diuretics?
loop inhibitors (Lasix), potassium sparing (aldactone), thiazide diuretics (Lopressor)
34
ACE Inhibitors
Angiotension converting enzyme inhibitors. Inhibit vaso constriction. Captopril
35
Angiotension II Receptor Blockers (ARBs)
Cause vasodilation. Cozaar, Hyzaar Benicar, Micardis, Diovan
36
Beta-adrenergic blocking agents
block beta-receptors in the heart to decrease HR and CO. propanolol, atenolol (tenormin), acebutolol
37
a-Recptor antagonists
Block the vascular muscle that normally respond to sympathetic stimulation and thus will reduce stroke volume. Cardura, Minipress, Hytrin
38
Ca Channel Blocking Agents
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
Aldosterone Antagonist
Suppressor the actions of aldosterone. ex. Spironolactone, eplernone
40
Direct renin inhibitors
By blocking renin, increases vaso dilation
41
Lifestyle Modifications to treat BP
Maintain a healthy BMI, DASH diet, reduce Na+ intake, Aerobic physical activity, alcohol in moderation
42
Nutrition therapy goals for treatment of HTN
wt reduction, assess dietary intake, meet DASH goals, tailor PA goals
43
Which lifestyle modification has the greatest effect in regard to reducing systolic blood pressure?
wt loss
44
The success of the DASH diet in helping to control BP results from which characteristic of the diet?
Increased intake of fruits, vegetables, and low-fat dairy.
45
Which type of medications are the most effective in lowering LDL-C levels?
HMG-CoA reductase inhibitors.
46
The regulation of MAP involves what three systems
The SNS, the RAAS, & renal function.
47
Parasympathetic nervous system ? blood pressure?
Decreases HR via the vegas nerve and the SA and AV nodes. Acetylcholine is released
48
The sympathetic nervous system ? BP?
Increases HR
49
What neurotransmitter is released by the SNS to increase HR?
norepinephrine
50
When there is a water deficit what hormone is released by the hypothalamus
Vasopressin is released. It acts to increase water reabsorption, increasing blood volume and thus BP.
51
Role of angiotensin II in BP regulation?
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
Long term regulation of BP is regulated by?
Urine output, and thirst
53
Short-term BP regulation is accomplished by?
The baroreceptor reflex, the autonomic nervous system, which increases CO and total peripheral resistance.
54
Hypertension (HTN)
A chronic elevation in BP.
55
HTN can lead to
HF, kidney failure, MI, stroke, and aneurysms. Also, vision problems, decreased ejection fraction, arrhythmias, sudden cardiac death.
56
Primary HTN
aka essential HTN. Is idiopathic = 90% of all cases.
57
Secondary HTN
Result of other disease including: renal disease, CVD, and endocrine or neurogenic disorders
58
Standard aspects of the HTN nutrition intervention
DASH, wt loss, Na+, Alcohol, K+, Ca2+, Mg, PA, smoking cessation
59
Benefits of wt loss and HTN
A 10% wt loss lowers BP
60
JNC-7 recommendation for PA
30 minutes /day to reduce BP by 4-9mmHg.
61
One teaspoon of table salt contains X sodium
2300mg
62
Atherosclerosis
Thickening of the blood vessel walls specifically caused by the presence of plaque.
63
Arteriosclerosis
General term for thickening of the blood vessel walls with a resulting loss of vascular elasticity and narrowed lumen.
64
infarct
cellular necrosis due to lack of oxygen
65
What caused increased dyslipidemia in hypothyroidism?
A lipogenic enzyme that down-regulates LDL receptors has decreased activity.
66
apolipoprotein
The protein portion of the lipoprotein, allows for recognition of the lipoprotein.
67
Borderline high and High cholesterol numbers
200-239 mg/dL = borderline high. 240mg/dL and above = high cholesterol
68
HDL Cholesterol Levels
< 40mg/dL = major risk factor. 40-59mg/dL Normal. HDL > 60 mg/dL = protective against CVD
69
LDL Cholesterol Levels
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
Triglyceride Levels
TG < 150 mg/dL = normal. 150-199mg/dL = borderline. 200-499 mg/dL = high. TG > 500 mg/dL = Very high.
71
Nitric oxide (NO)
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
foam cells
Macrophage cells containing lipid; found within the fatty streaks in the development of AS.
73
thrombus
blood clot
74
Plaques are made up of?
Exterior is fibrous. Interior: connective tissue, lipids, macrophages smooth muscle cells, thrombus, Ca++.
75
Currently accepted nutrition therapy for the prevention of AS
TLC as part of the ATP III.
76
stearic acid
An 18-carbon saturated fatty acid found in beef.
77
Effect of stearic acid on LDL
Has neither a positive nor negative effect on cholesterol and LDL levels.
78
Trans-fats contribute to atherogenic process how?
Associated with an increased inflammatory response which may contribute to the atherogenic process.
79
HMG CoA reductase
Enzyme of the rate limiting step in the synthesis of cholesterol. Target of Rx intervention.
