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S2 Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

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
Q

loop diuretic targets

  • how does it work
  • useful in what patients?
  • most common one
A 
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)
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26
Q

potassium sparing diuretics - aldosterone antagonists

  • how does it work
  • used for
  • common ones
A 
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
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27
Q

ACE inhibitors

-how does it work?

A

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

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28
Q

ACE inhibitors

-therapeutic uses

A

hypertension
post MI (with LVSD) - remodeling
HF
diabetic patients

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29
Q

ACE inhibitors

-monitoring

A

BP
K+
renal function (BUN/SCr)

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30
Q

ACE inhibitors

-side effects

A

angioedema
cough (dry)
orthostasis/hypotension
hyperkalemia

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31
Q

ACE inhibitors

-cautions/contraindications

A

acute kidney injury
bilateral renal artery stenosis
hypotension
history of angioedema

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32
Q

angiotensin receptor blocker

-how does it work?

A 
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
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33
Q

angiotensin receptor blockers

-therapeutic uses

A

same as ACE inhibitors
hypertension post MI - remodeling
HF
diabetic patients

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34
Q

angiotensin receptor blockers

-monitoring

A

same as ACE inhibitors
BP
K+
renal function

35
Q

angiotensin receptor blockers

-side effects

A

angioedema
orthostasis/hypotension
hyperkalemia
NO COUGH

36
Q

angiotensin receptor blockers

-cautions/contras

A

acute kidney injury
bilateral renal artery stenosis
hypotension
history of angioedema

37
Q

angiotensin receptor blockers

-what ending

A

-sartan

38
Q

calcium channel blockers

  • what does it do
  • mechanisms
  • examples
A 
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
Q

calcium channel blockers

-results of the mechanisms

A

vasodilation of vasculature
-decreased BP
-alleviates chest pain/spasm
first line option for HTN

40
Q

calcium channel blockers

-therapeutic uses

A 
hypertension
-causes less orthostatic HTN than any othe vasodilator
angina
atrial fibrillation
subarachnoid hemorrhage
Raynaud's Phenomenon
41
Q

calcium channel blockers

-monitoring

A

BP

HR

42
Q

calcium channel blockers

-side effects

A 
hypotension
AV block
reflex tachycardia
headache, dizziness, flushing, drowsiness
Pedal edema
nausea
constipation
43
Q

calcium channel blockers

  • ends in…
  • most common
A 
-pine
amlodipine
-dihydropyridine
diltiazem, verapamil
-non-dihydropyridine
44
Q

common use of verapamil

A

cerebral vasospasm

  • after sub-arachnoid hemorrhage
  • allows them to relax and effectively perfuse the brain
45
Q

sympatholytics - beta blockers

-how do they work?

A 
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
Q

sympatholytics - beta blockers

-place in therapy

A

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
Q

beta blocker targets

-Beta 1 blockade

A

“cardioselective”
inhibits sympathetic contractility, inotropy, and conductivity of the heart
inhibits sympathetic renin secretion in the kidneys

48
Q

how to remember which beta 1 blockers are selective

A

near beginning of alphabet

49
Q

beta blocker targets

-beta 2 blockade

A

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
Q

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
A 
alpha 1 blockade
-causes peripheral vasodilation
lowers blood pressure more compared to w/ no alpha blockade
commonly used
-carvedilol
-labetalol
51
Q

alpha 1 blockers and place in therapy

A

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
Q

impact of hypertenion management on rehab

A

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
Q

non-pharmacological management of HTN

A 
diet modificatiion
-low fat
-low sodium
-Omega-3 fatty acids
exercise 
-limit alcohol
-smoking cessation
weight loss
54
Q

special considerations for a patient with HTN

  • watch for…
  • use cauteion when doing…
  • be aware of…
A 
orthostasis
hypotension
dizziness
fatigue
use caution when doing activites that may cause vasodilation and further drops in BP
55
Q

ischemic heart disease

  • what is it
  • 2 solutions
A

cardiac muscle has insufficient oxygen
two solutions
-reduce cardiac oxygen demand
-increase cardiac oxygen supply

