Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm 2 > Test 5: CV Drugs pt. 2 > Flashcards

Test 5: CV Drugs pt. 2 Flashcards

1
Q

What is Ephedrine?

A

A synthetic non-catecholamine.

Mixed actions:
-Mild direct (A1, B1, B2). Weakly agonizes these receptors on the postsynaptic side.
-Mostly Indirect actions: Increases NE release to the post synaptic receptors. Relies on endogenous NE stores for results. Greater effect on venous side. Both Alpha and Beta.

-Increases CO and PL
-Not metabolized by MAO or COMT
-Renal elimination (mostly unchanged)
-Administered IV, IM, and PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the dose of Ephedrine?

A

IVP: 5 - 10 mg
IM: 25 - 50 mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the uses of Ephedrine?

A

-Can be given IM before placing a spinal to counteract hypotension
-Used in OB since it doesn’t compromise uterine blood flow
-Used post-induction to buy time to adequately fluid resuscitate
-Can use instead of Neo if pt is already bradycardic.
-Hypotension with low CO + HR
-Tx of Sympathectomy
-Temporary tx of hypovolemia
-Treat transient myocardial depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the advantages of Ephedrine?

A

Similar to epinephrine:
-Epinephrine is 250X more potent
-Ephedrine 10X longer duration

SBP, DBP, HR and CO increase (inotrope and pressor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the disadvantages of Ephedrine?

A

-Tachyphylaxis
-Reduced efficacy with depleted NE stores
-R/O malignant HTN with MAOIs (If pt is on MAOI anti-depressants, can lead to malignant HTN (nothing to get rid of it).
-Increased HR

Caution use in:
-Patients on NDRIs and MAOIs
-CV dz or HOCM
-Closed angle glaucoma
-Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Phenylephrine?

A

-Direct acting alpha adrenergic agonist
-Some indirect with NE release
-Mainly Alpha 1 stimulation (arterial > venous)
-Just vasoconstriction
-Metabolized by MAO (not COMT). Short DOA (<5 minutes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the dose of Phenylephrine?

A

-40 to 80 to 160 mcg IV push
-Watch for reflex bradycardia
-Can be given as infusion: 20-200 mcg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the uses of Phenylephrine?

A

-Anesthesia-induced hypotension (Both GA and SAB)
-Nasal decongestant
-Hypotension with low SVR
-Temporary tx for hypovolemia

Decreased risk of fetal acidosis associated with phenylephrine when used for tx of hypotension r/t spinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the effects of Phenylephrine?

A

CV effects:
-Reflexive DECREASE in HR
-↑ SVR, ↓ CO
-Short duration (quick on/off)
-During hypotension: will increase CBF without increase in CO
-MVO2 does not ↑↑ if hypertension is avoided

Disadvantages
-May ↓ SV and ↑ PVR
-May ↓↓ renal, peripheral, and mesenteric perfusion
-RARELY may induce vasospasm: IMA, radial, gastroepiploic artery

Metabolic effects:
-Can interfere with K+ loading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Vasopressin?

A

-Arginine vasopressin (AVP) also known as ADH
-Endogenous regulation of osmolality, cardiovascular stability, blood coagulability
-Intense peripheral vasoconstriction via V1 receptors in vascular smooth muscle (peripheral, mesenteric vasoconstriction)
-Can restore vasomotor tone in refractory arterial hypotension or relative AVP deficiency
-Refractory shock states/CPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical uses for Vasopressin?

A

Adjunct vasopressor in the perioperative setting.
-Vasoplegia (post bypass and ACE-I; septic shock)
-Sympathetic blunting by GA or high SAB
-Post-pheochromocytoma resection
-Post CPB vasodilatory shock
-Alternative to Epi in ACLS
-Concomitant use with corticosteroids in septic shock
-Adjunct to catecholamines in septic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is vasoplegia?

A

When the post-synaptic receptors stop being receptive to Norepi/Epi.
-Occurs with patients on ACE-I therapy and post-CPB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the dosing for Vasopressin?

A

-2-4 units IVP
-10-20 unit bolus followed by infusion at 0.03- 0.1U/min
-Resuscitation dose 40 units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the cautions associated with Vasopressin?

A

-Withdrawal hypotension, DI after discontinuation
-Hyponatremia, pulmonary vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Digoxin?

A

-Cardiac glycoside
-Perioperative use for supraventricular tachydysrhythmias and last line in CHF
-Renal elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA of Digoxin?

A

-Inhibition of Na/K ATPase
-Increased Ca2+ in myocardium increases inotropy without increasing HR
-Some negative chronotropic and dromotropic effects via parasympathetic enhancement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the cautions with the use of Digoxin?

A

-Narrow therapeutic index

Toxicity most common in setting of renal dysfunction and hypokalemia:
-Nausea, vomiting, arrhythmias
-Correct causes, administer antiarrhythmics, temporary pacer, digoxin antibodies

Many drug-drug interactions
-Amiodarone - MAJOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Milrinone?

