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Pharm II > Lecture 5 (Valvular)-Exam 2 > Flashcards

Lecture 5 (Valvular)-Exam 2 Flashcards

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1
Q

Stable angina/Stable ichemic heart disease
* What is one of the strategies and what are the goals?

A

Risk factor modification
* Slow progression of atherosclerosis and prevent complications
* Minimum effect on symptom control or QOL

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2
Q

Which drug for risk factor modification for stable angina, does decrease mortality rates but does not improve symtoms

A

ACE-i and ARBs

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3
Q

Fill in for stable angina?

A
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4
Q

What is the other general treatment approach for stable angina?

A
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5
Q

What is the first line for STMPTOMATIC txt of stable angina? What is the primary and secondary effects?

A

Nitroglycerin = first-line
* Onset of acute anginal symptoms or prophylaxis against episodes
* Primary effect: reduce ischemia primarily via reduction in myocardial oxygen demand (preload)
* Secondary effect: coronary artery vasodilation (including stenotic vessels)

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6
Q

Nitroglycerin:
* What is the MC route and the dose?

A

MC = sublingual tablets

Dose:
* 0.3 to 0.4 mg every 5 minutes PRN chest pain
* May repeat x 3 doses total

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7
Q

What is the first line for preventation of angina?
* How does it work?
* What agents are preferred and not as effect?
* Not indicate for what?

A

Beta-blockers First-line – reduce angina episodes and increase exercise tolerance
* Decrease HR and contractility -> decrease myocardial O2 demand
* All beta-blockers equally effective -> cardioselective agents preferred
* Agents with intrinsic sympathomimetic activity not as effective
* NOT indicated for vasospastic or Prinzmetal angina

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8
Q

Management of angina: prevention
* What is second line? When is it used?
* How does it work?
* What is preferred?

A

Calcium channel blockers: Second-line – patients who cannot tolerate beta-blockers or still have symptoms on a beta-blocker
* Decrease HR and contractility -> decrease myocardial O2 demand
* Coronary and peripheral vasodilation ->increase O2 supply
* Verapamil, diltiazem preferred

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9
Q

Besides BB and CCB, what else can be given for prevention of angina?

A
  • Nitrates
  • Ranolazine
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10
Q

Class 5 digoxin
* What are the two primary cardiac effects?

A
  • Slows cardiac conduction – pacemaker cells
  • Increases cardiac contractility – cardiac myocytes
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11
Q

How does digoxin slow cardiac conduction via pacemaker cells?

A
  • Stimulates increased acetylcholine release from the Vagus nerve
  • Slows conduction through the AV node
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12
Q

How does digoxin increase cardiac contractility via cardiac myocytes?

A

Increases cardiac contractility – cardiac myocytes
* Inhibits sodium/potassium ATPase pumps
* Increases intracellular Na
* Na leaves cell via Na / Ca exchanger
* Ca accumulates inside the cell
* Increases myocardial contractility

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13
Q

Digoxin
* What are the SE?

A
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14
Q

Digoxin:
* What are the therapeutic and toxic levels?
* What are the risk factos for toxicity?

A
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15
Q

Digoxin toxicity treatment:
* What is the treatment of digoxin toxicity?

A
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16
Q
A
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17
Q

What are the digoxin effects on ECG?

A
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18
Q

What valvular disease txt?

A

Definitive treatment – surgical repair
* Aortic (Surgery)
* Pulmonary (Surgery)
* Tricuspid
* Mitral

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19
Q

Aortic stenosis:
* What is the txt (general)

A

Medical management – awaiting valve replacement

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20
Q

Aortic stenosis:
* What are the recommend minimal intervention due to risk of destabilizing the patient? (3)

A
  • Diuretics reduce preload->patient may depend on for maintenance of cardiac output
  • Vasodilators->in the presence of a fixed valvular stenosis may excessively reduce systemic blood pressure and reduce coronary artery perfusion pressure
  • Positive inotropic agents (eg dobutamine)->induce tachycardia->mmyocardial ischemia
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21
Q

aortic stenosis:
* What are the sxs?

A
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22
Q

Aortic stenosis: What does palliative care for severe symptomatic inoperable AS include?

