PHARM: Heart Failure + Hypertension Flashcards
1
Q
what is cardiac output and what is the formula?
A
- amt of blood pumped by a ventricle per minute
- CO = HR x SV
2
Q
what is stroke volume and what is the formula?
A
- volume of blood pumped by a ventricle in a single contraction
- SV = EDV - ESV
3
Q
Sx of right heart failure
A
- pressure back to systemic circulation
- oedema in extremities
- elevated JVP
- hepatomegaly
4
Q
Sx of left heart failure
A
- pressure back to pulmonary circulation
- dyspnoea
- orthopnoea
- oedema
- tachycardia
5
Q
causes of heart failure
A
- HTN (inc. pulmonary)
- heart issues: valves, ischaemia, arrhythmia, CHD, atherosclerosis
- renal failure, diabetes
6
Q
preload vs afterload
A
- preload: vol of blood in ventricles @ end of diastole (EDV)
- afterload: pressure the LV must overcome to pump blood to the body
7
Q
what happens to cardiac output if there is increased preload or afterload?
A
- increased preload (EDV) = increased CO
- increased afterload = more pressure to overcome = decreased CO
8
Q
what happens in heart failure with preserved ejection fraction (HFpEF)
A
- impaired diastole b/c ventricular hypertrophy = space inside can’t feel w/ blood
- e.g. HTN, cardiac tamponade
9
Q
what happens in heart failure with reduced ejection fraction (HFrEF)
A
- dilated ventricle due to more fibrotic tissue = fewer cardiomyocytes
- impaired systole b/c thinner walls can’t pump as hard
- e.g. dilated cardiomyopathy, AMI
10
Q
4 main drug classes for hypertension
A
- A = ACE inhibitors + ARBs
- B = beta blockers
- C = DHP Ca2+ channel blockers
- D = diuretics
11
Q
4 main drug classes for heart failure
A
- A = ACE inhibitors + ARBs
- B = beta blockers
- C = contractility increasers (Digoxin, Dobutamine - B1 agonist)
- D = diuretics
12
Q
MOA and indications of ACE inhibitors
A
- end in -pril
- prevents conversion of angiotensin I to II and inhibit bradykinin breakdown = vasodilation and increased salt and water excretion (decreased BP)
- indications: HTN, heart failure
13
Q
MOA and indications of angiotensin receptor blockers (ARBs)
- what suffix do they end in?
A
- end in -sartan
- antagonists @ AT1 receptors = inhibit USE of angiotensin II = vasodilation and increased salt/water excretion (decreased BP)
- indications: HTN, heart failure (used when Pt is intolerant to ACE inhibitors)
14
Q
adverse effects and contraindication of ACE inhibitors and ARBs
A
- dry cough (due to increased bradykinin) but ONLY for ACE inhibitors (ARBs don’t change bradykinin so no cough)
- marked hypotension
- hyperkalaemia
- sometimes rash, itch, angioedema
- contraindicated during pregnancy
15
Q
vasopeptidase inhibitors MOA and indications
A
- inhibits AT1 receptor and NEP (enzyme which breaks down natriuretic peptides) = vasodilation and increased Na+/H2O excretion = decreased BP
- indications: HTN, heart failure
16
Q
MOA and indications of B blockers
A
- blocks B1 receptors = decreased rate (-ve chronotrope) and force of contraction (-ve inotrope) = prevent arrhythmias
- leads to decreased BP (for HTN)
- decreased O2 consumption (for HFrEF + angina)
- indications: HTN, HFrEF, angina, tachyarrhythmias
17
Q
adverse effects and contraindication of B blockers
A
- A/Es: cold extremities, bradycardia, bronchoconstriction
- contraindicated in asthma, UNSTABLE heart failure and with class IV anti-arrhythmics (non-DHP Ca2+ channel blockers)
18
Q
digoxin MOA and indications
A
- binds to K to inhibit Na/K pump = indirectly increases intracellular calcium = increased contractility of heart (+ve inotrope) but decreased rate (-ve chronotrope)
- decreased O2 demand = heart beats slower but harder
- indications: HFrEF + arrythmias (last resort when ACE inhibitors, ARBs, B blockers and diuretics haven’t worked)
19
Q
adverse effects and contraindications of digoxin
A
- A/Es: arrhythmia, GIT, visual disturbances, hallucinations
- contraindications: hypokalaemia (e.g. thiazides + loop diuretics) > causes less Na/K pump competition = increased toxicity. also C/I in hypercalcaemia > arrhythmias
20
Q
digoxin pharmacokinetics
- Vd
- half life
- excretion
A
- very high Vd = distributes very well to body tissues = requires careful monitoring
- very long 1/2 life
- excreted by kidneys (creatinine clearance can be used to predict dosage)
21
Q
dobutamine MOA + indications
A
- MOA: B1 agonist = increased HR (+ve chronotrope) and force of contraction (+ve inotrope) = increased SV and CO
- indications: only acute HFrEF
22
Q
A/Es and C/Is of dobutamine
A
- A/Es: hypotension, tachyarrhythmias, nausea
- C/I: VF, tachyarrhythmia
23
Q
DHP Ca2+ channel blockers MOA + indications
A
- MOA: inhibit L-type Ca2+ channels in blood vessels = vasodilation = decreased afterload = decreased BP (for HTN) and decreased O2 consumption (for angina)
- indications: HTN, angina (stable + vasospastic)
24
Q
adverse effects + contraindications of DHP Ca2+ channel blockers
A
- A/Es: oedema, headache, flushing, dizziness, nausea
- C/Is: heart failure
25
loop diuretics MOA + indications
- end in -ide
- inhibit Na+ (and hence water) reabsorption in ascending loop of Henle (non-K+ sparing) = decreased BP (for HTN) and afterload (for HFrEF)
- indications: HTN, HFrEF
26
adverse effects and contraindications of loop AND THIAZIDE diuretics
- A/Es: hypokalaemia = increased digoxin toxicity and/or arrhythmia, hyponatraemia
- C/Is: hypokalaemia, hyponatraemia
27
thiazide diuretics MOA + indications
- promotes excretion of Na+/H2O @ DCT (non-K+ sparing) = decreased BP (for HTN) and afterload (for HFrEF)
- indications: HTN + HFrEF
28
MOA + indications of aldosterone antagonists
- end in -one
- aldosterone antagonists @ DCT/CD = increased Na+/H2O excretion (K+ sparing) = decreased BP (for HTN) and afterload (for HFrEF)
- indications: HTN, HFrEF
29
A/Es and C/Is of of aldosterone antagonists
- A/Es: hyperkalaemia = arrhythmias
- C/Is: hyperkalaemia
30
MOA and indications of sodium-glucose cotransporter 2 (SGLT2) inhibitors
- prevent reabsorption of glucose in PCT = decreased BP and BGL
- indications: diabetes, HTN, HFrEF
