Cardiovascular disorders

Cardiovascular disorders is the state in which blood flow and perfusion of peripheral tissues are insufficient to sustain life due to insufficient cardiac output or poor distribution of peripheral blood flow, generally accompanied by hypotension and oliguria.


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  • 1 General information
  • 2 Symptoms and signs
  • 3 Complications
  • 4 Diagnosis
  • 5 Prognosis and treatment
  • 6 External links
  • 7 Sources

General information

Shock may be due to hypovolemia , vasodilation, or cardiogenic causes (low cardiac output) or to a combination. The fundamental defect is the reduced perfusion of vital tissues due (generally) to hypotension, so that the release or uptake of O2 is insufficient for aerobic metabolism , leading to a shift towards anaerobic respiration, with increased production and accumulation of lactic acid. When shock persists, impaired organ function is followed by irreversible injury and cell death.

The degree of systemic hypotension required to cause shock varies, and often depends on pre-existing vascular causes. Thus, a small degree of hypotension that is well tolerated by a relatively healthy young person could lead to severe brain, cardiac, or renal dysfunction in a patient with significant arteriosclerosis .

  • Hypovolemic shock. Hypovolemic shock is associated with insufficient intravascular volume (absolute or relative), causing decreased ventricular filling and stroke volume . Unless compensated for by an increased heart rate, it results in decreased cardiac output. A common cause is acute bleeding (eg, from trauma, peptic ulcer, esophageal varices, or aortic aneurysm). The bleeding may be evident (eg, hematemesis or melena) or hidden (eg, ruptured ectopic pregnancy). Hypovolemic shock may also follow increased losses of bodily fluids other than blood.

Hypovolemia generally takes several hours to develop and may be accompanied by an increase in Hb or Ht (due to hemoconcentration). The hypovolemic shock may be due to inadequate fluid intake, which causes dehydration, often with increased fluid loss. Frequently, due to their neurological or physical disability, patients are often unable to respond to thirst by increasing fluid intake. In hospitalized patients it can be increased if the early signs of respiratory failure are incorrectly attributed to heart failure, suppressing fluids or administering diuretics .

  • Vasodilation shock. Vasodilation shock is a consequence of relative insufficiency of intravascular volume, caused by vasodilation. Circulatory blood volume is normal, but insufficient to adequately fill the heart. Several conditions can cause diffuse arterial or venous dilation; for example, traumatic brain injury or severe bleeding (neurogenic shock), liver failure, or the ingestion of certain drugs or toxins.

Shock associated with a bacterial infection (bacteremic or septic shock: this may be due in part to the vasodilatory effect of endotoxins or other chemical mediators on resistance vessels, thus reducing vascular resistance. In addition, some patients with acute MI and shock appear to have insufficient compensatory vasoconstriction in response to decreased cardiac output, if cardiac output does not rise in proportion to decreased vascular resistance, hypotension arises.

Below a critical systemic AP, the vital organs will be insufficiently perfused. Myocardial dysfunction secondary to insufficient coronary perfusion or other mechanisms (eg, release of myocardial depressor factor or other toxic substances) can complicate shock by vasodilation.

  • Cardiogenic shock. Relative or absolute reduction in cardiac output due to factors other than intravascular volume insufficiency can cause shock.

Symptoms and signs

Symptoms and signs may be due to shock itself or the underlying disease process. Mental activity may be preserved, but lethargy, confusion, and drowsiness are common. Hands and feet are cold, clammy, and often cyanotic and pale. Capillary filling time is prolonged and, in extreme cases, a bluish reticular pattern may appear on large surfaces. The pulse is weak and fast unless there is heart block or terminal bradycardia; sometimes only the femoral or carotid pulse can be palpated.

There is tachypnea and hyperventilation, but when the respiratory center fails due to insufficient cerebral perfusion, apnea can be a terminal episode. BP taken with a cuff tends to be low (<90 mm Hg, systolic) or cannot be obtained, but direct measurement by intra-arterial cannula often gives significantly higher values.

In septic shock, a type of vasodilation shock, there is usually fever, usually preceded by chills. High cardiac output is accompanied by a decrease in total peripheral resistance, possibly with hyperventilation and respiratory alkalosis. Thus, early symptoms may include a shaking chill, a rapid rise in temperature, skin with a heat surge, a pounding pulse, and a rising and falling BP ( hyperdynamic syndrome ).

