In this episode of IM Basics, Dr. Eric Acker and co-host Dr. Tark take a deep dive into right ventricular (RV) failure—a high-risk but often under-recognized cause of clinical deterioration. The discussion frames RV failure as a problem of both forward flow limitation and backward congestion, emphasizing that a preserved left ventricular ejection fraction does not rule out severe cardiogenic pathology.

The hosts walk through the typical clinical presentation, highlighting early altered mental status, lactic acidosis, acute kidney injury, hepatic congestion, and gastropathy as hallmark features. Unlike left-sided failure, RV failure often causes early end-organ hypoperfusion despite relatively preserved blood pressure, making “normotensive shock” a key concept.

Etiologies are divided into chronic and acute causes. Chronic drivers include pulmonary hypertension (pre- and post-capillary), COPD, chronic thromboembolic disease, and longstanding left-sided heart disease. Acute causes most notably include massive or submassive pulmonary embolism and acute right coronary artery infarction. The conversation emphasizes distinguishing acute from chronic RV failure, as this distinction directly affects management decisions.

Diagnostic evaluation extends beyond routine labs. While BNP, lactate, CMP, and liver enzymes help identify congestion and hypoperfusion, bedside ultrasound plays a central role. The hosts caution against relying solely on IVC size, instead advocating for venous Doppler assessment (portal and femoral veins) and focused echocardiography. Key echo findings include RV dilation, septal flattening (“D-sign”), reduced TAPSE, tricuspid regurgitation velocity, and features suggesting chronic remodeling versus acute strain.

Management is framed around “RV-specific do’s and don’ts.” Core principles include aggressive but thoughtful diuresis—even in the presence of AKI—correction of hypoxia and acidosis, and avoidance of negative inotropes. The episode strongly cautions against premature intubation due to the risks of sedation, positive pressure ventilation, and increased RV afterload. When shock develops, vasopressin is favored for hemodynamic support, often combined with inotropes such as low-dose norepinephrine or dobutamine.

Finally, the hosts discuss escalation of care, including when to involve the ICU, consider mechanical circulatory support, or pursue advanced therapies such as Impella RP or ECMO in select patients. The episode closes with practical bedside pearls and reinforces the importance of early recognition and RV-specific management strategies to prevent rapid clinical collapse.

Academic References & Guidelines

• Echocardiography: ASE Guidelines for the Echocardiographic Assessment of the Right Heart in Adults (Standards for TAPSE <17 mm and RV diameter >4.2 cm).
• Pulmonary Hypertension: ESC/ERS Guidelines for PH (Defined by mPAP >20 mmHg).
• Cardiogenic Shock: SCAI Clinical Expert Consensus (SCAI/SKY SHOCK Criteria) for staging severity.
• Management: AHA Scientific Statement: Evaluation and Management of Right-Sided Heart Failure.

Content Reviewed by Dr. Alejandro Chapa-Rodriguez

In this episode of IM Basics, Dr. Eric and Dr. Tark continue their shock series with a practical discussion of hypovolemic and hemorrhagic shock, focusing on bedside recognition, diagnostic strategies, and early management.

The episode begins with a review of shock pathophysiology, emphasizing reduced preload as the primary driver of both conditions. Loss of intravascular volume leads to decreased cardiac output and impaired end-organ perfusion, triggering a compensatory sympathetic response with vasoconstriction, tachycardia, and narrow pulse pressures.

The hosts highlight that hypotension is often a late finding. Earlier signs include tachycardia, cool extremities, delayed capillary refill, and altered mental status. The shock index (heart rate divided by systolic blood pressure) is introduced as a useful early marker, with values above 0.7 suggesting instability and values ≥1.0 indicating severe shock.

A major focus is on identifying the source of volume loss or bleeding. Hemorrhage is framed simply: patients bleed externally or into limited internal compartments such as the chest, abdomen, pelvis, or thighs. Point-of-care ultrasound (FAST exam) is emphasized as a first-line tool in unstable patients, with CT angiography and interventional radiology considered when patients can be stabilized.

For hypovolemic shock, common causes discussed include gastrointestinal losses, poor oral intake, diuretic use, osmotic diuresis (e.g., DKA), and third spacing from conditions like pancreatitis or advanced liver disease.

Management centers on early resuscitation, distinguishing fluid replacement for hypovolemia from early blood product administration for hemorrhagic shock. The hosts caution against excessive crystalloid use due to dilutional coagulopathy and DIC risk, and review massive transfusion principles, including balanced ratios of blood products and emerging data on whole-blood transfusion.

