exam 3: HTN& HF PCol - DUNN

What are the main determinants of blood pressure?

main determinants of blood pressure are cardiac output (CO), and systemic vascular resistance

What two main factors determine cardiac output?

cardiac output is determined by heart rate (HR) and stroke volume (SV)

What three primary factors influence stroke volume?

stroke volume is influenced preload, afterload, and contractility

What determines preload in the cardiovascular system?

preload is determined by venous return and blood volume

What determines afterload?

afterload is determined by systemic vascular resistance (SVR)

How does contractility affect stroke volume?

increased contractility increases stroke volume, while decreased contractility lowers it.

 Which medications can lower preload by reducing blood volume?

diuretics lower preload by reducing blood volume

Which medications reduce afterload by decreasing systemic vascular resistance?

vasodilators reduced afterload by decreasing systemic vascular resistance

Which drug classes directly affect heart rate to lower cardiac output?

beta blockers and non-dihydropyridine calcium channel blockers reduce heart rate, lowering cardiac output

Which drug classes reduce contractility to decrease cardiac output?

beta blockers and non-dihydropyridine calcium channel blockers reduced myocardial contractility

Which antihypertensive drugs primarily reduce systemic vascular resistance?

ACE inhibitors, ARBs, direct renin inhibitors, calcium channel blockers, and vasodilators reduce SVR

Which antihypertensive drugs primarily reduce blood volume and thereby preload?

diuretics and aldosterone antagonist reduce blood volume and preload

Which class of drugs reduces both preload and afterload through effects on the RAAS system?

ACE inhibitors, ARBs, and direct renin inhibitors reduce both preload (by decreasing aldosterone-mediated volume) and afterload (by vasodilation)

What is the overall equation for blood pressure?

blood pressure = cardiac output x systemic vascular resistance (BP = CO x SVR)

What are the major classes of diuretics used in hypertension?

the major classes are thiazide diuretics, loop diuretics, and potassium-sparing diuretics (including aldosterone antagonist)

What is the prototype thiazide diuretic commonly referenced in hypertension treatment?

hydrochlorothiazide is the prototype thiazide diuretic

What is chlorthalidone, and how does it compare to hydrochlorothiazide?

chlorthalidone is a thiazide-like diuretic; it has longer half-life than hydrochlorthiazide but not added efficiacy, and it may cause more side effects

Why might chlorthalidone’s longer half-life not be advantageous?

the longer half-life may increase the risk of side effects, outweighting benefits, without significantly improving blood pressure control

What are common side effects of thiazide diuretics?

common side effects include electrolyte disturbances (especially hypokalemia, hyponatremia, hypomagesemia) increased uric acid, and metabolic changes such as hyperglycemia

. What monitoring is required when prescribing thiazide diuretics?

monitoring should include blood pressure, electrolytes, and renal function

What time of day should thiazide diuretics generally be taken?

they should be taken in the morning to avoid nocturia

What are examples of loop diuretics used in hypertension?

furosemide (lasix), bumetanide, and torsemide

In what situations are loop diuretics particularly useful?

useful in patients with chronic kidney or heart failure where thiazides are less effective

What is an important potential side effect of loop diuretics?

ototoxicity (damaged to inner ear) can occur, especially at high dose or with IV use

What should patients on loop diuretics monitor daily?

patients should monitor daily weight to detect fluid overload or excessive diuresis

Under what circumstances might a dose of Lasix (furosemide) be held?

if a patient is not drinking or is vomiting, the dose may be held to prevent dehydration and worsening renal function

 What are examples of potassium-sparing diuretics?

amiloride and triamterene are true potassium-sparing diuretic, while spinrolactone and eplerenone are aldosterone antagonist

What is the major contraindication to potassium-sparing diuretic use?

they are contraindicated in patients with significant renal failure or hyperkalemia

Why should patients on potassium-sparing diuretics avoid salt substitutes?

salt subsitutues often contain potassium, which can worsen hyperkalemia and lead to life-threatening arrhythmias

How are magnesium and potassium linked with potassium-sparing diuretics?

magnesium tends to follow potassium levels, so disturbances in one often affect the other

What effect do calcium channel blockers (CCBs) have on the heart?

calcium channel blockers decrease the force of cardiac contractions, lowering myocardial contractility

In what type of heart failure are CCBs sometimes considered?

they may be considered in patients with heart failure with preserved ejection fraction (HFpEF), but not in those with reduced ejection fraction (HFrEF)

Which non-dihydropyridine CCB is more potent in its effects on contractility and conduction?

verapamil is more potent than diltiazem in decreasing contractility and slowing conduction through the AV node

Why might verapamil or diltiazem use be a concern in elderly patients?

these drugs can cause bradycardia and conduction abnormalities, which are more problematic in elderly patients

. How do non-dihydropyridine CCBs interact with statins?

they are moderate inhibitors of CYP3A4, which can increase statin concentration and risk of adverse effects