Urinary flow is decreased despite high cardiac output. Generally the mental state is affected and the mental confusion can be a premonitory sign that precedes hypotension ³24 h. However, these findings vary and may not be evident, even in patients whose markedly increased cardiac output and decreased vascular resistance are confirmed by direct hemodynamic measurements. In successive phases there may be hypothermia . Other causes of vasodilation shock (eg, anaphylaxis) may present with findings similar to those of septic shock.


Lung complications that often coexist or develop in patients with shock should not go unnoticed. Pulmonary edema after hypovolemia is generally caused by excessive fluid infusion during resuscitation, although it may be confused with pneumonia due to unrecognized sepsis or aspiration of gastric contents due to transient CNS depression.

Lung edema in septic shock generally results from increased patency of the pulmonary capillaries and alveolar epithelium, resulting in increased fluid exudation into the lungs. This complication ( adult respiratory distress syndrome ) is very serious. Hydrostatic pulmonary edema often complicates cardiogenic shock due to the marked increase in nailed pulmonary capillary pressure (PCPC).


For diagnostic evidence of insufficient tissue perfusion due to decreased cardiac output it is needed. Many consider that there is shock in any patient with predisposing factors that present a significant decrease in BP, a urine flow <30 ml / h and a progressive increase in arterial lactic acid concentration or an increase in anionic vacuum associated with reduced HCO3 levels. .

The diagnosis is supported by signs of hypoperfusion of specific organs (obctuation, oliguria, peripheral cyanosis ) or signs related to compensatory mechanisms (tachycardia, tachypnea, diaphoresis). In the earliest stages of shock many of these signs may be missing or go unnoticed if not specifically targeted. Thus, treatment should not be started until shock is advanced. None of these isolated signs is specific to shock; each of them must be assessed in the general clinical context.

In any type of shock, manifestations of the underlying disease can provide important diagnostic clues. Acute loss of blood or fluid from the aorta, spleen, or a ruptured tubal pregnancy or peritonitis may be suspected from physical findings. Signs of generalized dehydration are useful in diagnosing hypovolemia in patients with neurological, GI, renal, or metabolic disorders. Signs of lung disease, GI, or TU may be present in septic shock, as well as many signs of an underlying malignancy or debilitating disease that cause impaired immunity to infection.

Toxic shock syndrome may occur in women of gestational age due to the use of tampons; septic abortion, especially when performed illegally, can also produce septic shock. A systolic murmur may indicate a ruptured ventricular septum or mitral regurgitation, each of which can lead to shock after an acute MI.

Jugular venous distention, muffled heart sounds, pericardial rubbing, and a paradoxical pulse suggest pericardial tamponade. Massive pulmonary embolism is suspected in patients with parasternal elevation; a loud fourth noise to the left of the sternal border, increased on inspiration; a widely unfolded, accentuated closing noise, and distension of the jugular veins.

  • Hypovolemic shock. Normal or reduced ventricular filling pressure with low cardiac output in a patient in shock is diagnostic. A right ventricular filling pressure or a central venous pressure (PVC) <7 cm H2O (<5 mm Hg) indicates hypovolemia ; PVC can be higher than this when hypovolemic shock occurs in patients with pre-existing pulmonary hypertension . In some patients with chronic lung disease or cardiac dysfunction, end-diastolic pressure or PCPC measurements, both generally closely related to left ventricular pressure during diastole, is a better test.

Pulmonary end-diastolic pressure or PCPC <8 mm Hg (or <18 mm Hg in a patient with acute MI or pre-existing left ventricular disease) suggests hypovolemia. When hypovolemia is suspected, a therapeutic volume load test – rapid infusion (500 ml / 15 min) with 0.9% NaCl or colloid (see Prognosis and Treatment, below) – can help confirm the diagnosis. . Hypovolemia can be accepted when volume loading improves BP and urinary flow and reduces the clinical manifestations of shock , with small increases in PVC or PCPC. However, in septic shock there is also low PVC and low PCPC, so improvement after volume loading does not eliminate sepsis as the cause.