A
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23
Q

Aortic regurgitation:
* How do you txt Symptomatic patients with severe AR - candidates for valve surgery?

A

­ Intense medical treatment per HFrEF guidelines prior to surgery

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24
Q

AR
* how do you txt symptomatic patients with severe AR – NOT candidates for surgery?

A

Therapy as per patients with HFrEF
* Diuretics, ARNI (or ACE inhibitor / ARB), beta blocker, mineralocorticoid receptor antagonist, ± digoxin

Treat hypertension (systolic blood pressure >140 mmHg) in patients with chronic AR
* ACEI/ ARBs

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25
Mitral regurgitation * Limited role for hwat? * Who gets medical therapy? (2)
Limited role for medical therapy * Symptomatic patients with chronic primary MR, LVEF < 60% * Medical therapy recommended for patients awaiting surgery or patients not surgical candidates
26
What are all the different parts of Medical therapy for MR?(4)
* ­Diuretics – preload reduction * ­ACEI, ARB, ARNI – afterload reduction * ­± beta blockers * ­± mineralocorticoid receptor antagonists
27
MS medical management: * When and what do you anticoagulate?
Anticoagulation – warfarin (INR 2-3) for patients with: * Atrial fibrillation * History of primary embolic event * Atrial thrombosis
28
MS medical management * What is the txt? (3) What do they improve?
Symptomatic treatment – HF symptoms * Diuretics – relieve congestion symptoms * Beta blockers – HR control; improves dyspnea * Treatment of Afib if present
29
What should you prophylaxis when patients have MS?
Secondary rheumatic fever prophylaxis
30
MS medical management * What does primary pheumatic fever prophylaxis? * How do we eradicate GAS?
Primary Rheumatic Fever Prophylaxis * Prevent rheumatic fever after group A streptococcal pharyngitis GAS eradication: * Amox, penicillin, cefalexin (if pen allergic) * Clinda * Augmentin * Azithromycin
31
MS medical management * Who gets SECONDARY rheumatic fever prophylaxis?
­ Patients with documented RF or RHD
32
What can happen 1 to 6 weeks following GAS pharyngitis?
1. Carditis 2. Migratory large joint polyarthritis 3. Chorea 4. Subcutaneous nodules 5. Erythema marginatum ## Footnote J:joint involvement O: carditis N:Nodules E: erythema marginaum S: Sydenham chorea
33
* How do you dx Rheumatic fever?
* 2 major criteria or * 1 major criteria and two minor
34
MS medical management: * What is first line and alternatives for secondary Rheumatic Fever Prophylaxis?
First-line penicillin G benzathine * ≤27 kg 600,000 units IM q 4 wks * >27 kg 1.2 million units IM q4 wks Alternatives: * PO penicillin VK * Azithromycin
35
MS medical management * What is the duration of txt for no carditis, carditis without residual heart disease, and carditis with residual valvular disease?
36
mitral valve prolapse: * What is the txt for asymptomatic? * What is the txt for dysautonomia symptoms (anxiety, palpitations, chest pain)? * What is the txt for symptomatic with severe mitral regurgitation, systolic HF and symptom progression?
Asymptomatic – no treatment Dysautonomia symptoms (anxiety, palpitations, chest pain) * Beta blocker Symptomatic with severe mitral regurgitation, systolic HF and symptom progression * Surgical intervention
37
What is the txt for pulmonic stenosis and pulmonic regurgitation
Surgical interventions
38
Orthostatic hypotension (normal response to standing) * What happens normatls with the blood?
Standing causes blood pooling in splanic circulation and lower extremities * Decreases venous return and CO
39
Normal: * After blood pools, what does barorecptors detect? What are the responses?
40
Orthostatic hypotension * Decrease what? * What cannot compensate?
* Decreased volume * SNS cannot sufficiently compensate for gravitational blood pooling
41
Orthostatic hypotension * MC in who? * Why does it make it more common? (4)
MC in elderly * Decline in baroreceptor sensitivity * Increase in autonomic neurodegeneration * Incidence increases with increasing age * Exacerbated by disease states and medications
