Contents
Receptor Cheat Sheet
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- RECEPTOR β LOCATION β STIMULATION EFFECT β ANALOGY
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Alpha-1 β Vascular smooth β VASOCONSTRICTION β "Clamping the pipes"
- (Ξ±1) β muscle β βSVR, βBP β
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Beta-1 β Heart β βHeart Rate (chronotropy) β "Gas pedal for the heart"
- (Ξ²1) β β βContractility (inotropy) β
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Beta-2 β Bronchial/Vascular β Bronchodilation β "Opening airways and
- (Ξ²2) β smooth muscle β Mild vasodilation β relaxing vessels"
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- V1 β Vascular smooth β VASOCONSTRICTION β "Non-adrenergic clamp"
- (Vasopressin)β muscle β (non-adrenergic pathway) β
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
Vasoactive Medication Profiles
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- MEDICATION β RECEPTOR(S) β PRIMARY EFFECT β BEST FOR
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Phenylephrine β Pure Ξ±1 β βBP/SVR without βHR β Anesthesia-induced hypotension,
- (Neo-Synephrine) β β β when tachycardia contraindicated
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Norepinephrine β Strong Ξ±1 + β Strong vasoconstriction β SEPSIS (First-line)
- (Levophed) β Mild Ξ²1 β with mild cardiac kick β
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Epinephrine β Ξ²1 + Ξ²2 + β Potent cardiac stimulation β Cardiac arrest, Anaphylaxis,
- β Ξ±1 at high doses β + bronchodilation β Post-pump shock
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Dobutamine β Pure Ξ²1 β βContractility + βHR β Heart Failure/Cardiogenic
- β β (pump problem focus) β Shock - "Fix the pump"
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Vasopressin β V1 β Vasoconstriction via β Sepsis adjunct, Vasoplegia,
- β β non-adrenergic pathway β Refractory to catecholamines
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
- Milrinone β PDE3 Inhibitor β βContractility + Vasodilation β RV Failure, High SVR
- β (not a receptor) β "INODILATOR" β Heart Failure
- βββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββββ
Dopamine Dose-Dependent Effects
- βββ DOPAMINE DOSE LADDER βββ
- LOW DOSE (<5 mcg/kg/min): Dopaminergic receptors β Renal vasodilation (CONTROVERSIAL)
- β’ Historical belief: "renal dose dopamine" - now largely abandoned
- β’ No proven renal protective effect in clinical trials
- MEDIUM DOSE (5-10 mcg/kg/min): Ξ²1 predominates β Inotropy + βHeart rate
- β’ Increases cardiac contractility and heart rate
- β’ Similar effects to dobutamine at this range
- HIGH DOSE (>10 mcg/kg/min): Ξ±1 predominates β VASOCONSTRICTION
- β’ Mimics norepinephrine effects
- β’ Significant vasoconstriction, increased SVR
Test what you just learnedJump to CCRN-style practice questions on this topic β instant feedback with full rationales.
Start Free Practice βWhy Vasopressin Works in Refractory Septic Shock
- In prolonged septic shock, patients may become REFRACTORY to catecholamines
- PROBLEM: Metabolic acidosis causes adrenergic receptor DOWNREGULATION
- β’ Alpha and beta receptors become less responsive
- β’ Even high-dose norepinephrine loses effectiveness
- SOLUTION: Vasopressin stimulates V1 receptors (NON-adrenergic pathway)
- β’ Works effectively EVEN in acidosis where alpha/beta receptors fail
- β’ Provides alternative vasoconstriction mechanism
- CLINICAL USE: Add to norepinephrine when MAP remains <65 despite escalating doses
Milrinone: The "Inodilator" Concept
- MECHANISM: Phosphodiesterase-3 (PDE3) Inhibitor
- β’ Prevents breakdown of cAMP β increases intracellular calcium
- β’ NOT a receptor agonist - works inside the cell
- DUAL EFFECT:
- β’ INOTROPY: Increases cardiac contractility
- β’ VASODILATION: Decreases SVR and PVR
- BEST INDICATIONS:
- β’ Right Ventricular Failure (reduces pulmonary vascular resistance)
- β’ Heart Failure with HIGH SVR ("clamped down" patient)
- β’ Post-cardiac surgery with elevated afterload
- WHY MILRINONE over DOBUTAMINE in high SVR HF?
