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

Lecture 5 (Valvular)-Exam 2 Flashcards

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
Q

Mitral regurgitation
* Limited role for hwat?
* Who gets medical therapy? (2)

A

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

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26
Q

What are all the different parts of Medical therapy for MR?(4)

A
  • ­Diuretics – preload reduction
  • ­ACEI, ARB, ARNI – afterload reduction
  • ­± beta blockers
  • ­± mineralocorticoid receptor antagonists
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27
Q

MS medical management:
* When and what do you anticoagulate?

A

Anticoagulation – warfarin (INR 2-3) for patients with:
* Atrial fibrillation
* History of primary embolic event
* Atrial thrombosis

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28
Q

MS medical management
* What is the txt? (3) What do they improve?

A

Symptomatic treatment – HF symptoms
* Diuretics – relieve congestion symptoms
* Beta blockers – HR control; improves dyspnea
* Treatment of Afib if present

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29
Q

What should you prophylaxis when patients have MS?

A

Secondary rheumatic fever prophylaxis

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30
Q

MS medical management
* What does primary pheumatic fever prophylaxis?
* How do we eradicate GAS?

A

Primary Rheumatic Fever Prophylaxis
* Prevent rheumatic fever after group A streptococcal pharyngitis

GAS eradication:
* Amox, penicillin, cefalexin (if pen allergic)
* Clinda
* Augmentin
* Azithromycin

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31
Q

MS medical management
* Who gets SECONDARY rheumatic fever prophylaxis?

A

­ Patients with documented RF or RHD

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32
Q

What can happen 1 to 6 weeks following GAS pharyngitis?

A
  1. Carditis
  2. Migratory large joint polyarthritis
  3. Chorea
  4. Subcutaneous nodules
  5. Erythema marginatum

J:joint involvement O: carditis N:Nodules E: erythema marginaum S: Sydenham chorea

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33
Q
  • How do you dx Rheumatic fever?
A
  • 2 major criteria or
  • 1 major criteria and two minor
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34
Q

MS medical management:
* What is first line and alternatives for secondary Rheumatic Fever Prophylaxis?

A

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

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35
Q

MS medical management
* What is the duration of txt for no carditis, carditis without residual heart disease, and carditis with residual valvular disease?

A
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36
Q

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?

A

Asymptomatic – no treatment

Dysautonomia symptoms (anxiety, palpitations, chest pain)
* Beta blocker

Symptomatic with severe mitral regurgitation, systolic HF and symptom progression
* Surgical intervention

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37
Q

What is the txt for pulmonic stenosis and pulmonic regurgitation

A

Surgical interventions

38
Q

Orthostatic hypotension (normal response to standing)
* What happens normatls with the blood?

A

Standing causes blood pooling in splanic circulation and lower extremities
* Decreases venous return and CO

39
Q

Normal:
* After blood pools, what does barorecptors detect? What are the responses?

A
40
Q

Orthostatic hypotension
* Decrease what?
* What cannot compensate?

A
  • Decreased volume
  • SNS cannot sufficiently compensate for gravitational blood pooling
41
Q

Orthostatic hypotension
* MC in who?
* Why does it make it more common? (4)

A

MC in elderly
* Decline in baroreceptor sensitivity
* Increase in autonomic neurodegeneration
* Incidence increases with increasing age
* Exacerbated by disease states and medications

42
Q

What are is the most common medications that can cause or worsen orthostatic hypotension? 5

A
43
Q

What is first line for OH? Second line?

A
  • First line: Lifestyle changes
  • Second line: Pharm
44
Q

Lifestyle changes of OH:
* Slowly do what?
* Meals?
* Improve what?
* Avoid what?
* Discontinue what?

A
  • Rise slowly
  • Small frequent meals
  • Improve physical fitness
  • Avoid excess sweating/over heating
  • Discontinue or dose reduce exacerbating medications
45
Q

OH- lifesyle changes
* Increase what (2)
* what should they be wearing?
* Sleep with what?

A
  • 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
46
Q
A
47
Q

OH pharmacotherapy:
* What are two approaches?

A
  • Expansion of intravascular volume
  • Increased peripheral vascular resistance
48
Q

Are the specific agents used to tx OH? What do they cause?

A
49
Q

OH

Midodrine:
* What is the MOA?
* ADRs?

A
  • MOA: Alpha1-agonist; arterial and venous constriction
  • ADR: Piloerection, Pruritis, Urinary retention
50
Q

OH

Droxidopa:
* What is the MOA?
* What are ADRs?

A
  • MOA: NE precursor; alpha- and beta-adrenergic agonist
  • ADRs: HA, Supine hypertension, Nausea
51
Q

OH

Fludrocortisone:
* What is the MOA?
* What are the ADRs?

A
  • MOA: Mineralocorticoid Increases renal sodium and water reabsorption; expands intracellular volume
  • ADRs: Hypokalemia and ankle edema
52
Q

Shock syndromes:
* What is Distributive?
* What is Hypovolemic?

A

Distributive – plumbing problem (MC-2/3rds)
* Sepsis, anaphylaxis, neurogenic
* Decreased systemic vascular resistance

Hypovolemic – volume problem (16%)
* Blood loss, dehydration, burns
* Decreased preload

53
Q

Shock syndrome:
* What is cardiogenic?
* What is obstructive?

