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.

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High-YieldCardiology

Pulmonary Hypertension

Mean PAP ≥ 20 mmHg at rest by right heart catheterization. WHO Group 1 (PAH) is the classic form. RV failure is the primary cause of death. Avoid volume overload and systemic vasodilators.

🔍 Overview

WHO Classification

Group	Category	Examples
1	Pulmonary Arterial HTN (PAH)	Idiopathic, heritable, CTD-associated (scleroderma), HIV, portopulmonary, drugs
2	Left heart disease	HFrEF, HFpEF, valvular disease -MOST COMMON cause of PH
3	Lung disease/hypoxia	COPD, ILD, OSA
4	CTEPH	Chronic thromboembolic PH -potentially curable with pulmonary endarterectomy
5	Multifactorial	Sarcoidosis, hematologic, metabolic

Group 2 (left heart disease) is the most common cause of PH. PAH-specific therapies are CONTRAINDICATED in Group 2 -they worsen pulmonary edema.

Hemodynamic Definitions (6th World Symposium, 2018)

Type	mPAP	PAWP	PVR	Groups
Pre-capillary PH	≥20 mmHg	≤15 mmHg	>2 WU	Groups 1, 3, 4, 5
Isolated post-capillary PH (IpcPH)	≥20 mmHg	>15 mmHg	≤2 WU	Group 2
Combined pre- and post-capillary PH (CpcPH)	≥20 mmHg	>15 mmHg	>2 WU	Group 2 (with vascular remodeling) or Group 5

Updated 2022 definition: PH is now defined as mPAP >20 mmHg (lowered from ≥25). PVR threshold for pre-capillary PH lowered from ≥3 WU to >2 WU. These changes identify patients earlier in disease progression.

Vasoreactivity Testing

Feature	Details
Who gets tested?	All patients with idiopathic, heritable, or drug-associated PAH (Group 1 only). NOT for Groups 2-5
Agents used	Inhaled nitric oxide (10-20 ppm) or IV epoprostenol or IV adenosine during RHC
Positive response	Reduction in mPAP ≥10 mmHg to reach absolute mPAP ≤40 mmHg with maintained or increased cardiac output
If positive (~10% of IPAH)	Trial of high-dose calcium channel blockers (nifedipine, diltiazem, or amlodipine). NOT verapamil (negative inotropy)
If negative	Initiate PAH-specific therapy based on risk stratification (ERA + PDE5i for most; add prostacyclin if high-risk)
Long-term CCB responders	Only ~5-7% of IPAH patients are true long-term CCB responders. Must reassess at 3-6 months

Right Heart Catheterization, Key Values to Interpret

Parameter	Normal	Abnormal (PH)	Clinical Significance
mPAP	<20 mmHg	≥20 mmHg	Defines PH. Correlates with disease severity
PAWP (PCWP)	6-12 mmHg	>15 = post-capillary	Distinguishes Group 1 (pre-capillary) from Group 2 (post-capillary)
PVR	<2 WU	>2 WU = pre-capillary component	Elevated PVR with high PAWP = combined pre/post-capillary (CpcPH)
Cardiac output/index	CI >2.5 L/min/m²	CI <2.0 = severe RV failure	Low CI is a strong predictor of mortality
RAP	0-5 mmHg	>14 = severe RV failure	Elevated RAP indicates RV failure and volume overload
SvO2	65-75%	<60% = inadequate CO	Low mixed venous sat reflects poor cardiac output

🚨 Management

General Principles

Treat underlying cause -Group 2: optimize HF. Group 3: supplemental O₂. Group 4: anticoagulation ± PTE
PAH-specific therapy -only for Group 1 (and select Group 4/5). Based on vasoreactivity testing
Avoid: excessive IV fluids (RV cannot handle volume), systemic vasodilators (worsen V/Q mismatch), high-dose diuretics (RV is preload-dependent)

PAH-Specific Drug Classes

Pathway	Drugs	Notes
Endothelin receptor antagonists	Bosentan (Tracleer), Ambrisentan (Letairis), Macitentan (Opsumit)	Check LFTs monthly (hepatotoxicity). Teratogenic.
PDE-5 inhibitors	Sildenafil (Revatio), Tadalafil (Adcirca)	↑ cGMP → pulm vasodilation. Avoid with nitrates.
Prostacyclin pathway	Epoprostenol (Flolan), Treprostinil (Remodulin), Iloprost (Ventavis)	Epoprostenol = most potent. Continuous IV infusion. Line infection risk. Never abruptly stop -rebound PH crisis.
sGC stimulator	Riociguat (Adempas)	For PAH or inoperable CTEPH. Contraindicated with PDE-5i.

