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Patho & Pharmo > Disorders of the CV & Peripheral Vasc Systems > Flashcards

Disorders of the CV & Peripheral Vasc Systems Flashcards

1
Q

heart rate and force of contraction are controlled by

A

cardiac control center in medulla

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2
Q

amount of volume of blood ejected by a ventricle in one minute

A

cardiac output

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3
Q

volume pumped from one ventricle in one contraction

A

stroke volume

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4
Q

cardiac output is calculated with

A

heart rate and stroke volume

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5
Q

pressure of blood against the systemic arterial walls

A

blood pressure

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6
Q

Inner layer of the heart

A

endocardium

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7
Q

separated the left and right sides of the heart

A

septum

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8
Q

connections to prevent muscle cells from separating during contraction

A

Desmosomes

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9
Q

sympathetic innervation does what to the heart

A

increases heart rate

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10
Q

parasympathetic stimulation by vagus nerve

A

decreases heart rate

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11
Q

branch off the aorta immediately above the aortic valve

A

right and left coronary arteries

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12
Q

left coronary artery divides into

A

left anterior descending/interventricular artery.
left circumflex artery.

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13
Q

coronary artery that circles the exterior of the heart in the left atrioventricular sulcus

A

left circumflex artery

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14
Q

coronary artery that follows the anterior interventricular sulcus downward over the surface of the heart

A

left anterior descending

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15
Q

coronary artery that follows the right atrioventricular sulcus on the posterior surface of the heart

A

right coronary artery

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16
Q

anastosomes

A

direct connections between small branches of the left and right coronary arteries near the apex

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17
Q

collateral circulation

A

alternative source of blood and nutrients. vessels expand or extend to meet metabolic needs of the cells.

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18
Q

brings blood o the right side of the heart and inferior portion of the left ventricle, posterior interventricular septum

A

right coronary artery

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19
Q

brings blood to the anterior wall of the ventricles, anterior septum, bundle branches

A

left anterior descending artery

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20
Q

brings blood to left atrium, lateral and posterior walls of the left ventricle

A

circumflex artery

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21
Q

Blood supply to the SA node

A

mainly right coronary artery, left circumflex in some

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22
Q

AV node blood supply

A

right coronary artery

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23
Q

blockage of the right coronary artery results in disturbances to the

A

AV node - arrhythmias

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24
Q

blockage to the left coronary will impair

A

pumping capability of the left ventricle - CHF

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25
Q

illustrate the conduction activity of the heart

A

ECG

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26
Q

auscultation of heart murmurs reveals

A

valvular abnormalities

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27
Q

reflected sound waves to record the image of the heart and valve movement

A

echocardiography

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28
Q

assessing general cardiovascular function and checking for exercise-induced problems

A

exercise stress test

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29
Q

show the shape and size of the heart, pulmonary congestion associated with heart failure

A

chest x-ray

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30
Q

assesses the size of an infarct in the heart, the extent of the myocardial perfusion, and function of ventricles

A

nuclear imaging

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31
Q

illustrates various levels of a tissue mass

A

tomographic studies

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32
Q

can identify dead or damaged areas of myocardial tissues and may be used to assess the extent of myocardial damage after MI

A

nuclear imaging

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33
Q

assesses cardiac ischemia at test

A

SPECT - single proton emission computed tomography

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34
Q

visualizes the inside of the heart, measures pressures, assesses valve and heart function

A

cardiac catheterization

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35
Q

way of visualizing the blood flow in the coronary arteries

A

coronary angiography

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36
Q

visualizing blood in the peripheral vessels

A

doppler studies

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37
Q

assess serum triglyceride and cholesterol levels and levels of sodium, potassium, calcium, and other electrolytes

A

blood tests

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38
Q

current oxygen level and acid-base balance in patients with shock or myocardial infarction

A

arterial blood gas determination

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39
Q

drugs that resist peripheral resistance systemically, cause decrease in blood pressure, dizziness/syncope, flushed face

A

vasodilators

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40
Q

drugs used to treat hypertension and dysrhythmias, reduce number of angina events

