Antihypertensives Flashcards
3 main factors affecting blood pressure
CO
Blood volume
Resistance
- artery walls flexibility
- artery diameter
- blood viscosity or thickness
Causes of HTN
essential HTN is UNKNOWN
psychological and physiological stress
High Na and low K and Ca - facilitates RAAS increasing BP
metabolic syndrome - obesity, dyslipidaemia, diabetes - mainly affects afterload/SVR since larger body mass (excess fat and sugar) the longer the blood vessels, in response, the heart has to pump harder to get the same amount of pressure getting into the tissues putting a strain in the heart overtime increasing chance of having CADs
smoking - excess vasoconstriction
environmental factors - eg. pollution as air pollutants enter the systemic circulation and causes vasoconstriction
genetic factors
long-term consequences of HTN
heat performance gets overused leading to several CADs:
Heart failure - when RAAS gets overused causing blood retention in the systemic circulation (pulmonary/ peripheral oedema)
Accelerated atherosclerosis > MI
Renal failure - renal arteries are damaged overtime and narrows causing insufficient bladder perfusion in the kidneys
Stroke - blood vessels in the brain gets damaged
Weakened blood vessel walls > aortic/ cerebral aneurysms
Classes of Antihypertensive meds
ACE inhibitors
ARBs - ACE II receptor blockers
Beta-blockers
Calcium channel blockers
Diuretics
Centrally acting antihypertensives (methyldopa)
Peripheral vasodilators (hydralazine)
Pharmacodynamics of ACE inhibitors
inhibits conversion of ACE I to ACE II causing:
decreased vasoconstriction > decreased SVR
decreased aldosterone production > increasing Na+ and H2O excretion
decreased BP
increased renal blood pressure
indications: HTN, heart failure and nephropathy
Ace inhibitor meds
quinapril
lisinopril
enalapril
captropril
fosinopril
adverse effects of Ace inhibitors
Hypotension (monitor for orthostatic hypotension and dizziness)
Hyperkalaemia (since aldosterone is inhibited K+ are retained)
Angioedema (blocks airway, swelling underneath the skin)
Cough (ACE inactivates bradykinin - which mediates inflammation causing vasodilation)
Nursing considerations for Ace inhibitors
monitor hypotension
monitor K+ levels - avoid diet rich in K and Na
assess angiodema (swelling of the face and mouth)
educate NOT TO SUDDENLY STOP ACEIs as it causes REBOUND HTN
ACE inhibitors contradictions
pregnancy - teratogenic effects on foetus
Pharmacodynamics of ARBs/ Angiotensin II receptor blockers
Blocks angiotensin II receptors in the smooth muscles of the arteries inhibiting vasoconstriction
High affinity to AT II receptors causing vasodilation
Lowers BP and increase blood volume to the heart
Indicators:
HTN
alternative to ACE inhibitors to manage HF and diabetic nephropathy
AT II receptor blocker/ ARB meds
losartan
candesartan
adverse effects of ARBs
Hypotension
Hyperkalaemia
DO NOT CAUSE COUGH as it does not accumulate bradykinin
Pharmacodynamics of beta-blockers
Antagonist at sympathetic (noradrenaline) beta receptors
Blocks:
alpha-1 receptors: decreased SVR
beta-1 receptors:
- decreased HR and myocardial contractility > reduced myocardial O2 demand
- inhibits renin release > inhibit Na+ and H2O retention > reduce preload and decrease SVR
- slows development of atherosclerotic plaques
Indicators of beta blockers
HTN
Stable angina
Cardiac dysrhythmias after MI
HF
secondary prevention after MI
Beta blocker meds
Cardioselective Beta-1 blockers:
metoprolol
celiprolol
bisoprolol
Beta and Alpha-1 blockers:
labetalol
carvedilol
sotalol
Adverse effects of Beta blockers
Bradycardia
Bronchospasm
Drowsiness and fatigue
Worsen CHF
Contradictions for beta blockers
Pts with asthma/COPD - beta blockers can block beta-2 receptors in the lungs causing bronchospasm
Pts with DM - beta blockers inhibits beta cells in the pancreas preventing glycogenolysis causing hypoglycaemia
Nursing considerations for beta blockers
DO NOT STOP ABRUPTLY - risk of rebound HTN, instead decrease dose slowly
monitor hypotension - risk of falling from orthostatic hypotension
educate to change position slowly
monitor S&S of HF - wet lung sounds, weight gain, oedema
Pharmacodynamics of calcium channel blockers/ CCBs
blocks Ca channels by inhibiting Ca influx into smooth muscles and myocardial cells
- smooth muscle relaxation> vasodilation including coronary blood vessels
- reduce AV conduction
- decrease heart workload
CCB meds
3 classes:
Verapamil - myocardium
Nifedipine - smooth muscle
Diltiazem - myocardium & smooth muscle
CCBs indicators
HTN
Angina
Dysrhythmias
CCBs adverse effects
Constipation
Nocturia (waking up during the night and urinate)
Headache (cerebral vasodilation)
Hypotension, postural hypotension and fatigue (risk of falls)