Right Heart Failure Management (Acute Decompensation)

Volume management: RV is preload-sensitive BUT volume overload worsens RV dilation → septal bowing → LV impairment. Target gentle diuresis with IV furosemide. Avoid aggressive fluid boluses.
Vasopressors: Norepinephrine preferred (maintains systemic pressure without increasing PVR). Avoid phenylephrine (pure alpha = increases PVR). Consider vasopressin as adjunct.
Inotropes: Dobutamine or milrinone to augment RV contractility. Milrinone also reduces PVR (pulmonary vasodilator).
Pulmonary vasodilators: Inhaled NO or inhaled epoprostenol, reduce PVR without systemic hypotension. Avoid systemic vasodilators.
Avoid: Intubation if possible (positive pressure ventilation ↑ PVR → RV collapse). If needed, use low tidal volumes, avoid hypoxia/hypercarbia/acidosis.
Arrhythmia management: AF/flutter poorly tolerated in PH (loss of atrial kick devastating for stiff RV). Cardiovert early.

Intubating a PH patient can be fatal. Positive pressure ventilation increases RV afterload, and induction agents cause systemic hypotension → RV ischemia → cardiac arrest. If intubation is unavoidable: use ketamine (maintains SVR), push-dose epinephrine at bedside, and have inhaled NO/epoprostenol ready.

PAH-Specific Therapy, Comprehensive Table

Drug Class	Mechanism	Drugs	Route	Key Side Effects	Special Notes
Endothelin Receptor Antagonists (ERA)	Block ET-1 → reduce vasoconstriction + proliferation	Ambrisentan, Bosentan, Macitentan	PO	Hepatotoxicity (bosentan), peripheral edema, anemia	Teratogenic. Monthly LFTs for bosentan. SERAPHIN, NEJM 2013
PDE-5 Inhibitors	↑ cGMP → pulmonary vasodilation	Sildenafil, Tadalafil	PO	Headache, flushing, hypotension	Avoid with nitrates. Do NOT combine with riociguat
sGC Stimulator	↑ cGMP (NO-independent)	Riociguat	PO	Hypotension, dizziness	For PAH or inoperable CTEPH. Contraindicated with PDE-5i. PATENT-1, NEJM 2013
Prostacyclin Analogues	Vasodilation + antiproliferative + antiplatelet	Epoprostenol, Treprostinil, Iloprost	IV, SC, inhaled	Jaw pain, diarrhea, flushing, line sepsis (IV)	Epoprostenol = most potent, continuous IV. Never stop abruptly. Half-life 3-5 min
IP Receptor Agonist	Selective prostacyclin receptor agonist	Selexipag	PO	Headache, jaw pain, diarrhea, nausea	Oral alternative to parenteral prostacyclins. GRIPHON, NEJM 2015
Calcium Channel Blockers	Vasodilation (for vasoreactive patients ONLY)	Nifedipine, Diltiazem, Amlodipine	PO	Hypotension, edema, bradycardia (diltiazem)	ONLY for positive vasoreactivity test (~5-10% of IPAH). NOT verapamil

🧪 Workup

TTE -RV dilation/dysfunction, TR jet velocity, RVSP estimate, RA pressure
Right heart catheterization -diagnostic gold standard. mPAP ≥ 20 mmHg, PCWP, CO, PVR
Vasoreactivity testing -inhaled NO or IV epoprostenol during RHC. + response → trial of CCB
PFTs -exclude Group 3
V/Q scan -exclude Group 4 (CTEPH)
CT chest -parenchymal lung disease
Labs: BNP/NT-proBNP, HIV, ANA, LFTs
6-minute walk distance -functional assessment

💊 Medications

Drug	Dose	Route	Key Notes
Sildenafil (Revatio)	20 mg TID	PO	First-line oral. Avoid nitrates.
Tadalafil (Adcirca)	40 mg daily	PO	Once daily dosing advantage
Ambrisentan (Letairis)	5–10 mg daily	PO	ERA. Monthly LFTs.
Epoprostenol (Flolan)	2–16 ng/kg/min	Continuous IV	Most potent. Never stop abruptly. Half-life 3–5 min.
Riociguat (Adempas)	0.5–2.5 mg TID	PO	For PAH or CTEPH. Do not combine with PDE-5i.

📋 On Rounds

Pimp Questions

Why are PAH-specific therapies contraindicated in Group 2 PH?

Group 2 PH is caused by elevated left-sided filling pressures. PAH-specific vasodilators (prostacyclins, ERAs, PDE-5i) dilate the pulmonary vasculature → increased flow into an already congested left heart → worsening pulmonary edema and flash pulmonary edema. Treat the underlying LV dysfunction instead.

What happens if you abruptly stop epoprostenol?

Rebound PH crisis and death. Epoprostenol has a half-life of only 3–5 minutes. Abrupt cessation → acute pulmonary vasoconstriction → acute RV failure → death within minutes to hours. Patients need continuous infusion via dedicated central line. Line complications (infection, occlusion) are medical emergencies.