Hypovolemic shock from hemorrhage is usually accompanied by a decrease in Hb and Ht. However, since shock can develop in minutes of acute blood loss, normal Hb and Ht (before homeostatic hemodilution) do not eliminate bleeding. Elevation of Ht and Hb in hypovolemic shock indicate hemoconcentration due to loss of other body fluids.

  • Vasodilation shock . Vasodilation shock should be suspected in patients with traumatic brain injury, sepsis, drug intoxication, or exposure to heat with vasoregulatory failure and dehydration. Hypovolemia is also frequently present.
  • Cardiogenic shock. Cardiogenic shock is suggested by engorgement of the neck veins, signs of pulmonary congestion, and a gallop rhythm; however, in many patients with cardiogenic shock these signs are absent. In general, the diagnosis requires demonstration of decreased cardiac output with increased ventricular filling pressure.

Pericardial tamponade, tension pneumothorax, or massive pulmonary embolism can generally be confirmed by echocardiography , chest radiography, or pulmonary scintigraphy perfusion , respectively. When the acute MI myocardial injury is sufficient to produce shock, the ECG is usually diagnostic; however, anterior infarction, left bundle branch block, or atrioventricular block with idioventricular rhythm or pacemaker may exclude ECG diagnosis. In this case, the characteristic elevation of creatinine phosphokinase and myocardial bands in circulating plasma are useful.

The ECG also helps identify arrhythmias that, by themselves, cause or contribute to shock. As there may be hypovolemia with an acute MI or pre-existing heart disease , it cannot be assumed that the shock is entirely due to myocardial injury, especially inferior or posterior infarcts, which may affect the right ventricle or atrium.

Prognosis and treatment

Untreated shock is generally fatal. Even when treated, mortality from cardiogenic shock after massive MI and from septic shock is high. The prognosis depends on the cause, pre-existing or complicated diseases, the time between the start and the diagnosis, and the appropriateness of the treatment.

The first aid involves keeping the patient warm with the legs slightly raised to improve venous return. Bleeding should stop, check airway and ventilation, and administer respiratory aid, if necessary. Nothing should be given by mouth and the patient’s head should be turned to avoid aspiration if vomiting occurs.

Since tissue hypoperfusion makes absorption unreliable, all drugs should be administered iv, if possible. In general, narcotics should be avoided, but severe pain can be treated with 3 to 5 mg of morphine, administered in 2 min and repeating after 15 to 20 min, if necessary. Although cerebral hypoperfusion can cause anxiety, sedatives or tranquilizers should not be administered.

Supportive treatment stabilizes vital functions before diagnostic techniques can be performed. Nor-adrenaline or dopamine may be required . An O2 supplement can be administered immediately through a mask. If severe shock is present or ventilatory support is not indicated, endotracheal intubation is necessary to initiate positive pressure assisted ventilation with high O2 concentrations.

Outside the hospital or emergency department, a temporary increase in BP can be achieved with military (or medical) antishock pants (PASM). However, to avoid complications, experience with these pants is necessary.

A large catheter (16-18 gauge) should be inserted (especially if bleeding is suspected) into a peripheral vein (femoral, internal jugular, or antecubital) to transfuse blood or other fluids, and to administer medications. Direct infusion of fluids into the bone marrow provides alternative emergency access to the circulation when the veins are collapsed; In children, this route may be especially useful, although if there is severe hypovolemic shock, infusion through the femoral vein is preferable.

IV administration of 50 to 100 ml of an 8.4% (1 mEq / ml) solution of sodium bicarbonate may facilitate the treatment of metabolic acidosis, but treatment of the underlying cause of shock ( hypovolemia , sepsis, or low cardiac output ) it’s more important.

Patients in whom shock is not resolved immediately should be considered seriously ill and definitive treatment should be continued in a special care area (eg, an ICU, a coronary care unit). Careful monitoring should include ECG, systemic arterial PB – preferably by direct intra-arterial cannula; respiratory rate and depth; urinary flow (usually with a permanent bladder catheter); pH, Pao2 and Paco2; body temperature and clinical status, including sensory, pulse volume, temperature, and skin color. The measurement of PVC, PCPC, and cardiac output by thermodilution using a balloon-tipped pulmonary arterial catheter is also useful in patients with shock.of doubtful or mixed etiology, or severe, especially when accompanied by severe oliguria or pulmonary edema. A well-designed flow sheet is extremely valuable. Serial measurements of arterial blood gases, Hct, serum creatinine, and plasma lactate may also be helpful .

