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Pharmacotherapy > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the 3 pathological process in Virchow’s triad that contribute to clot formation?

A

venous stasis, vascular injury, hypercoagulability

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2
Q

What kind of factors activate the clotting cascade?

A

clotting factors

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3
Q

what kind of factors inhibit the clotting cascade?

A

anticoagulants

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4
Q

Unfractionated Heparin: mechanism, indications, adverse rxns, contraindications, pregnancy category

A

Mechanism: potentiates anti-thrombin III to block thrombin (IIa)(thus inhibiting fibrinogen), also blocks IXa, Xa, XIa, and XIIa, prevents coagulation, but DOES NOT affect an established thrombus
Indications: venous thromboembolism prevention and tx, unstable angina, MI, coronary bypass surgery, hemodialysis, angioplasty, IV line flushes
Adverse rxns: bleeding, Heparin induced thrombocytopenia (HIT–platelets
pregnancy category: C: does not cross placenta, caution with hemorrhage, osteoporosis, does not enter breast milk

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5
Q

UFH dosing, monitoring, reversal

A

dosing: Loading 80 units/Kg IV push, then continuous infusion of 18 units/Kg/hr (continuous because short half life) (lower in elderly) or subQ q8-12 hr if non acute
monitoring: aPTT (activated partial thromboplastin time) in 6 hr, platelets quod x 14 days
reversal: protamine(binds heparin) 1 mg to neutralize 90 units of UFH, max dose 50 mg, infused over 10 minutes (caution for hypotension and anaphylactoid rxns)

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6
Q

what are the pharmacokinetics of UFH?

A

Binds to endothelial cells, macrophages, and plasma proteins (low bioavailability), non linear clearance (saturable kinetics b/c large dose), half life increases with increasing doses (30-150 minutes, avg 90)

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7
Q

what is the reference range for aPTT and what should it be on UFH?

A

normal: 25-39 seconds, 45-75 seconds on UFH (1.5-2X control)

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8
Q

what are some of the advantages of Low molecular weight heparins as compared to UFH?

A

1/3 the size, higher subcutaneous bioavailability (92%), inhibit clotting factor Xa ONLY, very predictable dose response, longer half life, reduced need for lab monitoring

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9
Q

What’s an example of LMWH?

A

generic: enoxaparin; brand: lovenox

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10
Q

what are the indications for enoxaparin/lovenox?

A

DVT prophylaxis after hip or knee replacement surgery, or tx for VTE/TE

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11
Q

Is the dosing for prophylaxis (preventative measures) of blood clots higher or lower than dosing for treatment?

A

lower

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12
Q

what’s the dosing for enoxaparin/lovenox for DVT prophylaxis after hip or knee replacement surgery?

A

30 mg sc q 12 hr for 7-10 days until ambulatory

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13
Q

what is the dosing for enoxaparin/lovenox for VTE tx?

A

1 mg/kg sc q 12 h or 1.5 mg/kg sc Q24 hr

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14
Q

what disease would necessitate a lower dose of enoxaparin/lovenox?

A

severe renal impairment

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15
Q

what are the possible adverse rxns of LMWH?

A

bleeding, thrombocytopenia (lower incidence HIT than UFH, check on day 3 therapy), injection site hematoma, minor bleeding at site of injection, osteoporosis (less than UFH)

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16
Q

what/when do you monitor LMWH? what’s the therapeutic dose for VTE tx and VTE prophylaxis?

A

Baseline: PT, INR, APTT, CBC, serum, creatinine, platelets; steady state level 4 hrs after sub doseplatelets q3-5 days for 1st 2 weeks; anti factor Xa activity in pts with CrCl 14 days), no routine monitoring necessary
therapeutic dose VTE tx: 0.5-1 units/ml; VTE prophylaxis 0.2-0.4 units/ml

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17
Q

what’s the reversal for LMWH?

A

protamine 1 mg per 1 mg enoxaparin, although this cannot neutralize the anticoagulation effect of LMWH completely

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18
Q

What are some examples of other parenteral anticoagulants?

A

fondaparinux (Factor Xa inhibitor) and Argatroban (direct thrombin inhibitor)

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19
Q

what are fondaparinux’s mechanism, indications, and kinetics? is there a reversal? what are some drug intx?

A

Mechanism; inhibits factor Xa
indicated: for VTE prophylaxis for LE orthopedic procedures and tx of VTE, also indicated for HIT (unapproved)
kinetics: longer 1/2 life, so only dosed once daily
no reversal
few drug intros b/c not metabolized in liver

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20
Q

what is argatroban’s mechanism, indications, monitoring, adverse affects, and reversal agents?

A

directly inhibits circulating and bound thrombin (aka synthetic leech saliva), doesn’t bind plasma proteins=predictable dose response
indications: HIT, patient undergoing PTCA, HIT with PTCA, VTE prophylaxis in hip surgery
monitor: aPTT
adverse affects; high incidence of bleeding
no reversal agents

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21
Q

what is warfarin’s MOA, onset of effect, indications, and adverse reactions, and reversal?

A

MOA: vitamin K antagonist: interferes with hepatic synthesis of vitamin K dependent clotting factors, resulting in depletion of factors II, VII, IX, X, thus the half life is dependent on the half life of these clotting factors, no effect on est. thrombus or already formed clotting factors
onset of effect: 36-72 hours, full effect in 5-7 days
indications: VTE tx/prophylaxis, prosthetic heart valves, atrial fibrillation, TIA/stroke, acute MI, hyper coagulable states, peripheral arterial occlusive disease
adverse reactions: bleeding (minor in 2-10%), skin necrosis (rare, early, 3-8 days after starting–d/c drug, give Vit K and heparin), purple toe syndrome (later onset 3-10 wks, reversible but need to d/c drug)
reversal is vitamin K

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22
Q

What is warfarin’s pregnancy category and contraindications?

A

Pregnancy category X, CI: patients with add’l risk of hemorrhage, anyone at risk of noncompliance, surgery/dental work (before surgery go off it and after restart with LMWH which works faster), alcoholism (will cause liver damage), spinal anesthesia or spinal injections (don’t want blood in spinal cord)

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23
Q

what are the pharmacokinetics and metabolism of warfarin?

A

absorbed well in GI tract (97-99%), food in stomach may increase rate but not extent of absorption. >97% bound to plasma proteins like albumin, crosses placenta and through breast milk
metabolism: plasma half life is 1-2 days, longer in elderly with CHF (less blood flow, slower metabolism)

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24
Q

what is the dosing for warfarin?

A

4-5 mg qd, overlap with heparin for 4-5 days (shorter half-life for heparin, works faster than warfarin); NOTE: very wide range of doses depending on pt, age

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25
Q

What is the INR?

