bubble_chart Overview

Cardiogenic shock is an acute circulatory dysfunction caused by various cardiac pathologies that impair ventricular ejection or filling, leading to a sharp decline in cardiac output. This results in inadequate microcirculatory perfusion of vital organs, cellular damage, and metabolic disturbances. Clinically, it manifests as hypotension, cold and clammy skin, oliguria, and confusion or lethargy. The mortality rate is extremely high.

bubble_chart Etiology

Disease cause

1. Common disease causes of ventricular ejection dysfunction include acute myocardial infarction, acute myocarditis, acute heart failure, massive pulmonary embolism, rupture of chordae tendineae or papillary muscles, perforation of valve leaflets, and severe aortic or pulmonary stenosis (when accompanied by mild to grade II tachycardia).
2. Common disease causes of ventricular filling impairment include acute cardiac tamponade, tension pneumothorax, persistently rapid ventricular rate, atrial myxoma, and severe mitral stenosis (when accompanied by mild to grade II tachycardia).

Among the various disease causes listed above, acute myocardial infarction is the most common.

Pathophysiology

The most fundamental pathophysiological change in cardiogenic shock is a decrease in cardiac output. When acute myocardial infarction leads to cardiogenic shock, the severe weakening of myocardial contractility causes a sharp reduction in cardiac output and a drop in arterial pressure. This reflexively triggers an increase in catecholamines; the decline in arterial pressure can lead to renal ischemia, prompting the massive release of renin, which subsequently increases angiotensin II. Elevated catecholamines and angiotensin II cause constriction of small arteries in the skin and abdominal organs. In contrast, the α-receptors in cerebral blood vessels are less sensitive to catecholamines, so the reduction in microcirculatory perfusion in the brain is not significant. Catecholamines act on the β-receptors of the coronary arteries, causing them to dilate. Thus, under conditions of ischemia in the skin and abdominal organs, blood supply to the heart and brain is prioritized. However, the constriction of small arteries increases peripheral resistance, further burdening the heart's afterload and reducing output.

As shock progresses, microcirculatory perfusion in the skin and abdominal organs sharply declines, leading to persistent tissue ischemia, hypoxia, and acidosis. The local accumulation of acidic metabolites and the release of vasoactive substances such as histamine and kinins cause the precapillary sphincters and intermediate small arteries to dilate, significantly increasing blood perfusion in the microcirculatory vessels. However, because venules are more resistant and less reactive to stimuli such as vasoactive substances, hypoxia, and acidosis, they remain highly sensitive to catecholamines and stay constricted, obstructing the outflow of the microcirculation and resulting in microcirculatory stasis. At this stage, a large amount of blood pools in the true capillary network, drastically reducing effective circulating blood volume and lowering blood pressure. Additionally, during shock, the body produces significantly more histamine, serotonin, kinins, and acidic metabolites, increasing capillary permeability. In congested capillaries, not only does the arterial-end pressure rise, increasing fluid filtration, but the venous-end pressure also rises, causing fluid to filter out from the venous end rather than into the veins. These factors lead to hemoconcentration, increased blood viscosity, slowed blood flow, and a further decline in effective circulating blood volume. If the patient has used diuretics before or after the onset of illness, or experiences severe vomiting or excessive sweating, the reduction in effective circulating blood volume worsens. At this point, perfusion to not only the skin and abdominal organs but also vital organs like the heart and brain is severely diminished, potentially leading to necrosis in the kidneys, liver, gastrointestinal mucosa, and subendocardial tissues, exacerbating the shock.

When cardiogenic shock is caused by impaired cardiac filling, myocardial ejection function remains intact in the early stages. However, since coronary artery blood flow primarily depends on mean arterial pressure, impaired cardiac filling leads to sustained hypotension, reducing coronary blood flow. Myocardial hypoxia then weakens contractility and further decreases cardiac output.

Regardless of the cause of shock, if accompanied by tachyarrhythmia or severe bradycardia, cardiac output can decline further, worsening the shock.

bubble_chart Clinical Manifestations

1. Manifestations of the primary disease: Patients with cardiogenic shock caused by acute myocardial infarction mostly experience severe precordial pain, a sense of impending doom, and may be accompanied by nausea, vomiting, profuse sweating, listlessness, weakness, dysphoria, and restlessness. Most patients also present with various arrhythmias. Patients with cardiac tamponade may exhibit distended neck veins, hepatomegaly, a positive hepatojugular reflux sign, diminished heart sounds with a distant quality, and pulsus paradoxus.
2. The signs of shock include decreased blood pressure and a thready, rapid pulse. Due to insufficient organ perfusion, symptoms such as cold and clammy skin, pallor or cyanosis, sweating, impaired consciousness, or reduced urine output may occur.