A

-Phosphodiesterase 3 Inhibitor
-Inodilator: Provides inotropy and vasodilation
-Non-catecholamine inotrope and relaxation of arterial and venous beds
-Increases contractility and CO
-Decreases LVEDP, CVP, and PCWP
-Adverse effects: hypotension, arrhythmias
-Uses: Heart failure (Low CO with high PVR and LVEDP), bridge to transplant
-Preferred over dobutamine in patients with high risk of arrhythmia, pulmonary hypotension, and those on chronic beta-blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the dose of Milrinone?

A

Titrate as IV infusion:
-0.2 to 0.75 mcg/kg/min
-Requires renal adjustment
-Can do loading dose of 50 mcg/kg TRO 10 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the advantages to Milrinone?

A

Favorable myocardial profile:
-Decrease preload and afterload
-Minimal tachycardia
-Less arrhythmogenesis than Dopa or Epi

Retains efficacy when NE stores are depleted (chronic CHF)
No tachyphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the disadvantages to Milrinone?

A

Hypotension can occur with rapid IV bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the indications for the use of Milrinone?

A

-Low CO with high PVR and LVEDP
-Bridge to transplant
-Preferred over dobutamine in patients with high risk of arrhythmia, pulmonary hypotension, and those on chronic beta-blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are Beta 2 Agonists used for?

A

-Relax bronchioles and uterine muscles without tachycardia
-Slowly metabolized = long duration
-Inhalation as well as IV
-Tolerance may develop
-Increase lactic acid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are examples of Beta 2 Agonists?

A

-Albuterol: PO, inhalation – asthma
-Metaproterenol (Alupent ™) inhalation: asthma
-Terbutaline: IV, PO, SQ, inhalation - asthma or premature labor

