Cardiogenic shock in the elderly

Introduction to cardiogenic shock in the elderly Cardiogenic shock refers to cardiac pump failure caused by various reasons, which is manifested by a significant decrease in arterial pressure. Shock signs such as disturbance of consciousness, oliguria and sweating, mostly due to the reduction or loss of the contractile component of the heart (mainly the left ventricle), or due to the filling of the heart chamber, resulting in a sharp decrease in cardiac output and even shock. basic knowledge The proportion of illness: 0.003% Susceptible people: the elderly Mode of infection: non-infectious Complications: arrhythmia pulmonary edema

Etiology of cardiogenic shock in the elderly

(1) Causes of the disease

1. Cardiogenic shock: Most of them are elderly patients with myocardial infarction (80.64%), which is related to myocardial ischemic damage and myocardial degeneration in elderly patients.

2. Other causes: acute severe myocarditis can cause acute heart failure or cardiogenic shock, more common in children and young people, older people are less common, dilated (congestive) cardiomyopathy and heart valve patients usually cause chronic congestive heart Decline, if these patients have acute complications, such as tachyarrhythmia or pulmonary embolism, cardiac output can be drastically reduced and lead to cardiogenic shock, the elderly heart is less adaptable to sudden changes in heart rate, especially when the ventricular rate When the increase is obvious, the ventricular diastolic filling is reduced, the stroke volume and the heart index are significantly decreased, resulting in insufficient perfusion of the whole body tissues and organs, so atrial atrial fibrillation, atrial flutter, ventricular tachycardia and other tachyarrhythmias are The common cause of cardiogenic shock in elderly patients with heart disease. In recent years, cardiac surgery such as valve replacement, coronary artery bypass surgery indications have been extended to elderly patients, but compared with young people, elderly patients with complications and mortality during surgery High and low displacement syndrome is one of the main complications after surgery and is a common cause of cardiogenic shock.

(two) pathogenesis

Acute myocardial infarction cardiogenic shock can be divided into primary (myocardial) and secondary, and the former is more, accounting for 2/3 of the total.

Primary shock

Most of them occur within a few hours to 24 hours after myocardial infarction, mainly due to large myocardial infarction, reduced ventricular contraction components, which depends not only on the number of irreversible myocardial necrosis, but also on the size of reversible myocardial ischemia. A pathophysiological feature is essential for the prevention and treatment of cardiogenic shock. In the initial stage of myocardial infarction, if the ischemic myocardium is saved and protected from necrosis, the infarct size can be limited and reduced.

Pathological anatomical observation showed that myocardial infarction died of cardiogenic shock. The total area of fresh necrotic lesions and old lesions reached more than 40% of the total left ventricular area. Coronary artery lesions were severe and extensive, and the anterior descending branches were often involved, mostly complete. Sexual obstruction, 3 lesions in 2/3 cases, and 2 lesions in 1/3 of cases.

In recent years, studies have confirmed that there is an ischemic marginal zone around the infarcted area containing necrotic cells and cells that are damaged to varying degrees, but if the ischemia is further aggravated, the marginal zone may be completely or partially necrotic, and the infarct size may be expanded. Alonso et al. (1973) It has been found that 80% of cases of cardiogenic shock have an infarct enlargement, and one third of cases have an infarct enlargement before shock, one third is not sure of the onset time, and another 1/3 of the infarct is enlarged after shock. It indicates that a vicious circle may be formed during cardiogenic shock, that is, arterial pressure decreases during shock, coronary perfusion pressure decreases, myocardial ischemia worsens, and infarct area expands. This series of changes further impairs heart pump function and finally develops irreversible shock.

In addition to the size of the infarct size, there are other factors that can reduce the amount of left ventricular ejection:

1 Myocardial ischemia depends on anaerobic metabolism, myocardial ATP content decreases, lactic acid increases, causing lactic acidemia;

2 tachycardia reduces ventricular filling;

3 papillary muscle ischemia can cause mitral regurgitation;

4 abnormal wall motion of the lesion site or abnormal pulsatile pulsation.

The pathophysiology of cardiogenic shock may involve the regulation of peripheral blood vessels. In general, the reduction of cardiac output caused by any cause has an increase in reflex sympathetic tone, which increases peripheral resistance, but some patients with cardiogenic shock do not have peripheral resistance. Increased, even lower than normal, the results of experimental myocardial ischemia studies are very inconsistent. In the cardiogenic shock model, no vasoconstriction occurred in the peripheral area, which may be the result of a reflex induced by myocardial ischemic area. He Ruirong et al. In the experiment of blocking acute left myocardial infarction caused by left anterior descending coronary artery in dogs, it was also found that there was reflex inhibition of peripheral vascular activity, which was thought to be caused by activating afferent fibers of cardiac vagus nerve and inhibiting the activity of vascular movement center.

Myocardial infarction mainly affects the left ventricle, but the right ventricle can be infarction at the same time. The pathological anatomical data show that the incidence rate is 5% to 34%. It is mainly found in the inferior wall of the left ventricle. Among them, the posterior wall infarction involves the ventricular septum. Patients with right ventricular infarction can be up to 50%, and patients with right ventricular infarction are more serious and prone to cardiogenic shock.