bubble_chart Diagnosis

In the presence of an underlying primary disease, cardiogenic shock can be diagnosed if the following manifestations persist after correcting various factors that may cause hypotension, such as severe arrhythmia, pain, vasovagal reflex, hypoxia, acidosis, and hypovolemia: (1) Weak or impalpable peripheral pulses; (2) Cold, clammy skin and pale complexion; (3) Systolic blood pressure <10.7/6.67 kPa (80/50 mmHg), or in patients with pre-existing hypertension, a reduction of 10.7 kPa (80 mmHg) from baseline, even if the limit is not reached; (4) Urine output <20 ml/h; (5) Impaired consciousness or apathy; (6) Hemodynamic changes: cardiac index (CI) <2.0 L/min·m², pulmonary artery wedge pressure (PAWP) >2.4 kPa (18 mmHg), central venous pressure (CVP) >1.18 kPa (12 cmH₂

O), and total peripheral resistance >1400 dyn·sec·cm⁻⁵.

bubble_chart Treatment Measures

1. disease cause Treatment should aim to eliminate the causative factors as much as possible, such as timely pericardiocentesis to relieve cardiac tamponade; placement of a thoracic drainage tube to treat tension pneumothorax; rapid control of arrhythmias; and early reperfusion for acute myocardial infarction.
2. Monitoring
   1. Continuous ECG monitoring is essential to promptly detect various arrhythmias.
   2. Monitor arterial blood pressure. If conditions permit, it is preferable to directly measure arterial pressure, monitor central venous pressure, or capillary wedge pressure.
   3. Insert a urinary catheter and record hourly urine output.
   4. For severe cases, if conditions allow, measure cardiac output, serum pH, electrolytes, arterial oxygen partial pressure, and carbon dioxide partial pressure.
3. General Treatment

   (1) Sedation and Analgesia Anxiety and restlessness increase the patient's oxygen demand, exacerbating myocardial hypoxia. Sedatives that do not significantly suppress respiration or circulation may be used, such as hydroxyzine 50–100 mg IV or promethazine 25–50 mg IM. For myocardial infarction patients, severe chest pain can worsen shock; morphine 5–10 mg may be administered subcutaneously. If pain persists, another dose may be given after 10 minutes. For respiratory depression caused by repeated morphine use, nalorphine may be administered as an antidote at a dose of 2.5–5.0 mg, repeated every 2 hours if necessary.

   (2) Oxygen Therapy Due to factors such as pulmonary arteriovenous shunting and pulmonary edema, patients may experience hypoxia. Symptoms like dysphoria, restlessness, shortness of breath, disorientation, and arrhythmias indicate hypoxia. However, some patients may show no clinical signs of hypoxia despite reduced arterial oxygen partial pressure. Therefore, all cardiogenic shock patients should receive routine oxygen therapy at a flow rate of 5–6 L/min via mask or nasal cannula.

   (3) Correction of Acid-Base Balance Hyperventilation due to anxiety can lead to respiratory alkalosis. Reassure the patient to alleviate tension and anxiety. If ineffective, administer a sedative that does not suppress respiration or have the patient breathe into a paper bag to restore plasma pH and respiratory rate to normal. Metabolic acidosis, caused by shock itself, can be reversed once tissue perfusion is adequately restored. Thus, grade I acidosis does not require alkaline drugs. Severe acidosis can weaken myocardial contractility, reduce the effectiveness of vasoactive drugs, and cause arrhythmias. Administer 4–5% sodium bicarbonate 100–200 ml IV, repeating once or twice if necessary, but avoid complete correction. Excessive sodium can increase circulating blood volume, burden the heart, and lead to metabolic alkalosis, which shifts the hemoglobin oxygen dissociation curve leftward, impairing oxygen release in tissues.

   (4) Volume Expansion Some patients may experience hypotension due to reduced blood volume from vomiting, sweating, or diuretic use, rather than true cardiogenic shock. If the patient shows no clinical or X-ray signs of heart failure, a volume expansion test may be performed: infuse 200 ml of normal saline IV over 15–20 minutes. If blood pressure does not improve, guide further treatment based on central venous pressure or pulmonary capillary wedge pressure.