A

International normalized ratio, standardizes therapies since PT reagents vary in sensitivity

INR=PT (pt)/PT (control)

reference range is about 1

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26
Q

What are the INR goal ranges for VTE tx and prophylaxis, atrial fibrillation, acute MI? for which conditions is the goal range larger?

A

2.0-3.0; larger (2.5-3.5) for some mechanical valves like caged ball/disk, mitral tilting disk

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27
Q

how long do most people take warfarin?

A

3-6 months for tx of VTE or MI or a bioprosthetic heart valve with previous embolism; lifetime for prophylaxis or mechanical heart valves or atrial fibrillation

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28
Q

what’s a good rule of thumb for warfarin drug intx?

A

assumes interacts with warfarin until proven otherwise; have patients check with health care provider before starting any new meds

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29
Q

what are the 3 ways other drugs can interact with warfarin?

A

other drugs can dangerously increase the INR with warfarin; can decrease the anticoagulation effect/INR (these drugs induce CYP450); or they can increase the bleeding risk without changing the iNR (makes platelets more slippery)

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30
Q

what are 4 important drugs to remember that warfarin intx with?

A

aspirin (increase bleeding risk), vitamin K (antidote/decreases therapeutic effect), sulfamethoxazole aka bactrim/septrim for acne increases the anticoagulation effect

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31
Q

what kinds of foods can interfere with how warfarin works?

A

vitamin K prevents warfarin MOA: in green vegetables; tell patients its good to eat them just eat a consistent amount so we can keep their dose right; acute EtOH can increase the INR (gets fatty deposts in liver for a few days that prevents liver from working) and chronic EtOH can decrease the INR, cirrhosis can increase the INR

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32
Q

what are examples of “other’ oral anticoagulants and what are their MOAs?

A

Dabigatran (direct thrombin inhibitor), rivaroxaban (oral factor Xa inhibitor), Apixaban (oral factor Xa inhibitor), Edoxaban (Xa inhibitor)

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33
Q

Which “other” oral anticoagulant is a little safer in pregnancy? (the others are all Category C)

A

apixaban

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34
Q

what are the indications for the “other” oral anticoagulants?

A

VTE prophylaxis/tx, thromboembolism tx in Afib, DVT/PE tx/prevention with hip/knee replacement (for dabigatran and rivaroxiban)

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35
Q

which oral anticoagulant is best for people with CrCl

A

edoxaban

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36
Q

Which “other” oral anticoagulant is a prodrug that doesn’t require any monitoring, has no antidote, and that is a good substitute for warfarin in those that can’t tolerate it but whose capsules have some quirky sensitivities?

A

dabigatran

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37
Q

which drug is more effective than enoxaparin after total knee replacement, but its more expensive, with no specific antidote?

A

rivaroxaban

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38
Q

which drug is a good substitute for those who can’t tolerate warfarin or dabigatarn, but is not recommended in pots with prosthetic heart valves?

A

apixaban

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39
Q

what are the pros of other oral anticoagulants?

A

at least as effective as warfarin for stroke prophylaxis, have a faster onset, fewer drug intx, and cause less intracranial bleeding

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40
Q

what are the cons of other oral anticoagulants?

A

no specific antidote, require strict adherence–even stopping for a few days can put them back at risk for clots, more expensive, need dose adjustments with renal insufficiency, and should not be used in people with mechanical heart valves

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41
Q

what is the recommended tx for VTE treatment?

A

start on parenteral anticoagulat (like UFW, LMWH, or fondaparinux) for 5-7 days; after first dose of parenteral give oral anticoagulant (like warfarin) right after first dose, must have therapeutic INR for 2 days before stopping

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42
Q

in which case is a thrombolytic indicated?

A

for those with acute massive embolism who are hemodynamically unstable, plus lower risk of bleeding, and without risk of right ventricular injury

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43
Q

what gene may influence how warfarin is metabolized?

A

gene for CYP2C9, which normally metabolizes warfarin

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44
Q

which indications require a long term/lifetime duration of therapy of an anticoagulant?

A

second episode of VTE, or a first, unprovoked proximal DVT or unprovoked PE

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45
Q

what is the recommended duration of therapy for the first episode of VTE secondary to a transient risk factor?

A

3 months

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46
Q

what is the most common cause of death in the US and the leading cause of premature, permanent disability?

A

Coronary Heart Disease (CHD)

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47
Q

Lowering ________ reduces atherosclerotic progression and mortality from CHD

A

Cholesterol

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48
Q

T or F: Most patients at risk for CHD receive optimal treatment

A

False

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49
Q

What is something all HTN and dyslipidemia puts should be “prescribed”?

A

life style modifications: healthy food choices, weight reduction, increased physical activity, avoid tobacco

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50
Q

What are statins MOA, adverse effects, CIs, and drug intx, and monitoring?

A

MOA: 1) inhibit HGM co-reductase (rate limiting enzyme in endogenous cholesterol biosynthesis), 2) increase catabolism (break down) of LDL to clear it from plasma 3) anti-inflammatory (decrease C reactive protein)

adverse effects: hepatic toxicity: elevated transaminases in 1-2% of cases at high doses, myopathy in 1 in 10 pts with higher doses, neuropathy (very rare- 1/14000), small increased risk of DM, non serious and reversible cognitive side effects

CIs: pregnancy, active or chronic liver disease, concomitant use with CSA (cyclosporin–antirejection drug), gemfibrozil, and niacin

Drug intx: reports of myopahty with drugs above, + erythromycin and some antifungals, may potentiate oral anticoagulants, and increased effect of levothyroxine

monitoring: lipids, ALT baseline (liver), ALT as clinically indicated thereafter, CK prn if muscle pain

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51
Q

what is the relationship between LDL and CHD?

A

Log linear: for every 30 mg/dL increase in LDL there is a 30% increased risk of CHD (GOOD FOR PATIENT EDUCATION)

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52
Q

What is the relationship between MI and C reactive protein (CRP)

A

Increased CRP increases risk of MI because the plaques that burst and cause a clot have extra inflammation from CRP

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53
Q

What kind of dose/response relationship do statins have?

A

non linear–“get more bang for your buck at lower doses” Each doubling of dose only results in 6% reduction of LDL

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54
Q

which drug for dysplipidemia shows the best evidence for decreasing: LDL, mortality, cardiac risk, stroke incidence, and MIs?

A

statins

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55
Q

how are statins usually dosed?

A

lovastatin with evening meal, atorvastatin at any time, the rest at bedtime (HS)

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56
Q

why can grapefruit juice be a bad thing with statins?

A

It can inhibit the CYP450 enzyme that statins are metabolized by

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57
Q

What decrease in LDL and TG can diet alone provide?

A

10-15% for LDL, 10-20% for TG, it also decreases weight and BP which helps!

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58
Q

Which drug is the best at decreasing LDL? Which is second best?

