Silverstein and Hopper Chapter 6: Classification and Initial Management of Shock States

Shock

• Severe imbalance between oxygen supply and demand, leading to inadequate cellular energy production, cellular death, and multiorgan failure

  • Most commonly occurs secondary to poor tissue perfusion from low or unevenly distributed blood flow that causes a critical decrease in oxygen delivery (DO2) relative to oxygen consumption (VO2)

What are the four major mechanisms of shock?

• Loss of intravascular volume (hypovolemic shock)

• Maldistribution of vascular volume (distributive shock)

• Obstruction to diastolic filling (obstructive shock)

• Failure of the cardiac pump (cardiogenic shock)

Types of Shock Due to Inadequate Oxygen Delivery

Hypovolemic - decrease in circulating blood volume

Distributive - marked decrease or increase in systemic vascular resistance of maldistribution of blood

Cardiogenic - decrease in forward flow from the heart

Obstructive - Reduced diagnostic filling and preload

Hypoxic - decreased oxygen content in arterial blood

Types of Shock Due to Inappropriate Use of Oxygen by Tissues

Metabolic - deranged cellular metabolic machinery

Examples of Hypovolemic Shock

Hemorrhage

Severe dehydration

Trauma

Examples of Distributive Shock

Sepsis

Anaphylaxis

Catecholamine excess (pheochromocytoma, extreme fear)

Examples of Cardiogenic Shock

Congestive heart failure

Cardiac arrhythmia

Drug overdose (e.g. anesthetics, B-blockers, calcium channel blockers)

Examples of Obstructive Shock

Gastric dilatation - volvulus

Obstruction of the vena cava or aorta

Tension pneumothorax

Pericardial tamponade

High positive end-expiratory pressure mechanical ventilation

Examples of Hypoxic Shock

Anemia

Severe pulmonary disease

Carbon monoxide toxicity

Methemoglobinemia

Examples of Metabolic Shock

Hypoglycemia

Cyanide toxicity

Mitochondrial dysfunction

Cytopathic hypoxia of sepsis

Pathophysiology of Shock

• Inadequate cellular energy production leads to cell membrane ion pump dysfunction (e.g. Na-K ATPase), intracellular edema, leakage of intracellular contents extracellularly, and the inability to regulate intracellular pH

  • Leads to systemic acidemia, endothelial dysfunction, and activation of inflammatory and antiinflammatory cascades

Pathophysiology of Hypovolemic Shock

• Occurs secondary to a loss of intravascular fluid volume causing inadequate organ perfusion

• Insufficient oxygen delivery causes a shift from aerobic to anaerobic metabolism with accumulation of lactate, hydrogen ions, and oxygen free radicals

• DAMPs consisting of mitochondrial DNA, histones, heat shock proteins, and other mediators rise in response to damaged or dying cells

• DAMPs activate the innate immune system by interacting with PRRs and triggering a pathologic systemic inflammatory response

• Prolonged oxygen deprivation at the cellular level ultimately causes cellular necrosis and apoptosis, followed by end-organ damage and multiple organ dysfunction

Compensatory Mechanisms in Hypovolemic Shock

• Begin within minutes of an acute drop in venous return and cardiac output

• Baroreceptors communicate with the brain via the glossopharygneal nerve and vagus nerve to the nucleus of the solitary tract in the brainstem

  • Decrease in impulse firing to the medulla oblongata in response to low pressure or stretch in the carotid sinuses or aortic arch

  • This enables sympathetic activation while inhibiting parasympathtetic activation

  • Resultant response to shock-induced hypotension includes increased arteriolar ad venous tone, cardiac contractility, and heart rate

• Peripheral chemoreceptors are located in the aortic and carotid bodies and respond to changes in CO2, hydrogen ions (decreased pH, and to a lesser extent, the partial pressure of O2

  • Stimulation causes vasoconstriction and increased minute ventilation

• Central chemoreceptors in the respiratory center of the medulla oblongata sense an increase in CO2 or decrease in pH of the cerebrospinal fluid and cause an increase in respiratory rate and tidal volume

• Other changes associated with severe hypotension include an increase in circulating catecholamines and B endorphin release, which reduces perception to pain

• Over a period of hours, reduced capillary pressure results in a net shift in fluid from the interstitial to the intravascular compartment

• Reduced renal blood flow activates RAAS, which leads to an increase in norepinephrine and angiotensin II-mediated vasoconstriction as well as sodium and water retention via the release of aldosterone and ADH, respectively

Subclassifications of Hypovolemic Shock

• Hemorrhagic shock

• Traumatic hemorrhagic shock

• Hypovolemic shock without hemorrhage

• Traumatic hypovolemic (nonhemorrhagic) shock

What characterizes hemorrhagic shock and traumatic hemorrhagic shock?

• Hemorrhagic shock and traumatic hemorrhagic shock are characterized by an acute drop in circulating red blood cells causing tissue hypoxia

  • Traumatic hemorrhagic shock is further complicated by the inflammatory response that accompanies severe soft tissue injury resulting in worsened microvascular dysfunction, endothelial injury, and vasomotor tone derangement

Distributive Shock

• Refers to a state of relative hypovolemia due to the pathologic redistribution of fluid caused by changes in vascular tone or increased vascular permeability

Subcategories of Distributive Shock

Septic

Anaphylactic

Neurogenic

Sepsis Definition

Life-threatening organ dysfunction in response to infection

Septic Shock Defintion

Persistent hypotension requiring vasopressor therapy

What characterizes anaphylaxis?

Histamine-induced vasodilation

What causes vasodilation in neurogenic shock?

