Acute myocardial infarction (AMI) with cardiogenic shock is a clinical syndrome characterized by a series of ischemia, hypoxia, metabolic disorders, and damage to important organs due to a dramatic and significant decrease in cardiac output within a short period of time, which leads to severe perfusion deficits in all organs, and is one of the most critical complications and a major cause of death in AMI. The incidence of cardiogenic shock (about 15%-25%) and death rate (about 50% die within 10 h of shock onset and 80% die within 1 week) have decreased in AMI. Emergency revascularization supported by intra-aortic balloon counterpulsation (including emergency percutaneous transluminal coronary angioplasty and emergency coronary artery bypass grafting) and timely treatment of fatal arrhythmias reduce the morbidity and mortality rate (below 50%).
Pathogenesis of cardiogenic shock
Severe left ventricular (LV) dysfunction, right ventricular AMI (which accounts for only 5% of cases and is mainly due to a decrease in LV volume due to RV underfilling), and acute valvular disease (especially acute mitral valve insufficiency or septal perforation) can all cause cardiogenic shock. The proximal segment of the anterior descending branch occlusion is prone to combined left heart failure and cardiogenic shock, and the infarct size is usually more than 40% when cardiogenic shock occurs.
1.Systolic function impairment
The ischemic or necrotic myocardium may show asynchronous contraction with the normal myocardium nearby, reduced myocardial fiber shortening, myocardial fiber shortening arrest and paradoxical motion (also known as paradoxical expansion motion, i.e., necrotic myocardium completely loses its contractile function and protrudes out of the systolic phase of the myocardium), which seriously affects the work of the heart, while the non-infarcted myocardium is in a state of hyperdynamic contraction ( Frank-Starling mechanism and increased catecholamines in the blood circulation). The area of necrosis is small and myocardial depression can seriously impair cardiac function.
2.Diastolic impairment
Left ventricular end-diastolic pressure is excessively elevated resulting in decreased left ventricular diastolic compliance.
3. Hemodynamic changes
The low arterial pressure caused by the decrease of left ventricular beat volume can reduce coronary blood perfusion and further aggravate myocardial ischemia and enlarge the infarct scope, forming a vicious circle; the left ventricular emptying obstacle increases preload and increases ventricular wall tension, further reducing subendocardial myocardial perfusion; these “worsen” cardiac blood volume and thus constitute a “vicious circle”. These further “worsen” the cardiac output, thus constituting a “vicious circle”. If combined with atrioventricular block, mitral valve insufficiency or ventricular septal rupture, the hemodynamics deteriorate even more.
4.Cardiac arrhythmia
The ability of the ischemic heart to adapt to a larger range of heart rate changes is significantly reduced. Rapid arrhythmias can increase myocardial oxygen consumption and further aggravate myocardial hypoxia, while slow arrhythmias cannot increase cardiac reserve and further reduce cardiac output.
5.Other
During cardiogenic shock, the presence of a myocardial depressor factor (MDF) in the blood circulation can significantly weaken myocardial contractility and aggravate the progression of shock; nausea, vomiting and massive water loss lead to insufficient blood volume and promote the development of shock; hypoxemia caused by pulmonary ventilation and ventilation dysfunction during acute myocardial infarction may also be involved.
Clinical manifestations
Myocardial infarction with shock can occur immediately, but most of them occur gradually, i.e., within a few hours to 2-3 days after AMI, with the main manifestations being decreased perfusion of vital organs and pulmonary bruising. The risk is closely related to the presence of previous myocardial infarction, hypertension, congestive heart failure, and advanced age. Among them, infarct size and history of previous old myocardial infarction are important factors affecting prognosis.
Clinical features
1. early irritability, pallor, dry mouth, excessive sweating while the extremities are syncopal and cyanotic, late florid skin changes and extensive skin, mucosal and visceral bleeding, i.e., manifestations of diffuse intravascular coagulation, and multi-organ failure.
2. mental disorders, with still clear consciousness evolving into indifference, blurred consciousness, and confusion until coma.
3. decreased urine output (<20 ml/h) or even anuria, urine output <30 ml/h, urine specific gravity >1.02 suggesting hypovolemia, with a better prognosis for those who maintain urine output at 50 ml/min.
4. increased heart rate (often >120bpm) and weak pulse.
5, blood pressure decreased, systolic blood pressure below 90mmHg or the original hypertensive people systolic blood pressure drop more than 30mmHg, pulse pressure <20mmHg (Note: many patients can successfully recover from severe hypotension in the short term, so only hypotension is not enough to diagnose cardiogenic shock);
6, S1 decreases suggesting a decrease in left heart contractility, gallop rhythm that is an early sign of left heart failure, and monophonic rhythm in severe cases.
7, acute pulmonary edema manifestations.
8, pulmonary capillary wedge pressure (PCWP) >20mmHg, cardiac index (CI) below 2L/(min?m2).
Hemodynamics Cardiac work per beat and blood volume per beat decrease, cardiac index decreases, left ventricular end-diastolic pressure or filling pressure increases, and central venous pressure is no longer a reliable indicator of left ventricular filling pressure. Pulmonary capillary wedge pressure intermittently reflects left atrial and left ventricular filling pressures (or left ventricular end-diastolic pressure). Pulmonary capillary wedge pressure above 17 mmHg may lead to pulmonary congestion, and above 25 mmHg to alveolar pulmonary edema.
Diagnosis and differential diagnosis
The diagnosis of cardiogenic shock can be confirmed based on clinical features and hemodynamic changes, except for vasovagal reactions secondary to pain, hypoxia, etc. or hypovolemic shock.