A

Best is PCSK9, although this drug isn’t approved by FDA yet and is very expensive, the next best are statins

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59
Q

How do bile acid resins work? What’s an example? what are the adverse effects, monitoring CIs,?

A

they 1) stimulate LDL receptors to increase LDL catabolism 2) They bind bile acids and excrete them in stool, thus liver is forced to use cholesterol to make more which decreases LDL 3) may increase VLDL -> TG

example is cholestyramine (“chole-“ means bile or relating to bile ducts)

adverse effects are GI symptoms (can start at low dose and titrate to get GI to adjust, also increase fluid and fiber) -> this can cause noncompliance if they make them feel crummy–have them take 1 hr before or 2 hrs after meal to avoid intx

monitoring: lipids 6-12 wks after stable dose then q yr

CIs: already highly increased TGs (may increase TGS more and cause pancreatitis), familial dysbetalipoproteinemia (basically inheriting high TGs), h/o severe constipation

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60
Q

What are fibric acids MOA, example of one, effect on lipids, AE, monitoring, CIs

A

MOA: increase VLDL clearance and decrease VLDL synthesis (thus best at decreasing TGs)
example: fenofibrate
Mildy decrease LDL and increase HDL, tied for best at decreasing TGs
AE: GI, can increase bile lithogenicity (stones), can interfere with statins
monitoring: lipids 6-12 wks after dose change, q yr after; ALT baseline, 6-12 wks x2, then q yr; CK PRN myositis
CIs: h/o gallbladder disease or liver or kidney dysfunction (stones)

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61
Q

What is a common side effect of nicotinic acid? what is it best at lowering/increasing? how does it work? how do you monitor it?

A

flushing (tolerance develops over time, can be mitigated with ibuprofen during 1st 2 weeks and extended release niacin causes less flushing and is less hepatotoxic); best at increasing HDL, and tied for best at lowering TG
MOA: decreases LDL and VLDL synthesis
monitoring: lipids x2 months uric acid, glucose then q yr; baseline ALT, 6-12 wks, then q yr, CK prn myositis

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62
Q

How does ezetimibe work? what are some AE? what is it often combined with?

A

blocks cholesterol receptor and thus absorption on brush border of enterocytes, causing body to insert more LDL receptors which decreases LDL
AE: fatigue, abdominal pain, diarrhea, arthralgia, back pain
often combined with statins for pts with liver disease

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63
Q

How does PCSK9 work?

A

Works by preventing PCSK9 from degrading liver LDL receptors

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64
Q

what are some supplements for lowering cholesterol? how do they work?

A

plant stanol esters: competitively inhibit incorporation of cholesterol into micelles, decreasing total cholesterol and LDL in a dose dependent way, max LDL reduction 15%
fish oils: can reduce TGs by 20-50% with side effects of diarrhea and excess bleeding
others: oat bran, blond psyllium

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65
Q

what is a very important thing to educate patients on regarding the duration of their tx for HTN?

A

For most patents it is a life long tx

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66
Q

1 out of every _____ adults has HTN

A

3

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67
Q

In what ethnicity is HTN most prevalent?

A

african americans

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68
Q

what are the known causes of HTN?

A

known causes: sleep apnea, drug induced causes, CKD, primary aldosteronism, renovascular disease, chronic steroid therapy and cushing’s syndrome, pheochromocytoma, coarctation of the aorta, thyroid or parathyroid disease; meds that may increase it: NSAIDS, cox2, cocaine/amphetamines, sympathomimetics (decongestants, anorexiants), oral contraceptives, certain dietary supplements (ma haung, bitter oragne, guarana), corticosteroids, cyclosporine (anti rejection), erythopoietin, licorice

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69
Q

Diuretics: thiazides MOA, AE, special indications, example drug

A

MOA:at distal tubule: increases Na excretion and h20, which decreases plasma volume and CO, decreases extracellular fluid volume, some decrease in peripheral resistance over time
AE: hypokalemia, hypomagnesemia, hyperuricemia, hyperglycemia, slight increase of TGs but not significant (indapamide less of an effect)
special indications:effective in renal insufficiency if SCR >2.5
example: chlorthalidone

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70
Q

Chlorthalidone (thiazide) dosing

A

12.5-25 mg daily

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71
Q

diuretics: potassium sparing MOA, AE, special indications, example drug

A

weak diuretic effects at collecting duct, distal tubule. Conserves potassium, also aldosterone antagonists
AE: may cause hyperkalemia when given with K supplements or ACE inhibitors or in pts with renal insufficiency, gynecomastia
special indications: often used with thiazides to offset K loss for HTN tx
example: spironolactone

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72
Q

spironolactone (potassium sparing diuretic) dosing

A

25-200 mg/day in 1-2 divided doses

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73
Q

loop diuretics MOA, AE, special indications, example drug

A

MOA:more potent diuretic effect at loop of henle to increase Na excretion
AE:more potent effects than thiazides on K, Mg, overdiruesis, and metabolic alkalosis
special indications: used over thiazides esp for those with heart failure or renal sufficiency who need to get rid of more fluid
example: furosemide

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74
Q

furosemide (loop diuretic) dosing

A

10-160 mg daily in 1-2 divided doses

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75
Q

ACEi MOA, AE, CI, example

A

MOA: 1) block angiotensin converting enzyme to block angiotensin II (vasoconstrictor) and 2) decrease aldosterone to decrease sodium retention 3) increase bradykinin for vasodilation, possibly reduce hypertrophy of CV tissue (vessels, heart)
AE: may cause hyperkalemiam, monitor esp if on K supplement of K sparing diuretic, cough, hypotension, rash, angioedema, acute renal failure in pts with bilateral renal artery stenosis or significant dehydration
CI: 2 or 3 trimester of pregnancy
example: lisinopril

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76
Q

lisinopril dosing

A

5-40 mg daily, consider decreasing or d/c diuretic to avoid excessive hypotension

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77
Q

Angiotensin II receptor blockers (ARBS) MOA, AE, special indications, example

A

MOA: block angiotensin II receptor to cause vasodilation and decrease aldosterone (decreases sodium retention) (but no effect on bradykinin)
AE: may cause hyperkalemia, monitor esp if on K supplement of K sparing diuretic, , hypotension, angioedema, acute renal failure in pts with bilateral renal artery stenosis or significant dehydration
indication: for pts who cannot tolerate ACEi
example: losartan

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78
Q

losartan dosing

A

25-100 mg qday

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79
Q

direct renin inhibitors: MOA, AE, special indications, example

A

MOA: directly inhibit renin which leads to vasodilation and decreased sodium retention
AE: diarrhea (esp with higher dose), cough, angioedema (but less than ACEI)
CI: pregnancy
example: aliskiren

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80
Q

calcium channel blockers MOA, AE, CI, example, indications

A

MOA: block intracellular influx of calcium thereby preventing vascular smooth muscle contraction (leads to vasodilation/relaxation),
AE: possible severe HA, dizziness, peripheral (ankle) edema, eczema in elderly (3-6 mo after)
CI: pts with HF (heart needs the calcium for contractile force) if EF 2+pitting edema or with symptomatic hypotension
example: amlodipine
indications for dihyrdopyridines: contractility - , peripheral vasodilation +++, CSA if HR goal,

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81
Q

dihydropyridine class: amlodipine dosing

A

2.5-10 mg qday

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82
Q

non dihydropyridine class: diltiazem and verapamil dosing

A

diltiazem 30-90 mg tid; verapamil 40-240 mg bid

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83
Q

which CCB class is the best at vasodilation?