A

beta blockers

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41
Q

beta blockers mechanism of action

A

block the beta1-adrenergic receptors in the heart and prevent the SNS from increasing heart activity

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42
Q

drugs that block the movement of calcium ions into the cardiac and smooth muscle fiber

A

calcium channel blockers

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43
Q

drugs that decrease cardiac contractility, antiarrhythmic for atrial activity, antihypertensive, vasodilator

A

calcium channel blockers

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44
Q

CCB that is effective in selectivity for the myocardium and reduce both conduction and contractility

A

diltiazem

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45
Q

CCB that slows the heart rate by depressing the action of the SA and AV nodes

A

verapamil

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46
Q

CCB effective as peripheral vasodilators

A

nifedipine

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47
Q

CCB effective in lowering blood pressure

A

amlodipine

48
Q

cardiac glycoside, as a treatment for heart failure and as an antiarrhythmic drug for atrial arrhythmias, increases the contractility

A

digoxin

49
Q

drug that must be monitored for signs of toxicity and why

A

digoxin - effective dose is close to toxic dose

50
Q

examples of antihypertensive medications

A

adrenergic or sympathetic-blocking agents, calcium blockers, diuretics, ACE inhibitors, and angiotensin II receptor blocking agents

51
Q

may act on the SNS centrally (brain), may block peripheral alpha1-adrenergic receptors, may act as vasodilators

A

adrenergic-clocking agents

52
Q

preferred in the treatment of patients with hypertension and CHF

A

ACE inhibitors

53
Q

act by blocking the conversion of angiotensin I to angiotensin II by renin from the kidney

A

Angiotensin-converting enzyme inhibitors (ACE inhibitors)

54
Q

how do ACE inhibitors work?

A

reduce peripheral resistance (vasoconstriction) and aldosterone secretion (decreasing sodium and water retention) - decrease in preload and after load.

55
Q

remove excess sodium and water from the body through the kidneys by blocking the reabsorption of sodium or water

A

diuretics

56
Q

used to reduce the risk of blood clot formation in coronary or systemic arteries or damages or prosthetic heart valves

A

anticoagulants

57
Q

prescribed when diet and exercise are ineffective in reducing blood levels

A

statins

58
Q

how do statins work

A

reduce low-density lipoprotein (LDL) and cholesterol content of the blood by blocking synthesis in the liver

59
Q

relaxation phase of cardiac activity

A

diastole

60
Q

cardiac contraction

A

systole

61
Q

atria fill, all valves are closed

A

diastole

62
Q

increased atrial pressure opens AV valves, ventricles fill

A

diastole

63
Q

atria contract and empty, ventricles are full

A

systole begins

64
Q

ventricles begin contraction, pressure closes AV valves, atria relax

A

systole

65
Q

ventricles contract, increased pressure in ventricles, aortic and pulmonary valves open, blood ejected into aorta and pulmonary artery

A

systole

66
Q

ventricles empty, ventricles relax, aortic and pulmonary valves close

A

diastole

67
Q

lub corresponds with

A

closure of AV valves at the beginning of ventricular systole

68
Q

dub corresponds with

A

semilunar valves close with ventricular diastole

69
Q

heart rate measured at the heart itself

A

apical pulse

70
Q

difference in rate between the apical pulse and the radial pulse

A

pulse deficit

71
Q

volume of blood ejected by a ventricle in one minute

A

cardiac output

72
Q

volume pumped from one ventricle in one contraction

A

stroke volume

73
Q

Cardiac Output =

A

HR x SV (stroke volume)

74
Q

average cardiac output

A

4900-5000 mL/min (70bpmx70mL)

75
Q

Heart rate is influenced by

A

sympathetic nervous system, epinephrine

76
Q

stroke volume is influenced by

A

venous return, blood volume, sympathetic nervous system, peripheral resistance

77
Q

the ability of the heart to increase output in response to increased demand

A

cardiac reserve

78
Q

mechanical state of the heart at the end of diastole with the ventricles at their maximum volume

A

preload

79
Q

force required to eject blood from the ventricles

A

afterload

80
Q

determined by the peripheral resistance to the opening of the semilunar valves

A

afterload

81
Q

pressure exerted by the blood when ejected from the left ventricle

A

systolic pressure

82
Q

pressure sustained when the ventricles are relaxed

A

diastolic pressure

83
Q

difference between the systolic and diastolic pressures

A

pulse pressure

84
Q

force opposing blood flow, the amount of friction with the vessel walls encountered by the blood

A

peripheral resistance

85
Q

changes in blood pressure are detected by the

A

baroreceptors

86
Q

signals into the baroreceptors are relayed to

A

vasomotor control center in medulla

87
Q

what does the vasomotor control center in the medulla do?

