The shock state is precipitated by one of three cardiovascular states:

(1) severely depressed myocardial functional ability, interfering with pump function,

  1. Cardiogenic shock occurs whenever cardiac pumping ability is compromised (eg, as a result of severe arrhythmias, abrupt valve malfunction, coronary occlusions, or myocardial infarction). The direct consequence of any of these abnormalities is a significant fall in cardiac output.

 

(2) grossly inadequate cardiac filling due to low mean circulatory filling pressure,

Hypovolemic shock accompanies significant hemorrhage (usually greater than 20% of blood volume), or fluid loss from severe burns, chronic diarrhea, or prolonged vomiting. These situations can induce shock by depleting body fluids and thus circulating blood volume. The direct consequence of hypovolemia is inadequate cardiac filling and reduced stroke volume.

There are some situations that may result in reduced cardiac filling that are not related to hypovolemia. For example, cardiac tamponade, associated with fluid accumulation in the pericardial sac, prevents adequate diastolic filling as does the occurrence of a pulmonary embolus (a clot mobilized from systemic veins lodging in a pulmonary vessel).

 

(3) profound systemic vasodilation either due to the abnormal presence of powerful vasodilators or due to the absence of neurogenic tone normally supplied by the sympathetic nervous system.1

  1. Anaphylactic shock occurs as a result of a severe allergic reaction to an antigen to which the patient has developed a sensitivity (eg, insect bites, antibiotics, and certain foods). This immunological event, also called an “immediate hypersensitivity reaction,” is mediated by several substances (such as histamine, prostaglandins, leukotrienes, and bradykinin) that, by multiple mechanisms, results in substantial arteriolar vasodilation, increases in microvascular permeability, and loss of peripheral venous tone. These combine to reduce both total peripheral resistance and cardiac output.

  2. Septic shock is also caused by profound vasodilation but specifically from substances released into the circulating blood by infective agents. One of the most common is endotoxin, a lipopolysaccharide released from bacteria. This substance induces the formation of a nitric oxide synthase (called inducible nitric oxide synthase to distinguish it from the normally present constitutive nitric oxide synthase) in endothelial cells, vascular smooth muscle, and macrophages that then produce large amounts of the potent vasodilator nitric oxide. The term distributive shock is sometimes used to describe both the anaphylactic and septic shock states.

  3. Neurogenic shock is produced by loss of vascular tone due to inhibition of the normal tonic activity of the sympathetic vasoconstrictor nerves and often occurs with deep general anesthesia or in reflex response to deep pain associated with traumatic injuries. It may also be accompanied by an increase in vagal activity, which significantly slows the cardiac beating rate. This type of shock is often referred to a vasovagal syncope. The transient syncope evoked by strong emotions is a mild form of neurogenic shock and is usually quickly reversible.

Reference

https://www.nejm.org/doi/full/10.1056/NEJMra1208943

 

 

Shock is tissue perfusion inadequate to supply sufficient amounts of O2 and other nutrients to tissues to meet metabolic demands leading to cellular injury and dysfunction as well as decreased removal of waste byproducts of metabolism. 1

 

Even with all cardiovascular compensatory mechanisms activated, arterial pressure is usually (though not always) low in shock.Hypotension, although common in shock, is not synonymous to shock. One can have hypotension and normal perfusion, or shock without hypotension in a patient who is usually very hypertensive.

The approach to understanding the causes and selecting an appropriate treatment depends on determination of the underlying primary disturbance.

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Recall that arterial pressure is determined by cardiac output and total peripheral resistance, so any loss in blood pressure is a result of a decrease in either one or both of these variables.

 

In severe shock states of any etiology, inadequate brain blood flow leads to loss of consciousness often with sudden onset (called syncope).1

 

 

Progressive tissue hypoxia results in loss of cellular membrane integrity, a reversion to a catabolic state of anaerobic metabolism, and a loss of energy-dependent ion pumps and chemical and electrical gradients. Mitochondrial energy production begins to fail. Multiple organ dysfunction follows localized cellular death, and organism death follows.

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In early shock, compensatory regional vasoconstriction (skin, skeletal muscle, splanchnic circulation) may temporarily maintain normal blood pressure and adequate blood flow to vital organs. due to increase in sympathetic activity aimed at maintaining arterial pressure via augmented cardiac output and vascular resistance.

Endogenous compensatory mechanisms directed at reversing hypotension and shock include the release of catecholamines, cortisol, and activation of the renin–angiotensin–aldosterone axis.

As shock progresses, compensatory mechanisms fail and widespread cellular damage occurs. Insufficient O2 delivery to tissues causes anaerobic metabolism and lactic acidosis. If shock persists, irreversible injury to vital organs occurs; death ensues despite vigorous therapy that may temporarily return cardiovascular measurements to normal.

Even with all cardiovascular compensatory mechanisms activated, arterial pressure is usually (though not always) low in shock. Hypotension, although common in shock, is not synonymous to shock. One can have hypotension and normal perfusion, or shock without hypotension in a patient who is usually very hypertensive.

In severe shock states of any etiology, inadequate brain blood flow leads to loss of consciousness often with sudden onset (called syncope).