The episode also covers fluid selection, favoring balanced crystalloids such as lactated Ringer’s, and discusses vasopressors as adjuncts when hypotension persists despite adequate resuscitation or while definitive hemorrhage control is pending.

Key pitfalls are reviewed, including reliance on a normal initial hemoglobin, failure to reassess volume status, fluid overload causing pulmonary edema, and delays in specialist involvement. The episode closes with an emphasis on early communication with surgical, interventional, GI, and critical care teams to improve outcomes.

*Episode reviewed by Dr. Teshome Hailemichael, Core Faculty - Internal Medicine

Key References

1. Guyton AC, Hall JE. Textbook of Medical Physiology. 14th ed. Elsevier; 2021.
2. Advanced Trauma Life Support (ATLS®): Student Course Manual. 10th ed. American College of Surgeons; 2018.
3. Cannon JW. Hemorrhagic Shock. N Engl J Med. 2018;378:370–379. – Comprehensive review of hemorrhagic shock pathophysiology and resuscitation strategies.
4. Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Intensive Care Med. 2021.
5. Holcomb JB, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 ratio and mortality in patients with severe trauma. JAMA. 2015;313(5):471–482.
6. Semler MW, et al. Balanced Crystalloids versus Saline in Critically Ill Adults. N Engl J Med. 2018;378:829–839..

Episode Summary Dr. Eric Acker is joined by Drs. Amulya, Michael Bass, and Nicole Ebalo to discuss Inflammatory Bowel Disease (IBD). The team reviews presentation, diagnosis, imaging, pathology, and management from mild to fulminant disease.

Key Discussion Points

1. Presentation & Epidemiology Typical symptoms: diarrhea, abdominal pain, weight loss, fatigue.

• UC: Bloody diarrhea, urgency, tenesmus.
• Crohn’s: Non-bloody diarrhea, crampy pain; may have constipation
• Extraintestinal: Arthritis, erythema nodosum, uveitis, primary sclerosing cholangitis.
• Epidemiology: Bimodal (15–30 & 50–80 yrs); Crohn’s—slight female predominance, UC—slight male predominance.

2. Diagnostic Evaluation Initial workup: CBC, ESR, CRP, stool cultures (Salmonella, Shigella, Campylobacter, C. difficile) and fecal calprotectin.

• Colonoscopy: Diagnostic gold standard.
  • UC: Continuous mucosal inflammation from rectum.
  • Crohn’s: “Skip lesions,” transmural inflammation, often terminal ileum.
• Histology:
  • UC—mucosal/submucosal inflammation.
  • Crohn’s—non-caseating granulomas, transmural inflammation.
• Imaging: CT or MR enterography for strictures, fistulas, abscesses.

3. Treatment Approach Mild–Moderate:

• UC: 5-ASA (mesalamine) ± topical therapy.
• Crohn’s: Budesonide (if colonic involvement).

Moderate–Severe:

• UC: Corticosteroids → immunomodulators (6-MP, azathioprine, methotrexate) ± biologics (infliximab, vedolizumab).
• Crohn’s: Corticosteroids → biologics (infliximab, adalimumab) ± immunosuppressants.

Severe/Fulminant:

• UC: IV steroids (methylpred 60 mg/day or hydrocortisone 100 mg TID); add infliximab or cyclosporine if refractory.
• Crohn’s: IV steroids;

Notes:

• Screen for TB and hepatitis before anti-TNF therapy.
• Key complications: toxic megacolon (UC), short gut syndrome (post-surgery).
• Maintenance: Continue lowest effective biologic/immunosuppressive dose.
• Surveillance: Colonoscopy every 1–5 years

4. Lifestyle & Long-Term Care

• Smoking cessation: Improves Crohn’s outcomes; mixed data in UC but overall beneficial.
• Diet: GI soft, hydration, monitor B12, folate, micronutrients.
• Pregnancy: Adjust biologics/immunosuppressants before conception

💡 Clinical Pearls

• Fecal calprotectin is more specific for IBD activity than CRP/ESR.
• Crohn’s: Transmural, skip lesions → fistulas/strictures.
• UC: Continuous mucosal disease → toxic megacolon risk.
• Immunosuppressives: Used for maintenance, not induction.
• Multidisciplinary management GI, surgery, nutrition, primary care

References:

• The Washington Manual of Medical Therapeutics
• ECCO Guidelines on Pregnancy and IBD.
• UpToDate

In this episode of IM Basics, Dr. Eric Acker is joined by Dr. Harmandip Parmar for a deep dive into atrial fibrillation (AFib)—the most common sustained arrhythmia worldwide. They explore AFib’s definitions, staging, risk factors, clinical presentation, diagnostic strategies, and evidence-based management, with a focus on the latest 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial FibrillationAfib【ACC/AHA 2023 Guidelines†DOI:10.1161/CIR.0000000000001193】.