A

dihydropyridine

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84
Q

which CCB class is the best at contractility?

A

non dihydropyridine–drug is verapamil; diltiazem is second best

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85
Q

what are some adverse effects of beta blockers/

A

b2 blockers can aggravate asthma and other lung diseases, CI in pts with bradycardia, heart block, sinus node disease (can slow HR with b1 blockers), use caution in uncontrolled heart failure, can cause fatigue, insomnia, depression, nightmares, bradycardia, ED (decreased perfusion to periphery), aggravate peripheral vascular disease, mask signs of hypoglycemia, mildly lower HDL and mildly increase TG, do not stop abruptly in pts with ischemic heart disease: taper

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86
Q

what do alpha 1 receptors do?

A

smooth muscle contraction: vasoconstriction, up sphincter tone, hair erection, glycogenolysis, gluconeogenesis

87
Q

what do beta 1 receptors do?

A

cardiostimulation: up heart rate, up contractility, up renin (increasing excretion and vasodilation), up lipolysis

88
Q

what do beta 2 receptors do?

A

smooth muscle relaxation; bronchodilation, vasodilaion, uterine relaxation, liver: glycogenolysis, gluconeogenesis

89
Q

what are the AE of beta blockers?

A

b2 blockers can aggravate asthma and other lung diseases, CI in pts with bradycardia, heart block, sinus node disease (can slow HR with b1 blockers), use caution in uncontrolled heart failure, can cause fatigue, insomnia, depression, nightmares, bradycardia, ED (decreased perfusion to periphery), aggravate peripheral vascular disease, mask signs of hypoglycemia, mildly lower HDL and mildly increase TG, do not stop abruptly in pts with ischemic heart disease: taper

90
Q

what are the 4 kinds of beta blockers?

A

non selective (b1 and b2), cardioselective (b1), mixed alpha/beta, and intrinsic sympathomimetic activity

91
Q

what are non selective beta blockers MOA? whats an example and dose? what kind of pts are CI in this tx?

A

blocks beta 1 to decrease HR and thus decrease BP, also decreases plasma renin which increases vasodilation and excretion; example=propanolol 20-120 mg bid, CI in asthma

92
Q

what is the extra MOA that the cardioselective beta blocker uses?

A

also increases peripheral vasodilation via NO production and release from enodthelial cells

93
Q

what are cardioselective beta blockers MOA ? what’s an example and dosage?

A

work at b1 to decrease HR and contractility, higher doses affect b2; example: metoprolol (loppressor) 25-100 mg 1-2x/day and atenolol (tenormin) 25-100 mg qd

94
Q

what is the MOA of mixed alpha beta blockers? what’s an example and dosage?

A

like cardioselective: causes decrease in HR (and CO) and contractility, has additional alpha blocking effects (vasodilation) though; example: labetalol 100-600 mg bid

95
Q

what kinds of beta blockers are only indicated in those with HTn? why? what’s an example and dosage?

A

intrinsic sympathomimetic activity, provides slight agonist effect at beta receptors while blocking , example: acebutolol 200-800 mg qd

96
Q

how do centrally acting alpha agonists work? what’s an example? what are the adverse effects? what’s a special indication for them?

A

MOA: stimulates central alpha 2 receptors to decrease peripehral sympathetic activity which decreases BP
AE: sedation, dizziness, dry mouth, fatigue, orthostatic hypotension; avoid abrupt discontinuance as this may cause rebound HTN, methylodopa may rarely cause liver damage, fever, hemolytic anemia
example: clonidine patch q wk (helps compliance)
special indication: safe for pregnancy

97
Q

how do peripheral acting adrenergic antagonists work? what are the AE? CI?what is an example and dosing?

A

MOA: depletes catecholamine stores;
AE: orthostatic hypotension, nasal congestion, lethargy, depression,
CI: depression, active peptic ulcer
example: reserpine 0.1-0.25 mg qd

98
Q

what are the direct vasodilators MOA? AE? examples

A

MOA: direct vascular smooth muscle relaxation (vasodilation)
AE: may cause fluid retention, (consider adding diuretic), rebound tachycardia (consider beta blocker), HA, minoxidil can cause hirsutism, hydralizaine can cause lupus like syndrome

99
Q

alpha receptor blockers

A

MOA: blocks alpha 1 adrenergic stimulation of blood vessels to produce relaxation/vasodilation
AE: posturaleffects–orthostatic hypotension (titrate dose0, and 1st dose phenomenon syncope –initiate low dose at hs to start
pt ed: dangle legs at edge of bed first then slowly stand up, wait one minute before walking

100
Q

What 3 kinds of drugs can control atrial fibrillation/atrial flutter?

A

calcium channel antagonist (diltiazem or verapamil), beta blockers (esmolol or metoprolol), digoxin (IV or PO) or combos

101
Q

What options are there to convert an arrhythmia to a NSR

A

think about cardioversion if started

102
Q

after someone has been cardioverted, what do you do?

A

maintain normal sinus rhythm: can do rhythm control via drugs or sotalol to maintain, also consider anticoagulation and rate control drugs, consider ablation if fails

103
Q

in which case is an atrial fibrillation considered an emergency where they need immediate electrical cardioversion?

A

if hemodynamically unstable need to immediately cardiovert= significant hypotnesion, mental status change, chest pain

104
Q

what are the 3 steps to managing an atrial fibrillation with rapid ventricular response?

A

CONTROL RATE, PREVENT THROMBOEMBOLISM, CONVERT TO NSR AND MAINTAIN

105
Q

what are the two drugs used to control ventricular rate in a fib?

A

calcium channel blockers and beta blockers

106
Q

how do calcium channel blockers and beta blockers help a fib?

A

they slow the conduction velocity through the AV node, preventing such a high volume of signals getting through to ventricles..

107
Q

what should you monitor after giving calcium channel blockers in afib pts?