56
Q

how to reduce cardiac oxygen demand

A

decrease preload
reduce contractility
reduce afterload

57
Q

how to increase cardiac oxygen supply

A

increase coronary flow

increase oxygen extraction

58
Q

angina

  • what is it
  • due to…
  • -how is this seen
A 
chest pain due to ischemia
imbalance of O2 supply and demand to the myocardium
-EKG changes
-increase lactate
-wall motion abnormalities
59
Q

angina

-treatments

A 
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
Q

types of angina

A

stable angina
Prinzmetal’s angina (variant)
unstable angina

61
Q

stable angina

  • why
  • usually seen with…
A

O2 demand > O2 supply

usually seen with physical exertioin

62
Q

Prinzmetal’s angina

  • can occur…
  • caused by…
A

can occur at rest

caused by vasospasm –> decreased O2 supply

63
Q

unstable angina

  • cause
  • caused by…
A

decreased O2 supply (blocked artery) and increased O2 demand

caused by atherosclerotic plaque rupture

64
Q

angina pectoris

  • pharmacological management
  • how do they generally work?
A 
organic nitrates
beta blockers
CCBs
ranolazine
help to restore the balance between cardiac oxygen supply and cardiac oxygen demand
65
Q

beta blockers and ischemic heart disease

  • how does it work
  • place in therapy
A 
reduced cardiac O2 demand by limiting maximum stimulation (HR)
place in therapy
-first line for stable angina
-decreases morbidity (reduced Sx)
-decreases mortality
66
Q

angina pectoris and organic nitrates

  • how do they work?
  • short acting first line for…
  • long acting second line after…
A

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
Q

angina pectoris and CCBs

  • how does it work
  • agent of choice for…
  • examples
A 
blocks calcium re-entry
-reduced contractility, reduced HR
-agent of choice for Pinzmetal angina
examples
-amlodipine
-diltiazem
-verapamil
68
Q

ranolazine and angina pectoris

  • how does it work
  • does not impact…
  • generally considered second line based on…
A

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
Q

non-pharmacological management of angina

A 
underlying disease state needs to be addressed
-HTN
-CAD
-HF
-anemia
weight loss
smoking cesssation
stress reduction
PCI/CABG
70
Q

angina pectoris impact on rehab

-considerations

A

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
Q

special considerations for a PT concerning angina

A

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
Q

MI

  • all patients post-MI should be on the following medications unless contra’d…
  • patients should receive information regarding…
A 
aspirin
P2Y12 inhibitor for at least 12 months
beta blockers
statin +/- ACE inhibitor
info regarding
-weight management
-smoking cessation
-exercise
73
Q

what is acute coronary syndrome (ACS)

A

cardiac plaques rupture or fully occlude _________-

74
Q

ACS medication considerations

A 
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
Q

special considerations for a PT in regards to MI

A

S/S to look for

76
Q

special considerations for a PT in regards to MI

  • S/S to look for
  • what to do if S/S appear
A

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
Q

HF in 30 seconds

A

chronic overwork of the heart muscle causes hypertrophic remodeling
reduced CO
fluid retention

78
Q

HF treatment strategy

  • treat to…
  • types of drugs used
A 
treat to
-decrease cardiac load
-decrease resistance
-increase contractility
drugs
-cardiac glycosides
-ACE inhibitors
-beta blockers
-aldosterone antagonists
-vasodilators
-diuretics
79
Q

cardiac glycoside

  • how does it work
  • impact on mortality and hospitalizations
  • TI
  • S/S of toxicity
A 
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
Q

special considerations for a PT regarding HF

A

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
Q

arrhythmias

-categorized based on…

A 
heart rate
-bradyarryhythmia
-tachyarrhythmia
origin of irregular electrical activity
-supraventricular
-ventricular
82
Q

classes of antiarrhythmic drugs

-primary action

A 
class I
-drugs that block Na+ channels
class II
-beta blockers
class III
-drugs that prolong repolarization
class IV
-calcium channel blockers
83
Q

non-pharmacological management of arrhythmias

A 
underlying source of arrhythmia needs to be addressed
procedures/devices
-ablation
-AICD
-pacemakers

S2 Pharmacology (7 decks)

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