Key Topics Covered

• AFib staging and progression: The episode reviews the updated classification from the ACC/AHA guidelines, beginning with “at risk” and “pre-AFib” states (associated with modifiable risk factors such as obesity, hypertension, diabetes, and sleep apnea) through paroxysmal, persistent, longstanding, and permanent AFib.
• Clinical presentation & workup: While many patients present with palpitations, dyspnea, or fatigue, others are asymptomatic and diagnosed incidentally. Recommended evaluation includes ECG confirmation, transthoracic echocardiography, thyroid and metabolic panels, and exclusion of reversible causes (e.g., hyperthyroidism, acute illness). Not all patients require ischemic evaluation, aligning with Class III recommendations.
• Stroke prevention & anticoagulation: The team emphasizes CHA₂DS₂-VASc scoring as central to risk stratification. Direct oral anticoagulants (DOACs) are first-line for most, with apixaban favored over rivaroxaban due to lower GI bleeding risk (supported by observational data and network meta-analyses). Warfarin remains the standard for patients with mechanical prosthetic valves or moderate-to-severe mitral stenosis.
• Risk factor modification: Lifestyle interventions—weight loss ≥10%, regular exercise (≥210 min/week), alcohol reduction, smoking cessation, and blood pressure optimization—are strongly recommended to reduce AFib burden【Pathak 2014 JACC†DOI:10.1016/j.jacc.2014.03.058】. While caffeine restriction is not recommended (Class III), screening and managing sleep apnea may prevent AFib progression.
• Lifestyle vs. ablation: The PRAGUE-25 trial showed catheter ablation to be superior, but notably ~35% of patients in the lifestyle modification arm achieved sinus rhythm without invasive intervention.
• Rate vs. rhythm control: The discussion contrasts findings from AFFIRM (rate and rhythm strategies equivalent in older populations with EAST-AFNET 4 (early rhythm control associated with lower cardiovascular outcomes, particularly in younger patients or those with HF).
• Procedural & pharmacologic strategies: Management options include synchronized cardioversion (with anticoagulation protocols), catheter ablation (radiofrequency, cryoballoon, or emerging pulse-field technologies), and antiarrhythmic drugs such as amiodarone, flecainide, dofetilide, or propafenone. The CAST trial warns against Class IC agents in structural heart disease, though nuances remain in non-ischemic cardiomyopathy.

Takeaway: AFib is a progressive disease requiring early identification, aggressive risk factor management, stroke prevention, and individualized rhythm or rate control strategies. As new therapies (e.g., Factor XI inhibitors, pulse-field ablation) emerge, ongoing research continues to refine optimal care.

• Episode reviewed by Dr. Mathhar Aldaoud - Interventional Cardiologist

In this week’s episode, Eric is joined by Dr. Tark, now 3rd year resident, to break down the recognition and management of acute heart failure exacerbation.

Key Discussion Points:

• Patient Presentation: Common symptoms include peripheral edema, pulmonary congestion with dyspnea, and paroxysmal nocturnal dyspnea. Physical exam findings such as S3/S4 gallops, jugular venous distension, and hepatic jugular reflux play a critical role in making a clinical diagnosis.
• Workup: While BNP is frequently ordered, heart failure remains a clinical diagnosis. Supportive labs include CMP, renal function, troponins, ECG, and occasionally lactate in suspected shock. Chest X-ray can confirm pulmonary congestion, and echocardiography helps define the type of HF (HFrEF vs. HFpEF).
• Management:
  • Diuretics remain the cornerstone—IV loop diuretics with escalation as needed, targeting 2–3 L of diuresis in the first 24 hours.
  • Acetazolamide has emerged as a promising adjunct. The ADVOR Trial (Mullens et al., NEJM 2022) showed that adding acetazolamide to loop diuretics in acute decompensated HF increased decongestion rates and reduced hospital stay.
  • Non-invasive ventilation (CPAP/BiPAP) provides symptomatic relief in flash pulmonary edema by improving oxygenation and reducing preload/afterload.
• Guideline-Directed Medical Therapy (GDMT):
  • Beta-blockers should be continued in stable patients but held in cardiogenic shock.
  • ACE inhibitors/ARBs/ARNIs and SGLT2 inhibitors are central pillars of therapy in chronic HFrEF, with trials like DAPA-HF and EMPEROR-Reduced demonstrating mortality and hospitalization benefits.
  • SGLT2 inhibitors also benefit patients with HFpEF, as shown in EMPEROR-Preserved