A

in afib: HR, BP (this drug is a vasodilator and can cause BP to go down and HR to go up), signs of CHF in susceptible pts because it blocks contractility, rhyhtm to see if they convert to NSR

108
Q

what two drugs are available for afib in calcium channel blockers category? what is a ci?

A

diltiazem and verapamil; CI pts with HF (heart needs the calcium for contractile force) if EF

109
Q

what is the dosing for esmolol for fib?

A

IV infusion: loading dose of 200 mcg/kg over 1 minute then 50 mcg/kg/min and titrate to HR

110
Q

what is the dosing for metoprolol for afib?

A

more difficult to titrate dosing: 2.5-5 mg IV over 2 minutes; up to 3 doses at this time; then every 4-6 hrs; titrate to HR

111
Q

what is the dosing for diltiazem for a fib?

A

30-90 mg tid for HTN; for afib: 20 mg IV bolus over 2 minutes then start infusion at 10-15 mg/hr (5mg/hr in elderly); repeat bolus dose of 25 mg if necessary in 15 minutes, maintenance dose of 120-320 mg qd

112
Q

what is the dosing for verapamil for a fib?

A

40-240 mg bid for HTN; for afib: 5-10 mg IV over 2-3 minutes, then infuse at 5 mg/minute (lower in elderly) and maintenance dose of 120-480 mg qd

113
Q

what should you monitor for beta blockers for afib? what is a CI?

A

bradycardia, hypotension, exacerbation of CHF, CNS adverse effects: fatigue, lethargy, depression, sexual dysfunction
CI: asthma

114
Q

what are the advantages and disadvantages of using digoxin in a fib pts?

A

disadvantage in stress/exercise: increased sympathomimetic tone overrides digoxin vgagal effect; advantages esp in those with hypotension because it has no effect on BP, or those with CHF, because it doesn’t decreae hearts contractility,

115
Q

what are the dosing parameters for digoxin? who should you be careful giving it to?

A

loading dose IV or PO over 12-24 hours, then qday, very narrow window depending on person, be careful giving to those with impaired kidney function because it has a long half life

116
Q

what are the things to monitor for when using digoxin?

A

BP, HR, electrolytes (avoid hypokalemia, hypomagnesemia), rhythm for any new arrythmias/ectopy, sx of afib, signs of toxicity with chronic use: hallucinations, nause/vomiting, AV block, sinus pauses, arrythmias, vision changes, serum level

117
Q

what should be taken into consideration when thinking about converting someone to a NSR?

A

time of onset: if >48 hours, a new contractile activity in heart can cause a thrombus to dislodge and anticoagulation is need for 3 wks before cardioversion is attempted.

118
Q

how are persistent, long term a fibs tx for thrombi?

A

antithrombotic tx with warfarin, etc. based on CHADSVASc

119
Q

what is the difference between rate control and rhythm control? which is favored?

A

rate control just controls # of signals going through AV node and person will stay in fib; rhythm control attempts to convert them to NSR; rate control seems to be favored

120
Q

when is conversion to NSR recommended? what is it unfavorable?

A

recommended for those with sx, or for those whose rate can’t be controlled with drugs, or have CHF sx, younger pts, or those with lone afib. It can be unfavorable because ppl can go right back to afib, and often these things need to be taken long term and they can have some side effects. no proof that they improve mortality.

121
Q

how do type 1 a agents work to control rhythms? why are they not used today?

A

moa: inhibit fast sodium channels, depress conduction velocity, increase refractory time, decrease automaticitypotential arrythmia, negative inotropic effects, side effects (GI, anticholinergic) limit their use, monitor with EKG, can get excessive prolongation of QRS and qt and get torsade de pointes.

122
Q

what are some of the LT and ST risks of using amiodarone?

A

nO RISK of proarrythmia, LT risk of pulmonary fibrosis (

123
Q

how should amiodarone be monitored?

A

bradycardia, heart block, drug intx (warfarin, digoxin, statins), gi distrubances (nausea), lung fcn, CXR, LFTs, thyroid fcn

124
Q

how do you tx sinus bradycardia?

A

treat reversible causes; pacemaker if sx, atropine 0.5 mg q 3-5 minutes for acute sx control. If hemodynamically unstable and do not respond to atropine, use transcutaenous pacing.

125
Q

how can you treat acute 2nd degree type II or third degree AV block?

A

atropine, pacing (transvenous or transcutaneous) permanent pacemaker, if unresponsive to this: epinephrine (2-10 mcg/min titrated to response) or dopamine 2-10 mcg/kg/min can be administered

126
Q

what’s an example of a type 1 C agent for arrhythmias? in which pts should you avoid using this drug? what are its indications?

A

example: propafenone or flecanide. avoid in pts with structural heart disease like CAD, CHF indications: mostly for young people with lone a fib, not used very often

127
Q

how are ibutilide and dofetilide given?

A

ibutiilide: 1 time IV dose; dofetilide: oral

128
Q

ibutilide and dofetilide AE, CI, monitoring

A

AE may lead to QT elongation, proarrythmais, torsades de pointes
CI CrCl 500 msec, in initial dosing, cut dose in half. If stays this way, d/c the drug.

129
Q

which drug can be used for MAINTAINING NSR once converted (but not used for converting)

A

sotalol

130
Q

what are sotalol’s AE, and

A

AE: can prolong QT interval, proarrythmias, torsadesdp,

adjustd accoring to renal fcn

131
Q

what is adenosine used for? how do you give it/in what dosage? how long is the half life? what should you monitor for? what drugs accelerate/decelerate its effect? not for use in which type of pts?

A

for PVST or AV nodal reentry–Adenosine is drug of choice with 89-98% conversion drugs with effects to slow AV node. Adenosine is drug of choice with 89-98% conversion which briefly interrupts conduction at AV node to break reentry.
6 mg IV bolus :pump in very fast if at distant IV site followed with saline flush. May repeat with 12 mg in 2 minutes if needed.
half life of 5 seconds
monitor: peripehral vasodilation: hypotension, flushing, SOB, chest tightness, apprehension (all of short duration)
effects antagonized by theophylline, caffeine; increased by dipyridamole carbamazepine
not for use in heart transplant pts or those with severe obstructive lung disease

132
Q

what should you do if someone is hemodynamically unstable in a fib, PSVT, or atrial flutter?

A

immediate synchronized DCC

133
Q

how do you treat PSVT?

A

need to break re entry pathway and prolong the refractory period of the AV node–carotid sinus massage, vagal maneuvers (works in up to 25% of cases) drugs with effects to slow AV node. Adenosine is drug of choice with 89-98% conversion which briefly interrupts conduction at AV node to break reentry-may cause some heart pain that mimics MI for those few seconds while it is given. long term prevention of occurence via radiofrequence catheter ablation. synchronized cardioversoin if becomes unstable

134
Q

how should you handle someone in vtach?

