When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

Vasopressors & Inotropes -Dosing Guide -RoundsRx

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Inotropes ≠ vasopressors. Vasopressors increase SVR (squeeze vessels). Inotropes increase contractility (squeeze heart). Some agents do both. Picking the wrong one kills patients -a patient in cardiogenic shock who gets phenylephrine (pure vasoconstrictor, no inotropy) will get worse.

When to Use Inotropes

Clinical Scenario	Hemodynamic Profile	Agent of Choice
Cardiogenic shock (acute MI, decompensated HFrEF)	↓ CO, ↑ SVR, ↓ MAP, cold extremities, poor cap refill	Dobutamine (if BP adequate) or milrinone (if RV failure / pulm HTN). Add norepinephrine if MAP < 65.
Septic shock with cardiac dysfunction	↓ CO despite adequate MAP on NE, poor ScvO₂ (< 70%), elevated lactate despite fluids + pressors	Dobutamine added to norepinephrine. Or epinephrine (provides both inotropy + vasopressor). SSC, 2021
Acute RV failure (massive PE, pulm HTN crisis, RV infarct)	↓ CO, ↑ CVP/JVP, ↑ PVR, RV dilation on echo, septal bowing	Milrinone (↓ PVR + inotropy) or dobutamine. Add inhaled epoprostenol/iNO for selective pulmonary vasodilation. Avoid volume loading -worsens RV dilation.
Post-cardiac surgery (low CO syndrome)	↓ CO post-CPB, stunned myocardium	Milrinone (preferred -↓ afterload helps stunned heart, ↓ PVR). Or dobutamine. Epinephrine if hemodynamically significant.
Bridge to LVAD / transplant	End-stage HFrEF failing oral meds, awaiting mechanical support	Milrinone (continuous infusion, can use outpatient via PICC). Or dobutamine.
ADHF -"warm and wet" needing diuresis	Low CO limiting diuretic response, adequate BP	Low-dose dobutamine (2–5 mcg/kg/min) to augment renal perfusion for diuresis. Short-term only.

Inotrope Comparison

Agent (Brand)	Mechanism	Dose	Hemodynamic Effect	Best For	Watch Out
Dobutamine (Dobutrex) 1ST LINE	β₁ > β₂ agonist	2–20 mcg/kg/min IV	↑ CO, ↑ HR, mild ↓ SVR (β₂ vasodilation). Net MAP may be unchanged or slightly ↓.	First-line inotrope in most cardiogenic shock (if MAP adequate). Septic shock with cardiac dysfunction. Augments diuresis in acute HF.	Never use alone if MAP < 65 -can drop BP via β₂ vasodilation. Always pair with NE if hypotensive. Tachycardia dose-limiting. Arrhythmogenic (↑ O₂ demand). Tachyphylaxis after 72h (downregulation of β-receptors).
Milrinone (Primacor) 1ST LINE	PDE3 inhibitor (↑ cAMP)	0.125–0.75 mcg/kg/min IV (skip loading dose in ICU -causes hypotension)	↑ CO, ↓ SVR, ↓ PVR. "Inodilator" -inotropy + vasodilation. Better lusitropy (diastolic relaxation) than dobutamine.	RV failure / pulmonary HTN (↓ PVR is key advantage). Post-cardiac surgery. Bridge to LVAD/transplant. Works when β-receptors are downregulated (chronic HF on BB) -bypasses β-receptor.	Hypotension (vasodilation) -more than dobutamine. Renally cleared -dose-adjust in AKI/CKD. Thrombocytopenia (rare). Longer half-life (2–3h) -effects persist after stopping. Do NOT give loading dose in ICU (severe hypotension).
Epinephrine (Adrenalin) 2ND LINE	α₁ + β₁ + β₂ agonist	Low dose: 0.01–0.1 mcg/kg/min (β₁/β₂ dominant → inotropy + vasodilation) High dose: 0.1–0.5 mcg/kg/min (α₁ dominant → vasoconstriction + inotropy)	↑ CO, ↑ HR, dose-dependent SVR. Low dose = inotrope. High dose = inopressor.	Refractory cardiogenic shock (need both inotropy + pressor). Cardiac arrest. Post-arrest low CO. Anaphylaxis.	Falsely elevates lactate (β₂-mediated aerobic glycolysis) -cannot use lactate to guide resuscitation. Arrhythmogenic. ↑ myocardial O₂ demand. Hyperglycemia. Mesenteric ischemia at high doses.
Dopamine (Intropin) AVOID	Dose-dependent: D₁ (low) → β₁ (mid) → α₁ (high)	"Renal dose" 1–3 → "cardiac" 3–10 → "pressor" 10–20 mcg/kg/min	Variable. Unpredictable hemodynamics.	Avoid. Inferior to NE in shock SOAP II, 2010. Only remaining role: symptomatic bradycardia if no pacing.	More arrhythmias and higher mortality vs NE. "Renal-dose dopamine" is a myth -no renal protection Bellomo, 2000. Unpredictable dose-response. Avoid in ICU.
Levosimendan (Simdax) SPECIALIZED	Calcium sensitizer + K-ATP channel opener	0.05–0.2 mcg/kg/min IV × 24h	↑ CO, ↓ SVR, ↓ PVR. Inotropy without ↑ O₂ demand (unique). Active metabolite lasts 7–9 days.	Decompensated HF (Europe -not FDA-approved in US). Post-cardiac surgery. Bridge. Does not increase myocardial O₂ demand (unlike all other inotropes).	Not available in the US. Hypotension. Effect lasts days after stopping (long-acting metabolite). Limited data vs milrinone.
Isoproterenol (Isuprel) SPECIALIZED	Pure β₁ + β₂ agonist (no α)	2–20 mcg/min IV	↑ HR, ↑ CO, ↓ SVR. Potent chronotrope.	Symptomatic bradycardia (bridge to pacing). Torsades de Pointes (↑ HR shortens QT). Beta-blocker overdose. Post-heart transplant (denervated heart -atropine doesn't work).	Severe hypotension (↓ SVR via β₂). Massively increases myocardial O₂ demand. Arrhythmogenic. Never use in ischemia.
Digoxin (Lanoxin) ADJUNCT	Na⁺/K⁺-ATPase inhibitor → ↑ intracellular Ca²⁺	0.125–0.25 mg PO/IV daily Load: 0.25–0.5 mg IV	Mild ↑ CO, ↓ HR (vagotonic). Weak inotrope compared to IV agents.	Chronic HFrEF with persistent symptoms on GDMT. Afib rate control adjunct (especially HFrEF). DIG, 1997: reduced HF hospitalizations, no mortality benefit.	Narrow therapeutic window (target 0.5–0.9 ng/mL). Toxicity: any arrhythmia -classically "regularized Afib" (junctional rhythm), bigeminy, bidirectional VT. Hypokalemia potentiates toxicity. Renally cleared -dose-adjust. Reversal: digoxin-specific Fab (DigiFab).

