Cardiovascular Pharmacology Flashcards

(83 cards)

1
Q

hypertension in 30 seconds

A

excessive vascular volume
low compliance of vasculature
increased activity of the renin angiotensin system

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2
Q

renin

  • what is it
  • release stimulated by
A

proteolytic enzyme that is released into the circulation primarily by the kidneys
release stimulated by
-sympathetic nerve activation
-renal artery hypotension (due to systemic hypotension or renal artery stenosis)
-decreased sodium delivery to the distal tubules of the kidney

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3
Q

essential vs. secondary HTN

A

essential (primary)
-no clear cause
secondary
-increase in BP due to a specific, known cause (head trauma, cancer, renal, endocrine disorders)

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4
Q

first line medication classes for hypertension

A

thiazide diuretics
angiotensin-converting enzyme (ACE) inhibitors
angiotensin receptor blockers (ARBs)
calcium channel blockers (CCBs)

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5
Q

second line and third line medication classes for hypertension

A

beta-blockers
aldosterone antagonists
loop diuretics
direct vasodilators, alpha-1 blockers, alpha-2 blockers

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6
Q

basic targets for treating HTN

A

direct cardiac agents
peripheral vascular agents
renal agents

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7
Q

direct cardiac agents

-affect…

A

HR
contractility
conductivity

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8
Q

peripheral vascular agents

-affects…

A

peripheral resistance
pre-load
vascular health
vasodilation

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9
Q

renal agents

-affect

A

fluid volume

metabolites

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10
Q

direct cardiac agents

-types of drugs

A

beta blockers

calcium channel blockers

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11
Q

peripheral vascular agents

-types of drugs

A

hydralazine
alpha 1 antagonists
alpha 2 agonists

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12
Q

renal agents

-types of drugs

A

ACE inhibitors
angiotensin 2 inhibitors
diuretics

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13
Q

classes of diuretics

A
carbonic anhydrase inhibitors
loop
thiazide diruetics
aldosterone antagonists
potassium sparing diuretics
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14
Q

antihypertensive drug categories

A
diuretics
sympatholytics
vasodilators
inhibiton of renin-angiotensin (ACE-inhibitors)
calcium channel blockers
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15
Q

diuretics

  • primary action sites
  • anti-HTN effects
A

action
-kidneys
effects
-decrease plasma fluid volume

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16
Q

sympatholytics

  • primary action sites
  • anti-HTN effects
A

action
-various sites within sympathetic nervous system
effects
-decreased sympathetic influence on heart

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17
Q

vasodilators

  • primary action sites
  • anti-HTN effects
A

action
-peripheral vasculature
effects
-lower vascular resistance

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18
Q

ACE inhibitors

  • primary action sites
  • anti-HTN effects
A

action
-peripheral vasculature and certain involved organs
effects
-various

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19
Q

calcium channel blockers

  • primary action sites
  • anti-HTN effects
A

action
-vascular smooth muscle and cardiac muscle
effects
-decreased contractility, cardiac force, and rate

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20
Q

diuretics

-therapeutic uses

A

hypertension - thiazides are first line
HF
edema (pulmonary/peripheral)

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21
Q

diuretics

-monitoring

A

BP
electrolytes
ins/outs, weights

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22
Q

diuretics

-side effects

A

hypotension
renal dysfunction
volume depletion
electrolyte disturbances

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23
Q

diuretics

-cautions/contras

A

sulfa allergy (loops)
anuric patients
concomitant use of other nephrotoxic agents

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24
Q

thiazide diuretic agents

  • how does it work
  • when it is used
A

inhibition of sodium/chlorine reuptake
-excretes sodium
-loosely coupled with potassium excretion
-moderate diruesis and afterload reduction
therapeutic value appears to be beyond diuresis
first line option

