Death Review: 90-Year-Old Male with Cardiogenic Shock

CLINICAL SUMMARY AT PRESENTATION

RECONSTRUCTED PATHOPHYSIOLOGY: WHY THIS PATIENT DIED

The Perfect Storm - Multiple Converging Mechanisms

• Giddiness and fall 3 days prior were almost certainly the FIRST presentation of hemodynamic compromise - likely an early syncopal/pre-syncopal episode from the same underlying cardiac pathology.
• The RT intertrochanteric fracture from the fall added significant additional physiological burden: pain, blood loss (up to 1-1.5L can collect in the thigh/pelvis with IT fractures), immobility, inflammation, and the neurohumoral stress response.

1. Massive Pulmonary Embolism - 90 year old, fractured hip, 3 days immobility, tachypnea (RR 32), hypoxia, hypotension, syncope: this is a HIGH-probability Wells/Geneva scenario. PE and cardiogenic shock can be clinically indistinguishable.
2. ACS/NSTEMI-STEMI with acute LV failure
3. Hypovolemic shock superimposed on cardiac failure (blood loss from IT fracture)
4. Acute aortic syndrome

WHAT SHOULD HAVE BEEN DONE IN THE ED: MINUTE-BY-MINUTE PROTOCOL

IMMEDIATE (0-5 minutes): Simultaneous Actions

• High-flow O2 - increase to 15L via non-rebreather mask, target SpO2 >94%
• Consider early Non-Invasive Ventilation (NIV/BiPAP) given RR 32 - reduces work of breathing and improves oxygenation in acute cardiogenic pulmonary edema
• Prepare for possible RSI and intubation - have drugs drawn up (ketamine 1-2 mg/kg preferred as it is vasopressor-sparing; succinylcholine 1.5 mg/kg). NOTE: intubation in this setting carries severe risk of further BP drop from sedation and loss of sympathetic drive. Only if absolutely necessary.

• 2x large-bore IV access (16G or 14G bilateral antecubital)
• Continuous cardiac monitoring (rhythm strip)
• 12-lead ECG - STAT (must look for ST changes, STEMI, BBB, RV strain pattern suggesting PE)
• Arterial line for continuous BP monitoring (non-invasive BP unreliable in shock)
• Urinary catheter for hourly urine output monitoring

• Epinephrine push-dose: 10-20 mcg IV boluses (phenylephrine 100 mcg IV boluses is an alternative if cardiac output is adequate)
• This buys time while setting up vasopressor infusion

INVESTIGATIONS (order all simultaneously within first 10 minutes):

PHARMACOLOGICAL MANAGEMENT

1. Norepinephrine - FIRST LINE vasopressor
   • Dose: Start at 2 mcg/min, titrate to effect (target MAP >65 mmHg)
   • Preferred over dopamine as it has lower arrhythmia risk; evidence from SOAP II trial supports this
   • Via central line (or peripherally as temporary measure until CVC placed)
2. Dobutamine - Add if LV dysfunction confirmed on echo and SBP is >70-80 mmHg
   • Dose: 2-5 mcg/kg/min, titrate to 20 mcg/kg/min
   • Works as inotrope; avoid as sole agent when SBP <90 mmHg due to vasodilatory effect
   • CAUTION in AF: can increase ventricular rate
3. Combination NE + Dobutamine is the most rational approach when SBP is <70 and LV function is poor
4. Dopamine: Use only if NE unavailable; higher arrhythmia risk in AF patients - Washington Manual explicitly notes it is NOT a preferred first-line agent in shock
5. Epinephrine 0.1-0.5 mcg/kg/min: Second-tier, particularly useful if RV dysfunction present

• Beta-blockers (even if AF with high rate appears) - will worsen cardiogenic shock
• ACE inhibitors, ARBs, nitrates - vasodilators contraindicated with unrecordable BP
• Calcium channel blockers for rate control in AF (diltiazem, verapamil) - profoundly negative inotropic
• Digoxin for rate control - onset too slow; relative contraindication in acute setting
• NSAIDS for hip fracture pain - worsen renal perfusion

• Rate control is appropriate ONLY if hemodynamically stable
• This patient is in cardiogenic shock with AF - DO NOT attempt pharmacological rate control with nodal agents
• If AF is thought to be the precipitant (new onset AF causing pump failure), electrical cardioversion after ruling out intracardiac thrombus (TEE or if onset clearly <48h) can be considered
• Amiodarone 150 mg IV over 10 minutes (then 1 mg/min infusion) is the only rate-control/rhythm agent relatively safe in hemodynamically compromised AF

• This patient scores at minimum 5 on CHA2DS2-VASc (age 75+: 2 points, male: 0, vascular disease likely: 1, age 65-74: already counted, heart failure: 1+)
• BUT: acute shock and possible need for urgent procedures means anticoagulation decision is complex - hold until hemodynamics stabilize

• Small judicious crystalloid boluses 250 mL at a time ONLY if POCUS shows IVC collapse (volume responsive) and no pulmonary edema
• Avoid blind aggressive fluid resuscitation in cardiogenic shock - will cause flash pulmonary edema
• If IT fracture hemorrhage suspected (Hb drop on labs) - packed RBCs after cross-match