Why is immediate-release nicardipine avoided in clinical practice?

immediate-release nicardipine works too quickly, causing rapid reduction in blood pressure that can compromise blood flow to tissues and increase the risk of ischemia

Why is nicardipine’s long half-life not beneficial in the acute setting?

a long half-lie mean it cannot be quickly adjusted or withdrawl if blood pressure drops excessively

What unique side effect is associated with dihydropyridine CCBs, particularly nifedipine?

gingival hyperplasia, or overgrowth of the gums, can occur

Are dihydropyridine calcium channel blockers substrates of CYP3A4?

yes, dihydropyridines are substrates of CYP3A4, though drug interactions are usually not clinically signficiant

What is angiotensin II’s primary effect on blood vessels?

angiotensin II is potent vasoconstrictor

. What class of medications prevents the formation of angiotensin II?

ace inhibitors prevent the conversion of angiotensin I to angiotensin II

What additional substance is affected by ACE inhibitors besides angiotensin II?

ACE inhibitors increase bradykinin levels because ACE normally degrades bradykinin

What common adverse effect of ACE inhibitors is caused by increased bradykinin?

a dry cough is common adverse effect caused by elevated bradykinin

When can ACE inhibitor–induced cough occur during therapy?

the cough can occur at any point in therapy, not just early on

What serious but rare adverse effect is associated with ACE inhibitors?

angioedema is a serious adverse effects associated with ACE inhibitors

What should be monitored at baseline and within 1–2 weeks of starting or adjusting ACE inhibitors or ARBs?

serum creatinine, blood urea nitrogen (BUN), and potassium should be monitored

At what potassium level should clinicians begin to worry when a patient is on ACE inhibitors or ARBs?

a potassium level of 5.5 mEq/L or higher is concerning and requires monitoring

What should be done if serum creatinine rises slightly after starting an ACE inhibitor or ARB?

a small increase in serum creatinine is expected due to reduced intraglomerular pressure and is usually not a reason to discontinue therapy

What drug directly inhibits renin?

aliskiren directly inhibits renin

Why is aliskiren not commonly used?

aliskirens is avoided because it has added concerns, such as increased risk of advese effects, without added clinical benefit over ACE inhibitors or ARBs

What receptor subtypes are targeted by beta-blockers?

beta blockers target B1 receptors in the heart and B2 receptors in the lungs

How does dose affect receptor selectivity with beta-blockers?

at higher doses, beta blockers lose selectivity and can block both B1 and B2 receptors

Why is beta-blocker use a concern in patients with asthma?

nonselective beta blockers block b2 receptors, causing bronchonstriction that can worsen asthma

How do beta-blockers affect heart rate and blood pressure?

beta blockers lower heart rate, reduce blood pressure, and decrease energy and sexual function

What additional receptor activity does carvedilol have compared to metoprolol?

carvedilol blocks alpha receptors in addition to beta receptors, providing additional vasodilation

Why is patient counseling important when starting beta-blockers?

patients should be counseled about possible fatigue, sexual dysfunction, and bradycardia, and instructed not to stop the drug abruptly

Which beta-blocker is sometimes used for both hypertension and benign prostatic hyperplasia (BPH)?

beta blockers like carvedilol can lower blood pressure and may help in patients with BPH due to added alpha-blocking effects

What is a risk of abrupt discontinuation of beta-blockers?

abrupt discontinuation can cause rebound hypertension, angina, or myocardial infarction due to upregulation of beta receptors

What type of beta-blocker activity can help in patients with bradycardia?

beta blockers with partial agonist activity (intrisinc sympathomimetic acitvity, ISA)may be useful in patients prone to bradycardia

How do beta-blockers affect exercise tolerance?

beta blockers may reduce excerise tolerance by limbing heart rate and cardiac output response during exertion

 What are examples of centrally acting α2-adrenergic agonists used in hypertension?

clonidine, guanfacine, and methyldopa

How do central α2-agonists lower blood pressure?

they stimulate alpha 2 receptors in the brainstem, reducing sympathetic outflow and decreasing systemic vascular resistance and heart rate

What cardiovascular adverse effect can central α2-agonists cause?

they can cause notable bradycardia

What is a risk of abrupt discontinuation of clonidine?

abrupt discontinuation can cause rebound hypertension, which may precipitate mycoardial infraction

How should clonidine be discontinued to avoid rebound effects?How should clonidine be discontinued to avoid rebound effects?

clonidine should be tapered gradually to avoid rebound hypertension

What is a unique feature of the clonidine transdermal patch regarding tapering?

a low dose clonidine patch may taper itself naturally because the medication is released gradually over time

How do central α2-agonists reduce cardiac workload?

they reduce afterload by lowering systemic vascular resistance through decreased sympathetic activity

What long-term effect can occur with chronic use of central α2-agonists?

desenitization to the drug’s effects can occur over time, reducing its effectiveness

