In this episode of Hospital Medicine Unplugged, we sprint through atrial flutter—spot the sawtooth, choose the fastest safe path to sinus, and keep strokes off the table.

We open with the do-firsts: confirm the rhythm and triage the “why.” Grab a 12-lead ECG—regular narrow tachycardia with classic sawtooth F-waves (atrial ~240–300 bpm, often 2:1 AV → ~150 bpm). Don’t confuse variable conduction with AF. Put the patient on telemetry; replete K/Mg (K ≥4, Mg ≥2). Hunt triggers (infection, hypoxia, decomp HF, stimulants, post-op). Get an echo to size up structure/valves; plan TEE if cardioversion and duration ≥48 h or unknown.

Acute decisions—match stability to action:

Anticoagulation—same rules as AF: use CHA₂DS₂-VASc for long-term decisions. If duration ≥48 h or unknown, choose ≥3 weeks of therapeutic anticoagulation or TEE-guided cardioversion, and continue OAC ≥4 weeks post-cardioversion. Many hospitalized adults meet OAC criteria—don’t skip stroke prevention.

When to favor rhythm early: persistent rapid rates despite meds, ischemia/HF, poor tolerance, or procedural timing needs. A quick shock back to sinus simplifies everything.

Think definitive: CTI ablation for typical (isthmus-dependent) flutter is >90–95% effective with low risk—strong option after a first significant hospitalization or if recurrent. Expect incident AF (~50%) after flutter—monitor and keep OAC per risk, not just rhythm appearance.

ICU/complex plays: in decompensated HF or shock, cardiovert early; if meds needed, amiodarone is often the hemodynamically friendliest for rate control. Correct hypoxemia, fever, and volume—they’re gasoline on the circuit.

Special populations, quick hits:

Procedure pearls (make it boring-safe): Anterior–posterior pad placement, sedation ready, sync ON, start low energy (flutter needs less than AF), and re-check rhythm + anticoagulation plan before leaving the bedside.

We close with the system moves: an atrial-flutter bundle that (1) auto-flags sawtooth at ~150 bpm and fires a cardioversion pathway for instability; (2) hard-stops electrolytes to K ≥4/Mg ≥2; (3) blocks NDHP-CCBs in HFrEF and blocks AV-nodal agents if pre-excitation seen; (4) offers ibutilide with QT/Mg guardrails and dofetilide inpatient-initiation checklist; (5) forces TEE-or-≥3-weeks-OAC when duration ≥48 h/unknown, and locks in ≥4 weeks post-CV OAC; (6) auto-consults EP for CTI ablation after first significant admission or recurrence; (7) adds AF-surveillance plan (patch/tele) and leaves OAC tied to CHA₂DS₂-VASc, not wishful thinking.

Fast, ECG-led, and stroke-savvy—see the sawtooth, fix the rate or flip the rhythm, and never miss the anticoagulation.

In this episode of Hospital Medicine Unplugged, we blitz inpatient atrial fibrillation (AF)—fix the trigger, pick rate vs rhythm, and prevent stroke—so you can move fast and safely.

We open with the do-firsts: vitals + hemodynamics, bedside ECG, labs (electrolytes, Mg, CBC, TSH when relevant), pulse oximetry/ABG, and a deliberate hunt for reversible triggers—infection, hypoxia, electrolyte derangements, volume shifts, ACS/PE, surgery, alcohol/withdrawal, stimulants. Treat the cause; the rhythm often follows.

Unstable? (hypotension, shock, ischemia, pulmonary edema) → immediate synchronized DCCV. While prepping: oxygen, gentle fluids/pressors as needed, avoid AV-nodal blockers if WPW suspected.

Stable? Rate or rhythm are both reasonable.

Cardioversion anticoagulation rules (no preexcitation/WPW):

Stroke prevention—don’t miss it. Use CHA₂DS₂-VASc to guide therapy; check HAS-BLED to modifiable risks—not to deny needed OAC. Prefer DOACs over warfarin for most nonvalvular AF (dose-adjust for renal function). Warfarin for mechanical valves or moderate–severe mitral stenosis. In sepsis, avoid routine acute anticoagulation (↑bleeding, no stroke benefit). LAAO is a niche option when long-term OAC is truly not possible.

Post-op AF (CABG/valve): β-blockers first; rhythm control (amiodarone or DCCV) if poorly tolerated; consider OAC for ~6–8 weeks if bleeding risk acceptable, then reassess.

We close with the hospital bundle that sticks:

Screen & treat triggers (sepsis, hypoxia, electrolytes, ACS/PE, meds).

