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Shock Loring W. Rue, III, MD, FACS Professor and Vice Chairman Department of Surgery University of Alabama at Birmingham

Shock
What is it?
How to deal with it

Shock- Surgical Legacy
G.J. Guthrie was the first to use the term shock in the context of physiologic instability
Surgeon for Duke of Wellington in Peninsula campaign against Napoleon

George Crile
Developed experimental models of hemorrhagic shock
First to describe the decrease in CVP and cardiac output associated with hemorrhage
An Experimental Research into Surgical Shock (1899)

Alfred Blalock
Demonstrated the hypovolemia associated with hemorrhage resulted in:
HYPOTENSION
METABOLIC ACIDOSIS
IMPAIRED OXYGEN DELIVERY TO TISSUES
Physiologic derangements corrected by volume resuscitation

What is Shock?
Inadequate provision of oxygen to peripheral tissues resulting from either insufficient perfusion or abnormal extraction of oxygen
Results in anaerobic metabolic pathways

Shock- Pathophysiology
In the setting of adequate oxygen:
Glucose metabolized via citric acid cycle yielding a net of 36 ATP
In the setting of inadequate oxygen:
No citric acid cycle-lactate generated yielding 2 ATP

Shock- Anaerobic Metabolism
Results in significant intracellular energy deficits:
Cell membrane repair mechanisms altered
Electrolyte disturbances occur
Rupture of endoplasmic reticulum
Mitochondrial dysfunction occurs
Rupture of lysosomes

Shock and Reperfusion Injury
Resuscitation and tissue reperfusion in this setting results in free radical generation
Can lead to cell death and organ dysfunction

Shock and Metabolic Acidosis: Not A Good Thing
Cardiac Effects:
Blood flow is redistributed from endocardium to epicardium with potential myocardial dysfunction
Poor response to systemic catecholamines

Pulmonary Effects
Impairment of central respiratory drive
CNS Effects
Autoregulatory mechanisms of cerebral blood flow overridden with MAP < 60

Renal Effects
Afferent arteriolar vasoconstriction with RBF redistributed from cortex to medulla
GFR decreases: oliguria / anuria
Gastrointestinal Effects
Gut ischemia > mucosal necrosis > bacterial translocation

Shock- Systemic Compensatory Mechanisms
Intravascular volume
Baroreceptor activity
Mechanoreceptor activity
CNS Response Pituitary releases -ADH -ACTH Na/Water retention Cortisol released Sympathetic nervous stimulation
Epinepherine
Norepinepherine
Renin/Angio/Aldo
Enhanced cardiac function Peripheral vasoconstriction Na/Water retention Peripheral vasoconstriction

Shock- Clinical Features
Hypotension
Tachypnea
Oliguria / Anuria
Impaired Mental Status
Depending upon cause, may also demonstrate
Narrowing of pulse pressure
Tachycardia

Shock- Management Priorities
Airway adequacy
Breathing restoration
Circulatory support- method dependent upon cause of shock

Shock - Resuscitation Endpoints
Classic
Restoration of blood pressure
Normalization of heart rate and urine output
Appropriate mental status
Improved
All of the above plus
Normalization of serum lactate levels
Resolution of base deficit

Shock- Judging the Adequacy of Resuscitation
Monitor resuscitation with serial ABGs (attention to base deficit) and serum lactate levels.

Shock Causality
Hypovolemic
Cardiac Tamponade
Tension Pneumothorax
Cardiogenic
Neurogenic
Septic

Approach to the Trauma Patient - Appropriate for Any Patient in Shock
Triage
Primary Survey
Resuscitation
Secondary Survey
Monitoring and Re-evaluation
Definitive Care

Initial Assessment of the Trauma Patient– Primary Survey
A – AIRWAY with C-SPINE CONTROL
B – BREATHING
C – CIRCULATION with BLEEDING CONTROL
D – DISABILITY, NEUROLOGIC STATUS
E – EXPOSURE and ENVIRONMENT
Life threatening problems identified and managed simultaneously