What are examples of direct vasodilators used in hypertension?

hydralazine and minoxidil

How do direct vasodilators lower blood pressure?

they act directly on vascular smooth muscle to cause vasodilation, lowering systemic vascular resistance

What compensatory response can occur with direct vasodilators?

reflex tachycardia and fluid retention can occur due to baroreceptor-mediated sympathetic activation

What additional medications are often co-administered with vasodilators to counter side effects?

a beta blocker (to control reflex tachycardia) and a diuretic (to prevent fluid retention) are often added

What unique adverse effect is associated with hydralazine?

can cause drug-induced lupus like syndrome, especially at higher dose

What is minoxidil also used for outside of hypertension?

minoxidil is used topically to promote hair growth rogaine)

What is “coronary steal” in relation to vasodilators?

coronary steal is a phenmenon where vasodilation diverts blood away from ischemia areas of the heart to non-ischemic regions

What rare but serious toxicity is associated with sodium nitroprusside?

sodium nitroprusside can cause cyanide toxicity, especially prolonged infusion or high doses

How is the risk of cyanide toxicity minimized with nitroprusside?

by using the lowest effective dose for the shortest possible duration

. What classes of antihypertensives are commonly compared in therapy selection?

ace inhibitors, arbs, dihdyropyridine CCBs, non-dihydropyridine CCBs, loop diuretics, thiazides, and aldosterone antagonists

What is the overall treatment goal with antihypertensives in terms of vascular resistance and volume status?

the goal is to reduce systemic vascular resistance and/or blood volume to lower blood pressure safely without compromising perfusion

What is the main mechanism by which ACE inhibitors lower blood pressure?

ACE inhibitors lower BP by blocking conversion of angiotensin I to angiotensin II, reducing vasoconstriction and alodsterone-mediated sodium retention

How do ARBs differ from ACE inhibitors in their mechanism?

ARBs block the angiotensin II receptors (AT1 receptor), preventing angiotensin II from exerting its effects, but does not bradykinin

Which class is associated with bradykinin-related cough and angioedema?

ACE inhibitors are associated with cough and angioedema due to bradykinin accumulation

How do dihydropyridine CCBs differ from non-dihydropyridine CCBs?

dihydropyridines mainly cause vasodilation, while non-dihyropyridines also reduce heart rate and myocardial contractility

Why must non-dihydropyridine CCBs be used cautiously in heart failure with reduced ejection fraction (HFrEF)?

they reduce contractility and can worsen heart failure with reduced ejection fraction

 What is the major clinical use for loop diuretics compared to thiazides?

loop diuretics are mainly used in patients with chronic kidney disease or heart failure, while thiazide are first life for essential hypertension

What monitoring is essential for patients on diuretics?

blood pressure, renal function, and electrolytes should be monitored regularly

What is the mechanism of aldosterone antagonists (e.g., spironolactone, eplerenone)?

they block aldosterone receptors in distal nephron, preventing sodium and water reabsorption while sparing potassium

In what patient population are aldosterone antagonists especially beneficial?

they are particularly beneficial in patients with resistance hypertension and heart failure with reduced ejection fraction

What is the most important safety concern with aldosterone antagonists?

hyperkalemia is the most significant safety concern

What drug–drug interaction is particularly concerning with potassium-sparing drugs?

the use of potassium supplements or salt substitues can dangerously increase potassium levels, leading to hyperkalemia

What is the target organ system for α1-adrenergic antagonists in hypertension?

alpha-1 adrenergic antagonist target vascular smooth muscle, causing vasodilation and lowering blood pressure

What are examples of α1-adrenergic antagonists used in hypertension?

prazosin, doxazosin, and terazosin

Why are α1 blockers not first-line for hypertension?

they are not first line because they increase the risk of heart failure and are associated with orthostatic hypotension

In what patients might α1 blockers still be useful?

they may be useful in patients with hypertension and benign prostatic hyperplasia (BPH), since they relax smooth muscle in the prostate and bladder neck

What is the “first-dose phenomenon” with α1 blockers?

the first-dose phenomenon refers to significant orthostatic hypotension after first dose, which may cause dizziness or fainting

How can the first-dose phenomenon with α1 blockers be minimized?

it can be minimized by giving the first dose at bedtime

What adverse effects can α1 blockers cause besides orthostatic hypotension?

they may cause dizziness, fatigue, and reflex tachycardia

What role do direct renin inhibitors like aliskiren play in hypertension?

aliskiren directly inhibits renin, lowering angiotensin I and II levels, but it has no added benefit over ACE inhibitors or ARBs

Why are direct renin inhibitors rarely used?

they are rarely use because of safety concerns, limited outcomes data, and lack of additional benefit compared to ACE inhibitors or ARBs

Can aliskiren be combined with ACE inhibitors or ARBs?

no, aliskiren should not be combined with ACE inhibitors or ARBs due to increased risk of renal impairement, hyperkalemia, and hypotension