Default to rate control (β-blocker or diltiazem; digoxin add-on) with HR <110 unless symptomatic.

Escalate to rhythm control for symptoms, HF, or failure of rate—DCCV early; pick AA drug by substrate; consider ablation in HFrEF or recurrent.

Anticoagulation pathway: DOAC-first, valve disease exceptions; TEE vs 3-week rule before cardioversion; ≥4 weeks after.

Monitoring: telemetry, daily K/Mg goals (K ≥4.0, Mg ≥2.0), watch QT/AV block, drug-drug interactions.

Risk-factor remix: weight loss, BP control, OSA treatment (CPAP), diabetes optimization, alcohol moderation, exercise, smoking cessation—these cut AF burden and recurrences.

Discharge plan: clear OAC plan, rate/rhythm meds with doses, red-flags, follow-up ECG/Holter, renal/hepatic labs for drug safety, and referral to AF clinic when available.

Bottom line: Treat the trigger, stabilize the rate, choose rhythm wisely, and anticoagulate by risk. Build a system that’s fast, safe, and recurrence-proof—so your patients leave in rhythm (or with a controlled rate) and a plan that lasts.

In this episode of Hospital Medicine Unplugged, we sprint through hepatorenal syndrome–AKI (HRS-AKI)—exclude look-alikes fast, start albumin + vasoconstrictor early, watch the lungs, and loop in transplant.

We open with the do-firsts: clinical diagnosis by exclusion—rule out hypovolemia, nephrotoxins, structural kidney disease. Pull diuretics/ACEi/NSAIDs, check UA/sediment (should be bland), kidney US (should look normal), and hunt triggers (SBP, GI bleed, overdiuresis). Albumin challenge (≈1 g/kg/day, max 100 g for 24–48 h): no renal improvement → HRS-AKI. Urine biomarkers (e.g., NGAL) may help ATN vs HRS but aren’t ready for routine.

Call AKI early using ICA criteria: ↑Cr ≥0.3 mg/dL/48 h or ≥1.5× baseline/7 d and/or low urine output. Don’t chase urine Na/FeNa alone (diuretics confound). Treat the precipitant (especially SBP: antibiotics + albumin).

Treatment—build the hemodynamic fix:

Special plays & edge cases:

Monitoring that matters:

Medication pitfalls you don’t want to meet:

We close with the HRS bundle that sticks: (1) Exclude hypovolemia/nephrotoxins/structural disease fast; (2) Albumin challenge (24–48 h) → if no improvement, start vasoconstrictor + albumin; (3) Prefer terlipressin, use norepinephrine in ICU/shock or contraindications; (4) Hard stop/check at day 4 for response; (5) Prevent/ treat SBP (antibiotics + albumin); (6) Protect the lungs—watch SpO₂, CXR/POCUS, adjust albumin; (7) Early transplant activation ± RRT as bridge; (8) Multidisciplinary liver–kidney–ICU collaboration.

Bottom line: HRS-AKI is a race against time—diagnose by exclusion, pair albumin with the right vasoconstrictor, watch for respiratory hits, and escalate to transplant pathways early.

In this episode of Hospital Medicine Unplugged, we blitz cardiorenal syndrome (CRS)—define fast, subtype smart, decongest early, protect kidneys, and tighten the cardio–nephro handshake.

We start with the frame: CRS = bidirectional heart–kidney dysfunction where trouble in one organ triggers or worsens the other. Know the five plays: Type 1 (acute cardiorenal), Type 2 (chronic cardiorenal), Type 3 (acute renocardiac), Type 4 (chronic renocardiac), Type 5 (secondary/systemic). Classification isn’t trivia—it drives workup and therapy.

Pathophys in one breath: venous congestion > low forward flow; RAAS/SNS surge, vasopressin, inflammation & endothelial dysfunction; sodium avidity → diuretic resistance. CKD stacks the deck toward higher mortality and rehospitalization.

Bedside diagnosis—do-firsts and don’t-miss:

Risk & admit cues: refractory hypoxemia, rising JVP/edema, oliguria, shock/low MAP, refractory hyperK/acidosis, suspected Type 1 or 3 CRS, or diagnostic uncertainty.

Treatment—make decongestion the north star:

Monitoring that matters:

Etiology threads—treat the cause:

Pitfalls to dodge: underdosing loops, stopping diuresis for mild Cr rise, ignoring RV failure/venous hypertension, delayed escalation to combo diuretics/UF, and premature RAAS/SGLT2 withdrawal without a clear reason.

We close with the hospital CRS bundle that sticks:

Classify type (1–5) and rule intrinsic kidney disease (UA/sediment, albuminuria, renal US).

Default to loop + natriuresis-guided titration; add thiazide-type early for resistance; consider MRA.

Track congestion multimodally (exam + weights + VeXUS ± TTE).

Guard rails: daily labs, K/Mg repletion, renal & hemodynamic checks.

RAAS/SGLT2 smart use—continue/initiate when safe; hold for hypotension, hyperK, true AKI.

Escalation pathway: UF/RRT for refractory overload or life-threatening derangements; CRT/MCS in select HF.

Team sport: cardiology + nephrology + ICU/pharmacy from day one; discharge with diuretic plan, labs, and early follow-up.

Bottom line: Congestion kills kidneys—decongest completely, use RAAS/SGLT2 wisely, monitor like a hawk, and move fast together.

In this episode of Hospital Medicine Unplugged, we cut through the Mallory-Weiss tear—spot it fast, stop the bleed, stabilize smart, and endoscope right.

We open with the why and who: a longitudinal mucosal laceration at the gastroesophageal junction, triggered by vomiting, retching, or sudden pressure surges. Alcohol, reflux esophagitis, hiatal hernia, NSAIDs, coagulopathy, and liver disease stack the odds. It’s uncommon but not benign—~7.5/100,000 hospitalized patients, with a small but high-risk subset landing in the ICU.

Presentation pearls: classic sequence—retching then hematemesis—appears in <1/3 of cases. Hematochezia or shock = severe bleed. Keep an eye on cirrhotics, dialysis patients, and the elderly—they hide blood loss until they crash.

Diagnosis: stabilize first, scope early. EGD within 24 hours confirms the tear and rules out ulcers, varices, or Dieulafoy’s lesion. Imaging? Rarely needed unless endoscopy fails or perforation’s on the table.

Stabilization priorities:

Endoscopic game plan—mechanical first:

Medical and supportive backbone:

Special populations:

Complications: bleeding anemia (26%), shock (3%), AKI, sepsis, and rare death (~2–3%). Rebleeding 2–12%, mostly in coagulopathic or cirrhotic patients.

Prevention & long game:

We close with the system moves:

Fast scope, tight stabilization, and mechanical mastery—that’s how you keep Mallory-Weiss tears from turning catastrophic.

In this episode of Hospital Medicine Unplugged, we tackle portal hypertension in hospitalized cirrhosis—find it fast, control bleeding, dry the belly, clear the brain, and pick the right patients for TIPS and transplant.

We open with the diagnosis play: suspect it in cirrhosis with splenomegaly/ascites/varices. Gold standard is HVPG; CSPH = ≥10 mmHg. In real life, lean on liver stiffness + platelets for risk (rule-in ≥25 kPa or rule-out <20 kPa with high platelets), and confirm with varices on endoscopy or collaterals on imaging.

When blood hits the basin—acute variceal bleed—move fast:

Between bleeds, prevent the next one:

Ascites management that sticks:

Encephalopathy, SBP, and kidneys:

Imaging & surveillance you shouldn’t skip:

Who gets a shunt (and who doesn’t):

Medication & system pitfalls:

We close with the big picture: portal hypertension is the engine of decompensation—catch it, treat bleeds aggressively, use NSBBs/banding wisely, control ascites, and pull the TIPS lever early in the patients who benefit. And never forget the destination for many: timely transplant evaluation once major-index complications appear.

In this episode of Hospital Medicine Unplugged, we blitz acute peptic ulcer bleeding—risk fast, resuscitate right, scope within 24 hours, secure hemostasis, run high-dose PPIs, and crush recurrence.

We open with the do-firsts: airway/breathing/circulation, 2 large-bore IVs, orthostatics, urine output, type & cross, and labs (CBC, BMP, INR/LFTs). Risk-stratify with Glasgow–Blatchford (GBS)—≤1 may go outpatient; everyone else is inpatient/urgent care.

Resuscitation that matters: balanced crystalloids, permissive targets while bleeding, and a restrictive transfusion strategy (Hb <7–8 g/dL; <10 g/dL if active CAD). Correct coagulopathy pragmatically; reverse only when it changes decisions.

Pre-endoscopic moves: start IV PPI immediately, consider IV erythromycin 250 mg 30–60 min pre-EGD to clear the field. No tranexamic acid. If cirrhosis/portal hypertension is on the table: prophylactic antibiotics + vasoactive therapy.

