Antihypertensive Drugs, Treatment of Angina, Arrhythmias, and CHF Flashcards

(85 cards)

1
Q

Which 2 factors influence blood pressure

A

-cardiac output (CO)
-total peripheral vascular resistance (TPR)

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2
Q

What does the baroreceptor reflex control?

A

BP- it monitors and corrects changes in BP within seconds by altering cardiac output and peripheral vascular resistance

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3
Q

How do antihypertensive drugs work?

A

By affecting CO and TPR

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4
Q

What are the two categories of hypertension?

A
  1. Primary/essential HTN
  2. Secondary HTN
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5
Q

Secondary HTN

A

Attributed to an abnormality in the body (chronic kidney disease, renal stenosis, endocrine disorders)
<10% of HTN

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6
Q

Primary or Essential HTN

A

There is no clear cause
90% of HTN

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7
Q

What are possible causes of essential HTN

A

-diet
-stress
-genetic predisposition
-cigarette smoking
-alcohol abuse
-obesity

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8
Q

What is metabolic syndrome?

A

All the following characteristics together:
-impaired glucose metabolism
-hyperinsulinemia
-abdominal obesity

**associated with HTN

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9
Q

The drugs used to treat HTN

A

-diuretics
-sympatholytics
-vasodilators
-drugs that inhibit the renin-angiotensin system
-calcium-channel blockers

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10
Q

How do diuretics work?

A

They increase renal excretion of water and sodium which decreases fluid volume in the vascular system and helps to lower BP

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11
Q

What do we need to be aware of if a pt is taking diuretics?

A

That potassium is also excreted so they should be taking a potassium supplement or be getting blood levels drawn regularly to check levels

**low potassium will lead to arrhythmias and no energy

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12
Q

Types of Diuretics

A

-Thiazide diuretics: needs good kidney function, not good for geriatric population
-Loop diuretics: more potent than thiazide diuretics
-Potassium sparing diuretics: reduces the loss of potassium and prevents hypokalemia, not as potent

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13
Q

Adverse effects of diuretics

A

-fluid depletion
-electrolyte imbalance
-hyponatremia
-hypokalemia (thiadize and loop diuretics)
-orthostatic hypotension
-impaired glucose and lipid metabolism
-fatigue
-“up all night peeing”

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14
Q

How do sympatholytic drugs work?

A

they interfere with sympathetic discharge

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15
Q

Examples of sympatholytic drugs

A

-beta blockers
-alpha blockers
-presynaptic adrenergic inhibitors
-centrally acting agents

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16
Q

How do Beta-blockers work?

A

-They decrease HR and myocardial contraction force and cardiac output which lowers BP (antihypertensive)
-The work of the heart is decreased and thus the myocardial oxygen demand is decreased (angina)
-decreases effects of sympathetics nervous system which slows HR and controls HR (arrhythmias)

**typically used in combination with other antihypertensive meds

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17
Q

ending of beta blockers

A

-lol

Carvedilol
Propranolol
Metoprolol

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18
Q

Side effects of beta blockers

A

-excessive HR depression
-OH
-impair glucose and lipid metabolism
-depression
-fatigue
-GI disturbances
-allergic reactions
-blunted HR response with exercise
-bronchoconstriction in patients with asthma or other respiratory issues (taking nonselective beta blockers)

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19
Q

How do alpha blockers work?

A

They block the alpha-1 adrenergic receptors on vascular smooth mm which promotes a decrease in vascular resistance
-they also improve blood lipid profiles (decrease triglycerides and total cholesterol)

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20
Q

Adverse effects of alpha blockers

A

-reflex tachycardia: baroreceptor reflex may kick in when peripheral resistance drops and cause an increase in HR
-OH
-increase in cardiac disease and CHF: vasodilation increases blood volume and thus increases the workload on the heart
**those at risk for heart failure should avoid alpha blockers

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21
Q

How do presynaptic adrenergic inhibitors work?

A

Inhibit the release of norepinephrine from the persynaptic terminals which decreases sympathetic excitation of the heart and peripheral vascular resulting in decreased BP

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22
Q

Adverse side effects of presynaptic adrenergic inhibitors

A

-bradycardia
-arrhythmias
-drowsiness
-GI disturbances: nausea, vomiting, diarrhea

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23
Q

How do centrally acting agents work?