Progressive tissue hypoxia results in loss of cellular membrane integrity, a reversion to a catabolic state of anaerobic metabolism, and a loss of energy-dependent ion pumps and chemical and electrical gradients. Mitochondrial energy production begins to fail. Multiple organ dysfunction follows localized cellular death, and organism death follows.Shock leads to multisystem end-organ hypoperfusion characterized by decreased cellular oxygen delivery and utilization as well as decreased removal of waste byproducts of metabolism.

The end result is tissue hypoxia, often with accompanying lactic acidosis.

The end result of multiorgan hypoperfusion is tissue hypoxia, often with accompanying lactic acidosis. Since the MAP is the product of cardiac output and systemic vascular resistance (SVR), reductions in blood pressure can be caused by decreases in cardiac output and/or SVR. Accordingly, once shock is contemplated, the initial evaluation of a hypotensive patient should include an early bedside assessment of the adequacy of cardiac output (Fig. 321-2). Clinical evidence of diminished cardiac output includes a narrow pulse pressure—a marker that correlates with stroke volume—and cool extremities with delayed capillary refill. Signs of increased cardiac output include a widened pulse pressure (particularly with a reduced diastolic pressure), warm extremities with bounding pulses, and rapid capillary refill. If a hypotensive patient has clinical signs of increased cardiac output, it can be inferred that the reduced blood pressure is from decreased SVR.

 

A hyperadrenergic state results from the compensatory response to shock, physiologic stress, pain, and anxiety. Shivering frequently results when a patient is unclothed for examination and then left inadequately covered in a cold resuscitation room. The combination of these variables increases V̇ o2. Pain further suppresses myocardial function, further impairing Do2 and V̇ o2. Providing analgesia, muscle relaxation, warm covering, anxiolytics, and even paralytic agents, when appropriate, decreases this inappropriate systemic oxygen consumption.

 

 

 

 

 

The initial derangement precipitating a state of shock might be (1) vasodilation (causing a decreased SVR) from sepsis, anaphylaxis, drugs, or cervical cord lesion, (2) extremes of HR, (3) loss of preload volume (causing decreased EDV) from blood or volume loss, or (4) loss of contractility (increasing the ESV) from heart failure. Compensatory mechanisms come into play and provide many of the clinical clues to early shock.

The initial compensatory mechanisms depend on the initial insult. (1) Vasodilation with loss of SVR generally causes a compensatory tachycardia and thirst. Despite systemic tissue hypoxemia, the skin remains perfused and is warm initially. (2) Blood or fluid loss (decreasing EDV) causes a reflex increase in SVR, which increases diastolic BP, narrowing the pulse pressure, increases sympathetic cholinergic sweating and makes the patient pale, thirsty, and cool. As volume loss increases, tachycardia and hypotension ensue. (3) Loss of contractility also is compensated by increases in SVR to maintain blood pressure with similar symptoms.

Once compensatory mechanisms fail, irreversible shock occurs with irreversible cell death, microcirculation plugging, and free radical generation. There is loss of autonomic regulation due to local nitric oxide vasodilator generation, and even with complete correction of blood volume (for example, in hypovolemic shock), tissue function, and organ function are not restored, causing eventual death.

 

Content 9

 

History

 
 
 
 

 

Physical Exam

 

Laboratory Tests

X-ray

 

Essentail Criteria to Establish Diagnosis

 

 

1. Establish Airway

2. Establish Breathing

3. Establish Circulation

4. Determine the cause (see Hypotension)

 

 

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Approach to the patient in shock.
 EGDT, early goal-directed therapy; JVP, jugular venous pulse.

Image not available.

Clinical evaluation : narrow pulse pressure, cool extremities, and delayed capillary refill suggestive of reduced cardiac output.

Indicators of high cardiac output (e.g., widened pulse pressure, warm extremities, and rapid capillary refill) associated with shock suggest reduced systemic vascular resistance.

Reduced cardiac output can be due to intravascular volume depletion (e.g., hemorrhage) or cardiac dysfunction. Intravascular volume depletion can be assessed through changes in right atrial pressure with spontaneous respirations or changes in pulse pressure during positive pressure mechanical ventilation. Reduced systemic vascular resistance is often caused by sepsis, but high cardiac output hypotension is also seen in pancreatitis, liver failure, burns, anaphylaxis, peripheral arteriovenous shunts, and thyrotoxicosis. Early resuscitation of septic and cardiogenic shock may improve survival; objective assessments such as echocardiography and/or invasive vascular monitoring should be used to complement clinical evaluation and minimize end-organ damage.

 

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A goal-directed approach of MAP >65 mm Hg, central venous pressure of 8 to 12 mm Hg, Scvo2 >70%, and urine output >0.5 mL/kg/h during ED resuscitation of septic shock has been shown to decrease mortality, but which of the metrics accounts for the mortality decrease remains in question.16,19,20,25 Source control, whether with infection, hemorrhage, or other state of shock, is essential in the initial stages of management. If shock or hypotension persists, reassessment at the patient's bedside is essential while considering the important issues in Table 12–8.

 

Content 4

Despite recent advances in treatment, mortality remains high: > 50% in cardiogenic shock and > 35% in septic shock.

Content 11

 

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