Endoscopy: within 24 hours after stabilization; sooner if unstable once perfusing. Treat high-risk stigmata (Forrest Ia/Ib/IIa/IIb):

Post-EGD pharmacotherapy—build the acid-suppression backbone:

Monitoring & rebleeding: watch vitals q2–4h, H/H q6–12h for 24–48h, and the stool/NG story. Rebleed? → repeat endoscopy first. If failure or early re-rebleed, transcatheter arterial embolization; surgery if IR/EGD fail.

Etiology plays—prevent the encore:

Antithrombotics without fear:

Nutrition, level of care, disposition: early feeding after control is safe and shortens LOS. Step-down/ICU for major stigmata or instability (first 24 h). Low-risk ulcers can go home early with clear return precautions and a PPI plan.

Medication pitfalls you don’t want to meet: epinephrine monotherapy (never), under-dosed PPIs, premature endoscopy before resuscitation, and stopping secondary-prevention aspirin without a plan.

We close with the systems bundle that sticks:

Triage with GBS + ABCs + IV PPI ± erythromycin;

EGD ≤24 h with dual-modality for high-risk stigmata; OTSC/powders for select cases;

72-hour high-dose PPI (infusion or BID—equivalent), then tailored step-down;

Rebleed pathway: repeat EGD → IR embolization → surgery if needed;

Etiology track: test/treat/confirm H. pylori, NSAID strategy, idiopathic high-dose PPI;

Antithrombotic game-plan: early aspirin for secondary prevention, timely anticoagulant resumption;

Early enteral nutrition, targeted monitoring, and clear discharge instructions.

Fast, hemostasis-focused, and recurrence-proof—stabilize, scope, suppress acid, fix the cause, and never miss a rebleed.

In this episode of Hospital Medicine Unplugged, we take on acute peptic ulcer bleeding (PUB)—triage fast, stabilize smart, scope early, seal the vessel, and lock in acid suppression + secondary prevention.

We start at the door with risk stratification: use the Glasgow–Blatchford Score (GBS)—≤1 means very-low risk and potential outpatient management; everyone else gets admitted and prepped for urgent endoscopy. Pull CBC, chemistries, INR, type & cross.

Resuscitation that helps, not harms: large-bore IVs, balanced crystalloids, and a restrictive transfusion strategy—transfuse at Hgb <7–8 g/dL (consider <10 g/dL in active coronary disease). Aim for hemodynamic stability before the scope. Early enteral feeding once controlled shortens LOS.

Pre-endoscopic moves: start IV PPI immediately; give IV erythromycin pre-scope to clear the stomach (better visualization). Skip tranexamic acid. If the patient has cirrhosis, flip to the variceal bundle (antibiotics + vasoactive agents) while you clarify source.

Endoscopy timing & targets: perform within 24 hours (earlier only after stabilization in the unstable). Treat high-risk stigmata—active bleeding, non-bleeding visible vessel, adherent clot. Use dual-modality therapy (epi injection + thermal or clips) as your default. Deploy OTSC or hemostatic powder for difficult lesions or poor visualization. Clean base/flat spots? No therapy; plan early discharge.

Post-endoscopic pharmacotherapy (the acid wall): run high-dose PPI for 72 hours—either 80 mg IV bolus → 8 mg/h infusion or intermittent high-dose IV/PO (equally effective). Then step down: once-daily PPI for most; BID for 10–14 days in high-risk, then daily 2–4 weeks.

Monitoring & rebleeding rescue: watch closest in the first 72 hours—vitals, H/H every 6–12h, stool color, symptoms. Suspect rebleed? Resuscitate → repeat endoscopy (works ~75%). If bleeding persists, escalate to transcatheter arterial embolization (TAE); surgery if IR/endoscopy fail.

Etiology matters (prevent the sequel):

Antithrombotics without chaos: hold during active bleed, but restart early after hemostasis to avoid thrombotic events—continue/restart aspirin for secondary prevention and reintroduce anticoagulants promptly based on thrombotic risk (multidisciplinary call). Use PCC/vitamin K or specific DOAC reversal only for life-threatening bleeds.

Discharge playbook:

Bottom line: assess risk fast, resuscitate right, endoscope within 24h, use dual-modality hemostasis, and run high-dose PPI for 72h. Then fix the cause (H. pylori, NSAIDs, antithrombotics) to prevent the rematch.

In this episode of Hospital Medicine Unplugged, we blitz acute diverticulitis—spot it early, stage it right, treat what matters, and prevent the encore.

