Acute Heart Failure Explained: Diagnosis, Workup, and Treatment

Right Ventricular Failure: The Forgotten Side of Cardiogenic Shock

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

Running on Empty: Hypovolemic and Hemorrhagic Shock

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..

Infammatory Bowel Disease Overview with Drs. Amulya Anumolu, Nicole Ebalo, and Michael Bass

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

AFib Basics: Staging, Stroke Prevention, and Management Strategies

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

Acute Heart Failure Explained: Diagnosis, Workup, and Treatment

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)