HTN and Arrhythmia Flashcards
Name the non-pharmacological strategies to reduce blood pressure
-Dietary salt restriction
-Potassium supplementation preferably by dietary modification
-Weight loss
-DASH diet (dietary approaches to stop HTN)
-Exercise - aerobic
ACE inhibitors MOA
-prils
-inhibits Ang II formation → decreased vasoconstriction → lower BP
-Inhibits aldosterone secretion → decreases Na and H2O retention → lowers BP
-Prevents remodeling of blood vessels and heart
ACE inhibitors AE
-dry cough (common)
-hyperkalemia
-acute kidney damage
-angioedema
-fetotoxic (poisonous for fetus; don’t use these by pregnant women)
ARBs MOA
-sartan
-blocks Ang II receptors to prevent vasoconstriction, release aldosterone from adrenal glands
-Same therapeutic effect as ACE inhibitors
-Prevents remodeling of blood vessels and heart
ARBs AE (5)
-cough
-angioedema (swelling of deeper layers of skin)
-fetotoxic
-acute kidney damage
-hyperkalemia
Calcium channel blockers MOA
-blocks calcium entry into cells of vascular smooth muscle and heart —> decreases BP and work of heart
-Influx of extracellular Ca releases stored Ca from the sarcoplasmic reticulum (SR)
-Increased intracellular calcium concentration binds to calmodulin (a protein), which activates myosin light chain kinase (MLCK)
-Activation of MLCK enables myosin to interact w/ actin to induce contraction
Calcium channel blockers AE (5)
-dizziness
-flushing
-headache
-fatigue
-peripheral edema
Common calcium channel blockers (5)
verapamil, diltiazem, amlodipine, felodipine, nifedipine
Diuretics MOA
act on kidneys to increase excretion of sodium and water
Thiazide diuretics MOA
inhibits Na reabsorption (distal convoluted tubule)
Loop diuretics MOA
-semide
inhibit Na and chloride reabsorption (loop of Henle)
K+ sparing diuretics MOA
prevent secretion of K+, not as good as diuretic but prevents K+ loss (hypokalemia)
Describe phase 0 of the cardiac action potential
Phase 0: opening of fast Na channels and rapid depolarization
Na+ goes into cell, changing membrane potential
Describe phase 1 of the cardiac action potential
initial rapid repolarization
Closure of fast Na+ channels
Describe phase 2 of the cardiac action potential
plateau phase
Balance between inward movement of Ca+ and outward movement of K+
Describe phase 3 of the cardiac action potential
repolarization
K+ channels remain open, allows K+ to build up outside the cell, causing the cell to repolarize
Describe phase 4 of the cardiac action potential
resting phase
Subclass IA antiarrhythmic drug MOA
moderate blockade of sodium channels; delay repolarization
Subclass IA antiarrhythmic drug AE
-diarrhea
-nausea
-thrombocytopenia (platelet # too low)
-torsades de pointes (polymorphic vtach)
Subclass IB antiarrhythmic drug MOA
mild blockade of sodium channels; accelerate repolarization
Subclass IB antiarrhythmic drug AE
CN effects (drowsiness, seizures), hypoTN
Subclass IC antiarrhythmic drug MOA
pronounced blockade of sodium channels
Subclass IC antiarrhythmic drug AE
visual disturbances, dizziness, risk of proarrhythmia
Class III (potassium channel blockers) MOA
blockade of potassium channels; delay repolarization; also has Class I, II and IV effects
Class II (beta blockers) antiarrhythmic drug AE
fatigue, bradycardia, hypoTN
Class II (beta blockers) antiarrhythmic drug MOA
blockade of beta-adrenergic receptors, reducing sympathetic effects
Class III (potassium channel blockers) AE
Pulmonary toxicity, thyroid dysfunction, hepatotoxicity, corneal deposits
Class IV (calcium channel blockers) MOA
blockade of calcium channels in cardiac tissue
Class IV (calcium channel blockers) AE
constipation, hypoTN, bradycardia, heart failure exacerbation
PT considerations for anti-hypertensive drugs
-monitor BP
-OH
-fatigue and dizziness; gradually progress ex
-intensity: beta blockers blunt HR response to ex
-dehydration w/ diuretics
-electrolyte imbalances w/ diuretics