42
What are is the most common medications that can cause or worsen orthostatic hypotension? 5
43
What is first line for OH? Second line?
* First line: Lifestyle changes * Second line: Pharm
44
Lifestyle changes of OH: * Slowly do what? * Meals? * Improve what? * Avoid what? * Discontinue what?
* Rise slowly * Small frequent meals * Improve physical fitness * Avoid excess sweating/over heating * Discontinue or dose reduce exacerbating medications
45
OH- lifesyle changes * Increase what (2) * what should they be wearing? * Sleep with what?
* Increase water intake – 1.5 to 3 L / day (500 ml in am) * Increase sodium intake – 2 to 3 grams / day (minimum) * Compression stockings / abdominal binders * Sleep with head of bed elevated 30 degrees or greater
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47
OH pharmacotherapy: * What are two approaches?
* Expansion of intravascular volume * Increased peripheral vascular resistance
48
Are the specific agents used to tx OH? What do they cause?
49
# OH Midodrine: * What is the MOA? * ADRs?
* MOA: Alpha1-agonist; arterial and venous constriction * ADR: Piloerection, Pruritis, Urinary retention
50
# OH Droxidopa: * What is the MOA? * What are ADRs?
* MOA: NE precursor; alpha- and beta-adrenergic agonist * ADRs: HA, Supine hypertension, Nausea
51
# OH Fludrocortisone: * What is the MOA? * What are the ADRs?
* MOA: Mineralocorticoid Increases renal sodium and water reabsorption; expands intracellular volume * ADRs: Hypokalemia and ankle edema
52
Shock syndromes: * What is Distributive? * What is Hypovolemic?
Distributive – plumbing problem (MC-2/3rds) * Sepsis, anaphylaxis, neurogenic * Decreased systemic vascular resistance Hypovolemic – volume problem (16%) * Blood loss, dehydration, burns * Decreased preload
53
Shock syndrome: * What is cardiogenic? * What is obstructive?
Cardiogenic – pump problem (16%) * Decompensated CHF, MI, arrythmia * Decreased cardiac output Obstructive – plumbing or pump problem (6%) * Cardiac tamponade, PE, tension pneumothorax * Decreased cardiac output
54
Fill in for shock
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56
Vasopressor: * Agents what do what?
Agents that either increase SVR or CO
57
Recepotor effects: agonist * What does beta 1 and 2 cause?
58
Recepotor effects: agonist * What does alpha 1 cause?
* Arteriole vasoconstriction->increase SVR->increase AL * Venule vasoconstriction->increase venous return->increase PL
59
Recepotor effects: agonist * What does D1 and D2 cause?
60
Vasopressors: * Choice of vasopressor depends on what? * Many vasopressors cause what?
* Choice of vasopressor depends on underlying shock pathophysiology and goals of treatment * Many vasopressors cause adverse peripheral vasoconstriction and decreased splanchnic perfusion
61
Many vasopressors cause adverse peripheral vasoconstriction and decreased splanchnic perfusion * What does that cause?
Ischemia / necrosis IV infiltrations common * ­ Larger vein or intraosseous access preferred for administration
62
Vasopressors: * What does catecholamines vasopressors cause? * What is the half life? What is required?
* Catecholamine vasopressors - dysrhythmogenic * Short half-lives – continuous infusions required
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Inodilators: * PDE normally breaks down what? * What does milrinone inhibits? Where? * What does it decrease?
PDE normally breaks down cAMP Milrinone specifically inhibits PDE3 * PDE 3 located in cardiac myocytes Decreased breakdown of cAMP
66
Inodilators: * What happens when cAMP accumulates?
* More cAMP -> increased activation of protein kinase A (PKA) * PKA phosphorylates calcium channels on cardiac myocytes -> increased Ca influx ->increased cardiac contraction cAMP build up -> vasodilation
67
Norepinephrine: * What is the dose? * What receptor is most activated? * How does it affect SVR/MAP? CO/HR? * What are the indications? * What can happen?