   1. When the central venous pressure is less than 1.2 kPa (12 cmH₂O) or the pulmonary capillary wedge pressure is less than 2 kPa (15 mmHg), administer 5% glucose in normal saline intravenously at a rate of 20 ml per minute, and measure the central venous pressure every 3 minutes. If there is no significant change in central venous pressure, but the stirred pulse blood pressure rises, shock symptoms improve, and urine output increases, the intravenous drip can be continued. If the central venous pressure increases by more than 0.294 kPa (3 cmH₂O), the infusion should be temporarily stopped. If the central venous pressure returns to the original level after 3 minutes, the infusion can be resumed while closely monitoring changes in central venous pressure.
   2. When the central venous pressure is between 1.2–1.5 kPa (12–15 cmH₂O), the infusion rate should be reduced to 10 ml/min. Special attention should be paid to observing whether signs of pulmonary edema, such as dyspnea or moist rales at the lung bases, appear. Excessive fluid infusion can lead to pulmonary edema, and central venous pressure may not promptly reflect left ventricular filling pressure. That is, when left ventricular filling pressure begins to rise, central venous pressure may still be within the normal range.
   3. If the central venous pressure exceeds 1.5 kPa (15 cmH₂O) or the pulmonary capillary wedge pressure exceeds 2.4 kPa (18 mmHg), and signs of pulmonary edema appear, fluid infusion should be stopped. Alternatively, inotropic agents such as dopamine or dobutamine may be added to the fluid. If the central venous pressure decreases after medication, fluid infusion may still be continued based on clinical conditions.
   (5) Selection of Fluids: In the initial stage, it is advisable to use normal saline or 5% glucose solution, as these fluids can be rapidly excreted from the body in case of overdose. If volume expansion is effective, appropriate amounts of plasma, whole blood, dextran, or normal saline may be selected for continued intravenous infusion based on the patient's history (e.g., severe vomiting, profuse sweating, blood loss, etc.).
4. Black Catechu Phenolic Amines: After excluding hypovolemia and other factors causing hypotension, if blood pressure still does not recover, Black Catechu phenolic amines should be selected to maintain blood pressure and enhance myocardial pumping function.

   (1) Dobutamine: This is the drug of choice for cardiogenic shock. It directly acts on myocardial β1 receptors, and its inotropic effect is stronger than that of digitalis or dopamine. It can increase cardiac output, reduce left ventricular filling pressure, and selectively dilate mesenteric and renal vessels, with no significant effect on heart rate or blood pressure. It rarely causes arrhythmias. Administer 100–250 mg in 500 ml of 5% glucose solution for intravenous infusion, with an initial dose of 200 μg/min and a maximum dose of 1,500 μg/min.

   (2) Dopamine: Its pharmacological effects are similar to those of dobutamine. It is often administered at a concentration of 10–30 mg/dL, infused at a rate of 1 mg/min, which can be doubled if necessary. Its drawback is its stimulatory effect on α receptors. When the dose exceeds 10 μg/kg·min, it can cause tachycardia, increased peripheral resistance, increased myocardial oxygen consumption, and may induce arrhythmias due to heightened ventricular irritability.

   Currently, the combined use of dopamine and dobutamine is widely advocated. The dosage of each agent is 9.5 μg/kg·min. Combined therapy not only reduces the dose of each drug but also increases pulse pressure, maintains pulmonary capillary wedge pressure within the normal range, and mitigates the increased oxygen consumption caused by dopamine.

5. Vasodilators should not be used alone for the following reasons: when cardiac output decreases, the small arteries in the skin and abdominal organs constrict to redistribute blood flow, ensuring blood supply to the heart and brain. The use of vasodilators leads to widespread dilation of small arteries, resulting in reduced blood flow to the heart and brain; meanwhile, the decrease in systemic diastolic pressure reduces coronary artery perfusion pressure and blood flow. When combined with catecholamine vasopressors, adjusting the dosage based on indicators such as central venous pressure, pulmonary capillary wedge pressure, and arterial blood pressure often yields better results. For milder cases, phentolamine and dopamine can be used together, with the addition of aramine if necessary. The concentrations of dopamine, aramine, and phentolamine should be 200, 20–400, and 50–100 mg/L, respectively, administered at a rate of approximately 1 ml/min. If the heart rate is elevated, phentolamine should be replaced with sodium nitroprusside. The latter acts directly on vascular smooth muscle, dilating both arteries and veins, increasing tissue blood perfusion, improving microcirculation, and reducing both preload and afterload on the heart. Typically, 50 mg of this agent is added to a 5% glucose solution, with a usual dosage of 20–100 μg/min. Continuous intravenous infusion should not exceed 72 hours. The solution must be freshly prepared, and the infusion bottle should be wrapped in black paper to avoid light exposure, preventing decomposition into toxic thiocyanate.
6. The main risk of using Rehmannia-based preparations in cardiogenic shock caused by acute myocardial infarction is the increased excitability of the ischemic area, which can induce severe ventricular arrhythmias. Therefore, Rehmannia-based preparations should not be used within 24 hours of the infarction. They should only be considered when shock is accompanied by clear manifestations of congestive heart failure that do not respond to inotropic drugs like dobutamine, or when accompanied by rapid supraventricular tachycardia such as atrial fibrillation or paroxysmal supraventricular tachycardia.
7. Treatment of Arrhythmias Myocardial ischemia and acid-base imbalances can cause arrhythmias, and excessively fast or slow heart rates further reduce cardiac output. For sinus bradycardia, 1 mg of atropine can be administered intravenously. If bradycardia persists, atrial or ventricular pacing may be initiated based on whether the patient has atrioventricular block. Ectopic tachycardia can rapidly worsen cardiac function and expand the infarct area. For paroxysmal ventricular tachycardia, lidocaine, procainamide, bretylium, or verapamil may be used. For torsades de pointes, magnesium salts are preferred. For supraventricular tachycardia, digoxin, adenosine triphosphate, quinidine, or electrical cardioversion are commonly used.
8. Interventional Therapy