A

adjusts the distribution of blood to maintain normal blood pressure

88
Q

Two ways in which blood pressure is elevated by increased SNS stimulation

A
  1. SNS and eps act at the beta1-adrenergic receptors in the heart to increase rate and force contraction.
  2. SNS, epi, and norepi increase vasoconstriction by stimulation the alpha1-receptors in the arterioles of the skin and viscera. Reducing capacity of the system and increases venous return.
89
Q

increases water reabsorption through the kidney, thus increasing blood volume

A

Antidiuretic hormone (ADH)/Vasopressin

90
Q

increases blood volume by increasing reabsorption of sodium ions and water

A

aldosterone

91
Q

cause for angina

A

deficit of oxygen to the hear

92
Q

deficiency of blood

A

ischemia

93
Q

death of myocardial tissue due to ischemia

A

myocardial infarction

94
Q

right heart failure

A

right ventricle cannot maintain its output, less blood proceeds to left side of heart and systemic circulation - forward effect

95
Q

left heart failure

A

normal blood volume of blood returning from lungs cannot enter left side of heart - causes congestion in pulmonary circulation, increased capillary pressure, possible pulmonary edema

96
Q

structural defects in the heart that develop during the first 8 weeks of embryonic life

A

cardiac anomalies

97
Q

acute systemic inflammatory condition resulting from abnormal immune reaction occurring weeks after an untreated infection

A

rheumatic fever

98
Q

what causes rheumatic fever

A

certain strains of group A beta-hemolytic streptococcus

99
Q

general term for all types of arterial changes

A

arteriosclerosis

100
Q

arterial changes characterized by the presence of atheroma

A

atherosclerosis

101
Q

define atheromas

A

plaques consisting of lipids, cells, fibrin, and cell debris, often with thrombus attached

102
Q

lipid subgroups assessed in serum lipids

A

total cholesterol, triglycerides, low-density lipoproteins, high-density lipoproteins

103
Q

bad lipoprotein that promotes atheroma formation

A

low-density lipoprotein

104
Q

where does LDL transport cholesterol

A

from liver to cells

105
Q

where does HDL transport cholesterol

A

from peripheral cells to liver for catabolism and excretion

106
Q

a bulge in the material wall

A

aneurysm

107
Q

non modifiable atherosclerosis factors

A

age, gender, genetic of familial factors

108
Q

predisposing or modifiable factors for atherosclerosis

A

obesity, smoking, sedentary lifestyle, DM, HTN, combination of these.

109
Q

what causes angina

A

deficit of oxygen to the heart muscle

110
Q

prolonged pain at rest and of recent onset

A

unstable angina

111
Q

types of chest pain

A

classic/exertional angina, variant angina, unstable angina

112
Q

vasospasm occurs at rest

A

variant angina

113
Q

myocardial hypertrophy

A

heart has outgrown its blood supply

114
Q

tachycardia associated with hypothyroidism can increase

A

Oxygen demand

115
Q

pain described with angina

A

tightness or pressure that radiates to the neck and left arm

116
Q

7 emergency treatments for angina

A
  1. rest, stop activity.
  2. sit upright.
  3. nitro SL.
  4. check pulse and resp.
  5. admin o2 if needed.
  6. hx of angina, nonresolving angina 3x NGSL > 5 mins - treat as MI.
  7. no pmhx angina, nonresolving angina NSGL > 2 mins - treat as MI.
117
Q

three ways infarct may form

A
  1. thrombus obstructs an artery.
    2.

Patho & Pharmo (6 decks)

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