2. Secondary shock: more than 24 hours to 1 to 2 weeks after myocardial infarction, the main cause of shock is papillary muscle infarction or rupture leading to acute mitral regurgitation; ventricular septal perforation occurs left to right shunt; ventricle The formation of a wall tumor, the abnormal pulsation of the wall of the wall, and the rupture of the ventricular wall, etc., the mechanism of shock is different from the primary, mainly due to the existence of the above-mentioned mechanical complications, resulting in a sharp decrease in the amount of left ventricular ejection during systole and even shock, so Called secondary or mechanical shock.

(1) Papillary muscle rupture: usually occurs within the first week after onset, and the affected part of the rupture (the nipple body or head) can cause different degrees of mitral regurgitation.

(2) ventricular septal rupture: occurs within 1 to 2 weeks of onset, resulting in acute left to right shunt.

(3) ventricular aneurysm: mainly causes chronic heart failure, ventricular arrhythmia, systemic embolism, etc., but the acute phase of myocardial infarction, such as ventricular aneurysm formation, can significantly affect left ventricular ejection function, left ventricular contraction, The ventricular wall tumor bulges, and some of the blood stays in the ventricular aneurysm, reducing the stroke volume.

(4) left ventricular free wall perforation: more than 3 to 5 days after myocardial infarction, leading to acute pericardial tamponade, cardiogenic shock, rapid death, sometimes, blood flow into the pericardium is slow, forming a pericardial hematoma and pseudo-compartment A wall tumor, the latter can also be worn.

The common hemodynamic consequence of the above complications is that there is more blood shunting during systole, reflux or stagnation in the ventricular aneurysm, resulting in a significant decrease in stroke volume and ejection fraction, and even shock.

Elderly patients with cardiogenic shock prevention

Elder cardiogenic shock is an extremely critical cardiac emergency, and the mortality rate is very high. Cardiogenic shock is mostly caused by severe organic heart disease. In order to prevent the occurrence of cardiogenic shock, the focus should be on the primary disease. In the treatment and monitoring, medical staff engaged in cardiovascular disease, especially those working in the CCU, should have a comprehensive and in-depth understanding of the diagnostic monitoring and emergency treatment of cardiogenic shock, and should also master and non-cardiogenic shock. Differential diagnosis to avoid delay in treatment.

Elderly patients with cardiogenic shock complications Complications arrhythmia pulmonary edema

The main complications are arrhythmia, acute pulmonary edema, interventricular septal perforation and papillary muscle rupture.

Symptoms of cardiogenic shock in the elderly Common symptoms Indifferent expression Skin pale, slow response, irritability, discomfort, pale, electro-mechanical separation, phlegm, edema, papillary muscle, atrioventricular block

Early clinical signs of cardiogenic shock are due to heart pump failure, sympathetic excitation, increased release of catecholamines, and early hypoperfusion. There are increased heart rate, ventricular arrhythmia, wet bottom of the lungs, irritability, paleness Sweating, etc., the arterial pressure change is not obvious at this time, the systolic blood pressure is normal or low, and the diastolic blood pressure is slightly increased, but the early signs of shock may be caused by other symptoms of myocardial infarction.

Before the occurrence of secondary shock, there are generally clinical manifestations of mechanical complications, such as ventricular septal rupture or papillary muscle rupture caused by loud systolic murmur and pseudo heart failure symptoms, caused by left ventricular free wall perforation The pericardial tamponade develops rapidly, the diagnosis is not easy, and there is electro-mechanical separation in the clinic, that is, shock occurs suddenly, blood pressure and heart sound disappear, and ECG activity still exists. At this time, ECG monitoring can find that the heart rate suddenly slows down, and there is sinus slowness or Atrioventricular junction rhythm, or high atrioventricular block, or QRS wave gradually widened, and finally arrest, according to the above performance may consider the possibility of ventricular wall perforation.

After shock occurs, the main manifestations are arterial pressure drop, systolic blood pressure below 80mmHg, small pulse pressure, fine pulse rate, insufficient tissue and organ perfusion, brain: indifferent expression, unresponsiveness, coma; kidney: oliguria or anuria, low urine output At 20ml / h; skin: pale complexion and pale skin, lips and limbs cyanosis, limbs wet and cold, cold sweat; heart: heart rate increased, up to 110 ~ 140bpm, heart sounds low, ventricular galloping or fourth heart sound; Lung: shortness of breath, wet lungs in both lungs, acute pulmonary edema in severe cases, obvious cerebral arteriosclerosis in the elderly, when blood pressure drops, cerebral blood flow is significantly reduced, it is easy to be associated with central nervous system symptoms, such as cerebral thrombosis Form and so on.