Hypovolemic Shock
Must treat the source of hypovolemia and arrest ongoing fluid losses
The usual suspects:
Thorax (CXR or CT)
Abdomen (CT or Ultrasound)
Pelvis (CT or plain film)
Retroperitoneal (CT)
Extremities – fractures or open wounds (plain films)
All can be evaluated by operative intervention

Initial Assessment – Radiographs
Cervical spine
Chest
Pelvis

Hypovolemic Shock
Categorized by severity as Class I-IV

Hypovolemic Shock
Mainstay of therapy- Volume restoration
Crystalloids
Colloids
Blood
Plasma
Blood Substitutes

Hypovolemic Shock – Basic Management Principles-1
Immediate and rapid administration of 2 liters warm Lactated Ringers through large bore peripheral IVs
Check for response to therapy
If no response, either:
Not enough “treatment given”
Incorrect treatment

Hypovolemic Shock – Basic Management Principles-2
Consequently, repeat fluid bolus
Re-assess
If no response, either:
Massive exsanguinating hemorrhage
Other causes: think Cardiogenic or Neurogenic in the trauma patient

Progressive entry of air into pleural space
Collapse of ipsilateral lung
Mediastinal shift
Compromised venous return to heart
Hypotension / decreased cardiac output
Cardiovascular collapse
Needle decompression / chest tube

Hypotension
Absent breath sounds
Neck vein distension
Hyperresonant thoracic percussion note
Contralateral tracheal shift
Subcutaneous emphysema
Mechanism of injury
Clinical diagnosis

Cardiogenic Shock
The heart fails to deliver an adequate amount of blood to the body resulting in hypoperfusion of peripheral tissues
The heart cannot generate a sufficient stroke volume and cardiac output
Can be the result of impaired diastolic or systolic function or a combination of the two

Cardiogenic Shock
Most often due to myocardial ischemia or infarction or resultant complications of papillary muscle rupture or ventricular septal rupture
In trauma setting, think cardiac contusion in blunt force trauma and cardiac tamponade in penetrating trauma.

Cardiogenic Shock- Basic Management Principles
For pure “pump” failure, options include:
Pharmacologic agents
Re-perfusion strategies
Lytic agents
Stents
Coronary bypass
Mechanical assists (Intra-aortic balloon)
For tamponade physiology- surgery

Cardiac Tamponade

Penetrating Cardiac Injury

Penetrating Cardiac Injuries
Etiology usually knives or bullets on the streets, but
In the hospital lines, catheters

Relative role of tamponade vs. severe hemorrhage determined by :
Size of pericardial rent
Rate of bleeding from cardiac wound
Chamber of heart involved
STAB WOUNDS – TAMPONADE
GSW - BLEED

Tamponade Physiology:
Blood accumulates in pericardium
Stroke volume decreases
Right atrial pressure increases
Right ventricle distends
Ventricular septum shifts to left
Left ventricle filling compromised
Cardiac output decreases, hypotension ensues

Pre-hospital :
Get patient to hospital ASAP
Mattox / Feliciano study of 100 consecutive patients – if external CPR > 3 minutes- 100% mortality
Emergency department :
Hemodynamics stable- ECHO +/- subxyphoid window
Hemodynamics unstable – ED thoracotomy / OR *

Neurogenic Shock
A form of distributive shock caused by the sudden loss of CNS signals to vascular smooth muscle following spinal cord injury
Results in an immediate decrease in peripheral vascular resistance and hypotension
May be associated with normal heart rate or even bradycardia

Neurogenic Shock Basic Management Principles
Adequate oxygenation
Spine immobilization
Restore vasomotor tone after insuring adequate volume status
Alpha agonist pharmacologic agents
Often a role for early use of flow directed pulmonary artery catheter

Septic Shock
A type of distributive shock related to loss of vasomotor tone in response to severe systemic infection or inflammatory response
Results from release of multiple cellular mediators which stimulate a neurohormonal systemic response and influence vascular resistance

Septic Shock
Inadequate treatment can lead to ARDS and multiple organ failure
Mortality approaches 50%