A

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

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24
Q

Adverse side effects of centrally acting agents

A

-dry mouth
-dizziness
-sedation

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25
How do Vasodilators work?
Drugs that vasodilate the peripheral vasculature cause a decrease in peripheral resistance which decreases BP
26
Side effects of vasodilators
-reflex tachycardia -dizziness -OH -weakness -nausea -fluid retention -HA
27
How does the Renin-Angiotensin System work?
It is a system that regulates vascular tone as well as sodium and water balance in the body -rennin is an enzyme produced in the kidneys that is released into the blood stream when BP decreases -angiotensinogen is a peptide within the bloodstream -angiotensin I: a biproduct of when renin and antiotensinogen contact each other in the blood -angiotensin I is transformed into angiotensin II by angiotensin converting enzyme -angiotensin II: a potent vasoconstrictor
28
What are the different renin-angiotensin system inhibitors?
-ACE inhibitors (angiotensin converting enzyme) -ARBs (angiotensin II receptor blockers) -Direct renin inhibitors
29
How do ACE inhibitors work?
Inhibits the enzyme that allows angiotensin I to be converted into angiotensin II- allows for vasodilation and a decrease in BP
30
How do ARBs work?
Angiotensin II receptor blockers block the actual receptor where angiotensin II would bind to allow vasoconstriction to occur- allows for vasodilation and decrease BP
31
How do direct renin inhibitors work?
they inhibit renin's ability to convert angiotensinogen to angiotensin I- allows for vasodilation and decrease BP
32
Adverse effects of renin-angiotensin system inhibitors
1. ACE inhibitors: -allergic reaction- skin rash -persistent dry cough -angioedema- rashes, welts, burning/itching skin, face swelling, difficulty breathing -hyperkalemia 2. ARBs: -same as above expect dry cough 3. Direct renin inhibitors: -dry cough -GI problems
33
How do calcium channel blockers work?
They block the calcium entry into the vascular smooth mm cells which blocks the contractile process and leads to vasodilation and decrease vascular resistance -allows for an increase in coronary blood flow which increases myocardial oxygen supply **originally developed to treat angina and cardiac arrhythmias
34
Adverse side effects of calcium channel blockers
-excessive vasodilation: swelling in feet and ankles -OH -abnormalities in HR: too fast or too slow
35
Stages of HTN
-Normal: <120/<80 -Pre-hypertensive: 120-139/80-89 -Stage 1: 140-159/90-99 -Stage 2: >159/>99
36
What are the initial drugs of choice for those with stage 1 or stage II HTN?
-thiazide diuretic -calcium channel blocker -ACE inhibitor or ARBs **using 2 of these is a more aggressive and better first approach
37
PT considerations for patients on HTN meds
-be aware of OH and hypotension -avoid activities that cause widespread vasodilation: whirlpool and Hubbard tanks -be aware that exercise will cause further vasodilation -beta blockers will cause a blunted HR response to exercise (use RPE!) -encourage patients with be compliant with HTN meds
38
Why does angina Pectoris occur?
The supply of oxygen to the heart is insufficient to meet myocardial demands at a specific point in time, then lactic acid accumulates and the painful symptoms occur
39
Drugs to treat angina pectoris
-organic nitrates -beta blockers -calcium channel blockers
40
Examples of organic nitrates
-Nitroglycerin -Isosorbide dinitrate -Isosorbide mononitrate
41
How do organic nitrates work?
They convert nitric oxide within the vascular smooth mm which then causes vasodilation of the smooth mm throughout the body- this allows for a decrease in the amount of work the heart must do so the myocardial oxygen demand decreases
42
Administration of Nitroglycerin
Given for both the prevention and treatment of angina -can be taken orally, buccally, sublingually, transdermally, or via IV
43
What is the most common and best route for nitroglycerin?
Sublingual- placed under the tongue and drug is rapidly absorbed through the oral mucosa into the systemic circulation -therapeutic effect begins within 2 minutes -avoids first pass effect of liver
44
Adverse effects of organic nitrates
-HA -dizziness -OH
45
Why are some patients with angina prescribed an anticoagulant?
because angina is usually associated with some coronary artery occlusion, thus an anticoagulant will help to prevent coronary arteries from becoming completely blocked and causing an MI
46
Stable Angina
The myocardial oxygen demand greatly exceeds oxygen supply -often called exertional angina: occurs with a certain level of activity
47
Treatment for stable angina
-beta blockers -calcium channel blockers -nitrates
48
What are the first drugs used for the long term management of stable angina?
Beta blockers- they decrease the workload of the heart -must be taken daily to prevent episodes -calcium channel blockers are used if beta blockers aren't tolerated
49
Treatment of acute angina
Nitroglycerin
50
What is variant angina?
When the oxygen supply to the myocardium decreases because of coronary artery vasospasm -can be triggered by environmental and emotional stimuli
51
What is used to treat variant angina?
Calcium channel blockers are more effective -nitrates used if those are ineffective
52
What is the most severe form of angina?
Unstable angina- initiated by sudden rupture of atherosclerotic plaques within the coronary arteries and results in a decrease of myocardial oxygen supply
53
Which two things are within the category of Acute Coronary Syndromes?
-Unstable angina -MI
54
Which drugs are essential for preventing unstable angina to progressing into an MI?
anticoagulants and antiplatelet therapy **anticoagulants are given in the early stages of unstable angina
55
Which drugs are used for the management of unstable angina?
-ACE inhibitors -statin drugs
56
Concerns for PT with those with angina