A

tx if sustained: unstable/pulseless: begin cardiac arrest sequence( defib, CPR, epi, amiodarone), if pulse but unstable: synchronized cardioversion, if pulse but stable: IV antiarrthmic like amiodarone or lidocaine and go to synchonrized cardioversion if unstable, if no tx will go to vfib. Most have better LT success with an ICD + amiodaronea and beta blocker to prevent more shocks (improves QOL).

135
Q

what is the sequence for finding someone wit no pulse?

A

cardiac arrest sequence: activate emergency response and call for defibrillator or AED, assess pulse,if no pulse: begin CPR and attac the defib/AED:, assess rhythm, shockx1 if VF/VT, do not if in asystole, and continue CPR, give epi or vaso, continue CPR, assess rhythm after 2 minutes of CPR, if still in vfib/tach, shock x2. assess. consider antiarrythmics: amiodarone 300 mg IV push or lidocaine 1-1.5 mg/kg IV push. repeat x1 in 3-5 min. CPR sequence= airway (place), breathing (intubate), circulation (IV access), Drugs (epi 1 mg IV q3-5 minutes or vasopressin 40 units x1 attach defibrillator

136
Q

if you can’t get an IV in someone who is pulseless, what should you do?

A

inject iO IN tibia

137
Q

what is the sequence for if someone is in asystole?

A

cardiac arrest sequence: activate emergency response and call for defib or AED, assess pulse, if no pulse: begin CPR and attac the defib/AED:, assess rhythm, shockx1 if VF/VT, do not if in asystole, and continue CPR, give epi 1 mg IV q3-5 minutes or vasopressin 40 units x1, continue CPR x2 min, assess rhythm after 2 minutes of CPR, repeat epi and vaso if necessary. CPR sequence= airway (place), breathing (intubate), circulation (IV access), Drugs attach defibrillatorCPR sequence (no shocking) and epi 1 mg iV 3-5 min or vaso 40 units x1; Look for causes: 5 Hs and 5Ts, also consider transcutaneous pacing

138
Q

what are the 5 Ts and 5 Hs to keep in mind when evaluating what the cause of someone’s asystole is?

A

5 Hs and 5 Ts: hypovolemia, hypoxia, hydrogen ion, hyper hypokalemia, hypothermia; tabelts (OD), tamponade, tension pneumothorax, thrombosis, coronary (MI), thrombosis, pulmonary (PE)

139
Q

effective CPR can _____ a persons chance of survival

A

double

140
Q

what are the 1st priorities when taking care of someone with ventricular arrhythmias?

A

basic CPR, debrillation, and proper airway management

141
Q

what are the two kinds of drugs that are used to manage cardiac arrest?

A

drugs that increase perfusion, and drugs that fix the rhythm

142
Q

what are drugs that increase perfusion?

A

epinephrine or vasopressin

143
Q

what is epinephrines indication, MOA and dosing?

A

to increaes perfusion to heart in cardiac arrest, works on adrenergic nervous sytem (mixed alpha, beta 1 and beta 2 effects) and increases myocardial contractility, 1 mg IV q 3-5 min

144
Q

what is vasopressin’s indication, MOA and dosing?

A

alternative to epi to increaes perfusion to heart in cardiac arrest, vasoconstricts by stimulating smooth muscle receptors, 40 units by IV push (single dose) if no response go to epi

145
Q

what is the indication for atropine?

A

symptomatic bradycardia

146
Q

what is the indication for sodium bicarbonate?

A

for metabolic acidosis, clinically significant hyperkalemia, overdoses of certain drugs like aspirin and tricyclic antidepressants

147
Q

what is the indication for calcium chloride?

A

for cardiac arrest due to hyperkalemia

148
Q

what is then standard pharm. for heart failure with reduced ejection fraction? add ons/

A

diuretic with ACEI or ARB, then add beta blocker, then can add aldosterone antagonist

149
Q

what is then standard pharm. for post mI? add ons?

A

beat blocker, then can add ACEI (best), ARB, no add ons

150
Q

what is then standard pharm. for CAD? add ons?

A

beta blocker then add ace (best) or arb, add ons; CCB or thiazide diuretic

151
Q

what is then standard pharm. for DM? add ons?

A

ACE (best) or ARB, can add CCB or thiazide diuretic or beta blocker

152
Q

what is then standard pharm. for CKD? add ons

A

ACEI, ARB. no add ons

153
Q

what is then standard pharm. for recurrent stroke prevention? add ons?

A

thiazide diuretic or thiazide with ACEI

154
Q

52 yo with no c/o angina today and no cardiac hx. bp(hr)=169/90 (72) urine alb: Cr ratio=350 mg/g (macroalbuminurea)
what do you give him for CSA?
A. add LA nitrate to improve pain control B. add a BB to bring hR to goal C. do both D. do neither

A

D. do neither. he has no pain. tx the pt not the numbers!

155
Q 
52 yo male with no c/o angina today and no cardiac hx. BP(HR)=169/90 (72) urine able: cr ratio 350mg/g (macroalbuminurea)
how do you fix his bp?
A. add LA nitrate
B. add metoprolol
C. add lisinopril
D.cpm, BP at goal
E. add amlodipine
A

C. add lisinopril. he has bad cr output: the best drug for these is ACEI. LA nitrate will dilate veins. no hard indications for a BB.

156
Q 
50 yo female that' using SL NTG freq. for ADLS. currently on BB.. BP(HR)=138/83 (82). how should you manage her CSA?
A. CPM if 1 nitro has worked
B. increase her BB
C. Add LA nitro
D. add amlodipine
A

B. increase–taking nitro for ADLs sucks, you need to control that. nitro won’t help her HR (won’t help control the csa–guidelines say to control HR first)

157
Q 
50yo female using SL NTG freq for ADLS. currently on BB.. BP(HR)=159/93 (58). how should you manage her CSA?
A. CPM if 1 nitro has worked
B. increase her BB
C. Add LA nitro
D. add amlodipine
A

D. HR at goal, increasing BB won’t help and will increase her side effects. her HR is already low–so amlodipine (a dihydro) will work nicely.

158
Q 
52 yo male with new sx CSA. start him on initial tx: BP(HR)=165/97 (49)
A. diltiazem
B. amlodipine
C. metoprolol
D. labetalol
A

b. amlodipine. dilt (non dihydro) and metoprlol (BB) will lower his HR more. labetalol is a sympathomimetic BB.

159
Q 
given CP: which stable angina pt would you give a BB to?
A. type I DM 4 mo post mI
B. TYPE I DM status post hernia repair
c. neither
d. both
A

A. even though dM, you are going to have to give them a bb because they have a hard indication. hernia is not a hard indication for a bb.