  • Hypovolemic shock . Definitive treatment requires restoring intravascular volume and eliminating the underlying cause. Clearly, rapid infusion of fluids can precipitate pulmonary edema; therefore, control of PVC or PCPC is sometimes useful. BP and urinary secretion should also be controlled.

In general, PVC or PCPC should not rise> 12 to 15 mm Hg due to fluid substitution. Control of PVC alone can only lead to error in patients with significant pre-existing cardiac or pulmonary vascular disease. Care must be taken when interpreting filling pressures in patients during ventilatory care, especially when using end-expiratory pressure levels> 10 cm H2O, or in tachypneic patients with extensive negative pleural pressures.

Measurements should be made at the end of expiration and the transducer should be located at the atrial level (mid- chest ) and should be carefully calibrated. The exact mode and type of fluids to be administered are determined by clinical circumstances and guided by frequent determinations of Hto, serum electrolytes, urine flow, and arterial pH (i.e., a search for evidence of resolution of metabolic alkalosis).

0.9% NaCl is as good as other solutions. After approximately 40 to 50% of the calculated blood volume deficit has been replaced, whole blood or colloid solution should be administered. Whole blood should be checked, but in an urgent situation, giving 1 to 2 U of O, Rh negative blood is a good alternative.

Colloid substitutions – 6% hetastarch in 0.9% NaCl, plasma (fresh frozen plasma is at risk of transmitting infections), or 5% reconstituted human serum albumin – lack RBCs and dilute Ht. Hetastarch 6% in NaCl 0.9% is an osmotic expander that is generally well tolerated, but may prolong bleeding time.The usual maximum dose is 20 ml / kg / 24 h, although higher amounts have been used . Allergic reactions have occasionally been reported.

The shock that is unresponsive to volume substitution may be due to the administration of an insufficient volume in the presence of blood loss up, or due to complicating factors (p. G., Cardiogenic shock coexisting myocardial injury or septic shock ). When hypovolemia is not the probable cause or when systemic BP does not respond rapidly to volume administration, a vasopressor drug should be considered (see treatment of shock by vasodilation, below).

  • Shock due to vasodilation (for the treatment of patients with adrenal insufficiency. Intravascular volume depletion that occurs due to increased systemic vascular permeability, especially in sepsis, is always necessary to treat with fluid resuscitation of 0.9% NaCl. Vasopressor drugs ( norepinephrine , dopamine ) are often necessary , especially in deep hypotension.

Dopamine is an inotropic drug that, at small doses (2 to 5 mg / kg / min), is less vasoconstrictive than norepinephrine, but selectively improves mesenteric and renal blood flow ; it may have advantages over other vasopressors in selected patients. The dobutamine , a selective b-agonist, increases cardiac output without vasoconstriction and therefore may not be as useful in these patients. The norepinephrine or dopamine administered by controlled infusion can be used to raise systolic pressure to between 90 and 100 mm Hg.

Once BP has stabilized, steps should be taken to correct accompanying abnormalities (eg, hypoxemia , acidosis, hypovolemia, sepsis) so that vasopressor administration can be reduced or discontinued; the vasoconstriction prolonged due to stimulation of a-receptors may further worsen the microcirculation visceral and increase work myocardial and O2 demand.

In the presence of heart failure or sepsis, the inotropic and chronotropic effects of norepinephrine or dopamine can improve cardiac output and systemic perfusion. In the absence of adrenal insufficiency, corticosteroid treatment is of no interest. Little can be done when shock follows massive, irreversible brain injury.

  • Cardiogenic shock. The shock cardiogenic is improving cardiac function. Shock after acute MI should be treated with O2 inhalation, stabilization of heart rate and rhythm, and volume expansion if accompanied by normal PCPC. Shock after right ventricular MI sometimes responds favorably to rapid volume expansion, which should be considered after lower wall MI, when the right ventricular filling pressure (PVC) is significantly elevated in the absence of ventricular filling pressure. elevated left (end-diastolic pulmonary pressure or PCPC).