Pearls and Pitfalls:

• BNP should be interpreted in context
• Always rule out mimickers such as pulmonary embolism, ischemic events, arrhythmias, thyroid disease, and infections.
• Early and aggressive diuresis in the first 24–48 hours can shape the patient’s entire trajectory of recovery.

Takeaway: Acute heart failure requires a careful balance of clinical recognition, judicious use of diagnostics, and evidence-based diuretic strategies. Early intervention, guided by both bedside exam and trial evidence, makes the difference between stabilization and deterioration.

References:

1. Felker GM, et al. "Diuretic Strategies in Patients with Acute Decompensated Heart Failure" NEJM. 2011;364:797–805. (DOSE Trial)
2. Mullens W, et al. "Acetazolamide in Acute Decompensated Heart Failure with Volume Overload." NEJM. 2022;387:1185–1195. (ADVOR Trial)
3. McMurray JJV, et al. "Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction." NEJM. 2019;381:1995–2008. (DAPA-HF)
4. Packer M, et al. "Cardiovascular and Renal Outcomes with Empagliflozin in Heart Failure." NEJM. 2020;383:1413–1424. (EMPEROR-Reduced)
5. Anker SD, et al. "Empagliflozin in Heart Failure with a Preserved Ejection Fraction." NEJM. 2021;385:1451–1461. (EMPEROR-Preserved)

In this episode of "IM Basics," host Dr. Eric Acker is joined by Dr. Michael Bass to tackle the frequently encountered topic of alcohol withdrawal. They provide a comprehensive overview, starting with the fundamental definitions and pathophysiology, moving through patient presentation, workup, and the nuances of treatment. Learn to look beyond simply ordering a protocol and gain a deeper understanding of how to manage these complex patients dynamically.

In this episode, you will learn about:

• Defining and Scoring Alcohol Withdrawal:
  • Symptoms are categorized as mild (anxiety, tremors, insomnia, palpitations) or severe (hallucinations, seizures, delirium tremens). Only about 20% of patients develop severe symptoms.
  • The DSM-5 criteria for diagnosis require two or more specific symptoms following the cessation or reduction of alcohol use.
  • The CIWA is a common scoring system used by nursing staff to guide treatment based on symptom severity.
• The Pathophysiology of Withdrawal:
  • Chronic alcohol use enhances the effect of the inhibitory GABA receptors and inhibits the excitatory NMDA receptors.
  • The body adapts by decreasing the sensitivity of GABA receptors and increasing the sensitivity of NMDA receptors.
  • When alcohol is stopped, the brain is left in a state of uninhibited excitatory stimulation.
• Timeline of Symptoms:
  • 6-36 hours after last drink: Mild symptoms like tremors, sweats, and agitation may appear.
  • 6-48 hours: Seizures can occur.
  • 12-48 hours: Hallucinations (visual, auditory, or tactile) may develop.
  • 48-96 hours: The most severe manifestation, delirium tremens (DTs), can set in.
• Patient Workup:
  • A thorough history is the most critical part of the workup, especially the timing of the last drink and the quantity consumed.
  • Labs are essential to rule out other conditions and should include a blood glucose, CBC, electrolytes, and blood cultures.
  • An ethanol level can be checked, but a patient can be in withdrawal even with a detectable alcohol level.
• Treatment Strategies:
  • Symptom-Triggered Therapy: This is the most recommended approach, where benzodiazepines are given based on a CIWA score threshold (e.g., a score greater than 8 or 10).
  • Benzodiazepines: These are the mainstay of treatment and work by stimulating the GABA receptor.
    • Lorazepam (Ativan): Slower onset (15-30 mins) but shorter duration.
    • Diazepam (Valium): Faster onset (2-3 mins) but longer half-life, which can lead to accumulation.
  • Refractory Withdrawal: For patients who don't respond to high doses of benzodiazepines, phenobarbital is an option. It can be used as a dual therapy with benzos or as a monotherapy.
  • Front-Loading: For patients at high risk of severe withdrawal (e.g., history of DTs), proactively administering high doses of benzodiazepines can be considered.
• Pearls and Pitfalls:
  • Be aware that benzodiazepines can cause paradoxical agitation in elderly patients,
  • Don't get anchored on alcohol withdrawal, especially considering hepatic encephalopathy in patients with cirrhosis.
  • Remember supportive care: thiamine, along with a multivitamin and electrolyte repletion
  • Always reassess your patient if the treatment isn't working.

