Cardiovascular Pharmacology Flashcards
hypertension in 30 seconds
excessive vascular volume
low compliance of vasculature
increased activity of the renin angiotensin system
renin
- what is it
- release stimulated by
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
essential vs. secondary HTN
essential (primary)
-no clear cause
secondary
-increase in BP due to a specific, known cause (head trauma, cancer, renal, endocrine disorders)
first line medication classes for hypertension
thiazide diuretics
angiotensin-converting enzyme (ACE) inhibitors
angiotensin receptor blockers (ARBs)
calcium channel blockers (CCBs)
second line and third line medication classes for hypertension
beta-blockers
aldosterone antagonists
loop diuretics
direct vasodilators, alpha-1 blockers, alpha-2 blockers
basic targets for treating HTN
direct cardiac agents
peripheral vascular agents
renal agents
direct cardiac agents
-affect…
HR
contractility
conductivity
peripheral vascular agents
-affects…
peripheral resistance
pre-load
vascular health
vasodilation
renal agents
-affect
fluid volume
metabolites
direct cardiac agents
-types of drugs
beta blockers
calcium channel blockers
peripheral vascular agents
-types of drugs
hydralazine
alpha 1 antagonists
alpha 2 agonists
renal agents
-types of drugs
ACE inhibitors
angiotensin 2 inhibitors
diuretics
classes of diuretics
carbonic anhydrase inhibitors loop thiazide diruetics aldosterone antagonists potassium sparing diuretics
antihypertensive drug categories
diuretics sympatholytics vasodilators inhibiton of renin-angiotensin (ACE-inhibitors) calcium channel blockers
diuretics
- primary action sites
- anti-HTN effects
action
-kidneys
effects
-decrease plasma fluid volume
sympatholytics
- primary action sites
- anti-HTN effects
action
-various sites within sympathetic nervous system
effects
-decreased sympathetic influence on heart
vasodilators
- primary action sites
- anti-HTN effects
action
-peripheral vasculature
effects
-lower vascular resistance
ACE inhibitors
- primary action sites
- anti-HTN effects
action
-peripheral vasculature and certain involved organs
effects
-various
calcium channel blockers
- primary action sites
- anti-HTN effects
action
-vascular smooth muscle and cardiac muscle
effects
-decreased contractility, cardiac force, and rate
diuretics
-therapeutic uses
hypertension - thiazides are first line
HF
edema (pulmonary/peripheral)
diuretics
-monitoring
BP
electrolytes
ins/outs, weights
diuretics
-side effects
hypotension
renal dysfunction
volume depletion
electrolyte disturbances
diuretics
-cautions/contras
sulfa allergy (loops)
anuric patients
concomitant use of other nephrotoxic agents
thiazide diuretic agents
- how does it work
- when it is used
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
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)
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
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
ACE inhibitors
-therapeutic uses
hypertension
post MI (with LVSD) - remodeling
HF
diabetic patients
ACE inhibitors
-monitoring
BP
K+
renal function (BUN/SCr)
ACE inhibitors
-side effects
angioedema
cough (dry)
orthostasis/hypotension
hyperkalemia
ACE inhibitors
-cautions/contraindications
acute kidney injury
bilateral renal artery stenosis
hypotension
history of angioedema
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
angiotensin receptor blockers
-therapeutic uses
same as ACE inhibitors
hypertension post MI - remodeling
HF
diabetic patients
angiotensin receptor blockers
-monitoring
same as ACE inhibitors
BP
K+
renal function
angiotensin receptor blockers
-side effects
angioedema
orthostasis/hypotension
hyperkalemia
NO COUGH
angiotensin receptor blockers
-cautions/contras
acute kidney injury
bilateral renal artery stenosis
hypotension
history of angioedema
angiotensin receptor blockers
-what ending
-sartan
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
calcium channel blockers
-results of the mechanisms
vasodilation of vasculature
-decreased BP
-alleviates chest pain/spasm
first line option for HTN
calcium channel blockers
-therapeutic uses
hypertension -causes less orthostatic HTN than any othe vasodilator angina atrial fibrillation subarachnoid hemorrhage Raynaud's Phenomenon
calcium channel blockers
-monitoring
BP
HR
calcium channel blockers
-side effects
hypotension AV block reflex tachycardia headache, dizziness, flushing, drowsiness Pedal edema nausea constipation
calcium channel blockers
- ends in…
- most common
-pine amlodipine -dihydropyridine diltiazem, verapamil -non-dihydropyridine
common use of verapamil
cerebral vasospasm
- after sub-arachnoid hemorrhage
- allows them to relax and effectively perfuse the brain
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
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
beta blocker targets
-Beta 1 blockade
“cardioselective”
inhibits sympathetic contractility, inotropy, and conductivity of the heart
inhibits sympathetic renin secretion in the kidneys
how to remember which beta 1 blockers are selective
near beginning of alphabet
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
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
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
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
non-pharmacological management of HTN
diet modificatiion -low fat -low sodium -Omega-3 fatty acids exercise -limit alcohol -smoking cessation weight loss
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
ischemic heart disease
- what is it
- 2 solutions
cardiac muscle has insufficient oxygen
two solutions
-reduce cardiac oxygen demand
-increase cardiac oxygen supply
how to reduce cardiac oxygen demand
decrease preload
reduce contractility
reduce afterload
how to increase cardiac oxygen supply
increase coronary flow
increase oxygen extraction
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
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
types of angina
stable angina
Prinzmetal’s angina (variant)
unstable angina
stable angina
- why
- usually seen with…
O2 demand > O2 supply
usually seen with physical exertioin
Prinzmetal’s angina
- can occur…
- caused by…
can occur at rest
caused by vasospasm –> decreased O2 supply
unstable angina
- cause
- caused by…
decreased O2 supply (blocked artery) and increased O2 demand
caused by atherosclerotic plaque rupture
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
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
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
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
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
non-pharmacological management of angina
underlying disease state needs to be addressed -HTN -CAD -HF -anemia weight loss smoking cesssation stress reduction PCI/CABG
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
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
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
what is acute coronary syndrome (ACS)
cardiac plaques rupture or fully occlude _________-
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
special considerations for a PT in regards to MI
S/S to look for
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
HF in 30 seconds
chronic overwork of the heart muscle causes hypertrophic remodeling
reduced CO
fluid retention
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
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
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
arrhythmias
-categorized based on…
heart rate -bradyarryhythmia -tachyarrhythmia origin of irregular electrical activity -supraventricular -ventricular
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
non-pharmacological management of arrhythmias
underlying source of arrhythmia needs to be addressed procedures/devices -ablation -AICD -pacemakers
