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Pharm > 7: Antihypertensive (Angina, Arrhythmias, CHF) > Flashcards

7: Antihypertensive (Angina, Arrhythmias, CHF) Flashcards

1
Q

equation for blood pressure

A

BP = CO x TPR

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2
Q

what is the function of the baroreceptor reflex?

A

to monitor and correct changes in BP within seconds by altering cardiac output and peripheral vascular resistance

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3
Q

how do kidneys help with long term management of BP?

A

they control fluid balance

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4
Q

which type of hypertension is less common?

A

secondary hypertension (<10%)

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5
Q

which type of hypertension means there is no clear cause of the elevated BP?

A

primary hypertension

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6
Q

what are some causes of secondary hypertension?

A

chronic kidney disease, renal artery stenosis, endocrine disorders

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7
Q

how is secondary hypertension treated?

A

treatment focuses on correcting the abnormality –find the cause and address it specifically

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8
Q

what are possible causes of primary hypertension?

A

diet, stress, genetics, cigarette smoking, alcohol abuse, obesity

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9
Q

how are peripheral vessels impacted by consistently high BP?

A

vessels become less compliant and resistance increases

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10
Q

what are metabolic abnormalities associated with hypertension?

A

insulin resistance (impaired glucose metabolism), hyperinsulinemia, dyslipidemia, abdominal obesity (these characteristics all together are known as metabolic syndrome)

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11
Q

what classes of drugs are used to treat HTN?

A

diuretics
sympatholytics
vasodilators
renin-angiotensin inhibitors
calcium-channel blockers

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12
Q

what is the mechanism of diuretics?

A

they increase renal excretion of water and sodium, which decreases fluid volume in the vascular system

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13
Q

why do pts need a potassium supplements when taking diuretics?

A

potassium is also decreased with diuretics, which can lead to arrhythmias, decreased energy, and inability to tolerate PT

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14
Q

what are three types of diuretics?

A

thiazide, loop, and potassium-sparing

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15
Q

what is required for using thiazide diuretics?

A

good kidney function (often not a good choice for geriatrics)

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16
Q

are loop diuretics more or less potent than thiazides?

A

more potent

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17
Q

what are adverse effects of diuretics?

A

fluid depletion, electrolyte imbalance, low sodium, low potassium, orthostatic hypotension, impaired glucose or lipid metabolism, tired, up all night peeing

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18
Q

what are problems caused by fluid depletion (with use of diuretics)?

A

decrease in blood volume, increase in CO and peripheral resistance due to activation of the baroreceptor reflex

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19
Q

What are examples of sympatholytics?

A

beta blockers
alpha blockers
presynaptic adrenergic inhibitors
centrally acting agonists

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20
Q

What are sympatholytics?

A

drugs that block or interfere with sympathetic discharge

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21
Q

how do beta adrenergic blockers address HTN?

A

decrease CO and myocardial force, which slow down HR

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22
Q

suffix of sympatholytic beta blockers

A

(-lol)

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23
Q

side effects of beta blockers

A

excessive HR depression, orthostatic hypotension, impaired glucose and lipid metabolism, depression, fatigue, GI disturbances, allergic reactions, blunted HR response with exercise

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24
Q

what is the mechanism of alpha blockers?

A

they block alpha-1 adrenergic receptors on vascular smooth muscle, which decreases vascular resistance

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25
Q

adverse effects of alpha blockers

A

reflex tachycardia, orthostatic hypotension, increase in cardiac disease and CHF

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26
Q

what is reflex tachycardia?

A

when peripheral vascular resistance fails, the baroreceptor reflex may kick in and cause a compensatory increase in HR

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27
Q

why do alpha blockers increase risk of cardiac disease and CHF?

A

they allow vasodilation, which increases plasma volume and increases the workload of the heart (if they have a known risk of any cardiac disease, they should avoid alpha blockers)

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28
Q

what is the mechanism of presynaptic adrenergic inhibitors?

