Types of Shock

Types of Shock

Hypovolemic Shock

Hypovolemic shock is caused by decreased effective circulating blood volume. The most common cause of hypovolemic shock is major blood loss, such as occurs with trauma, burn, surgery, or massive gastrointestinal hemorrhage. Increased output caused by diarrhea, vomiting, accumulation of fluid in the gut following intestinal obstruction and drainage cause plasma volume deficit.

Signs, symptoms of hypovolemic/ hemorrhagic shock

• Classification and physiologic variables highlighted in Table 3.2
• Rapid heart rate: Take the pulse and/or use an electrocardiogram/pulse oximeter (if available).
• Decreased blood pressure: Feel the peripheral pulse for rate as well as quality. In general the lowest palpable systolic blood pressure for the carotid artery is 60 mmHg; femoral artery is 70 mmHg; and radial artery is 80 mmHg.
• Poor tissue perfusion:
Check capillary refill by applying pressure to the end of the patient's fingernail until the nail bed whitens. Release the pressure. Rapid pink coloring in the nail bed should return within two seconds.
Pull the lower eyelid down slightly. If the area is pale then circulation to the head is compromised.
• Low urine output: Insert a Foley catheter (if available). A low urine output is defined as less than 0.5 ml/kg/hr in adults and less than 1 ml/kg/hr.
• Changes in respiratory rate: will increase to greater than 20 respirations per minute, in the adult, during severe hemorrhagic shock.
• Changes in facial/extremity color: pale or ashen color, and may be cool to touch. Difficult to access in some races.
• Change in level of consciousness - Patient may present from being alert to being confused, sleepy, or even unconscious.

Table 3.2

Cardiogenic Shock

The circulatory shock syndrome caused by inadequate cardiac pumping is called cardiogenic shock

This form of shock is caused by failure of the heart as an effective pump. It occurs most commonly as a complication of acute myocardial infarction but it may also be seen in patients with severe brady- or tachyarrhythmia, valvular heart disease, significant cardiac contusion, or in the terminal stage of chronic heart failure of any cause, including ischemic heart disease. Cardiogenic shock is characterized by a low cardiac output, diminished peripheral perfusion, pulmonary congestion, and elevation of systemic vascular resistance. The ineffective contractile activity of either the right or left side of the heart leads to the accumulation of blood in the venous circulation upstream to the failing ventricle. Cardiogenic shock with left-sided heart failure increases fluid in the lungs that can overwhelm the capacity of the pulmonary lymphatics and causes interstitial and eventually pulmonary edema.

With compression, the heart and surrounding structures are less compliant and, thus, normal filling pressures generate inadequate diastolic filling. Blood or fluid within the poorly distensible pericardial sac may cause cardiac tamponade (pressure on the heart when the pericardial cavity fills with blood or serous fluid which reduce venous return). Any cause of increased intrathoracic pressure, such as tension pneumothorax, herniation of abdominal viscera through a diaphragmatic hernia, or excessive positive pressure ventilation to support pulmonary function, can also cause compressive cardiogenic shock while simultaneously impeding venous return.

The classic findings of pericardial tamponade include hypotension, neck vein distention, and muffled heart sounds. Pulsus paradoxus, i.e., an inspiratory reduction in systolic pressure >10 mmHg and heart rate, may also be noted. Treatment consists of immediate pericardiocentesis (surgical perforation of pericardium to remove accumulated blood or other fluid). A tension pneumothorax produces ipsilateral decreased breath sounds, tracheal deviation away from the affected thorax, and jugular venous distention. Chest decompression (drainage) must be carried out immediately to release air.

Distributive Shock

This type of shock is characterized by an increase in the vascular capacity. It is most commonly caused by sepsis, secondary to the release of inflammatory mediators. Other causes include anaphylactic shock, neurogenic shock, and acute adrenal insufficiency.

This form of shock is caused by the systemic response to a severe infection. It occurs most frequently in elderly or immunocompromised patients and in those who have undergone an invasive procedure in which bacterial contamination has occurred. Despite normal or increased cardiac output and oxygen delivery, cellular oxygen consumption is less than normal due to impaired extraction as a result of impaired metabolism. In early stages of septic shock, the patient usually does not have signs of circulatory collapse but only signs of the bacterial infection. As the infection becomes more severe, the circulatory system usually becomes involved either because of direct extension of the infection or secondarily as a result of toxins from the bacteria, with resultant loss of plasma into the infected tissues through deteriorating blood capillary walls.

Interruption of sympathetic vasomotor input after a high cervical spinal cord injury, inadvertent cephalad migration of spinal anesthesia or severe head injury may result in neurogenic shock. In addition to arteriolar dilatation, venodilation causes pooling in the venous system, which decreases venous return and cardiac output. The extremities are often warm, in contrast to the usual vasoconstriction-induced coolness in hypovolemic or cardiogenic shock.

The normal host response to the stress of illness, operation, or trauma requires that the adrenal glands hypersecrete cortisol in excess of that normally required. Hypoadrenal shock occurs in settings in which unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery. Adrenocortical insufficiency may occur as a consequence of the chronic administration of high doses of exogenous glucocorticoids. The shock produced by adrenal insufficiency is characterized by reductions in systemic vascular resistance, hypovolemia, and reduced cardiac output.

Anaphylaxis is an allergic condition in which the cardiac output and arterial pressure often decrease drastically. It results primarily from an antigen-antibody reaction that takes place immediately after an antigen to which the person is sensitive enters the circulation. One of the principal effects is to cause the basophiles in the blood and mast cells in the pericapillary tissues to release histamine or a histamine-like substance. The histamine causes

• An increase in vascular capacity because of venous dilation, thus causing a marked decrease in venous return
• Dilation of the arterioles, resulting in greatly reduced arterial pressure
• Greatly increased capillary permeability, with rapid loss of fluid and protein into the tissue spaces. The net effect is a great reduction in venous return and sometimes such serious shock cause that the person dies within minutes