A

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
Q

Fill in for shock

A
55
Q
A
56
Q

Vasopressor:
* Agents what do what?

A

Agents that either increase SVR or CO

57
Q

Recepotor effects: agonist
* What does beta 1 and 2 cause?

A
58
Q

Recepotor effects: agonist
* What does alpha 1 cause?

A
  • Arteriole vasoconstriction->increase SVR->increase AL
  • Venule vasoconstriction->increase venous return->increase PL
59
Q

Recepotor effects: agonist
* What does D1 and D2 cause?

A
60
Q

Vasopressors:
* Choice of vasopressor depends on what?
* Many vasopressors cause what?

A
  • Choice of vasopressor depends on underlying shock pathophysiology and goals of treatment
  • Many vasopressors cause adverse peripheral vasoconstriction and decreased splanchnic perfusion
61
Q

Many vasopressors cause adverse peripheral vasoconstriction and decreased splanchnic perfusion
* What does that cause?

A

Ischemia / necrosis

IV infiltrations common
* ­ Larger vein or intraosseous access preferred for administration

62
Q

Vasopressors:
* What does catecholamines vasopressors cause?
* What is the half life? What is required?

A
  • Catecholamine vasopressors - dysrhythmogenic
  • Short half-lives – continuous infusions required
63
Q
A
64
Q
A
65
Q

Inodilators:
* PDE normally breaks down what?
* What does milrinone inhibits? Where?
* What does it decrease?

A

PDE normally breaks down cAMP

Milrinone specifically inhibits PDE3
* PDE 3 located in cardiac myocytes

Decreased breakdown of cAMP

66
Q

Inodilators:
* What happens when cAMP accumulates?

A
  • 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
Q

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?

A
  • 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
Q

Dopamine:
* What is the dose?
* What receptor is most activated?
* How does it affect SVR/MAP? CO/HR?

A

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
Q

What are the SE of dopamine?

A
  • tachycardias
  • Dysrhythmias
  • Mesenteric hypoperfusion
70
Q

Epinephrine:
* What is the dose?
* What receptor is most activated?
* How does it affect SVR/MAP? CO/HR?

A

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
Q

What are the indications and SE of epinephrine?

A

Indications:
* Septic shock
* Add-on cardiogenic shock
* AV nodal dysfunction
* Anaphylactic shock

SE:
* Tachycardias
* Dysrhythmias
* Mesenteric hypoperfusion
* Increased lactate

72
Q

Vasopressin:
* What is the MOA?
* What does it cause to SVR/MAP, CO/HR?
* What is the indication?
* What can it cause ?

A
  • MOA: Arginine vasopressin receptor 1->Pure vasoconstriction
  • SVR/MAP: increase
  • CO/HR: no change
  • Indication: septic shock
  • SE: peripheral ischemia
73
Q

Phenylephrine:
* What is the MOA?
* What does it cause to SVR/MAP, CO/HR?
* What is the indication?
* What can it cause ?

A
  • MOA: A1 receptors -> pure vasoconstriction
  • SVR/MAP: increase
  • CO/HR: no change
  • Indications: septic shock
  • SE: peripheral ischemia
74
Q

Septic shock
* What is the primary problem?
* Need to increase what?

A
  • Vasodilation primary problem
  • Also need increased CO and BP
75
Q

Septic shock:
* What is the IVF of choice? What is the dose, goal and reassess what?

A

IVF of choice: isotonic crystalloids
* Dose: 30mL/kg within 3 hours
* Goal: MAP ≥ 65
* Reassess perfusion

76
Q

Septic shock
* What is the first line vasopressor? When do you give this? Less what?
* What is second line?

A

First-line vasopressor: norepinephrine
* Patients not responding to fluid resuscitation
* Less beta stimulation than epinephrine

Second-line vasopressor: epinephrine

77
Q

What was given for marik protocol? (3)

A
  • 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
Q

What was good about the marik protocal? What were limitations?

A

Good: Similar patients, safe, consecutive

Limitations:
* Small trial
* Not RCT – still significant difference
* Single site

79
Q
A
80
Q

How do get epinephrine?

A

Tyrosine -> L-Dopa -> Dopamine -> Norepinephrine -> Epinephrine

81
Q

Decompensated HF:
* What are multiple triggers?

A
82
Q

Decompensated HF
* What are the treatment goasl?

A
83
Q

Decompenstated HF

A
84
Q

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?

A
85
Q

Cold/Dry patients:
* What is going on with them?
* MC with what?

A
  • No fluid overload
    • peripheral hypoperfusion
      * Weakness, decreased UOP, weak pulses
  • MC with over aggressive diuresis
86
Q

What is first line and second line for cold/dry patients?

A

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
Q

Cold/Wet patients:
* What is going on with them?
* Good or bad prognosis? MC when?
* What is the txt?

A
88
Q

Cardiogenic shock
* What is the issue?
* What is the MCC?

A

Pump problem
* Pulmonary edema and hypoperfusion

In adequate oxygen to heart…
* MCC – myocardial infarction (80%)

89
Q

Cardiogenic shock:
* What is the goal?
* What do you need to treat?
* What should you give (2)

A
90
Q

Which vasopressors do you give with cardiogenic shock?

A
  • SBP > 90 – dobutamine
  • SBP < 90 – NE + dobutamine

Pharm II (14 decks)

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