A

they inhibit the release of norepinephrine from the presynaptic terminals, which decreases sympathy excitation of the heart and vasculature, resulting in decreased BP

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29
Q

what is the mechanism of presynaptic adrenergic inhibitors?

A

they inhibit the release of norepinephrine from the presynaptic terminals, which decreases sympathy excitation of the heart and vasculature, resulting in decreased BP

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30
Q

what are adverse effects of alpha blockers?

A

bradycardia, arrhythmias, drowsiness, GI disturbances (nausea, vomiting, diarrhea)

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31
Q

what is the mechanism of centrally acting agents?

A

they inhibit sympathetic discharge from the brainstem by acting on central receptors, which causes a decrease in cardiovascular stimulation and BP

32
Q

what are adverse effects of centrally acting agents?

A

dry mouth, dizziness, sedation

33
Q

how do vasodilators decrease BP?

A

they dilate the peripheral vasculature, which decreases peripheral resistance, therefore decreasing BP

34
Q

what are side effects of vasodilators?

A

reflex tachycardia, dizziness, orthostatic hypotension, weakness, nausea, fluid retention, headache

35
Q

what is the mechanism of renin-angiotensin system inhibitors (in general)?

A

prevents renin’s ability to convert angiotensinogen to angiotensin II, which is a vasoconstrictor, in order to keep vasculature dilated and decrease BP

36
Q

What are three types of renin-angiotensin system inhibitors?

A

ACE inhibitors, ARBs (angiotensin II receptor blockers), and renin inhibitors

37
Q

what are adverse effects of ACE inhibitors?

A

allergic reaction (skin rash), persistent, dry cough, angioedema (rashes, welts, burning, swelling, difficulty breathing), hyperkalemia (can lead to irregular HR)

38
Q

what are adverse effects of ARBs?

A

no benefit over ACE inhibitors except that they don’t cause the dry cough

39
Q

what are adverse effects of direct-acting renin inhibitors?

A

dry cough, GI problems (diarrhea, upset stomach, abdominal pain)

40
Q

what is the mechanism of calcium channel blockers?

A

they block calcium entry in the vascular smooth muscle cells which blocks the contractile process, leading to vasodilation and decreased vascular resistance

41
Q

what are adverse effects of calcium channel blockers?

A

excessive vasodilation (swelling in feet and ankles), orthostatic hypotension, abnormalities in HR (too fast or slow)

42
Q

What are the systolic and diastolic values for each stage of hypertension?

A

normal: <120/<80
pre-HTN: 120-139 / 80-89
stage 1 HTN: 140-159 / 90-99
stage 2 HTN: >159 / >99

43
Q

what are the initial drug choices for stage 1 HTN?

A

thiazide diuretic, calcium channel blocker, ACE inhibitor or ARB

44
Q

what is the drug choice for stage 2 HTN?

A

use two of those “first line of defense” drugs in combination

45
Q

what are PT implications for HTN?

A
  • orthostatic hypotension is common
  • avoid activity that causes widespread dilation (whirlpool)
  • use RPE scales with beta blockers
  • exercise causes vasodilation
46
Q

why does angina occur?

A

imbalance between myocardial oxygen supply and demand leads to ischemia, which causes metabolic, electrophysiological, and contractile changes in the heart
lactic acide accumulaties and painful symptoms occur

47
Q

which drugs are used to treat angina pectoris?

A

organic nitrates, beta blockers, and calcium channel blockers

48
Q

what is the mechanism of organic nitrates?

A

they convert nitric oxide within the vascular smooth muscle, which causes vasodilation of the smooth muscle (in the periphery as well as the coronary arteries, which decreases both cardiac preload and after load)

49
Q

what is the best and most common route for nitroglycerin?

A

sublingual

50
Q

what are adverse effects of nitroglycerin and other organic nitrates?

A

headache, dizziness, orthostatic hypotension

51
Q

why are patients with angina prescribed an anticoagulant?