25
What is Methylene Blue?
A drug used for vasoplegia. -Reduces morbidity & mortality -Interrupts inflammatory cascade of Nitric oxide -> Guanylyl Cyclase -> cGMP -> Vasoplegia/vasodilation -Vasopressin and methylene blue are the 2 drugs used for vasoplegia
26
What are the advantages to Methylene Blue?
-Improves MAP in certain types of shock -Patients require less pressors and have shorter ICU LOS -Mortality benefits -Cheap and readily available
27
What are the disadvantages to Methylene Blue?
-Can cause paradoxical methemoglobinemia (data from case reports and small RCTs) -Potentially life-threatening side effects in patients on SSRIs
28
When would you use Methylene Blue?
If patient is on high dose Norepi/Epi AND Vasopressin and still not meeting goal MAP (vasoplegia). -Give Methylene Blue 1-2 mg/kg IV -If first bolus works, can repeat bolus and start drip
29
When is Methylene Blue contraindicated?
In patients taking SSRIs/SNRIs/MAOIs
30
What drugs can you give as alternatives to Methylene Blue if it's C/I?
-Angiotensin II (consider if high risk of renal failure) -Hydroxocobalamin (consider if high risk of thrombosis)
31
What is Calcium?
-Necessary for neurotransmission, coagulation, muscle contractility -Potent inotrope: Used to treat cardiac depression. Good post CPB -Ionized calcium responsible for physiologic effect -Calcium sensitizers – drugs that increase myocardial contractility. Ex: Levosimendan (Increases our response to calcium)
32
When is Calcium used?
Reverses hypotension: -Anesthetic induced -CCBs -Hypocalcemia -CPB -BBs Hyperkalemic cardiotoxicity
33
What are the effects of Calcium administration?
-No change or decrease in HR -Increased contractility -Increased BP -Increase SVR -Variable CO
34
What is Glucagon?
-Peptide hormone -Increases intracellular cAMP -Clinical offset: redistribution and proteolysis -Duration of action: 20-30 minutes -Side effects: headache, severe nausea, hyperglycemia and hypokalemia -Dose: 1-5mg IV slowly
35
What is Glucagon used for (CV)?
-Treatment of beta-blockade overdose due to increase cAMP in the myocardium -Bypasses the inhibitory effect of beta-blockade
36
What is the MOA of Nitrates?
Indirect acting: Nitroglycerin (Has to be activated by enzymes before releases NO) Direct acting: Nitroprusside (releases NO spontaneously) Work on the NO pathway. -NO is released by blood vessel capillary endothelial cells, cause relaxation by entering cell. Guanylyl Cyclase converts GTP to GMP, cGMP causes relaxation. -Nitric oxide activates smooth muscle soluble guanylyl cyclase (GC) to form cGMP. -Increased intracellular cGMP inhibits calcium entry into the cell, thereby decreasing intracellular calcium concentrations and causing smooth muscle relaxation -NO also activates K+ channels, which leads to hyperpolarization and relaxation. -NO acting through cGMP can stimulate a cGMP-dependent protein kinase that activates myosin light chain phosphatase, the enzyme that dephosphorylates myosin light chains, which leads to relaxation.
37
How are Nitrates removed?
Nitrates are removed (De-nitrated) by: -Smooth muscle: glutathione S-transferase -Mitochondrial enzyme: aldehyde dehydrogenase
38
What are the effects of Nitrates?
-Vascular Smooth Muscle dilation (gradient of response). Arteries vs veins -Increased venous capacitance/decreased PL = risk of orthostatic hypotension -Baroreceptor and hormonal responses to 🡻 arterial pressure -Redistribution of blood flow -Slight positive inotropic effect via nitric oxide (due to PDE) -Can work on Erectile tissue and Pulmonary HTN (Sildenafil) -Inc cGMP = decreased platelet aggregation -Nitrates react to form Methemoglobin (not a huge issue in adults unless long-term therapy)
39
What are the toxicity S/Sx of Nitrates?
Directly related to the extent of vasodilation that occurs. -Headache, flushing, tachycardia, orthostatic hypotension -Contraindicated with increased ICP
40
How does Tolerance to Nitrates form?
Mechanisms not completely understood: -Reduced bioactivation +/- loss of soluble guanylate cyclase -Systemic compensation Variable tolerance depending on which nitrate is used -Nitroprusside (SNP) not as affected -NTG > SNP
41
What is Nitroglycerin?
An indirect acting vasodilator. -Activation of cGMP causes vasodilation -Affects venous > arterial -Clinical offset: redistribution, metabolism in smooth muscle and liver -Duration 5-10 minutes -Onset 2-3 minutes
42
What is the dosing of Nitroglycerin?
Bolus dosing (profound HOTN): -40-80 mcg IVP IV infusion: -0.1-7 mcg/kg/min or 5 mcg/min and up
43
What are the effects of Nitroglycerin?
Marked vasodilation causing: -Reflex increased HR and Contractility -Decreased BP, PL, SVR/PVR -Variable CO
44
What are advantages to Nitroglycerin?
-Preload reduction -No metabolic toxicity (compared to SNP) -Effective for myocardial ischemia (vasodilates coronaries) -Effective for CHF -Increases vascular capacity (useful post CPB) -Dilates pulmonary vascular bed
45
What are disadvantages to Nitroglycerin?
-↓ BP = ↓Coronary Perfusion Pressure (CPP) -Reflex tachycardia (Dose related) -Inhibits HPV (less than NTP) -May increase ICP -May be absorbed by PVC tubing (titrate to effect) -Tolerance -Dependence -Methemoglobinemia
46
What are clinical uses for Nitroglycerin?
-Relief of Coronary Artery vasospasm -Redistribution of blood flow to ischemic coronary areas (MI) -Reduced ischemia = improved inotropy and increased VF threshold -At high doses (up to 10 mcg/kg/min) has Arterial effects (Decreased SVR = reduced wall stress and MVO2)
47
What is Nitroprusside?
Direct acting vasodilator. -Dilates both venous and arterial but slightly more arterial at usual doses -Clinical onset <1min. -Duration 3-5 mins. -Longer half-life than NTG
48
What is the dosing for Nitroprusside?
Bolus dosing: (careful!) 20 mcg Infusion: -0.1-2 mcg/kg/min
49
What are the effects of Nitroprusside?
-Reflex increase in HR and Contractility -Dose-dependent decrease in BP and SVR/PVR -Decreases PL -Variable effect on CO
50
What are the advantages to Nitroprusside?
-Duration of action: Quick on & off -Systemic and pulmonary vasodilation -Highly effective for all types of HTN -More arterial vasodilation than NTG -Good for AL reduction
51
What are disadvantages to Nitroprusside?
-Cyanide toxicity -Unstable in light -Reflex tachycardia (responds to BB) -Blunts HPV (More than NTG) -Vascular steal -Caution with managing chronic hypertension -Rebound hypertension -Increased ICP -Inhibited platelet function
52
Why is there a risk of Cyanide toxicity with Nitroprusside?
-NTP rapidly metabolized to cyanide -Adults normally able to “detoxify” NTP -Issue in peds -Biggest issues with large, prolonged dosing and with hepatic and renal disease
53
How do you diagnose Cyanide toxicity?
-Challenging in anesthetized patients -Hypertension and metabolic acidosis (lactate >8) -Late signs: CV collapse with hypotension -Seizures/coma; mydriasis -Onset often preceded by tachyphylaxis -Elevated SVO2
54
What is the treatment for Cyanide toxicity?
-Stop the NTP -100% O2 -Sodium thiosulfate (150 mg/kg over 15 minutes)
55
What causes vasopressin to be released by the Posterior Pituitary?
-Hyperosmolarity -Decreased atrial receptor firing -Angiotensin 2 -SNS Stimulation
56
What are the actions of V1 receptor stimulation?
-Constriction of blood vessels (inc SVR) -Increases intracellular calcium -Tx of esophageal varices
57
What are the actions of the V2 receptor stimulation?
-Increased fluid reabsorption by the kidneys (increased blood volume) -Antidiuresis.
58
What are advantages/disadvantages of Vasopressin?
Advantages: -Independent of adrenoreceptors -Effective with vasoplegia unresponsive to usual means -ACLS: restore coronary perfusion without ↑HR Disadvantages: -Symptoms of ↓BF to mesentery, bronchoconstriction, etc -Decrease hepatic BF (esp. if used with α1 agonists) -Decreased platelet count -Lactic acidosis (?)

Pharm 2 (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions