Core Lecture Series: Shock Eric M. Wilson, MD September 22, 2009

Core Lecture Series:

Shock

Eric M. Wilson, MD

September 22, 2009

Definition

• A physiologic state characterized by– Inadequate tissue perfusion

• Clinically manifested by – Hemodynamic disturbances– Organ dysfunction

• Imbalance in oxygen supply & demand

• Conversion from aerobic to anaerobic metabolism

• Insult initiates neuroendocrine & inflammatory mediator reponses

Pathophysiology

Pathophysiology

• Hemodynamics maintained

• Continued hypoTN-> tissue injury; reversible w/resuscitation

• Cont’d volume loss / inadequate resuscitation -> hypoperfusion, cell injury-death

Compensated

Decompensation

Irreversible phase

Shock: Compensatory Mechanisms

• Neural response

• Hormonal response

Neural Response

- Decreased filling pressures lead to decreased output from left atrial stretch receptors to the vasomotor center of the medulla.

- Decreased frequency of impulses from the Carotid and aortic arch baroreceptors to the vasomotor center of the medulla.

- Result- Increased sympathetic output.

- Inhibition of the vagal center

Neural Response: Effects on cardiovascular function

• Larger arterioles constrict– Increases blood pressure

• Smaller arterioles dilate– Lowers capillary hydrostatic pressure resulting in fluid

shift from interstitial space into intravascular space

• Vasoconstriction minimal in brain & heart & most intense in peripheral tissues

Pathophysiology: Neuroendocrine Response

α1 & β1 Gluconeogenesis

Insulin resistance

Glycogenolysis

Lipolysis

The hormonal response to injury and shock

The hormonal response to injury and shock

Hormones with increased releaseHormones with decreased

release

Epinephrine Β-endorphin InsulinNorepinephrine Growth Hormone Estrogen

Dopamine Prolactin TestosteroneGlucagon Somatostatin Thyroxine

Renin Eicosanoids T3Angiotensin II Histamine TSHAVP (ADH) Kinins FSH

ACTH Serotonin LHCortisol Interleukin 1 IGF

Aldosterone TNF

• Cellular physiology– Tissue hypoxia -> decrease generation of ATP

anaerobic glycolysis– Pyruvate lactate decrease in pH

Intracellular metabolic acidosis– Cell membrane pump dysfunction

• Na & H2O in cellular swelling; K out

• Resultant systemic physiology– Cell death & end organ dysfunction– MSOF & death

Pathophysiology

• Shock– Initial signs of organ dysfunction

– Tachycardia– Tachypnea– Metabolic acidosis– Oliguria– Cool & clammy skin

Pathophysiology

• End organ dysfunction– Progressive irreversible dysfunction

– Oliguria, anuria– Progressive acidosis & depressed CO– Agitation, obtundation, & coma– Patient death

Pathophysiology

• Hypovolemic/Hemorrhagic

• Cardiogenic

• Vasodilatory/Septic

• Neurogenic

Classification

Distributive

Hypovolemic Shock

• Results from decreased preload

• Etiologic classes– Hemorrhage: trauma, GI bleed, ruptured

aneurysm– Fluid loss: diarrhea, vomiting, burns

Parameter I II III IV

Blood loss (ml) <750 750–1500 1500–2000 >2000

Blood loss (%) <15% 15–30% 30–40% >40%

Pulse rate (beats/min) <100 >100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate (bpm) 14–20 20–30 30–40 >35

Urine output (ml/hour) >30 20–30 5–15 Negligible

CNS symptoms Normal Anxious Confused Lethargic

Hypovolemic ShockHemorrhagic Shock

Elderly – blood thinners, meds masking compensatory responses to bleeding (beta-blockers)

Hemorrhagic Shock:Treatment

• Control the source of blood loss

• Intravenous volume resuscitation– Crystalloid solutions– If shock state is uncorrected after 2L,

transfuse blood

Cardiogenic Shock

• Inadequate blood flow to vital organs due to inadequate cardiac output despite normal intravascular volume status

Pump Failure

Cardiogenic Shock:Causes

• MI

• Arrhythmias

• Cardiomyopathy

• Myocarditis

• Mechanical– Acute mitral regurgitation– Acute aortic insufficiency– Ventricular septal defect

Cardiogenic Shock:Treatment

• Maintain adequate oxygenation

• Judicious fluid administration to avoid pulmonary edema

• Correct electrolyte abnormalities

• Treat dysrhythmias – reduce heart rate

• Inotropic agents

• Intra-aortic balloon counterpulsation

Cardiogenic Shock:Intra-aortic balloon pump

-Improves coronary blood flow

-Decreases afterload

-Decreases myocardial oxygen demand

Vasodilatory Shock

• Hypotension from failure of vascular smooth muscle to constrict

• Vasodilation

• Causes– Sepsis– Anaphylaxis – Systemic inflammation

SIRS 2 or more of the following: Temp >38 or <36 HR > 90 RR > 20 WBC > 20K >10% bands

Sepsis SIRS in the presence of suspected or documented infection

Severe Sepsis Sepsis with hypotension, hypoperfusion, or organ dysfunction

Septic Shock Sepsis with hyotension unresponsive to volume resuscitation, and evidence of hypoperfusion or organ dysfunction

MODS Dysfunction of more than one organ

Vasodilatory Shock

Vasodilatory Shock:Treatment

• Treat source of infection

• Maximize intravascular volume status

• Intubation, if necessary

• Vasopressors

• Immune modulators– Activated protein C (Xigris)

• Promotes fibrinolysis• Inhibits thrombosis & inflammation

Neurogenic Shock

• Usually caused by an injury to the spinal cord

• Not caused by an isolated brain injury

Neurogenic Shock:Clinical Presentation

• Hypotension

• Bradycardia

• Sensory loss

• Motor paralysis

• Warm, dry skin

Neurogenic Shock:Pathophysiology

• Hypotension– Loss of sympathetic tone to arterial system resulting

in decreased systemic vascular resistance– Loss of sympathetic tone to venous system resulting

in pooling of blood in venous capacitance vessels with decreased cardiac filling and diminished cardiac output

• Bradycardia– Loss of sympathetic input from spinal cord– Tonic parasympathetic input to heart unopposed

leading to bradycardia

Neurogenic Shock:Pathophysiology

• Sensory loss– Loss of efferent communication from the sensory

organs to the brain

• Motor paralysis– Loss of afferent communication from the brain to the

voluntary muscles

• Warm, dry skin– Loss of sympathetic input to sweat glands leads to

failure to produce sweat– Failure of peripheral vasoconstriction maintains flow

of warm blood to periphery and “warm skin”

Neurogenic Shock:Treatment

• Fluid replacement

• Pressor agents to restore vascular tone once volume status restored

Obstructive Shock

• Reduced filling of the right side of the heart resulting in decreased cardiac output

• Tension pneumothorax– Increased intrapleural pressure secondary to

air accumulation

• Pericardial tamponade– Increased intrapericardial pressure precluding

atrial filling secondary to blood accumulation

Distinguishing Types of Shock

ShockCVP/

PCWPCO SVR

Hypovolemic

Septic

Cardiogenic

Neurogenic

Which of the following is an appropriate definition of the shock state?

A. Low blood pressure

B. Low cardiac output

C. Low circulating volumes

D. Inadequate tissue perfusion

E. Abnormal vascular resistance

In cases of hemorrhagic shock, what initial alteration in blood pressure is seen?

A. Increase in systolic pressure

B. Decrease in systolic pressure

C. Increase in diastolic pressure

D. Decrease in diastolic pressure

Class II shock – decrease in pulse pressure, which is generally related to increase in diastolic component, which in turn is related to elevation of catecholamines produced by neural response to shock