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