   (1) Thrombolytic Therapy If papillary muscle or chordae tendineae rupture or aortic dissection can be ruled out, 500,000 units of urokinase should be slowly injected intravenously, followed by an infusion of 1–1.5 million units. Alternatively, 750,000–1.5 million units of streptokinase can be added to a 5% glucose solution and infused over 1 hour, followed by a continuous infusion of 100,000 units per hour for 24–72 hours.

   (2) Percutaneous Transluminal Coronary Angioplasty (PTCA) This procedure may be considered for patients with contraindications to or poor response to thrombolytic therapy. The method involves inserting a balloon catheter into the diseased coronary artery and injecting contrast medium to dilate the narrowed lumen, restoring blood flow. Laser ablation of the stenotic lesion can also achieve the same goal.

9. Counterpulsation This includes intra-aortic balloon counterpulsation and external counterpulsation. The principle is similar: the procedure increases diastolic pressure in the aorta, thereby enhancing coronary artery blood flow. During systole, aortic pressure decreases, peripheral resistance vessels dilate maximally, reducing left ventricular ejection impedance, lowering left ventricular systolic pressure, increasing cardiac output, and decreasing myocardial oxygen consumption.

Counterpulsation has a clear short-term effect on cardiogenic shock. It is currently mainly used for patients with complications such as papillary muscle rupture or ventricular septal perforation, or those preparing for coronary artery bypass surgery, to improve their clinical condition and create opportunities for surgical intervention.

bubble_chart Prevention

Active prevention and treatment of primary diseases is the most fundamental measure to prevent various types of cardiogenic shock. For patients with acute myocardial infarction, in addition to providing symptomatic treatments, reperfusion should be performed within 2 to 4 hours after the onset of chest pain. Early reperfusion is a crucial means to salvage ischemic myocardium, prevent the expansion of the infarct area, and avert the occurrence of shock. Common methods include thrombolytic therapy and percutaneous transluminal coronary angioplasty. In recent years, the successful promotion of these measures has significantly improved the survival rate of cardiogenic shock.

bubble_chart Differentiation

Shock from any cause can lead to a decrease in coronary {|###|} artery blood flow. On the other hand, patients with pre-existing coronary heart disease are more prone to myocardial injury if hypotension occurs. Therefore, unless the patient has a typical history of myocardial infarction, clinical manifestations, and electrocardiographic changes, a diagnosis of cardiogenic shock should not be made hastily for patients with only ischemic myocardial injury on electrocardiogram combined with shock.

Cardiogenic shock should be differentiated from the following conditions:

1. Hypovolemic shock Loss of blood can cause hypovolemic shock. The most common cause in internal medicine is duodenal ulcer. Various traumas can lead to severe internal bleeding, with bleeding in the mediastinum and retroperitoneal space being the most frequent. In aortic {|###|} dissection, blood enters the dissected aortic {|###|}, accumulating in the aortic {|###|} media, thoracic cavity, or retroperitoneal space as an abdominal mass. Patients present with severe chest pain, which is very similar in nature to that of acute myocardial infarction. Aortic {|###|} dissection can extend to the pericardium, leading to cardiac tamponade. Additionally, aortic {|###|} dissection may obstruct the coronary {|###|} artery ostium, resulting in myocardial infarction. Echocardiography is of decisive value in diagnosing this condition.
2. Pulmonary embolism is more common in the elderly and chronically bedridden patients with sexually transmitted diseases, with thromboembolism caused by deep vein vasculitis being the most frequent. Pulmonary embolism obstructs pulmonary blood flow, reducing left ventricular return and preload, thereby decreasing cardiac output and coronary {|###|} artery blood flow. Severe cases may complicate shock. Main symptoms include dyspnea and chest pain; half of the patients experience cough and anxiety. Wheezing may be heard on lung auscultation. Diagnosis primarily relies on chest X-rays, computed tomography (CT), etc.
3. Neurogenic shock Severe pain or major trauma can both lead to shock. On the other hand, patients with major trauma may suffer massive hemorrhage, resulting in concurrent neurogenic and hemorrhagic shock. Most cases are relatively easy to correct by treating the primary cause and precipitating factors (e.g., analgesia), oxygen therapy, subcutaneous epinephrine injection, and intravenous fluid resuscitation to expand blood volume. Differential diagnosis is not difficult when combined with clinical history.