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25
loop diuretic targets - how does it work - useful in what patients? - most common one
``` inhibits Na, K, Ca, Mg reabsorption in the loop of Henle powerful diuresis and volume reduction decreased afterload not sued much for BP reduction useful in patients with edema and HF most common is furosemide (Lasix) ```
26
potassium sparing diuretics - aldosterone antagonists - how does it work - used for - common ones
``` inhibits aldosterone by inhibiting sodium-potassium exchange site in the distal tubule -excretes sodium -excretes water -retains potassium used for resistant hypertension used to treat HF aldosterone antagonists -spironolactone -eplerenone ```
27
ACE inhibitors | -how does it work?
inhibition of angiotensin converting enzyme -inhibition of the conversion of angiotensin I to angiotensin II peripheral vasodilation -ATII causes peripheral vasoconstriction reduced antidiuretic hormone (ADH) production -reduced fluid volume reduced aldosterone production -reduced fluid volume first line option
28
ACE inhibitors | -therapeutic uses
hypertension post MI (with LVSD) - remodeling HF diabetic patients
29
ACE inhibitors | -monitoring
BP K+ renal function (BUN/SCr)
30
ACE inhibitors | -side effects
angioedema cough (dry) orthostasis/hypotension hyperkalemia
31
ACE inhibitors | -cautions/contraindications
acute kidney injury bilateral renal artery stenosis hypotension history of angioedema
32
angiotensin receptor blocker | -how does it work?
``` inhibition of angiotensin II receptor -action of angiotensin II is blocked despite its production peripheral vasodilation -ATII causes peripheral vasoconstriction reduced ADH production -reduced fluid volume reduced aldosterone production -reduced fluid volume first line option -should not be combined with ACE inhibitors ```
33
angiotensin receptor blockers | -therapeutic uses
same as ACE inhibitors hypertension post MI - remodeling HF diabetic patients
34
angiotensin receptor blockers | -monitoring
same as ACE inhibitors BP K+ renal function
35
angiotensin receptor blockers | -side effects
angioedema orthostasis/hypotension hyperkalemia NO COUGH
36
angiotensin receptor blockers | -cautions/contras
acute kidney injury bilateral renal artery stenosis hypotension history of angioedema
37
angiotensin receptor blockers | -what ending
-sartan
38
calcium channel blockers - what does it do - mechanisms - examples
``` inhibition of sympathetic stimulation of vascular smooth muscle -reduce afterload -reduced cardiac muscle contractility mechanisms -reduced contractility, reduced HR -preserve renal function in those with HTN-related renal disease examples -diltiazem -amlodipine -nicardipine ```
39
calcium channel blockers | -results of the mechanisms
vasodilation of vasculature -decreased BP -alleviates chest pain/spasm first line option for HTN
40
calcium channel blockers | -therapeutic uses
``` hypertension -causes less orthostatic HTN than any othe vasodilator angina atrial fibrillation subarachnoid hemorrhage Raynaud's Phenomenon ```
41
calcium channel blockers | -monitoring
BP | HR
42
calcium channel blockers | -side effects
``` hypotension AV block reflex tachycardia headache, dizziness, flushing, drowsiness Pedal edema nausea constipation ```
43
calcium channel blockers - ends in... - most common
``` -pine amlodipine -dihydropyridine diltiazem, verapamil -non-dihydropyridine ```
44
common use of verapamil
cerebral vasospasm - after sub-arachnoid hemorrhage - allows them to relax and effectively perfuse the brain
45
sympatholytics - beta blockers | -how do they work?
``` primarily a function of beta 1 blockade -inhibition of sympathetic carciad stimulation of the SA node -inhibition of renin secretion secondary effects of Beta 2 Blockade -vasodilation of GI vasculature ```
46
sympatholytics - beta blockers | -place in therapy
second line for hypertension when first line agents are optimized can decrease exercise tolerance initially important agent for HTN with other cardiovascular co-morbidities -ischemic heart disease -MI -CHF
47
beta blocker targets | -Beta 1 blockade
"cardioselective" inhibits sympathetic contractility, inotropy, and conductivity of the heart inhibits sympathetic renin secretion in the kidneys
48
how to remember which beta 1 blockers are selective
near beginning of alphabet
49
beta blocker targets | -beta 2 blockade
beta 2 receptors inhibit smooth muscle contractions in the lungs and GI tract beta 2 blockade is useful for restricting hepatic blood flow for patient with liver cirrhosis, but generally not a therapeutic effect for CVD beta 2 blockade may cause bronchospasm
50
combined alpha and nonselective beta-blockers - alpha 1 blockade function - effects vs. beta blockers without alpha blockade - commonly used combined alpha and nonselective beta-blockers
``` alpha 1 blockade -causes peripheral vasodilation lowers blood pressure more compared to w/ no alpha blockade commonly used -carvedilol -labetalol ```
51
alpha 1 blockers and place in therapy
inhibition of sympathetic stimulation of vascular smooth muscle -reduced afterload alternative sympatholytic -has some synergistic effects for people with CVD -reduced BP -reduced afterload and increased CO -resulting tachycardia via baroreceptor response as side effect
52
impact of hypertenion management on rehab
primary concern is the presence of hypotension and postural-related hypotension reduced CV response to exercise, especially with beta-blockers and CCBs physical therapists can increase compliance through education -emphasize "silent killer" nature of HTN
53
non-pharmacological management of HTN
``` diet modificatiion -low fat -low sodium -Omega-3 fatty acids exercise -limit alcohol -smoking cessation weight loss ```
54
special considerations for a patient with HTN - watch for... - use cauteion when doing... - be aware of...
``` orthostasis hypotension dizziness fatigue use caution when doing activites that may cause vasodilation and further drops in BP ```