80
Folate and Vit B12 are required for the conversation of ? to ?
homocysteine to methionine
81
ischemic heart disease (IHD)
Heart disease characterized by inadequate blood supply to the heart.
82
hypertrophic cardiomyopathy
A genetic disorder causing abnormal thickening of the left ventricular wall.
83
Acute coronary syndrome
Condition characterized by an episode of acute unstable angina
84
Unstable angina
Occurs at rest. Chest pain caused by oxygen deficit to the heart.
85
What four mechanisms can initiate an MI or angina in pt with IHD?
Sudden blockage of a coronary artery. Hemorrhage into an atherosclerotic plaque. Arterial spasm. Increase in Myocardial oxygen demand
86
emboli
A blood clot that breaks from the cellular surface and freely moves through the circulation.
87
ventricular fibrillation
Can cause heart to come to a stop. Uncontrolled contraction of the ventricle; often associated with MI.
88
Pericarditis
Complication of MI. Infarcts of the epicardium may cause fluid accumulation in the pericardial sac.
89
Cardiac rupture
Complication of MI. Leak develops due to transmural infarct and blood leaks into the pericardium.
90
Cardiac tamponade
The heart can not expand in diastole to receive blood due to pressure from a cardiac rupture.
91
ventricular aneurysm
It fills with blood during systole, and impacts ejection fraction. Leads to HF.
92
Stable angina
Chest pain associated with increased oxygen demand such as occurs with physical exertion, or emotional stress.
93
Cellular contents that are markers of MI
MB isoenzyme of creatine kinase (CK MB). Lactate dehydrogenase isoenzyme (LD I). Cardiac troponin I (cTnI). Cardiac troponin T (cTnT). myoglobin.
94
Bedrest after an MI in indicated for how long?
The first 24-48 hours.
95
Initial oral intake post MI
Clears. No caffeine. Decreases risk of aspiration, and arrhythmia.
96
Peripheral Arterial Disease (PAD)
Occlusion of blood flow in non-coronary arteries, and in general refers to the lower extremities.
97
Claudication
Pain in arms and legs due to inadequate blood flow to those muscles.
98
Ankle Brachial Index (ABI)
A measure of peripheral vascular disease. Ratio of Doppler-recorded systolic blood pressures between upper and lower extremities.
99
Claudication
A measure of peripheral vascular disease. Ratio of Doppler-recorded systolic blood pressures between upper and lower extremities. Used to diagnose PAD.
100
Mean Arterial Pressure (MAP) is determined by?
A combination of CO and total peripheral resistance.
101
Cardiac Output (CO) is influenced by?
Heart rate (HR), and stroke volume.
102
Peripheral Resistance is influenced by?
Arteriolar radius, and blood viscosity
103
Heart rate is controlled by what two mechanisms?
Parasympathetic activity ↓. Sympathetic activity and epinephrine
104
Stroke Volume is influenced by?
Sympathetic activity and epinephrine. Venous return.
105
Venous return is influenced by?
Sympathetic activity and epinephrine. Blood volume. Respiratory activity. Skeletal muscle activity. Cardiac-suction effect.
106
Blood Volume is influenced by?
Salt and water balance. Passive bulk-flow fluid shifts between vascular and interstitial fluid compartment.
107
Arteriolar radium is influenced by?
Skeletal muscle via local metabolic control. Extrinsic vasoconstrictor control: sympathetic activity and epinephrin, vasopressin and angiotensin II.
108
Blood Viscosity is directly related to?
Number of RBCs.
109
Hypertension (HTN)
Condition of chronically elevated blood pressure.
110
Diagnostic Criteria for HTN
Access risk factors, target organ damage. Find IDable causes. Hx and physical exam. ECG
111
Lab for diagnostic criteria for JNC-7 for HTN
Lipid profile. Glucose. Urinalysis. Hematocrit. K+. Creatinine. Ca+.
112
Risk factors for CVD
Obesity. HTN. Smoking. DM. Dyslipidemia. Age >55men, >65women. Microalbuminuria GFR <60 mL/min. Family history.
113
Identifiable causes of HTN
Sleep apnea. Drug induced. Chronic kidney disease. Primary aldosteronism. Renovascular disease. Cushing's /steroid use. Thyroid disease. Pheochromocytoma.
114
Diuretics
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
Ace Inhibitors
Angiotensin-converting enzyme inhibitors. Inhibit vasoconstriction. (Captopril)
116
Angiotensin II Receptor Blockers (ARBs)
Cause vasodilation (Cozaar, Hyzaar, Benicar, Micardis, Diovan). 2nd line drugs
117
Beta-adrenergic blocking agents
beta-blockers. Block B-receptors in the heart to decrease HR and CO. (propanolol, atenolol, acebutolol.