160
Q

give cp: which stable angina pt do you give a bb to?
A. type I DM 4 mo post mI (hR 47)
B. TYPE I DM status post hernia repair (hr 88)
c. neither
d. both

A

c. neither. A’s HR is too low. B has no hard indications.

161
Q 
which med should you give to a DM pt after hernia with CP. HR: 88, CrCl 102 no proteinura
a. lisinopril
B. amlodipine
C. diltiazem
D. isdn
E. metoprolol
A

C. dilt. lisinopril is good for kidney pts but won’t help CP. amlodopine is good for CSA but he has room to lower his hr a bit. don’t give BBs (metoprolol) to DM if you can help it. he has no hard indications for one

162
Q

what are the indications and dosing for LA and SA nitrates?

A

SA: CSA to terminate acute anginal attack or prevent stress induced attacks; if CP: sit down, take one SL NTG. If not significant better or gets worse, take another and call 911. If it did improve, take a 2 and 3rd dose and call 911 if sx don’t completely resolve. Call 911 if dizzy, sweating, short of breath, nauseated.
LA: long term prophylaxis of CSA, generally added to other tx. Add to BB or non DHP to improve sx control. Combine with DHP if pt can’t tolerate BB or NDHP.can use over DHP if pts have cautions for DHPs. ; need nitrate free period of at least 8-12 hrs. sustained release need nitrate free interval of 15-17 hours to avoid tolerance. Generally give at 8 am and 2 pm.

163
Q 
63 YO c/o daily angina and 3+ pitting edema. currently on bb. 125/77(57)
A. add dilt
B. add amlod.
C. add iSDN (isosorbide denigrate)
d. add sl NTG
E. increae BB
A

C. add ISDN. dilt and more BB will lower HR more. amlodipine is CI in people with 2+ pitting edema. it happens daily so a long nitrate will work.

164
Q 
63 yo male c/o daily angina and left shoulder pain. currently on bb. 168/89 (59)
A. add dilt
B. add amlod.
C. add iSDN (isosorbide denigrate)
d. add sl NTG
E. increae BB
A

B. add amlodipine. dilt and more BB will lower hR more. long acting nitrates are good for pain but best to add DHP first.

165
Q 
63 yo male c/o occasional left shoulder pain. currently on BB and amlodopine for CSA. 150/79 (58). how should you tx his pain
a. add APAP (tylenols) 1 gram tid
B. add tramadol 50 mg bid
c. add oxycodone 2.5 mg q 6 hr
d. add salsa late 500 mg ti
. add naproxen 250 mg BID
A

a. start small first. these are in the order of how AHA wants you to use them.

166
Q

49 yo CSA pt with no cp. 155/90 (70). CRCL: 55 mL/min K:4. 2+ pedal edema. how do you manage him?

a. start BB
b. start ACEI
c. start NDHP
d. start DHP

A

b. ACEI . he has no chest pain right now. a DHP would be CI because of the edema. ACE indicated because he has crappy renal fcn

167
Q

do patietns with CSA have ASCVD

A

yes, by definition

168
Q

what is the guidelines for addressing CSA with pharmacotherapy?

A

is there chest pain? are there hard indications? then choose beta blocker. are there CIs or cautions for BB? then try adding or substiting CCB. CIs for CCB or cautions? consider adding or substiting LA nitrate. Also consider if they need a better BP med or BB replacement?

169
Q

what is the algoirthm for treating new or changed CP?

A

EKG first: if STE then treat with PCI or lytics. If NO st eleveation, check enzymes. if enzymes positive then=NSTEMI and evaluate risk score with TIMI. if no enzymes then its unstable angina.

170
Q

what does the timi score evaluate?

A

predicts risk of death or MI in the next 14 days. risk varies from 5-41%.

171
Q

how should you treat CP pts with high timi scores? low scores?

A

high=coronary angiogram. low=med manage

172
Q

which ACS pts should be on anticoagulant tx? what should you use?

A

everyone. use UFH, enoxaparin, fondaparinux. use UFH esp in pts >65, wt150 kg and crappy crcl.

173
Q

what are the indications for using the p2y12 receptor inhibitor prasugrel?

A

antiplatelet for high risk MI (not USA) pts at the time of PCI with DM or hx of MI or stent, more effective, but more bleeding

174
Q

which antiplatelet drug is more potent than clopidrogel/plavix?

A

prasugrel

175
Q

choose an antiplatelet for 62 yo with NSTEMI, PMH HTN, DM, hx MI and stroke. undergoing PCI wt: 90 kg, crcl is 110 mg/min
A. prasugrel 60 mg
B. clopidogrel 300 mg (low)
C. clopidrogel 600 mg (high)

A

C. give higher dose clopidogrel because the lower dose is for older pts or for pts with crummy renal fcn. prasugrel is CI in those with stroke.

176
Q

choose antiplatelet for 82 yo with TIMI risk of 1. PMH HLD, GI bleed. wt: 43 kg. crcl 25 ml/min. ASA naive.

  1. prasugrel 60 mg
  2. clopidogrel 300 mg
  3. clopidrogel 600 mg
A
  1. clop 300 mg because prasugrel is CI in those with lower weight and over 75 and crummy renal fcn. give him the lower dose clopidrogel because he’s older.
177
Q

what are the indications for using IIbIIIa inhibitors?

A

not rec’d for upstream use, use is provisional or when there is not enough time for clopidrogel to take effect

178
Q

why is ticragrelor better than clopidrogel and plasugrel?

A

it is reversible, but its BID tx which is harder for pts

179
Q

what are the 3 goals of tx for UA/NSTEMI?

A

dimish coagulability with drugs (antiplatelets (ASA, P2Y12, IIBIIA inhib) anticoags (heparin, bivalrudin), thrombolytics not used), relieve pain with drugs (antiischemics/analgesics: SL and IV nitro, morphine), prevent morbitidy and mortality(BB, ACEI, aldosterone antagonists)

180
Q

what dose does someone take for SA nitro? CIs?

A

0.4 mg SL q 5 min x3 or IV after SL
CI: hypotension, tachycardia, phosphodiesterase inhibitor within 24 h of sildenafil or 48 h of tadalafilnot for replacing mortality reducing meds like BB, ACEI

181
Q

when do you use IV morphine sulfate?

A

if CP uncontrolled despite IV NTG. don’t use without mortality reducing meds liek BB, ACEI or in people with hypotension or tachycardia

182
Q

which pts req BB?s

a. everyone
b. HF pts
c. everyone who can
d. HTN pts

A

c. everyone who can. they are not for those with HF or low HRs. they are good for HTN though

183
Q

what should you give to patients with pulm congestion or LVEF

A

oral ACEI/ARB

184
Q

in treating an ACS pt with systolic HF (EF 30%) on IV nitro and a BB you should? 90/60 (65)

a. d/c bb, start acei
b. do not start acei
c. dc nitro; start acei
d. start acei

A

c. b/c if you get rid of the nitro their BP may go up into a good range and ACEI won’t hurt their Lvef.