Treatment
Treatment strategy: Identify cardiogenic shock as early as possible and treat it on the basis of AMI intervention before irreversible metabolic changes and organ damage or microcirculatory disorders, with the aim of improving cardiac function, preventing infarct extension, and ensuring that cardiac output and perfusion pressure can meet the effective perfusion requirements of target organs. Treatment indicators: mean arterial pressure maintained at 70-80 mmHg, heart rate 90-100 bpm; left ventricular filling pressure <20 mmHg, reduced cardiac work, gold indicator is the increase in heart beat volume. Arterial partial pressure of oxygen (PaO2), blood pressure and urine volume can be used as indicators for determining disease regression.
1.General treatment
Extra-cardiac factors can induce or aggravate cardiogenic shock, which should be corrected.
(1) Sedation and pain relief: The severe chest pain of AMI can induce and aggravate shock, and is even one of the reasons why shock is difficult to reverse. The preferred choice is morphine intravenous administration (3-5mg, respiration and blood pressure without significant effect on the state of chest pain is not relieved, can be repeated after 15-30min), AMI thrombolytic therapy is contraindicated. The combination of nitroglycerin, analgesics, oxygen and β-blockers can effectively relieve pain.
(2) oxygenation: AMI and cardiogenic shock due to reduced tissue blood perfusion are varying degrees of hypoxemia, intractable cardiogenic shock is particularly, arterial oxygen partial pressure is often reduced earlier than the pulmonary edema X-ray signs. Depending on the patient’s status, oxygen can be administered by nasal cannula, semi-open mask or ventilator (high flow rate 5-10L/min) to make the arterial oxygen saturation greater than or equal to 90% (partial pressure of oxygen maintained above 60mmHg). Continuous bedside monitoring of skin oxygen saturation per beat.
(3) Appropriate supplemental blood volume: AMI complications of cardiogenic shock when the body’s blood volume is absolutely or relatively insufficient is also one of the causes of shock difficult to treat, so it is important to improve hypovolemia. In the absence of acute pulmonary edema, a fluid tolerance test is feasible, i.e., the therapeutic response (blood pressure, heart rate, urine output, and pulmonary improvement or not) to isotonic volume expanders such as saline administered intravenously at 200 mL within 30 min. Clinical improvement suggests insufficient blood volume and should be rehydrated (250-500mL intravenously over 1h). The rate of infusion may be based on urine volume, venous pressure, blood pressure, pulmonary signs or pulmonary capillary wedge pressure, and cardiac output. Monitor hemodynamics as much as possible, with PCWP controlled at 20 to 24 mmHg and the rise in venous pressure limited to about 15 to 20 cmH2O.
In right ventricular infarction combined with cardiogenic shock, vasodilator therapy can improve the shock state by increasing left ventricular preload and cardiac output. However, rapid rehydration of 1000 mL without significant reversal of shock should be followed by immediate hemodynamic monitoring (excessive rehydration may not help to correct the shock and may cause pulmonary edema) and application of vasoactive drugs. In view of the fact that once the input of excessive glucose solution is easily excreted by the kidneys, 5% glucose solution is preferred, and various other crystalloid solutions, low-molecular dextrose, plasma, etc. can also be used.
(4) Acidosis
The accumulation of acid in anaerobic metabolism and the decrease of renal H+ excretion can cause metabolic acidosis, which can inhibit myocardial contractility and cardiac arrhythmia and reduce the responsiveness of the heart to vasoactive drugs, so the acidosis should be improved in time. Treatment target: blood pH ≥ 7.30, blood bicarbonate 20 mmol/L. Excess alkali and sodium may cause increased left ventricular end-diastolic pressure and further worsen shock, so caution should be exercised.
(5) Arrhythmia control
Tachycardia or bradyarrhythmia can reduce cardiac output and expand the infarct, induce and aggravate cardiogenic shock, so it should be actively controlled. Avoid negative inotropic effects such as propafenone and pyridostigmine as much as possible.
2.Vasoactive drugs
Dopamine and dobutamine can improve the patient’s hemodynamics, but both can increase myocardial oxygen consumption and aggravate myocardial ischemia, and vasodilators can increase cardiac output and lower left ventricular filling pressure and lower coronary artery perfusion pressure, forming a vicious circle. Sodium nitroprusside reduces LV end-diastolic pressure by uniformly dilating small arteries and veins, and dobutamine increases the cardiac index and the maximum rate of increase of LV intraventricular pressure. However, more evidence-based medical evidence is needed to verify this.
3.Intra-aortic balloon counterpulsation (IABP)
IABP is more suitable for acute myocardial infarction combined with cardiogenic shock. Combined with vasodilators and positive inotropic drugs, it can increase cardiac output and maintain or even increase coronary perfusion pressure.
4.Blood flow reconstruction
Early coronary reperfusion (thrombolysis, emergency PCI, CABG or even heart transplantation) can reverse cardiogenic shock. However, late cardiogenic shock is mostly irreversible injury, and revascularization is not only difficult to achieve the therapeutic purpose, but also increases the risk of intraoperative death.
Prognosis
The risk of myocardial infarction with shock is closely related to the presence of previous myocardial infarction, hypertension, congestive heart failure, and age over 60 years. In addition, the presence of cardiac enlargement, peripheral edema, and pulmonary edema increases mortality; the size of the infarct and the presence of previous myocardial infarction are important factors in the prognosis. Patients with severe cardiogenic shock who are treated with aggressive volume expansion and vasoactive drugs but whose blood pressure does not recover have a higher mortality rate.