- β’ Milrinone directly reduces the elevated afterload while increasing contractility
- β’ Dobutamine only addresses contractility, not the afterload problem
Preload vs Afterload Management
- βββ PRELOAD (Volume returning to heart) βββ
- INCREASE PRELOAD: IV fluids, blood products, Trendelenburg
- DECREASE PRELOAD: Diuretics, Venodilators (Nitroglycerin)
- MONITORED BY: CVP (right side), PAOP (left side)
- βββ AFTERLOAD (Resistance heart pumps against) βββ
- DECREASE AFTERLOAD: Arterial dilators (Nitroprusside), Milrinone, ACE inhibitors
- INCREASE AFTERLOAD: Vasopressors (Norepinephrine, Phenylephrine, Vasopressin)
- MONITORED BY: SVR (systemic), PVR (pulmonary)
- βββ KEY CONCEPT βββ
- Nitroglycerin: Primarily VENO-dilator β reduces PRELOAD (pulmonary congestion)
- Nitroprusside: ARTERIAL dilator β reduces AFTERLOAD (high BP, high SVR)
Phenylephrine Danger in Low EF Patients
- PHENYLEPHRINE = Pure Alpha-1 agonist = Potent VASOCONSTRICTION
- EFFECT: Dramatically increases SVR and Blood Pressure
- DANGER IN WEAK HEART (Low EF):
- β’ Heart must pump against MUCH greater resistance (afterload)
- β’ Already compromised ventricle cannot overcome increased SVR
- β’ May lead to cardiac decompensation, worsening cardiac output
- β’ Can precipitate acute heart failure or cardiac arrest
- SAFER ALTERNATIVES for hypotension in low EF:
- β’ Norepinephrine (has Ξ²1 to support contractility)
- β’ Dobutamine if hypotension is from pump failure
- β’ Volume if preload is low
Quick Reference: Vasoactive Selection
- βββ CLINICAL SCENARIO β DRUG CHOICE βββ
- Septic shock, first-line β NOREPINEPHRINE
- Septic shock, refractory to catecholamines β Add VASOPRESSIN
- Cardiogenic shock (pump failure) β DOBUTAMINE
- Cardiogenic shock with high SVR β MILRINONE
- Anesthesia-induced hypotension β PHENYLEPHRINE
- Cardiac arrest β EPINEPHRINE
- Anaphylaxis β EPINEPHRINE (IM 0.3-0.5mg)
- Post-cardiac surgery, low BP β NOREPINEPHRINE or VASOPRESSIN
- RV failure with pulmonary HTN β MILRINONE (reduces PVR)
Can you answer these 3 CCRN questions?
Here are 3 questions from our premium bank. The full rationale explains exactly why the right answer is right β and why the 3 distractors trap most test-takers.
Premium Practice Question
A 71-year-old arrives with dyspnea and chest pressure. Skin is cool and clammy. VS: HR 118, BP 78/44, SpOβ 92% on 4 L NC. Crackles present bilaterally. Hemodynamics: CI 1.7, CVP 18, PAOP 24, SVR 1750, SvOβ 54%. Which shock type best fits?
- Hypovolemic
- Distributive (early septic)
- Cardiogenic
- Neurogenic
Rationale: Low CI + high CVP/PAOP + high SVR + low SvOβ with pulmonary congestion is classic cardiogenic shock (pump failure with backup and compensatory vasoconstriction)....
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Premium Practice Question
A patient on an IABP reports worsening chest pain. The arterial waveform shows balloon deflation occurring after the next systolic upstroke begins, and assisted systolic pressure appears higher than expected. What is the most likely problem/effect?
- Early inflation β decreased coronary perfusion
- Late inflation β decreased diastolic augmentation
- Late deflation β increased afterload and myocardial oxygen demand
- Early deflation β improved unloading
Rationale: Late deflation means the balloon is still inflated as systole starts, which increases afterload and myocardial Oβ demandβcan worsen ischemia and hemodynamics....
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Premium Practice Question
A 63-year-old is 24 hours postβinferior MI. Suddenly develops acute respiratory distress, frothy sputum, hypotension, and a new loud holosystolic murmur at the apex. SpOβ 84% on NRB. What is the most likely cause?
- Acute pericarditis
- Papillary muscle rupture β acute severe mitral regurgitation
- Right ventricular infarct causing preload collapse
- Dressler syndrome
Rationale: Sudden pulmonary edema + shock + new holosystolic murmur post-MI strongly suggests papillary muscle rupture leading to acute severe MR (a surgical emergency)....
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