-make sure they have their nitroglycerin tablets with them -be aware of cardiac limitations -HR will be blunted- adjust workloads carefully -at risk for hypotension
57
What things can result in arrhythmias?
-electrolyte imbalance -metabolic imbalances -toxicity to drugs -autonomic influences -cardiac diseases -genetic factors
58
What are the three basic abnormalities that will cause an arrhythmia?
1. Abnormal impulse generation: normal rhythm of SA and AV nodes has been disrupted 2. Abnormal impulse conduction: impulses through myocardium has been disrupted (heart blocks) 3. Simultaneous abnormalities of impulse generation and conduction: combo of above
59
Classes of Arrhythmic Drugs
-Class I: sodium channel blockers -Class II: beta blockers -Class III: drugs that prolong repolarization -Class IV: calcium channel blockers
60
How do sodium channel blockers work?
They bind to sodium channels in various tissues which inhibits the channels and decreases the membrane excitability and normalizes the rate of firing
61
What are the different categories of Class I drugs?
Sodium Channel Blockers -Class IA -Class IB -Class IC
62
What is the pro-arrhythmic effect?
A side effect of anti-arrhythmic drugs by actually increasing rhythm disturbances (another arrhythmia can be triggered while trying to treat another one)
63
Side effects of sodium channel blockers
-pro-arrhythmic effect -dizziness -visual disturbances -GI problems
64
How do drugs that prolong repolarization work?
They delay repolarization of cardiac cells which lengthens the time interval between action potentials and ultimately slows and stabilizes HR
65
what is the most widely used anti-arrhythmic drug?
Amiodarone -has properties of class I, II, and III drugs -controls many types of arrhythmias Side effects: -pulmonary toxicity -thyroid problems -liver damage
66
Which types of arrhythmias do class III drugs treat?
Ventricular arrhythmias: v-tach, v-fib, and supraventricular arrhythmias
67
Side effects of class III drugs?
Initial increase in arrhythmias (pro-arrhythmic effect)
68
why do calcium channel blockers help with arrhythmias?
Calcium entry plays a role in the generation of cardiac action potentials- by inhibiting the calcium influx into myocardial cells the excitability and conduction of cardiac tissue is altered -they decrease the rate of SA node discharge and inhibit conduction velocity through the AV node
69
What type of arrhythmia are class IV drugs useful in treating?
a-fib
70
Examples of nonpharamcological treatment for arrhythmias
-pacemakers -cardioverter defibrillators -surgical electrode catheter ablation **reduce long term complications and may be a more effective way to manage arrhythmias
71
PT considerations for arrhythmia medications
-faintness and dizziness can be signs of cardiotoxic drug effects (a sign that further arrhythmias are developing)- REFER! -hypotension can occur- monitor BP and HR
72
What are the 2 primary goals of CHF drugs?
1. improve myocardial contraction force (positive inotropic agents) 2. decrease cardiac workload: by affecting the heart or peripheral vasculature or by controlling fluid volume
73
Which drugs increase myocardial contraction?
Cardiac Glycosides: improves pumping action of the heart which increases cardiac output at rest and exercise
74
Which drugs decrease cardiac workload?
-ACE inhibitors -ARBs -Beta blockers -Diuretics -Vasodilators
75
What are the two types of cardiac glycosides?
1. Digoxin - used in the US 2. Digitoxin **digitalis refers to both of these drugs
76
How does Digitalis work?
Increases intracellular calcium concentrations which facilitates interaction between actin and myosin filaments in myocardial cells and decreases the symptoms of heart failure and number of hospitalizations -it also has an inhibitory effect on the sympathetic nervous system: slows HR and slows impulse conduction through heart
77
What is digitalis toxicity
A potentially fatal reaction to high doses of digitalis Signs: -GI disturbances -CNS disturbances (drowsiness, fatigue, confusion, visual disturbances) -Abnormalities in cardiac function -toxicity increases V-fib and death can occur
78
How is the Renin-Angiotensin System used for CHF?
The renin-angiotensin system is often activated in patients who have CHF which causes vasoconstriction and causes the heart to work even more- also stimulates aldosterone production which stresses the cardiovascular system more due to salt and water retention
79
ACE inhibitors for CHF
Very successful in treating CHF when heart failure is due to reduced L ventricular function and decreases mortality in those with CHF -early use of them can prevent or delay disease progression
80
Why is it important for ACE inhibitors to inhibit aldosterone secretion?
Angiotensin II promotes aldosterone secretion which promotes water retention- this beneficial because it reduces fluid volume
81
Which drugs are used if CHF patients cannot tolerate ACE inhibitors?
ARBs- are as effective as ACE inhibitors in treating heart failure and reducing mortality
82
Why are beta blockers beneficial for CHF?
they lessen the increased sympathetic activity that occurs with CHF- also reduces mortality and morbidity associated with this disease -used along with ACE inhibitors, digitalis, and diuretics to provide optimal treatment
83
Purpose of Diuretics for CHF
Increases the excretion of sodium and water which decreases the amount of fluid the heart must pump which reduces the heart's workload
84
PT Implications for CHF patients
-watch for s/s of acute congestive heart failure -watch for s/s of digoxin toxicity -fatigue and weakness may be early signs of fluid and electrolyte imbalance -watch those taking vasodilators for hypotension or postural hypotension
85
Vasodilators for CHF
these drugs vasodilate peripheral vessels which reduces peripheral resistance- thus the amount of blood returning to the heart is decreased and the pressure against which the heart must beat against is reduced