How do you differentiate pre-capillary from post-capillary PH?

Right heart catheterization. Pre-capillary (Groups 1,3,4,5): mPAP ≥ 20, PCWP ≤ 15, PVR ≥ 3 Wood units. Post-capillary (Group 2): mPAP ≥ 20, PCWP > 15. Combined: PCWP > 15 AND PVR ≥ 3 (out-of-proportion PH).

What defines a positive vasoreactivity test and who should get it?

Vasoreactivity testing is performed only in idiopathic, heritable, or drug-associated PAH (Group 1). NOT for other groups. Agents: inhaled NO, IV epoprostenol, or IV adenosine during RHC. Positive response: fall in mPAP ≥10 mmHg to absolute mPAP ≤40 mmHg with maintained or increased cardiac output. Only ~10% of IPAH patients are vasoreactive, and only ~5-7% are true long-term CCB responders.

Why is intubation dangerous in pulmonary hypertension?

Intubation in PH is extremely high-risk for several reasons: (1) Positive pressure ventilation increases RV afterload (increases intrathoracic pressure → compresses pulmonary vasculature). (2) Induction agents cause systemic hypotension → decreased RV coronary perfusion → RV ischemia. (3) Hypoxia, hypercarbia, and acidosis all increase PVR. The result is acute RV failure and PEA arrest.

How do you manage volume status in acute RV failure from PH?

The RV is preload-dependent but volume-intolerant. Excess volume → RV dilation → interventricular septum bows into LV → decreased LV filling → decreased cardiac output (ventricular interdependence). Management: gentle diuresis with IV furosemide (goal net negative 0.5-1L/day). Avoid aggressive fluid boluses. If hypotensive, use vasopressors (norepinephrine preferred) rather than fluids.

What is CTEPH and why is it important to diagnose?

Chronic thromboembolic pulmonary hypertension (CTEPH, Group 4) occurs when organized thrombus persists in pulmonary arteries after PE, causing mechanical obstruction + vascular remodeling. Incidence: 2-4% after acute PE. It is the only potentially curable form of PH. Screen with V/Q scan (NOT CT angiography, CTA can miss chronic disease). Treatment: pulmonary endarterectomy (PTE) at experienced centers is potentially curative.

What is the initial combination therapy approach for newly diagnosed PAH?

Based on AMBITION Trial, NEJM 2015, upfront dual combination therapy (ERA + PDE-5i) is now standard for most newly diagnosed PAH patients. The trial showed ambrisentan + tadalafil reduced clinical failure events by 50% compared to monotherapy. Risk stratification guides further escalation: low-risk patients may start with oral combination; intermediate/high-risk patients should receive triple therapy including parenteral prostacyclin.

Clinical Examples

📋 Case 1, Group 1 PAH Workup in Young Woman with Scleroderma

Patient: 38F with limited systemic sclerosis (CREST) presents with progressive exertional dyspnea over 6 months. Now WHO FC III (dyspnea with minimal activity). No orthopnea or PND. 6MWD: 310 meters (reduced). SpO2 drops to 88% with walking.

Workup:

TTE: RV dilation with moderate dysfunction, RVSP 68 mmHg, moderate TR, RA enlarged, TAPSE 14mm (reduced), small pericardial effusion. LV normal. No valvular disease.
Labs: BNP 480, ANA 1:640 (centromere pattern), anti-Scl-70 negative. HIV negative. Normal PFTs (no restrictive disease).
V/Q scan: Normal perfusion (excludes CTEPH).
RHC: mPAP 48 mmHg, PAWP 12 mmHg, PVR 8.5 WU, CI 2.1 L/min/m², RAP 12 mmHg, SvO2 58%.
Vasoreactivity testing: Not performed (CTD-associated PAH, not idiopathic, vasoreactivity testing only for IPAH/heritable/drug-associated).

Assessment: Group 1 PAH (CTD-associated, scleroderma). Pre-capillary PH confirmed (mPAP 48, PAWP 12, PVR 8.5). High-risk features: WHO FC III, low CI, low SvO2, elevated RAP, pericardial effusion.

Management:

Upfront triple therapy: Ambrisentan 5mg PO daily + tadalafil 40mg PO daily + IV treprostinil (started in ICU, titrated up).
Supportive: Supplemental O2 to maintain SpO2 >90%, gentle diuresis for fluid overload, anticoagulation (patient-specific decision in CTD-PAH).
Follow-up: 3-month reassessment: 6MWD improved to 385m, BNP decreased to 180, WHO FC II. Continued current regimen.