However, the administration of fluids alone will rarely correct the hemodynamic alteration and additional treatment with vasopressors may be necessary. Morphine, at a dose of 3 to 5 mg iv, administered every 2 min, can relieve severe chest pain, facilitate the reduction of high levels of catecholamines and reduce insufficient preload and afterload of the heart; the response should be closely monitored because morphine causes respiratory depression, is a venodilator, and can cause BP to drop.

The initial dose can be repeated after 10 min if there is no evidence of respiratory depression or adverse BP response. Occasionally, 1 mg iv atropine is effective in the treatment of severe bradycardia (heart rate <50 beats / min) and hypotension that often occurs very early after the onset of symptoms , especially in posteroinferior MI. The noradrenaline or dopamine is used to maintain systolic blood pressure> 90 mm Hg (but not> 110 mm Hg) that markedly increases the demand for O2 isoproterenol is contraindicated in patients with shock after the acute MI, unless temporarily necessary for complete heart block.

When shock is complicated by bradycardia or advanced atrioventricular block, restoration of BP with norepinephrine or dopamine and correction of acidosis generally produce an adequate ventricular rhythm.

Temporal transvenous pacing may be necessary in patients with evidence of persistent high-grade atrioventricular block or severe sinus node dysfunction. Short-term administration of isoproterenol (2 mg / 500 ml 5% d / a, 1 to 4 mg / min [0.25 to 1 ml / min]) may occasionally be necessary before stimulation in patients with prolonged periods of asystole or tachycardia or recurrent ventricular fibrillation accompanied by severe bradycardia .

The digoxin is not used routinely in shock, but may have value in patients with supraventricular tachycardia. In the absence of severe systemic hypotension, infusion of dobutamine or amrinone (0.75 mg / kg iv in 2 to 3 min, followed by infusions of 5 to 10 mg / kg / min) can be used to improve cardiac output and reduce left ventricular filling pressure.

Tachycardia and arrhythmias can sometimes occur during administration of dobutamine, especially at high doses. Since amrinone is inotropic and vasodilator, arrhythmias and hypotension may occur during its administration. This drug can also cause thrombocytopenia and the platelet count must be monitored. Vasodilators (eg, nitroprusside, nitroglycerin), which increase venous capacitance or decrease systemic vascular resistance, reduce the burden of an injured myocardium and may be of value in patients without severe arterial hypotension.

Combination therapy (eg, dopamine or dobutamine with nitroprusside or nitroglycerin) may be especially helpful, but requires careful ECG and systemic pulmonary and hemodynamic monitoring . The early use of intra-aortic balloon counterpulsation seems to be valuable for temporarily reversing shock in patients with acute MI and it should be considered in patients who require vasomotor support (norepinephrine or dopamine) for> 30 min and in those with acute MI. complicated by ventricular septal rupture or severe acute mitral regurgitation. The development of percutaneous techniques for introduction to the head of the bed makes balloon counterpulsation available to community hospitals.

Emergency surgical correction of mechanical defects (eg, ruptured intraventricular septum, pseudoaneurysm, severe mitral regurgitation, large dyskinetic segment) may also be necessary. If emergency percutaneous transluminal coronary angioplasty (PTCA) is performed a few hours after the start of acute MI to open an occluded coronary artery, cardiogenic shock may be reversed.

The use of IV thrombolytic drugs before emergency PTCA or cardiac surgery has not been established; Thrombolytic therapy should be considered as soon as possible, unless contraindicated.

  • Other considerations. Pericardial tamponade requires pericardiocentesis, and in life-threatening situations, pericardial fluid must be removed at the head of the bed. In less urgent circumstances, surgical creation of a pericardial window or pericardiectomy may be advisable to prevent recurrence.

Massive pulmonary embolism that ends in shock is treated with supportive measures, such as supplemental O2, intratracheal intubation with assisted ventilation, vasopressor support (norepinephrine, dopamine), and heparin to prevent recurrent thrombosis. In patients who cannot be stabilized with these measures, emergency pulmonary angiography should be considered.

The use of urokinase or streptokinase to liquefy clots appears to be of value and is preferable to attempts at embolectomy, unless contraindicated (eg, due to recent major surgical intervention, especially neurosurgical). When pulmonary edema complicates shock, rapid resolution often results from treatment of coexisting heart failure with diuretics while O2 is administered, as well as positive pressure ventilation. Pulmonary edema that develops in septic shock should simply be treated with O2 and positive end-expiratory pressure ventilation.

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