We open with the why: ~200,000 US admissions/year and >$6.3B in costs. Risk stacks with age >65, obesity, NSAIDs/steroids/opioids, HTN/DM2, connective-tissue disease, and genetics. Patients roll in with LLQ pain, fever, leukocytosis, N/V.

Do-firsts in the ED/ward: IV access, analgesia (acetaminophen first; minimize opioids; avoid routine NSAIDs), antiemetics, IV fluids, and labs (CBC, BMP, UA, CRP). CT A/P with IV contrast is the diagnostic gold standard—~99–100% sensitivity/specificity—to confirm diverticulitis and flag complications.

Call the type:

Who needs a bed? Admit for complicated disease, high fever (>38.5°C), marked leukocytosis, can’t tolerate PO, immunosuppression, serious comorbidity, or no home support. Outpatient is reasonable for low-risk, imaging-confirmed uncomplicated cases with reliable follow-up.

Treatment—build the supportive core:

If the core buckles—manage complicated disease:

Special populations you won’t want to miss:

Complication radar: abscess/phlegmon, perforation/peritonitis, fistula (look for pneumaturia/fecaluria), obstruction/stricture, bleeding, sepsis/AKI. Risk rises with CRP >140 mg/L, WBC >15 ×10⁹/L, extraluminal air/fluid on CT, long inflamed segment, and major comorbidity.

Colonoscopy after the dust settles:

Secondary prevention that sticks:

We close with the diverticulitis bundle: (1) confirm with contrast CT; (2) supportive care first (fluids, pain control, diet advance); (3) selective antibiotics—don’t overuse; (4) drain abscess ≥3 cm; (5) call surgery for peritonitis/obstruction/failed nonop care; (6) reassess at 48–72 h, re-image if stalled; (7) plan post-acute colonoscopy (complicated: 6–8 weeks); (8) lock in lifestyle prevention.

Imaging-led, selective with antibiotics, decisive with source control—treat what’s complicated, spare what isn’t, and keep patients out of the readmit loop.

In this episode of Hospital Medicine Unplugged, we dive into acute variceal bleeding—a high-stakes emergency in cirrhotic patients where seconds count and outcomes hinge on rapid, coordinated care.

We start with the crash course in recognition and stabilization: ICU-level monitoring, two large-bore IVs, and cautious transfusion—targeting a hemoglobin around 7 g/dL to avoid portal pressure spikes and rebleeding. Protect the airway early; intubate if hematemesis or encephalopathy loom.

Pharmacologic therapy doesn’t wait for endoscopy. Hit fast with octreotide (50 μg bolus → 50 μg/h infusion) or terlipressin/somatostatin if available, and start ceftriaxone 1 g IV daily to cover against bacterial translocation and sepsis. These moves—simple but evidence-based—slash early mortality and infection risk.

Then comes the endoscopic moment: perform urgent EGD within 12 hours. Band the culprit—endoscopic variceal ligation (EVL) is first-line for esophageal varices, while cyanoacrylate injection (± coils) dominates for gastric or ectopic sites. Visualization gets a boost from IV erythromycin pre-procedure. If bleeding laughs in your face—bridge with balloon tamponade or self-expanding stent while prepping for TIPS.

TIPS saves lives when all else fails or when the odds are stacked: Child-Pugh C (10–13) or B >7 with active bleeding—go early (within 24–72 hours). It decompresses the portal system, quells refractory bleeding, and buys survival time.

Once the storm calms, secondary prophylaxis takes over. Combine nonselective beta-blockers (carvedilol preferred at 12.5 mg daily) with repeat EVL every 2–4 weeks until varices vanish. No monotherapy—combo therapy halves rebleeding and boosts survival. For gastric or ectopic varices, keep repeating glue injection or move to BRTO or TIPS if anatomy and expertise allow.

Avoid the traps:

Complications hit early and hard—shock, infection, encephalopathy, AKI, and early rebleeding top the list. Six-week mortality can reach 40% in advanced cirrhotics, but drops sharply with prompt vasoactive therapy, antibiotics, and endoscopic control.

Predict death early: Child-Pugh C, MELD ≥19, active bleeding at endoscopy, transfusion >4 units, or renal/hepatic failure—each turns the curve downward. These patients may benefit from pre-emptive TIPS and aggressive ICU support.

Special plays:

We close with the system bundle that keeps patients alive:

Rapid, protocolized, and team-driven—control the bleed, decompress the pressure, and protect the liver. This is how you turn variceal crisis into survival.