Septic Shock Basic Management Principles
Remove the source of infection or nidus for unlimited inflammatory response
Antimicrobial therapy directed against offending organisms
Support organ function
Alpha agonists to maintain vasomotor tone
Aggressive use of flow directed pulmonary artery catheters

Shock A Guide to Resuscitation Flow Directed Pulmonary Artery Catheter
AKA the Swan- Ganz catheter, introduced into clinical practice in 1970
Integrates cardiopulmonary physiologic data of the patient
Aides in determining appropriate theraputic interventions when cause of shock unknown
Allows resuscitation to physiologic endpoints

Shock Flow Directed PA Catheters

Shock The Role of the PA Catheter
Most often used in conjunction with standard intravascular monitoring devices (central venous line, arterial line) , EKG and pulse oximetry
Provide both measured and calculated physiologic indices

Shock The Role of the PA Catheter, etc
Measured physiologic indices:
Mean arterial pressure (a-line)
Heart rate (EKG, a-line)
Central venous pressure (CVL, PA catheter)
Pulmonary artery occlusion pressure, AKA the “wedge pressure” (PA catheter)
Oxygen saturation (pulse oximetry, ABG)

The measured indices enable calculation of other parameters:
Systemic Vascular Resistance
[(MAP-CVP) x 80] / CO
Stroke Volume
CO / HR
Usually “indexed” by patient BSA (SV / BSA)

Invasive hemodynamic monitoring can provide insight into the principal determinants of CO and hence tissue perfusion:
Preload : (CVP, better yet PAOP)
Afterload : (SVR and MAP)
Contractility : (SI)

Shock- How Can the PA catheter help?
Hypovolemic shock-
Low CO, low PAOP and CVP, high SVR
Cardiogenic shock-
Low CO, high PAOP and CVP, low SI
Septic shock-
High CO, low PAOP and CVP, low SVR

Therapy can be directed where intervention needed:
Inadequate Preload = Hypovolemia
Volume- either crystalloids or colloids depending upon patient Hb and coagulation parameters
Excess Preload = Congestive Heart Failure
Diuretics +/- Inotropes

Inadequate afterload = neurogenic or septic shock
Alpha agonists AKA Pressors (Norepinephrine or Neosynephreine)
Excessive afterload = Hypertensive CVD
Vasodilators ( Sodium Nitroprusside, Nitroglycerine)

Inadequate contractility = cardiogenic shock
Beta agonists AKA Inotropes
Epinepherine
Dobutamine (good if increased afterload as well)

Shock- Pitfalls in Management
Assuming blood pressure equates to cardiac output
Extremes of age
Hypothermia
Athletes
Pregnancy
Medications / Pacemakers

Points for the Student
Understand the rationale for the pitfalls in shock management as listed on slide
What is the optimal and most efficient diagnostic modalities for the patient with presumed hypovolemic shock?
Understand the clinical features of the 6 major causes of shock.
Trivia question: Who is depicted on the slide “Penetrating Cardiac Injury” ?

Patient Scenario - 1
42 yo woman ejected from car following collision with a tree. Pre-hospital data:
HR 110 BP 88/46 RR 26
Confused, skin cold and clammy
Is she in shock? If so what are potential etiologies? How do we assess and treat?

42 yo woman involved in MVC arrives in ED with full spine protection and supplement oxygen
HR 120 BP 80 /46 RR 32
Is she in shock? If so what are potential etiologies? How do we assess and treat?

After 2000cc warm lactated Ringers:
HR 90 BP 110 / 80 RR 22
How has the patient responded? What are the diagnostic implications?

What if the same patient, after 2000cc warm lactated Ringers:
HR 130 BP 80 / 60 RR 40
Clinical interpretation?

18 yo man stabbed in the left chest with large kitchen knife
BP 80 / 60 HR 130 RR 30
Is he in shock ? Diagnostic possibilities ? How do you quickly evaluate and treat ?

56 yo man now 6 days after undergoing a left hemicolectomy for cancer. Develops oliguria and altered sensorium. Transferred to the ICU- PA catheter placed
Several hours later, patient is hypotensive BP 80 / 60 HR 140
What are the diagnostic possibilities ? What would the PA catheter data look like for the various diagnostic possibilities?

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