Shock Clinical Correlation

• Shock-Acute circulatory failure with inadequate or inappropriately disturbed

tissue perfusion resulting in generalized cellular hypoxia
○ Caused by disruption of the cardiovascular system and inadequate
compensation to maintain tissue perfusion
○ Indication of:
 1) abnormality of heart rate, stroke volume, or peripheral
resistance
 2) Failure of the others to compensate
• Cardiovascular System:
○ Pump-cardiac shock (problems with the heart)
○ Fluid-hypovolumic shock (loss of circulating volume)
○ Tubing-distributive shock (problems with vascular system)
○ Obstructive shock-outflow or inflow obstruction
• Types of shock:
○ Cardiogenic Shock
 Problem with the heart
 Myocardial
 Dysrrhythmia
○ Distributive
 Anaphylactic
 Neurogenic
 Septic
○ Hypovolemic
 Hemorrhage
 Serum/plasma loss
 Dehydration
○ Obstructive
 Tension
 Pneumothorax
 Cardiac Tamponade
 Pulmonary Embolism
• Failure of Cardiac Output due to (Q=HR X SV) & Q=BP/TPR:
○ Heart rate
 Tachycardia reducing filling time
 Inappropriate rate
○ Decreased Stroke Volume
 Absolute
• Occurs in Hemorrhage dehydration
○ Inadequate fluid intake and excessive fluid loss
•
 Relative
 • Occurs in inflow obstruction
○ Mitral stenosis
○ Tapenade
• Occurs in relative 3rd space fluid loss:
○ Compartment syndrome
 Failure to Eject
• Muscle dysfunction, vascular/septal failure, outflow
obstruction
 Failure of peripheral resistance
• Vasodilation
○ Anaphylaxis, spinal shock
• Vasodiation & microvascular injury
○ Systemic sepsis
 “capillary leak syndrome”
• Pathophysiology of shock
○ Microcirculatory dysfunction
 Platelet aggregation
 Decreased capillary blood flow
○ Tissue ischemia
 Anaerobic metabolism leading to lactic acidosis
○ Biochemical mediators
 Vasoactive: prostaglandinsincreased capillary permeability
 Inflammatory mediators: fever, increased capillary permeability
• End-organ damage
○ Cellular damage
 Dysfunction of membrane transport
 Depressed mito activity
○ Organ damage:
 Liver
• Due to high rate of metabolism and exposure to systemic
toxins
 Lungs
• Capillary leakage and pulmonary eduema
 Myocardium
• Reduced contraction
 Kidneys
• Damage to tubules
• Stages of shock
○ Nonprogressive (compensated)
 BP and vitals maintained
• Baroreceptros, chemoreceptors, rennin-angiotensin
system, humoral responses (catecholamines leading to
 vasoconstriction), autotransfusion (reabsorption of
interstitial fluid)
○ Progressive (uncompensated)
 Hypotension and organ deterioration
 Need intervention to survive
○ Irreversible
 Patient will die despite treatment
• Prognosis
○ Shock is life threatening
○ Prognosis depends on severity and duration of shock
○ Time matters
○ Best if treatment is initiated within an hour
• Early Recognition of Shock
○ Shock patients may initially look well because of their compensatory
mechanisms but their condition can deteriorate rapidly
○ Increased heart rate (first sign)
○ Increased respiratory rate
 Increases o2 to vital organs and compensates for metabolic
acidosis
○ Physical exam should focus on tissue perfusion
 Vasoconstriction occurs to maintain perfusion to vital organs
○ Hypotension is a late and premorbid sign
 Frequently shock exists without hypotension
• Late shock decompensation:
○ Decreased blood pressure and respirator rate
○ Altered mental status
• Clinical manifestations of shock:
○ Increased heart and respiratory rate
○ Cool, clammy (sweaty) skin
○ Cyanosis
○ Poor capillary refill (>2 secs)
○ **BP by itself is not a good indicator of shock**
• Classes of shock (adult)
○ I: blood loss
○ II: elevated heart rate, mild increase in respiration, BP may be
orthostatic
○ III: Heart rate b/w 120 and 140, BP is reduced, Cap refill is long,
respiration is increased
○ IV: BP is decreased markedly, HR is above 140 and there is no urine
output
• Early detection of shock in the pediatric population:
○ Greater ability to compensate!
  Doesn’t stop until they reach pre-morbid rate
○ Increased heart rate is the earliest sign of shock
 Respiration rate increases as well
○ BP does not fall until 20-30% of blood volume is lost
 Respirations are still high here
 Systolic reduces by more than 40mmHg
 Decrease in BP is a very bad sign and indicative of late stages of
shock
• Co-existing medications and or conditions adds complexity to diagnosis:
○ Medications may mask shock
 Ex: beta blockers prevents the increase in heart rate
○ Prior medical conditions may present as shock
 Ex: MI that reduced left ventricular CO
• Athletes verse poor baseline physical condition
• Diagnosing shock in the field:
○ Physical exam findings:
 BP and vital signs
• Monitoring shock in hospital:
○ Fluid levels:
 Urine output
 Blood values
○ Central Venous Pressure
 Pressure in thoracic vena cava
• Estimates preload
 Normal in healthy individual : 0-8mmHg, goal if spontaneously
breathing: 8-12mmHg, goal with PPV: 11-16mmHg
 Values in shock patient:
• Less than 8
○ Volume depleted, negative pressure inspiration
• Greater than 12
○ Heart failure, volume overlaod
○ Mean arterial Pressure:
 Goal=65mmHg
 Measured directly or indirectly
○ Golden Hour of Trauma:
 Right patient, right place, right time
 Survival from severe trauma falls after 60 minutes
○ Community’s response to trauma is designed to intervene and stabilize
prior to onset of irreversible shock
• Management:
○ ****First: Airway, then breathing, then circulation
○ Circulation
  Stop bleeding and replace volume
• Hemorrhagic Shock
○ Pure hypovolemia
○ Treatment: stop bleeding, replace volume
○ Never ever give a vasoconstrictor to a hypovolemic shock patient
• This will decrease end organ perfusion
• Septic Shock is a combination of:
○ Hypovolemia due to inappropriate vasodilation
○ Distributive
○ Cardiogenic
○ Most common form of shock
 10th leading cause of death in the US
○ TRT: treat hypovolemiafist to optimize CVP. If patient is still
hypotensive, give vasoconstricting drugs
• Cardiogenic Schock
○ Reduced contractility due to myopathies and arrhythmias
 Treatment:
• Replace volume then vasoconstrictors
• Neurogenic Schock
○ Decreased heart rate and vasodiation due to unopposed
parasympathetic system
○ Paralysis of sympathetic chain
 No control of vascular tone
○ Treatment: Replace volume then vasoconstrict
• Anaphalyctic Shock
○ Severe allergic reaction from histamine release
○ Severe vasodilation, decreased venous return
○ Death due to obstructed airway and decreased perfusion in end organs
○ Treatment: replace volume and give epinephrine simultaneously