Upload
karley-rowden
View
214
Download
0
Tags:
Embed Size (px)
Citation preview
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