• IV Paracetamol (Acetaminophen) 1g IV - safe, no hemodynamic effects
• Femoral nerve block or fascia iliaca compartment block - excellent pain control without systemic hypotension
• Low-dose IV morphine 1-2 mg titrated IF BP responds to vasopressors (CAUTION - vasodilatory)
• AVOID NSAIDs, ketorolac

• Aspirin 300 mg PO/nasogastric if ACS suspected (and not contraindicated)
• IV Heparin infusion if STEMI or massive PE confirmed (coordinate with cardiology/interventional)
• Thiamine 100 mg IV (elderly + sick = nutritional deficiency risk)
• PPI (Pantoprazole 40 mg IV) for stress ulcer prophylaxis

CONSULTATIONS (initiate within 15-30 min of arrival):

1. Cardiology - Urgent for ACS/CS workup, echo, possible PCI
2. Cardiothoracic surgery - If mechanical complication suspected
3. Interventional Radiology/Vascular - If aortic pathology
4. ICU/Critical Care - For vasopressor management, mechanical circulatory support (IABP, Impella, VA-ECMO)
5. Orthopaedics - For ongoing IT fracture management (surgery is on hold given haemodynamics)
6. Palliative Care - Given age 90, frailty, and severity; goals of care discussion with family MUST be initiated early

CENTRAL VENOUS ACCESS AND MONITORING:

• Central venous catheter (CVC) - Internal jugular or subclavian for reliable vasopressor delivery and CVP monitoring
• Arterial line - Radial preferred for continuous invasive BP
• Urinary catheter with hourly urine output (target >0.5 mL/kg/hr = >35 mL/hr for a 70 kg patient)

BEFORE FIRST ARREST: TARGETS

JUSTIFICATION OF DEATH (Death Review Statement)

Why this patient died despite all interventions:

• Pre-renal/renal injury (likely)
• Myocardial stunning and ischemia
• Hepatic congestion
• End-organ dysfunction already established before arrival

• Estimated 500-1500 mL concealed blood loss into thigh/pelvis
• Severe pain driving catecholamine surge and increased myocardial oxygen demand
• Immobility for 3 days raising PE risk
• Systemic inflammatory response

• Blunts catecholamine response to vasopressors
• Promotes arrhythmias
• Reduces myocardial contractility
• This patient almost certainly had severe metabolic acidosis on arrival (given >3 sec CRT, unrecordable BP, drowsiness)

DOCUMENTATION FOR DEATH CERTIFICATE

• Right intertrochanteric femur fracture with blood loss
• Multi-organ hypoperfusion (cerebral, renal, hepatic)
• Extreme age (90 years) with reduced physiological reserve
• Syncope x1 day with hemodynamic instability

LEARNING POINTS FOR DEATH REVIEW COMMITTEE

1. Syncope in elderly + fall = cardiac emergency until proven otherwise. The 3-day delay from initial giddiness/fall to definitive cardiac evaluation allowed disease progression.
2. "Rate-controlled AF" with unrecordable BP is NOT stable. The combination of AF, cardiogenic shock, and inability to record BP was a terminal hemodynamic state.
3. POCUS is mandatory within 10-15 minutes of any undifferentiated shock. It would have immediately identified LV function, ruled in/out PE (RV strain), and pericardial effusion.
4. Massive PE must always be in the differential. This patient had a hip fracture, 3 days immobility, tachypnea, hypoxia, syncope - classic massive PE presentation. If PE was the cause, heparin and possible thrombolysis (with all its risks) would have been the intervention.
5. Goals of care conversation should have begun on arrival. At 90 years with unrecordable BP, cardiogenic shock, and a background of 3 days of deterioration, the family should be counseled early about the extremely poor prognosis and goals of care. This is not giving up - it is providing complete, compassionate care.
6. SCAI shock staging should be applied on arrival. This patient was SCAI Stage D-E. Institutions should have pre-agreed escalation protocols for each stage.
7. Despite optimal ED management, this patient's outcome was likely terminal. The combination of extreme frailty, 90 years of age, 3-day pre-hospital deterioration, unrecordable BP, IT fracture blood loss, and prolonged first cardiac arrest (25 min to ROSC) represented a physiological state beyond the point of reversibility. The death, while tragic, was not preventable at the time of ED arrival. The question this case raises for systems improvement is whether earlier intervention (day of fall, day of first syncope) could have changed the trajectory.