A

to prevent coronary arteries from becoming completely blocked and causing an MI

52
Q

what is stable angina?

A

myocardial oxygen demand greatly exceeds oxygen supply, typically occurs with a certain level of exertional activity

53
Q

what is the typical drug for treating acute episodes of stable angina?

A

nitroglycerin

54
Q

what drugs are usually the first drugs used in long term management of stable angina?

A

beta blockers

55
Q

when are calcium channel blockers used in the treatment of stable angina?

A

when beta blockers aren’t tolerated

56
Q

what causes variant angina?

A

vasospasms that cause oxygen supply to decrease even though the oxygen demand has not changed (can occur even at rest; potential for environmental and emotional stimuli)

57
Q

what drug is most effective for variant angina?

A

calcium channel blockers

58
Q

what is the most severe form of angina?

A

unstable angina

59
Q

what is essential to prevent unstable angina from progressing to MI?

A

anticoagulant and antiplatelet therapy

60
Q

PT implications for angina pectoris?

A
  • be aware of what medications they take
  • exercise will increase demand of myocardial oxygen
  • be aware of cardiac limitations, keep nitroglycerin tablets with them for acute attacks
  • orthostatic hypotension
61
Q

three basic abnormalities that cause an arrhythmia:

A
  1. abnormal impulse generation
  2. abnormal impulse conduction
  3. simultaneous abnormalities
62
Q

what are the four categories of drugs that treat arrhythmias?

A

class 1: sodium channel blockers
class 2: beta blockers
class 3: drugs that prolong repolarization
class 4: calcium channel blockers

63
Q

what are general side effects of antiarrhythmic drugs?

A

pro-arrhythmic effect (increased rhythm disturbances, potential for another arrhythmia)
dizziness, visual disturbances, GI problems

64
Q

what arrhythmias are treated by drugs that prolong repolarization?

A

VTach, VFib, supraventricular arrhythmias

65
Q

what is the most widely used anti arrhythmic drug?

A

amiodarone

66
Q

what are non pharmacological treatment options for arrhythmias?

A

pacemakers, cardioverter defibrillators, surgical electrode catheter ablation

67
Q

PT implications for arrhythmia drugs:

A
  • risk of increased/new arrhythmias
  • faintness and dizziness = signs of cardiotoxicity
  • hypotension → monitor vitals
68
Q

two goals of CHF drugs:

A
  1. improve myocardial contraction force
  2. decrease cardiac workload (by affecting vasculature or controlling fluid volume)
69
Q

what drugs increase myocardial contraction force?

A

cardiac glycosides (digoxin and digitoxin)

70
Q

what types of drugs decreased cardiac workload?

A

ACE inhibitors, ARBs, beta blockers, diuretics, vasodilators

71
Q

What is the function of digitalis?

A

to improve pumping action of the heart, by increasing CO at rest and within exercise, which would lead to increased exercise tolerance

72
Q

what is the mechanism of digitalis?

A

it increases intracellular calcium concentration which facilitates interaction between actin and myosin filaments in the myocardial cell

73
Q

how does digitalis affect the sympathetic nervous system?

A

inhibits the sympathetic nervous system, which decreases the stress on the heart, which slows the HR as well as impulse conduction through the heart

74
Q

what are signs of digitalis toxicity?

A

GI distress (N&V, diarrhea)
CNS disturbances (fatigue, drowsiness, confusion, visual disturbances)
Abnormalities in cardiac function (arrhythmias, premature ventricular contractions, V-Tach, heart blocks)
V-fib and death

75
Q

what is the mechanism of ARBs?

A

they prevent angiotensin II from binding to the receptors on vascular tissues, which limits vasoconstriction (and causes vasodilation)

76
Q

are beta blockers good for treating CHF?

A

yes, although they used to be considered detrimental. now they are known to lessen the increase of sympathetic activity seen with CHF.

77
Q

what is the mechanism of diuretics?

A

Pharm (18 decks)

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