• Vasodilation seen in neurogenic shock results from abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscle

Cardiogenic Shock

• Characterized by systolic or diastolic cardiac dysfunction resulting in hemodynamic abnormalities that include increased heart rate, decreased stroke volume, decreased cardiac output, decreased blood pressure, increased peripheral vascular resistance, and increased right atrial, pulmonary arterial, and pulmonary capillary wedge pressures

  • Result in diminished tissue perfusion and increased pulmonary venous pressures, resulting in pulmonary edema and increased respiratory effort

Obstructive Shock

• Compression of the heart or a great vessel compromising venous return, diastolic filling, and cardiac preload

• Causes include severe gastric dilation (with or without volvulus), decreasing preload and tension pneumothorax or cardiac tamponade, reducing diastolic filling

• High PEEP can also negatively affect venous return and cardiac output

• Reduced cardiac output results in reduced perfusion and oxygen delivery, ultimately resulting in tissue hypoxia and organ failure

Clinical Presentation of Compensated Shock

• Animals with compensated shock commonly exhibit mild to moderate mental depression, tachycardia, normal or prolonged CRT, cool extremities, fair to moderate pulse quality, tachypnea, and abnormal blood pressure

Clinical Presentation of Decompensated Shock

• As the animal progresses to decompensated shock pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent

Hyperdynamic Shock

• Initial hyperdynamic phase

  • Characterized by tachycardia, fever, bounding peripheral pulse quality, and hyperemic mucous membranes secondary to cytokine mediated peripheral vasodilation (NO)

    • Often referred to as vasodilatory shock

Hypodynamic Shock

• Hypodynamic stage

  • If septic shock or SIRS progresses unchecked, a decreased cardiac output and signs of hypoperfusion often ensue secondary to cytokine effects on the myocardium or myocardial ischemia

  • Clinical changes may include tachycardia, pale (and possibly icteric) mucous membranes with a prolonged CRT, hypothermia, poor pulse quality, and a dull mentation

  • Decompensatory stage of sepsis

  • Without intervention will result in organ damage and death

What is a key predictor of the outcome in shock patients?

Magnitude of the oxygen deficit

Goal of Treatment of Shock

Optimizing oxygen delivery and tissue perfusion

What characteristics does a well perfused patient possess?

• CVP between 0 and 6 cmH2O

• Urine production of at least 1 ml/kg/hr

• Mean arterial pressure between 70 and 100 mmHg

• Normal body temperature, heart rate, heart rhythm, and respiratory rate

• Moist, pink mucous membranes with a capillary refill time of less than 2 seconds

Measurement of Indices of Systemic Oxygen Transport

• Measurement of indices of systemic oxygen transport is a direct method of assessing the progress of resuscitation in shock patients, but it is rarely utilized in clinical patients due to its invasive nature, potential risks, and questionable benefit

• A right-sided cardiac catheter or pulmonary artery catheter is typically used to monitor these parameters

  • PAC allows for measurement of central venous and pulmonary arterial pressure, mixed venous blood oxygen parameters (PvO2 and SvO2), pulmonary capillary wedge pressure, and cardiac output

How can changes in the global tissue oxygenation (oxygen supply demand) be assessed?

Using mixed venous oxygen saturation (SvO2) measurements?

Assuming VO2 is a constant, what is SvO2 determined by?

Cardiac output, hemoglobin concentration, and SaO2

When is SvO2 decreased?

SvO2 is decreased if DO2 decreases (i.e. low CO, hypoxemia, severe anemia) or if VO2 increases (i.e. fever, seizure activity)

When is SvO2 increased?

With conditions such as the hyperdynamic stages of sepsis and cytotoxic tissue hypoxia, SvO2 is increased

Central Venous Oxygen Saturation

• Ideally, venous oxygen saturation is measured in a blood sample from the pulmonary artery

  • In animals without a PAC, venous oxygen saturation can be measured from the central circulation, using a central venous catheter in the cranial or proximal caudal vena cava

    • Central venous oxygen saturation (ScvO2)

    • ScvO2 values are generally higher than SvO2 in critically ill patients with circulatory failure, the two measurements closely parallel each other in patients with less severe disease

    • A pathologically low ScvO2 likely indicates an even lower SvO2

What is a higher SvO2 associated with?

A lower risk of mortality

Treatment for Shock

• Mainstay of therapy for all forms of circulatory shock except cardiogenic shock is based on rapid administration of intravenous fluids to restore an effective circulating volume and tissue perfusion

• Administered fluid spreads rapidly into the extravascular space so that only approximately 25% of the delivered volume remains in the intravascular space 30 minutes after infusion

• Hypotensive resuscitation (to a mean arterial pressure of approximately 60 mmHg) may prove beneficial in the treatment of hemorrhagic shock since aggressive fluid therapy prior to control may worsen bleeding and outcome

• Shock patients that remain hypotensive despite intravascular volume resuscitation often require vasopressor or inotrope therapy

• Because oxygen delivery to the tissue is dependent on both cardiac output and systemic vascular resistance, therapy for hypotensive patients includes maximizing cardiac output with fluid therapy and inotropic drugs or modifying vascular tone with vasopressor agents

• Commonly used vasopressors include catecholamines (epinephrine, norepinephrine, dopamine) positive inotropic agents, and the sympathomimetic drug phenylephrine

  • Vasopressin, corticosteroids, and glucagon have been used as adjunctive pressor agents

Therapy for Cardiogenic Shock

• Oxygen therapy and minimal handling are extremely important to avoid further decompensation in patients with cardiogenic shock

• Furosemide is the mainstay of therapy for congestive heart failure

• Animals that fail to show clinical signs of improvement after repeated doses of diuretics may require more specific therapy targeting the underlying cardiac abnormality

• Ultimately, the dyspneic patient in cardiogenic shock that fails to respond to therapy should either be treated with high flow nasal oxygen or be anesthetized, intubated, and positive pressure ventilated with 100% oxygen to stabilize the animal