Pathophysiology
II-25. Possible causes of cardiogenic shock
心原性ショックの原因
Cardiogenic Shock — Causes
- Occurs because the pumping function of the heart decreases
- Prevalence order of shock: septic > cardiogenic > hypovolemic
Most frequent causes
- Myocardial infarction (MI)
- Heart valve failure
- Arrhythmia
- Cardiomyopathy
- Myocarditis, pericarditis
Mechanism of Progression (after MI)
- Occlusion of a large coronary artery → hypoxia shifts the cardiac function curve downward (same preload → smaller CO)
- Myocardial dysfunction: systolic (impaired contraction) + diastolic (impaired relaxation)
Self-aggravating vicious cycles
- ↑SYM tone (baroreflex): ↑HR shortens diastole → ↓coronary perfusion (filling occurs in diastole) + ↑myocardial O₂ demand
- ↑LVEDP: weak diastole → ↑end-diastolic pressure → wall stretch → compression of coronaries → ↓O₂ supply
- Diastolic dysfunction: → pulmonary congestion → pulmonary edema → arterial hypoxia → less oxygenated blood to myocardium → ↓O₂ supply
- All converge on progressive myocardial dysfunction → death
No-Reflow Phenomenon & Treatment
- MI treatment: reopen the occluded coronary (stent); sometimes flow does not restart = no-reflow
- Causes of no-reflow:
- Hypoxia-induced edema compressing vessels (swollen smooth-muscle/cardiac/endothelial cells)
- Hypercoagulable state (hypoxia + endothelial dysfunction) → platelet adhesion/aggregation → emboli
- Sludging of leukocytes/RBCs in small vessels → microvascular occlusion
- → even after reopening the large artery, the microcirculation may fail to perfuse
- Note: avoid vasoconstriction in cardiogenic shock → prefer dobutamine (β1 inotrope) without peripheral vasoconstriction
一問一答
▶What are the most frequent causes of cardiogenic shock?
Myocardial infarction (most frequent), heart valve failure, arrhythmia, cardiomyopathy, and myocarditis/pericarditis.
▶How does coronary occlusion shift the cardiac function curve?
Hypoxia shifts the cardiac function curve downward, so the same preload produces a smaller cardiac output.
▶What is the basic mechanism of cardiogenic shock?
The pumping function of the heart decreases, lowering cardiac output.
▶What two types of myocardial dysfunction occur in cardiogenic shock?
Systolic (impaired contraction) and diastolic (impaired relaxation) dysfunction.
▶What is the prevalence order of the major shock types?
Septic > cardiogenic > hypovolemic.
▶How does increased sympathetic tone worsen cardiogenic shock?
↑HR shortens diastole → ↓coronary perfusion (which occurs in diastole) and ↑myocardial O₂ demand.
▶How does increased LVEDP create a vicious cycle in cardiogenic shock?
Weak diastole → ↑end-diastolic pressure → wall stretch → compression of coronaries → ↓O₂ supply.
▶How does diastolic dysfunction lead to reduced myocardial oxygenation?
Diastolic dysfunction → pulmonary congestion → pulmonary edema → arterial hypoxia → less oxygenated blood reaching the myocardium → ↓O₂ supply.
▶What is the primary treatment of MI causing cardiogenic shock?
Reopening the occluded coronary artery (e.g., stent).
▶What is the no-reflow phenomenon?
After reopening the occluded large coronary artery, blood flow sometimes fails to restart in the microcirculation.
▶What causes the no-reflow phenomenon?
Hypoxia-induced edema compressing vessels, a hypercoagulable state causing platelet adhesion/emboli, and sludging of leukocytes/RBCs occluding small vessels.
▶Why is dobutamine preferred over vasoconstrictors in cardiogenic shock?
Vasoconstriction should be avoided; dobutamine is a β1 inotrope that improves contractility without peripheral vasoconstriction.
▶Why is coronary perfusion especially sensitive to tachycardia?
Coronary filling occurs during diastole, so a faster heart rate shortens diastole and reduces coronary perfusion.
▶Why does the baroreflex paradoxically harm the heart in cardiogenic shock?
It raises sympathetic tone and HR, which shortens diastole and increases O₂ demand, worsening the supply-demand imbalance.
▶What is the common endpoint of the vicious cycles in cardiogenic shock?
They all converge on progressive myocardial dysfunction leading to death.
▶How does a hypercoagulable state contribute to no-reflow?
Hypoxia plus endothelial dysfunction promotes platelet adhesion/aggregation forming emboli that block the microcirculation.
▶Why can microcirculation fail to perfuse even after the large artery is reopened?
Edema, microthrombi, and cell sludging obstruct the small vessels, so flow does not reach the tissue despite a patent large artery.
▶How does pulmonary edema in cardiogenic shock feed back on the heart?
It causes arterial hypoxia, so less oxygenated blood reaches the myocardium, further reducing pump function.
▶Why does cell swelling (edema) cause vascular compression in no-reflow?
Swollen smooth-muscle, cardiac, and endothelial cells physically compress the small vessels, impeding flow.
▶Besides MI, which intrinsic cardiac diseases can precipitate cardiogenic shock?
Heart valve failure, arrhythmia, cardiomyopathy, myocarditis, and pericarditis.