Probable 2D Echocardiography Findings in This Patient

1. LEFT VENTRICLE (LV) - The Core of the Story

Global Systolic Function:

• Severely reduced EF (<30%, possibly <20%) - The hallmark of cardiogenic shock from LV failure
• Global LV hypokinesia or akinesia - diffuse contractile impairment from ischemia/infarction
• A dilated, poorly contracting LV that barely moves between systole and diastole - sometimes called a "bag of blood" appearance

Regional Wall Motion Abnormalities (RWMA):

• These are the most diagnostically important finding for ACS
• Akinesia or hypokinesis in a coronary territory depending on the culprit vessel:
  • LAD territory: anterior wall, apex, interventricular septum
  • RCA territory: inferior wall, posterior wall, RV free wall
  • LCx territory: lateral wall, posterior wall
• Per the Textbook of Clinical Echocardiography: "Akinesis or hypokinosis of the myocardium supplied by the occluded vessel with normal wall thickness" in acute ACS; in old MI: "thinning, increased echogenicity, and akinesis"
• Hyperkinesis of uninvolved segments may be seen as a compensatory response - this suggests the event is acute rather than chronic

LV Dimensions:

• LV dilation - volume overload from failing pump
• Possible LV thrombus at the apex - seen in large anterior MIs with apical akinesia; appears as an intracavitary mass with layered, fixed structure

Diastolic Function (even if EF is preserved):

• In a 90-year-old, Grade 2-3 diastolic dysfunction is almost universal (impaired relaxation + increased filling pressures)
• Elevated E/e' ratio (>15) indicating high LV filling pressures - this is a marker of pulmonary congestion
• This matters greatly: even if EF looks borderline, diastolic failure alone can cause cardiogenic shock in the elderly (HFpEF crisis)

2. LEFT ATRIUM (LA) - The AF Story

• Markedly enlarged left atrium - LA dilation is the structural substrate for AF and also a marker of chronically elevated LV filling pressures
• A dilated LA in AF with cardiogenic shock indicates this is NOT new-onset AF - this is long-standing structural disease
• Left atrial appendage (LAA) thrombus - critically important to look for. In AF, especially when cardiac output is low, the LAA acts as a dead-end chamber where stagnant blood clots. The "smoke" appearance (spontaneous echo contrast) in the LA/LAA suggests very low flow and imminent thromboembolism
• Absent atrial contraction (as expected in AF)

3. MITRAL VALVE - Critical Finding

• Mitral regurgitation (MR) - likely present, possibly severe:
  • In ACS with inferior/posterior infarction, papillary muscle ischemia or rupture causes acute MR - this is a mechanical complication of MI and an echocardiographic emergency
  • Even without papillary rupture, LV dilation displaces papillary muscles, causing functional/ischemic MR (tenting of leaflets, incomplete coaptation)
  • Color Doppler shows a regurgitant jet into the LA
  • Severe acute MR is a cause of cardiogenic shock in its own right
• In elderly with longstanding hypertension/AF: mitral annular calcification is extremely common; may restrict leaflet motion and cause relative MS

4. AORTIC VALVE

• Aortic stenosis - must actively exclude. Severe AS is common in the elderly and can be overlooked. A gradient >40 mmHg with reduced valve area (<1 cm²) can cause syncope and cardiogenic shock
• In shock states, the gradient may be deceptively LOW because the LV can no longer generate pressure - so even severe AS may appear "mild" on Doppler - this is low-flow, low-gradient severe AS and requires dobutamine stress echo or CT calcium scoring to unmask
• In this patient, if a calcified, barely-opening aortic valve is seen - this changes the entire management plan

5. RIGHT VENTRICLE (RV) - The PE vs. RV Infarct Clue

• RV dilation - RV appears larger than LV (normally RV:LV ratio <0.6; in massive PE it can be >1.0)
• RV free wall hypokinesia with preserved RV apex - this is the McConnell's sign, which is >90% specific for acute PE
• Paradoxical septal motion (D-sign on parasternal short axis) - the IV septum bows into the LV during systole because RV pressure exceeds LV pressure
• Flattened interventricular septum on short-axis view (D-shaped LV)
• Dilated, non-collapsing IVC (see below)
• Estimated high RVSP on TR jet velocity (if measurable)
• Absent DVT sign in legs (POCUS)

• RV dilation + RV free wall akinesia (all walls equally affected, including apex - helps distinguish from PE)
• Tricuspid regurgitation
• IVC plethora

6. PERICARDIUM

• Pericardial effusion - possible in ACS setting; if myocardial free wall rupture has occurred (catastrophic complication of STEMI), this appears as a large hemopericardium
• Cardiac tamponade - if effusion is large, look for RV diastolic collapse and RA systolic collapse - these are the earliest echo signs of tamponade
• In a patient with unrecordable BP, tamponade must be actively excluded on the first echo view

7. INFERIOR VENA CAVA (IVC) - Volume Status Assessment

8. AORTA

• Aortic dissection must be excluded - a proximal dissection (Type A) can cause:
  • AR (flap undermining the aortic annulus)
  • Pericardial effusion (blood tracking into pericardium)
  • Cardiogenic shock
  • Limb ischemia
• Look for a dilated aortic root (>40 mm) and an intimal flap in the aortic root/ascending aorta (parasternal long-axis view)

SUMMARY TABLE: What to Look for and What to Expect

THE MOST IMPORTANT SINGLE ECHO VIEW IN THIS PATIENT

1. Confirmed the mechanism of shock
2. Identified any treatable mechanical complication
3. Excluded tamponade and aortic dissection
4. Guided vasopressor vs. volume strategy via IVC assessment
5. Informed goals-of-care discussion with clear, objective findings