55
ischemic heart disease - what is it - 2 solutions
cardiac muscle has insufficient oxygen two solutions -reduce cardiac oxygen demand -increase cardiac oxygen supply
56
how to reduce cardiac oxygen demand
decrease preload reduce contractility reduce afterload
57
how to increase cardiac oxygen supply
increase coronary flow | increase oxygen extraction
58
angina - what is it - due to... - -how is this seen
``` chest pain due to ischemia imbalance of O2 supply and demand to the myocardium -EKG changes -increase lactate -wall motion abnormalities ```
59
angina | -treatments
``` nitrates -decrease O2 demand beta-blockers -decrease O2 demand calcium channel blockers -increase O2 supply and decrease O2 demand ranolazine -no effects on O2 supply or demand; mechanisms unknown ```
60
types of angina
stable angina Prinzmetal's angina (variant) unstable angina
61
stable angina - why - usually seen with...
O2 demand > O2 supply | usually seen with physical exertioin
62
Prinzmetal's angina - can occur... - caused by...
can occur at rest | caused by vasospasm --> decreased O2 supply
63
unstable angina - cause - caused by...
decreased O2 supply (blocked artery) and increased O2 demand | caused by atherosclerotic plaque rupture
64
angina pectoris - pharmacological management - how do they generally work?
``` organic nitrates beta blockers CCBs ranolazine help to restore the balance between cardiac oxygen supply and cardiac oxygen demand ```
65
beta blockers and ischemic heart disease - how does it work - place in therapy
``` reduced cardiac O2 demand by limiting maximum stimulation (HR) place in therapy -first line for stable angina -decreases morbidity (reduced Sx) -decreases mortality ```
66
angina pectoris and organic nitrates - how do they work? - short acting first line for... - long acting second line after...
peripheral vasodilation by promoting nitric oxide release -veins, arteries, arterioles decrease preload short acting line for angina attacks (nitroglycerin) long acting second line after beta blockers for Sx relief
67
angina pectoris and CCBs - how does it work - agent of choice for... - examples
``` blocks calcium re-entry -reduced contractility, reduced HR -agent of choice for Pinzmetal angina examples -amlodipine -diltiazem -verapamil ```
68
ranolazine and angina pectoris - how does it work - does not impact... - generally considered second line based on...
blocks sodium channels but mechanisms for treating angina is not fully known does not impact blood pressure or HR second line based on cost and potential side effect of arrhythmias
69
non-pharmacological management of angina
``` underlying disease state needs to be addressed -HTN -CAD -HF -anemia weight loss smoking cesssation stress reduction PCI/CABG ```
70
angina pectoris impact on rehab | -considerations
ensure proximity and availability of drug during rehab sessions avoid over-challenging the heart during sessions artificial increase in tolerance to exercise guard against orthostatic hypotension
71
special considerations for a PT concerning angina
therapy may disturb the myocardial oxygen balance make sure patients with stable angina have SL nitro available may have to adjust exercise based on patient's medication regimen be aware of hypotension and dizziness use caution when doing activities that may cause vasodialtion and further drops in BP help with compliance
72
MI - all patients post-MI should be on the following medications unless contra'd... - patients should receive information regarding...
``` aspirin P2Y12 inhibitor for at least 12 months beta blockers statin +/- ACE inhibitor info regarding -weight management -smoking cessation -exercise ```
73
what is acute coronary syndrome (ACS)
cardiac plaques rupture or fully occlude _________-
74
ACS medication considerations
``` aspirin -antiplatelet agent may cause bruising P2Y12 inhibitors - also antiplatelet agents which may cause bruising -clopidogral -prasugrel -ticagrelor statins -most common side effect is myopathy ```
75
special considerations for a PT in regards to MI
S/S to look for
76
special considerations for a PT in regards to MI - S/S to look for - what to do if S/S appear
S/S to look for -diaphoresis -chest pain (often radiates to jaw or arm -shortness of breath what to do -call 911 -administer nitro if patient uses -administer 325 mg of aspirin - chew and swallow -if O2 available, administer via NC if O2 sat is <90% -hospital acronym: MONA
77
HF in 30 seconds
chronic overwork of the heart muscle causes hypertrophic remodeling reduced CO fluid retention
78
HF treatment strategy - treat to... - types of drugs used
``` treat to -decrease cardiac load -decrease resistance -increase contractility drugs -cardiac glycosides -ACE inhibitors -beta blockers -aldosterone antagonists -vasodilators -diuretics ```
79
cardiac glycoside - how does it work - impact on mortality and hospitalizations - TI - S/S of toxicity
``` positive inotrope - will increase contractility of heart no impact on mortality but can reduce hospitalizations narrow TI medications S/S -visual disturbances -bradycardia and heart block -anorexia -nausea and vomiting ```
80
special considerations for a PT regarding HF
know signs of HF exacerbations -dyspnea -cough be aware of medication side effects, especially digoxin be aware of hypotension and dizziness use caution when doing activites that may cause vasodilation and further drops in BP
81
arrhythmias | -categorized based on...
``` heart rate -bradyarryhythmia -tachyarrhythmia origin of irregular electrical activity -supraventricular -ventricular ```
82
classes of antiarrhythmic drugs | -primary action
``` class I -drugs that block Na+ channels class II -beta blockers class III -drugs that prolong repolarization class IV -calcium channel blockers ```
83
non-pharmacological management of arrhythmias
``` underlying source of arrhythmia needs to be addressed procedures/devices -ablation -AICD -pacemakers ```