Inotrope vs Vasopressor -Know the Difference

Feature	Inotrope	Vasopressor	Inopressor (Both)
Primary effect	↑ Contractility (↑ CO)	↑ SVR (↑ MAP)	↑ CO + ↑ SVR
Main receptor	β₁, PDE3	α₁, V1	α₁ + β₁
Examples	Dobutamine, milrinone	Phenylephrine, vasopressin	Norepinephrine, epinephrine
Effect on SVR	↓ or neutral	↑↑	↑
Use when	CO is low, MAP is OK	MAP is low, CO is OK	Both MAP and CO are low
Cardiogenic shock	Yes (primary)	Only as adjunct for MAP	NE is first-line pressor in CS
Septic shock	Add if ↓ CO despite MAP-targeted NE	NE is first-line	Epi if refractory

Decision Flowchart

Is MAP < 65? → Start norepinephrine first (inopressor). You need MAP before you add a pure inotrope.

MAP adequate but CO is low? (cold extremities, poor cap refill, ↑ lactate, low ScvO₂) → Add dobutamine (first-line inotrope).

RV failure or pulmonary HTN? → Milrinone preferred (↓ PVR). Consider inhaled epoprostenol or iNO for selective pulmonary vasodilation.

Patient on chronic beta-blocker? → β-receptors are downregulated. Milrinone works better than dobutamine (PDE3 pathway bypasses β-receptor).

Need both inotropy + vasopressor? → Epinephrine (inopressor). Or NE + dobutamine as separate drips (more titratable).

Refractory to all above? → Mechanical circulatory support: IABP, Impella, ECMO. Call your interventional cardiology / cardiac surgery team early.

Key Pearls

All inotropes increase myocardial O₂ demand (except levosimendan). In ischemic cardiogenic shock, this is a double-edged sword -you're helping the pump but potentially worsening the ischemia. Keep doses as low as effective.

"Renal-dose dopamine" is a myth. Bellomo, 2000: no renal protection. SOAP II, 2010: more arrhythmias + higher mortality than NE. There is no role for dopamine as an inotrope in modern ICU care.

Dobutamine tachyphylaxis occurs after ~72h due to β₁-receptor downregulation. If the patient stops responding, switch to milrinone (PDE3 pathway) or add mechanical support.

Milrinone has a 2–3h half-life. If the patient drops their BP on milrinone, the effect persists for hours after stopping -unlike dobutamine (t½ ~2 min). Plan accordingly. Also: renally cleared -dose-reduce in AKI.

Epinephrine falsely elevates lactate via β₂-mediated aerobic glycolysis. If you're running epi for inotropy, you cannot use lactate clearance to assess resuscitation adequacy. Use ScvO₂, echo, or CI instead.

Digoxin toxicity = "any arrhythmia." Classic: regularized afib, bigeminy, bidirectional VT. Hypokalemia potentiates it. Always check K⁺ with dig level. Reversal: DigiFab (digoxin-specific Fab fragments).