Pathophysiology · ELI Explains: Cardiovascular Pathophysiology (book 2)

Cardiogenic Shock and Reduced Perfusion

On this page 5 sections
  1. The college version
  2. Key takeaway
  3. Check yourself
  4. Quick check
  5. Study tools

The college version

Clinical Orientation

A 62-year-old man with an anterior STEMI is in the cardiac ICU. Despite successful LAD stenting, his BP is 78/48 on high-dose vasopressors. His lactate is 8.2 and rising. His extremities are cold and mottled. His urine output is 5 mL/hour. His cardiac index is 1.6 L/min/m2. He has cardiogenic shock. This chapter answers: What mechanism links cardiogenic shock to bedside findings, tests, red flags, and nursing priorities?

Cross-reference: Book 10 provides the complete shock integration volume. This chapter focuses on the cardiogenic mechanism.

What Goes Wrong?

Cardiogenic shock: Severe pump failure → cardiac output inadequate to meet tissue oxygen demand despite adequate intravascular volume. The defining hemodynamics: low cardiac output, elevated filling pressures (high PCWP), high SVR (vasoconstriction). This distinguishes it from distributive shock (low SVR) and hypovolemic shock (low filling pressures).

The downward spiral:

Severe pump dysfunction → reduced CO → hypotension → reduced coronary perfusion pressure → worsened myocardial ischemia → further reduced contractility → further reduced CO

Plus, systemic hypoperfusion → lactic acidosis (depresses myocardium) + release of inflammatory mediators (cause vasodilation and further myocardial depression). This is why mortality is so high (40-50%).

Causes: Most commonly acute MI (especially large anterior MI → >40% LV mass). Also: acute severe mitral regurgitation (papillary muscle rupture), ventricular septal defect, acute aortic regurgitation, end-stage cardiomyopathy, myocarditis, post-cardiotomy.

What the Nurse May See

Hemodynamic profile:

  • Hypotension: SBP <90 mmHg or MAP <65 mmHg, or drop >30 mmHg from baseline.
  • Low cardiac output: Tachycardia, weak pulses, narrow pulse pressure, cool/mottled extremities, delayed capillary refill.
  • Elevated filling pressures: Pulmonary congestion (crackles, hypoxia, frothy sputum), JVD, hepatomegaly.
  • End-organ hypoperfusion: Altered mental status, oliguria (<0.5 mL/kg/hr), rising lactate, rising creatinine.

Key distinction from other shock types:

  • Hypovolemic: Low filling pressures (flat JVD, dry), usually responds to fluids.
  • Distributive (septic): Warm extremities (early), bounding pulses, wide pulse pressure, low SVR.
  • Cardiogenic: Elevated filling pressures (JVD, crackles), cold extremities, narrow pulse pressure, high SVR.

Tests and Monitoring

  • Echocardiogram: EF, wall motion, mechanical complications (papillary muscle, VSD, tamponade).
  • Invasive hemodynamics (PA catheter): Cardiac output/index, PCWP (wedge), PAP, CVP, SVR.
  • Lactate: Rising = inadequate oxygen delivery. Trend is key.
  • Mixed venous oxygen saturation (SvO2): Low (<60%) = increased oxygen extraction (inadequate delivery). Continuously falling = worsening.
  • End-organ function: Renal (BUN/Cr, urine output), hepatic (LFTs), neurologic (mental status).

Nursing Priorities

  1. ABC assessment: May need intubation (respiratory failure from pulmonary edema, altered mental status). Mechanical ventilation also reduces oxygen consumption of respiratory muscles.
  1. Hemodynamic optimization:
    • Inotropes (dobutamine, milrinone): Increase contractility. Milrinone also vasodilates → reduces afterload. Monitor for hypotension and arrhythmias.
    • Vasopressors (norepinephrine): Increase SVR to maintain perfusion pressure. But they increase afterload → increase myocardial oxygen demand.
    • Afterload reduction (nitroprusside if BP allows): Reduces ventricular workload.
    • This is the tightrope: you need enough pressure to perfuse but not so much afterload that the failing heart cannot eject.
  1. Fluid management: Unlike other shock types, fluids may worsen cardiogenic shock (increase filling pressures, worsen pulmonary edema). However, RV infarction is volume-dependent. Assessment is key.
  1. Mechanical support (if available): Intra-aortic balloon pump (IABP), Impella, ECMO. Bridge to recovery, transplant, or LVAD.
  1. Continuous monitoring: HR, BP (arterial line), SpO2, urine output (hourly), lactate, cardiac rhythm, PA catheter parameters.
  1. Family communication: Cardiogenic shock has high mortality. Keep family informed. Facilitate provider-family discussions about goals of care.

Red Flags

Red FlagWhy Dangerous
Refractory hypotension despite escalating vasopressorsPump failure is overwhelming — without mechanical support, death is imminent.
Rising lactate despite all interventionsOxygen delivery remains inadequate — all treatments are failing.
New arrhythmia (VT/VF)Failing heart is electrically unstable. Cardiac arrest imminent.
Multi-organ failure developing (rising Cr, LFTs, coagulopathy)Shock has progressed beyond the heart — systemic organ failure. Mortality extremely high.

Key takeaways

  • Cardiogenic shock = severe pump failure → low CO, high filling pressures, high SVR, end-organ hypoperfusion.
  • The downward spiral: Low CO → hypotension → reduced coronary perfusion → worse pump function.
  • Fluids may worsen (except RV infarction).
  • Inotropes + vasopressors + possible mechanical support.
  • Lactate trending = best indicator of whether treatment is working.
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  • End of Book 2 Chapters
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Check yourself

1 review question from the chapter. Try each one, then open the answer.

  1. Q1 (Mechanism): In cardiogenic shock, why does SVR increase while it decreases in septic shock? A. The heart releases vasodilating hormones in cardiogenic shock B. In cardiogenic shock, baroreceptors detect low CO and trigger massive sympathetic vasoconstriction. In septic shock, inflammatory mediators cause pathologic vasodilation C. Cardiogenic shock patients are always dehydrated D. Septic shock patients have stronger hearts

    Show answer

    B. Low CO triggers baroreceptor-mediated SNS activation → vasoconstriction (increased SVR). The skin is cool and mottled. In septic shock, cytokines cause vasodilation (decreased SVR). The skin may be warm initially. This is the key hemodynamic distinction.

Quick check

2 questions here. Answers stay hidden until you check.

Question 1 of 2

In cardiogenic shock, why does SVR increase while it decreases in septic shock?

Choose an answer, then check it.
Question 2 of 2

A post-MI patient becomes hypotensive (82/50), confused, oliguric. Crackles are present. JVD is elevated. What should the nurse do?

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