* Dose: 0.05 to 2 mcg/kg/min ->Titrate to MAP ≥ 65 * Receptor: **a1** then B2, B1 * SVR/MAP: increase * CO/HR: not really changing it * Indications: Septic shock, add on cardiogenic shock * Cause peripheral ischemia
68
Dopamine: * What is the dose? * What receptor is most activated? * How does it affect SVR/MAP? CO/HR?
Dose: * 2-5 mcg/kg/min (low) * 5 to 10mcg/kg/min (mod) * > 10 mcg/kg/min (high) Receptors (SVR/MAP) : * Low: DA (no change) * Mod: B1 and DA (increase) * High: a1 and B1 (increase) CO/HR: * Low: increase * Mod: increase * High: no change
69
What are the SE of dopamine?
* tachycardias * Dysrhythmias * Mesenteric hypoperfusion
70
Epinephrine: * What is the dose? * What receptor is most activated? * How does it affect SVR/MAP? CO/HR?
Dose: * low: ≤ 0.05 mcg/kg/min * high: > 0.05 mcg/kg/min Receptors (SVR/MAP) * Low: B1 (no change) * High: A1 (increase) CO/HR: * Low: increase * High: increase
71
What are the indications and SE of epinephrine?
Indications: * Septic shock * Add-on cardiogenic shock * AV nodal dysfunction * Anaphylactic shock SE: * Tachycardias * Dysrhythmias * Mesenteric hypoperfusion * Increased lactate
72
Vasopressin: * What is the MOA? * What does it cause to SVR/MAP, CO/HR? * What is the indication? * What can it cause ?
* MOA: Arginine vasopressin receptor 1->Pure vasoconstriction * SVR/MAP: increase * CO/HR: no change * Indication: septic shock * SE: peripheral ischemia
73
Phenylephrine: * What is the MOA? * What does it cause to SVR/MAP, CO/HR? * What is the indication? * What can it cause ?
* MOA: A1 receptors -> pure vasoconstriction * SVR/MAP: increase * CO/HR: no change * Indications: septic shock * SE: peripheral ischemia
74
Septic shock * What is the primary problem? * Need to increase what?
* Vasodilation primary problem * Also need increased CO and BP
75
Septic shock: * What is the IVF of choice? What is the dose, goal and reassess what?
IVF of choice: isotonic crystalloids * Dose: 30mL/kg within 3 hours * Goal: MAP ≥ 65 * Reassess perfusion
76
Septic shock * What is the first line vasopressor? When do you give this? Less what? * What is second line?
First-line vasopressor: norepinephrine * Patients not responding to fluid resuscitation * Less beta stimulation than epinephrine Second-line vasopressor: epinephrine
77
What was given for marik protocol? (3)
* Vitamin C 1500 mg IV q6h 4 days or ICU DC * Thiamine 200mg IV q12h x 4 days or ICU DC * Hydrocortisone 50mg IV q6h x 7 days or ICU DC
78
What was good about the marik protocal? What were limitations?
Good: Similar patients, safe, consecutive Limitations: * Small trial * Not RCT – still significant difference * Single site
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80
How do get epinephrine?
Tyrosine -> L-Dopa -> Dopamine -> Norepinephrine -> Epinephrine
81
Decompensated HF: * What are multiple triggers?
82
Decompensated HF * What are the treatment goasl?
83
Decompenstated HF
84
Warm/Wet patients: * What is going on with them? * What is goal? * What is first line? * What is second line? * What do you need to decrease?
85
Cold/Dry patients: * What is going on with them? * MC with what?
* No fluid overload * + peripheral hypoperfusion * Weakness, decreased UOP, weak pulses * MC with over aggressive diuresis
86
What is first line and second line for cold/dry patients?
First-line: * Small fluid bolus – improve LV filling pressures * Inodilators – dobutamine, milrinone Second-line: * Reduce afterload with arteriole dilators if hypoperfusion not improved with inodilators * Nitroprusside
87
Cold/Wet patients: * What is going on with them? * Good or bad prognosis? MC when? * What is the txt?
88
Cardiogenic shock * What is the issue? * What is the MCC?
Pump problem * Pulmonary edema and hypoperfusion In adequate oxygen to heart... * MCC – myocardial infarction (80%)
89
Cardiogenic shock: * What is the goal? * What do you need to treat? * What should you give (2)
90
Which vasopressors do you give with cardiogenic shock?
* SBP > 90 – dobutamine * SBP < 90 – NE + dobutamine

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