In this episode of "IM Basics," host Dr. Acker is joined by Dr. Harmandip Parmar, an intern with an interest in cardiology, to break down the essentials of heart block. They cover the full spectrum of atrioventricular (AV) blocks, from incidental findings on an ECG to symptomatic emergencies. Tune in to learn how to identify, investigate, and manage these crucial cardiac conditions.

What You'll Learn in This Episode:

• Patient Presentation:
  • While many patients with heart block are asymptomatic, some may present with symptoms like fainting (syncope), lightheadedness, or chest pain.
  • Myocardial infarction (MI) can be an underlying cause of these symptoms and the heart block itself.
• ECG Findings for Different Heart Blocks:
  • First-Degree AV Block: Identified by a prolonged PR interval of more than 0.20 seconds.
  • Second-Degree AV Block, Mobitz Type I (Wenckebach): Characterized by a PR interval that gets progressively longer until a QRS complex is "dropped".
  • Second-Degree AV Block, Mobitz Type II: Features a constant PR interval length with intermittently dropped beats. These patients are often more symptomatic.
  • Third-Degree (Complete) AV Block: Shows a complete dissociation between P waves and QRS complexes, with each marching out at its own regular rate.
• Investigating the Causes:
  • A thorough workup is essential to find the underlying cause.
  • Potential causes include MI, electrolyte imbalances (like hyperkalemia), and thyroid issues.
  • A patient's medication list should be reviewed for drugs like beta-blockers, digoxin, amiodarone, and certain calcium channel blockers.
  • Other causes can include Lyme disease, inherited conditions like sarcoidosis, or recent cardiac procedures.
• Treatment and Management:
  • First-Degree and Mobitz I: Often asymptomatic and may not require urgent intervention, aside from investigating the cause.
  • Mobitz Type II: These patients are at high risk of progressing to a third-degree block and require admission. Atropine should be avoided. Definitive treatment is often a permanent pacemaker.
  • Third-Degree Block: This is an urgent condition. Management includes:
    • Giving atropine.
    • Using beta-adrenergic agonists like dopamine or epinephrine.
    • Initiating temporary cardiac pacing, followed by evaluation for a permanent pacemaker.

    Special Cases: In patients with Lyme carditis, a permanent pacemaker is often avoided as the condition typically improves within weeks.

• Additional Insights:
  • The discussion touches on "Stokes-Adams attacks," which are episodes of fainting linked to heart block.
  • The hosts explore the theory that rate control in atrial fibrillation might bombard the AV node, potentially leading to third-degree heart block over time

This episode of "IM Basics" provides a concise yet comprehensive overview of Multiple Myeloma. Dr. Eric Acker and Dr. Vinh Dao discuss the disease's non-specific presentation, diagnostic criteria (CRAB and SLIM), and essential workup procedures, including laboratory tests and imaging. The podcast also differentiates between MGUS, smoldering myeloma, and full-blown Multiple Myeloma, outlining when treatment is initiated for each. Key aspects of managing Multiple Myeloma, such as treatment modalities, handling complications like hypercalcemia and lytic lesions, and addressing immunocompromise, are covered in detail. The episode concludes with practical "pearls and pitfalls," emphasizing the importance of recognizing the disease despite its subtle presentation in an older demographic.

Don't forget to check out Dr. Dao's podcast, "Bloom Pod," which focuses on oncology and its links to other medical fields!

In this episode of "IM Basics," Dr. Amulya Anumolu provides a comprehensive overview of managing GI bleeds.

Patients often present with signs of volume loss like hypotension, tachycardia, pallor, altered mental status, or dizziness. Common complaints include vomiting blood (hematochezia) or dark, sticky, foul-smelling stools (melena). Melena specifically indicates an upper GI bleed because blood darkens as it passes through the GI tract. A disproportionately high BUN (e.g., 30:1 ratio) on CMP can also suggest an upper GI bleed. Bright red blood per rectum can be a lower GI bleed or as simple as hemorrhoids.