185
Q

IN treating a ACS pt with systolic HF (ef65%) on IV nitro and a BB you should? 90/60 (65)

a. dc bb; start ACEI
b. don’t start acei
c. dc nitro; start acei
d. start acei

A

b. don’t start ACEI–not critical in this pt

186
Q

what are the goals of treating a pt with STEMI?

A

relieve pain with antiischemics/analgesics SL and IV nitro, morphine, reperfuse PCI preferred over lytic, dimish coagulability ((antiplatelets (ASA, P2Y12, IIBIIA inhib) anticoags (heparin, bivalrudin)

187
Q

when should a lytic be given?

A

if the 90 minute PCI window cannot be met (often in rural settings), most effective if used within 12 hrs of sx. small benefits between 12 and 24 hours. not beneficial

188
Q

what are the CIs for lytics?

A

active bleeding for 1 month or hx of intracranial hemorrhages, ischemic stroke within 3 months. relative CIs: uncontrolled HTN (bp>180/110), current anticoagulant use, pregnancy, surgery

189
Q

what is the aspirin tx for everyone discharged post MI with med management/PCI+stent or lytic?

A

go home on 81-325 mg/day aspirin indefinitely; push for 81. if with combo of ticagrelor use only 81 mg.

190
Q

what drug should post MI pts go home on along with aspirin if they got a DES?

A

p2y12 inhibitors

191
Q

what puts someone at a high clot risk?

A

STEMI, NSTEMI, hx of ACS or stent, DM

192
Q

what is considered a low clot risk?

A

CSA, unstable angina, not clot hx

193
Q

what puts someone at high bleed risk?

A

HTN >180/110, abnormal renal or liver, stroke of TIA hx, bleed hx, labile INRs, >75 yo, drugs

194
Q

ASA dose post sirolimus (DES) in an 82 yo with USA
PMHD; HLD, hx of GI bleed, wt 43 kg, crcl 25 ml/min, ASA naive
1. 325 mg indefinitely
2. 325 x 6 months
3. 325 x 3 months
4. 81 mg indefinitely

A
  1. 81 mg indefinitely
195
Q

clopidogrel duration post sirolimus (DES) in an 82 yo with USA
PMHD; HLD, hx of GI bleed, wt 43 kg, crcl 25 ml/min, ASA naive
1. 75 mg daily x 6 months
2. 75 mg daily x 12 months
3. 37. 5 mg daily x 12 months
4. 75 mg daily indefinitely

A
  1. 75 mg daily x 6 months. he is older, low clot risk, high bleed risk.
196
Q 
ticagrelor duration post bare metal stent in a 75 yo with NSTEMI
PMH: HLD, DM
wt: 87 kg
crcl 35 ml/min
ASA naive
1. 10 mg daily x 6 months
2. 10 mg daily x12 months
3. 5 mg daily x12 months
4. 10 mg daily indefinitely
A
  1. 75 daily x 12 months. he is a mixed picture. he is a bleed risk because he is over 75. but he is a high clot risk too.
197
Q

what are the discharge meds for all?

A

BB for all who can, PRN SL NTG for all who can , statins for all (high dosig for 75), ACE if EF

198
Q

72 yo post MI (1yr) with CP on metoprolol daily has fallen down x2 month. 102/65 (55) what should you do?

  1. dc metoprolol, try amlodipine
    b. continue present management
    c. decrease meoprolol dose
    d. dc metoprolol, try diltiazem
A

c. decrease the dose because he will still fall down on other agents

199
Q

syndrome caused by heart’s inability to generate a sufficient cardiac output to meet the metabolic needs of the body

A

heart failure

200
Q

what signs shows volume overload?

A

SOB, rales, edema

201
Q

what signs show inadequate tissue perfusion?

A

light headed, poor exercise tolerance, fatigue

202
Q

what dx does more medicare dollars go to than any other dx?

A

HF

203
Q

what is the underlying cause of left ventricular dysfunction in 2/3 of pts?

A

CAD

204
Q

what are causes of HF?

A

HTN, idiopathic dilated cardiomyopathy, alcohol abuse

205
Q

what are the 4 compensatory responses in HF/

A

increase preload (to optimize stroke volume), vasoconstrict (to maintain BP and perfusion) increase HR to increase CO, ventricular hypertrophy and remodeling (maintain CO and reduce myocardial stress)

206
Q

why are the heart’s compensatory responses bad?

A

most of them are good ST but increase demand on the heart LT. i.e. tachycardia increases work and decreases ventricular filling time, vasoconstriction increases after load and demand, increasing the preload in creases demand and causes edema and congestion, hypertrophy causes dysfunction and weird conduction=higher risk of MI.

207
Q

which 2nd line pharm tx for HF is specifically req’d for those who can’t tolerate ACEI and for those who are african american?

A

isosorbide/hydralizaine

208
Q

what are some of the sx of digoxin toxicity?

A

disadvantage in stress/exercise: increased sympathomimetic tone overrides digoxin vgagal effect. Toxicity: aorexica, N/V/D, tiredness, weakness, decreased HR yellow/green halo vision, confusion, HA

209
Q

what’s the req’d dose for digoxin?

A

always start after BB to control HR. 0.125 loading dose IV or PO over 12-24 hours, then qday, very narrow window depending on person

210
Q

what are some drugs intx of digoxin?

A

verapamil, captopril, diuretics, amiodarone, dronedarone, clarithromycin, erythromycin

211
Q

which new drug for HF is more effective than a ACEI alone? how does it work?

A

increases sodium loss and vasodilation and enhances ARB efficacy. More effective than an ACE alone to decreaes death and hospitaliztions.

212
Q

which new med for HF can cause bradycardia, temporary brightness of visual field early in tx and MOA inhibits the if or funny current in the hear to decreaes HR without decreasing BP (maintains perfusion while decreasing work for heart). does it decrease mortality?

A

ivabradine (corlanor). doesn;t decrease mortality. best when added to maximized std tx

213
Q

how do you manage decompensated HF?

A

hospitalize, IV loop diuretic if signif. fluid overload, add thiaizide if needed. IV dobutamine to increase renal blood flow and diuresis. IV nitro can be given for dyspnea if no sx hypotension.

214
Q

which new HF drug has a half life 18 minutes. Eliminated viaa cell surface clearance receptors, proteolytic cleavage, renal filtration, clerance proportional to body weight; and smooth muscle relaxation, dilates veins and arteries, dose dependent decreae in wedge pressure and systemic arterial pressure. who are the best pts for it?

A

BNP; IV tx of pts with acutely deceompensated HF with dyspnea at rest or with minimal activity

Pharmacotherapy (9 decks)

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