Key lesson: Scleroderma-associated PAH requires systematic workup. RHC is mandatory for diagnosis. Vasoreactivity testing is NOT done for CTD-PAH. High-risk patients warrant upfront triple therapy including parenteral prostacyclin per AMBITION Trial, NEJM 2015 principles.

📋 Case 2, Group 2 PH from Left Heart Disease

Patient: 72M with HFpEF (EF 55%), HTN, DM2, BMI 38, and OSA presents with worsening exertional dyspnea and lower extremity edema. Referred for "pulmonary hypertension" after TTE showed elevated RVSP.

Workup:

TTE: EF 55%, grade II diastolic dysfunction (E/e' 18), LA dilated, RVSP 55 mmHg, mild RV dilation, moderate TR.
Labs: BNP 320, Cr 1.4, HbA1c 7.8.
RHC: mPAP 38 mmHg, PAWP 22 mmHg, PVR 2.8 WU, CI 2.4 L/min/m².

Assessment: Combined pre- and post-capillary PH (CpcPH), Group 2. PAWP 22 (>15) confirms post-capillary component. PVR 2.8 (>2 WU) indicates additional pre-capillary vascular remodeling.

Management:

Treat the underlying cause: Aggressive diuresis (IV furosemide 40mg → net negative 1-1.5L/day), sodium restriction, CPAP for OSA.
HFpEF optimization: SGLT2 inhibitor started (EMPEROR-Preserved, NEJM 2021), MRA, BP control.
PAH-specific therapy: NOT initiated. PAH drugs (ERAs, PDE-5i, prostacyclins) are contraindicated in Group 2 PH, they increase pulmonary blood flow into an already volume-overloaded left heart → worsening pulmonary edema.
After optimization: Repeat TTE in 3 months showed RVSP decreased to 38 mmHg with euvolemia. RV function improved.

Key lesson: Always check PAWP before starting PAH therapies. Group 2 PH is treated by optimizing the underlying left heart disease, NOT with PAH-specific drugs. CpcPH (high PAWP + high PVR) is increasingly recognized but treatment remains focused on decongestion and LHD optimization.

📋 Case 3, Acute RV Failure from Pulmonary Hypertension

Patient: 45F with known idiopathic PAH on IV epoprostenol (via Hickman catheter), ambrisentan, and tadalafil. Presents with 3 days of worsening dyspnea, abdominal distension, and lower extremity edema. Found to have Hickman line exit site erythema. T 38.9°C, HR 120, BP 84/52, SpO2 85% on 4L NC.

Labs: BNP 2,400 (baseline ~400), lactate 3.8, WBC 18k, blood cultures drawn. Cr 1.8 (baseline 0.9).

Assessment: Acute RV failure from PAH, triggered by line infection (sepsis increases PVR) + possible subtherapeutic epoprostenol delivery (line dysfunction).

Management:

Critical: Do NOT stop epoprostenol. Verify pump function and line patency immediately. Increase epoprostenol dose by 2 ng/kg/min.
Hemodynamic support: Norepinephrine for MAP >65 (maintains coronary perfusion). Avoid fluid boluses, RV is already volume-overloaded.
Inhaled pulmonary vasodilator: Inhaled NO 20 ppm started via high-flow nasal cannula (reduce RV afterload without systemic hypotension).
Diuresis: Furosemide 80mg IV bolus then 20mg/hr drip (goal 1-2L net negative/day). Monitor urine output closely.
Infection: Vancomycin + cefepime empirically for line infection. IR consulted for line exchange over wire (cannot remove, need continuous epoprostenol access).
Avoid intubation: Managed with high-flow nasal cannula at 50L/min, FiO2 60%. SpO2 improved to 92%.
Outcome: Blood cultures grew MSSA. Antibiotics narrowed. RV function improved over 72h with diuresis and infection control. Hickman exchanged on day 4. Discharged on day 10 back to baseline.

Key lesson: Acute RV failure in PAH is a medical emergency. Identify and treat the trigger (infection, non-adherence, arrhythmia). NEVER stop epoprostenol. Avoid intubation and fluid boluses. Use norepinephrine (not phenylephrine) for systemic pressure, inhaled vasodilators for PVR reduction, and careful diuresis.

⚡ Summary

Definition

mPAP ≥ 20 mmHg by RHC. Group 2 (left heart disease) is most common overall.

Diagnosis

RHC is gold standard. TTE screens. V/Q scan for CTEPH. Vasoreactivity testing for CCB trial.

Group 1 Therapy

ERAs + PDE-5i ± prostacyclins. Combination therapy based on risk stratification.

Key Avoid

PAH drugs in Group 2 (worsens edema). Never stop epoprostenol abruptly (rebound crisis).

RV Management

Avoid volume overload. Careful diuresis. Maintain preload. Avoid systemic vasodilators.

Monitoring

6MWD, BNP, echo, WHO functional class. LFTs monthly on ERAs.