Initial Assessment & Stabilization:

• Ensure the patient has two large-bore IVs (16 or 18 gauge) in both forearms for rapid fluid and blood product administration. Central lines are too thin for emergencies.
• Cross-matching and blood typing are essential.
• Transfuse blood for hemoglobin below seven or with active bleeding, as hemoglobin can appear normal due to hemoconcentration from significant volume loss.
• Provide supplemental oxygen to all GI bleed patients to enhance the oxygen-carrying capacity of blood.
• Intubate altered patients unable to protect their airway immediately.

Workup & Management:

• Initial workup includes CBC, CMP, and INR.
• History taking should cover NSAID use, history of ulcers, prior scopes, and anticoagulant use.
• The Glasgow-Blatchford score can help risk stratify patients to determine if ICU admission is needed.
• For upper GI bleeds, administer an initial bolus of 80 mg IV Protonix, followed by 40 mg BID; there's no evidence a drip is better.
• For suspected variceal bleeds (e.g., in cirrhosis), give octreotide (50-100 mcg bolus followed by 25-50 mcg/hour infusion for 3-5 days) to reduce portal pressures. Terlipressin can also be used.
• Administer ceftriaxone for SBP prophylaxis (1g) or treatment (2g) in cirrhotic patients with ascites.
• Erythromycin (150-200 mg IV) can aid gastric emptying for better scope visualization in upper GI bleeds, but monitor for QTC prolongation.
• Correct coagulopathies. Stop anticoagulants like Eliquis or Warfarin in severe bleeds.

Diagnostic & Interventional Procedures:

• An EGD is used for upper GI bleeds to band varices or cauterize ulcers. A colonoscopy is used for lower GI bleeds and requires bowel prep.
• If the source isn't found endoscopically, a CT angiography (CTA) during active bleeding can localize it for IR embolization. Ensure it's a three-phase CT angiography, not just a CT with contrast.
• A tagged RBC scan can also help locate blood pooling.
• In severe, unstable upper GI bleeds where endoscopy is not feasible, a Blakemore or Minnesota tube can be placed to tamponade varices.

Pearls & Pitfalls:

• Hemoglobin should be considered as a concentration, not just a volume.
• For cirrhotic patients, have a lower threshold to start lactulose and rifaximin if hepatic encephalopathy is suspected.
• Bright red blood per rectum could also indicate mesenteric ischemia.
• Test for H. pylori if ulcers are found, ideally after being off PPIs for two weeks.
• Be aware of atrial-esophageal fistulas as a rare, serious complication post-AFib ablation.
• Constantly monitor GI bleeders, even stable ones, as they can decompensate rapidly

Sources:

• Washington Manual
• Up-to-date

In this episode of IM Basics, Dr. Eric Acker and Dr. Tark break down the essentials of recognizing and managing hyperkalemia, a potentially life-threatening electrolyte disturbance. They discuss common presentations—ranging from dialysis patients to those with tumor lysis syndrome—and highlight key decision points in diagnosis and management.

Topics Covered:

• Common presentations of hyperkalemia and when to suspect it even without classic symptoms.
• ECG findings in hyperkalemia: from peaked T waves to sine waves.
• When to act and how aggressively, based on potassium levels and clinical stability.
• The three pillars of treatment:
  • Cardiac membrane stabilization with calcium gluconate.
  • Potassium shift therapies (e.g., insulin with dextrose, high-dose albuterol).
  • Potassium elimination (e.g., dialysis, Lokelma®, loop diuretics, or rarely, Kayexalate®).
• A practical discussion on the timing of interventions—why and when to delay shifting before dialysis.
• Tips on avoiding overtreatment, interpreting lab errors like pseudohyperkalemia, and reassessing post-intervention.

Clinical Pearls:

• Use calcium gluconate to stabilize membranes, not to lower potassium directly.
• Watch for hyperkalemia in AKI, rhabdomyolysis, tumor lysis syndrome, and missed dialysis.
• Lokelma® has high sodium content—consider alternatives like patiromer in volume-sensitive patients.
• Always reassess potassium after treatment to guide further interventions.

References & Citations:

• Sterns RH. "Hyperkalemia." N Engl J Med. 2022;386(15):1426–1435. DOI: 10.1056/NEJMra2110952.
• Montford JR, Linas S. "How dangerous is hyperkalemia?" J Am Soc Nephrol. 2017;28(11):3155–3165. DOI: 10.1681/ASN.2016121344.
• Kayexalate safety concerns: Patel K, et al. "Sodium polystyrene sulfonate-induced colonic necrosis." Am J Med Sci.2012;343(2):155–157.