118
a-Receptor antagonists
Block vascular muscle that normally respond to sympathetic stimulation and thus will reduce stroke volume. (Cardura, Minipress, Hytrin)
119
Calcium channel blocking agents
Slow HR. By affecting movement of Ca, blood vessels relax and vasoconstriction is reduced. (Ca antagonists)
120
Aldosterone antagonist
Suppress the actions of aldosterone - prevent Na reabsorption. (Spironolactone)
121
Direct renin inhibitors
Block renin which increases vasodilation
122
What is the general Nutrition Therapy for HTN?
wt reduction. Access dietary intake. Meet DASH dietary goals. Tailor exercise goals.
123
Cardiovascular Disease (CVD)
Involves impeded blood flow to the network of vessels surrounding and serving the heart.
124
The major cause of CVD is?
Atherosclerosis - structural and compositional changes in the inner wall of the arteries.
125
CVD is manifested in the clinical endpoints of?
MI and sudden death.
126
atheroma
or plaques consisting of lipids, platelets, fibrin, and cell debris.
127
Pathophysiology of Arteriosclerosis
Plaques develop in response to local injury of the endothelium.
128
The initial lesions in arteriosclerosis are?
called fatty streaks & occur in response to penetration of the arterial endothelium by cholesterol containing particles.
129
Decreased density = ? lipid content
higher.
130
Drug treatment of angina?
Vasodilators such as nitroglycerin or isordil for acute attacks. For treatment of chronic use B-blockers to decrease O2 demand by the heart.
131
HMG CoA Reductase Inhibitors (Statins)
Inhibits HNG CoA reductase which catalyzes the rate limiting step for cholesterol. Reduces LDL and raises HDL
132
Therapeutic benefits of Statin drugs
Reduce major coronary events, and CVD mortality. Reduce coronary procedures, reduce stroke
133
Nicotinic Acid
Decreases lipolysis in adipose tissue.
134
Fibric Acids
Decrease synthesis of fatty acids and cholesterol. Increases biliary excretion of cholesterol.
135
Signs and symptoms of MI
pallor, diaphoresis, nausea, dyspnea. Hypotension, low grade fever
136
Pathophysiology of L-sided HF
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
Damage if L-ventricle from MI that leads to HF?
The left ventricle undergoes remodeling post MI to compensate for loss of contractility. Results in L-ventricle hypertrophy &/or dilation.
138
Pathophysiology of R-sided HF
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
Symptoms associated with R-sided HF.
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
Signs and symptoms of generalized hypoxia
Fatigue, weakness, dyspnea, exercise intolerance, cold intolerance.
141
Compensation symptoms in HF
pallor, tachycardia
142
Gi symptoms in HF
Epigastric fullness (early satiety). Anorexia. Cachexia. Ascites / hepatomegaly.
143
Symptoms of L-sided HF
Orthopnea. SOB. cough. hemoptysis
144
Nutrition Therapy for HF
Reduced sodium intake. Fluid restriction. Correction of nutrient deficiencies. Nutritional rehabilitation - assure adequate kcal and PRO to prevent cardia cachexia
145
Common Na+ restrictions for HF
2,000mg. 1500mg. 500mg
146
Diuretics may lead to the loss of what nutrients?
All water soluble nutrients
147
beriberi
Thiamin deficiency. Common in HF. 200mg/day for 6 weeks
148
Carnitine
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
L-arginine
Supplement prescribed for HF. It is a precursor to NO, and increases vasodilation.
150
Benefits of Cardiac Rehab in HF
Improves vasodilation and oxidation to muscles. Decreased cardiac workload. Increases exercise tolerance and so quality of life.
151
Major solid organ transplants done in the US
Liver, kidney, heart, pancreas, lung, small bowel
152
How are organ recipients matched to donors
Geographic location, blood type, body size, & in some instances human leukocyte antigen (HLA)
153
Why is HLA matching important in organ transplant?
Improves changes of successful transplant. Promotes engraftment. Reduces the risk of graft vs host disease (GVHD).
154
Engraftment
When the new cells (of an organ transplant) start to grow and make new blood cells.
155
Graft-vs-Host Disease
Occurs when the immune cells from the donated marrow or cord blood (the graft) attack the recipients body (the host).
156
In order to receive a transplant an recipient must meet what criteria?
The recipient must meet medical and psychosocial criteria determined by each transplant center.
157
UNOS
United Organ Sharing Network.
158
Four common reasons for heart transplant?
Cardiomyopathy. Ischemic heart disease (IHD). Congenital /valvular heart disease. Hypertensive heart disease
159
What measure is used to evaluate potential heart transplant pt & their long term risk?
VO2. A VO2 > 14mL/min/kg is considered "too well" for transplant.
160
Brain death
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
hypercapnea
A condition marked by an unusually high concentration of CO2 in the blood as a result of hypoventilation.
162
Heart donors can not older than?
55 years old
163
What are the goals of pharmacotherapy in heart transplant?
Prevent complications. Reduce morbidity. Reduce rejection.
164
What equations are used for mechanically ventilated pt?
Ireton-Jones. Also, a version for critically ill pt spontaneously breathing. This equation can also be used for the morbidly obese.