Right ventricular infarction is characterized by right heart failure, pulmonary congestion is not obvious, arterial pressure is reduced, tricuspid valve fluid sign (systolic murmur, jugular vein V wave), ECG can be seen in V4 R lead ST segment elevation, lower Wall and/or posterior wall infarction pattern with varying degrees of atrioventricular block or supraventricular arrhythmia, such as sinus sinus, atrial premature contraction, atrial fibrillation, etc., serum myocardial enzymes are significantly elevated, ultrasound Cardiogram can show enlargement of the right ventricle, ventricular septal motion, hemodynamic examination showed right ventricular filling pressure, that is, elevated right atrial pressure, pulmonary wedge pressure or pulmonary end-diastolic pressure (representing left ventricular filling pressure) only Mild increase, the ratio between the two increased (RAP / PAEDP> 0.8), right ventricular and pulmonary systolic pressure does not increase, the above pressure changes can also be seen in cardiac tamponade and constrictive pericarditis, must be identified, pulmonary embolism can also It affects right ventricular function but can be differentiated according to pulmonary systolic blood pressure and abnormal increase of pulmonary end-diastolic pressure caused by pulmonary arteriospasm with normal pulmonary wedge pressure. It should be noted that right ventricular infarction blood The changes in flow dynamics can be masked by a drop in arterial pressure during cardiogenic shock, which can be revealed after expansion of blood volume.

Examination of cardiogenic shock in the elderly

1. Red blood cell count, hemoglobin and hematocrit determination to see if there is blood concentration or reduced circulating blood volume.

2. Arterial blood gas analysis and pH determination, detection of hypoxemia and acidosis, observation of efficacy.

3. Determination of urine volume: The bladder indwelling catheter continuously observes the urine volume, and maintains the urine volume >30ml/h. If the urine volume <20mL/h, the renal function tends to be depleted.

4. Others: including blood electrolytes, lactic acid concentration, renal function tests, platelet, fibrinogen, prothrombin time, plasma protamine co-coagulation test (3P test) and fibrin degradation product (FDP) test if necessary , blood culture and bacteriological examination.

If conditions permit patients to be admitted to the intensive care unit (ICU), closely observe body temperature, respiration and pulse, and perform necessary hemodynamics and experimental examination and monitoring.

5. Arterial pressure monitoring: In addition to early shock, the patient's arterial pressure is reduced. If the blood pressure is measured by the cuff when the surrounding blood vessels contract, the measured value is often lower than the actual. If the blood pressure is directly monitored by transarterial intubation, the arterial systolic pressure is maintained at 90 mmHg. The average pressure of about 80mmHg is used as a basis for adjusting the drug, which is more practical.

6. Central venous pressure (CVP) and pulmonary wedge pressure (PWP) monitoring: CVP was measured from the peripheral venous cannula to the proximal right atrium adjacent to the vena cava, which reflected the right ventricular filling pressure, normal value 9 ~ 12cmH2O, lower than normal for blood volume deficiency, higher than normal, suggesting right heart dysfunction or excessive fluid volume, to help identify cardiac dysfunction and insufficient blood volume.

Pulmonary wedge pressure (PWP) was used to monitor left ventricular function. The swan-ganz was delivered from the peripheral vein to the pulmonary arterioles. The wedge was inserted into the PWP. The normal value was 6-12 mmHg, usually PWP and left ventricular end-diastolic pressure. LVEDP) is similar or equal. Below normal, it indicates insufficient blood volume. >18mmHg indicates left ventricular dysfunction. Monitoring PWP can estimate blood volume and monitor infusion rate. It is a useful indicator to prevent pulmonary edema.

7. Cardiac output (CO) and cardiac index (CI) CO normal range of 3.5 ~ 5.5L / min, CI is 3.0 ~ 4.5L / (min · m2), while monitoring PWP and CI, the purpose is not Under the premise of making PWP>18mmHg, guide the clinical selection of drugs and try to increase the CO level.

8. ECG monitors heart rate and recognizes arrhythmia.

Diagnosis and diagnosis of cardiogenic shock in the elderly

Diagnostic criteria

The clinical diagnosis of cardiogenic shock includes the following two points:

1. Arterial pressure reduction: systolic blood pressure is less than 80mmHg, or more than 30mmHg before myocardial infarction, and lasts for at least 30min.

2. Insufficient blood perfusion of tissues and organs Brain: irritability or indifference, kidney: urine volume is less than 20ml / h, skin: wet and cold.

Some authors have also proposed that the heart index is lower than 2.2L/(min·m2), and LVFP>18mmHg is listed as one of the diagnostic criteria. The symptoms of elderly patients with myocardial infarction are often atypical, without chest pain, and early performance can only drop blood pressure, breathing Difficulties or neurological symptoms, therefore, acute shock of cardiogenic shock may be considered in the elderly when sudden shock occurs.

Differential diagnosis

Acute myocardial infarction cardiogenic shock should be identified within the first 24 hours of the onset of the disease:

1. Hypotension and sinus tachycardia caused by vagus nerve excitability: mainly seen in inferior myocardial infarction, given atropine, blood pressure can quickly rise.

2. Ventricular arrhythmia: If ventricular tachycardia can suddenly drop blood pressure, blood pressure can return to normal after cardioversion.

3. Low blood volume: vomiting and sweating, eating too little can cause, may also be related to blood redistribution, this change is more likely to occur in the elderly, at this time for hemodynamic examination, left ventricular filling pressure and The heart index is reduced.

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