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SHOCK
Sevgi Bilgen
2014
Students should learn;
The definition of shock
Types of shock and differential diagnosis
Shock treatment
Introduction
In order to treat shock appropriately, it must
first be recognized, then identify the cause
In order to recognize it, it is important to
understand some of the physiology of the
disease process
The definition of shock
Shock is a physiologic state characterized by
systemic reduction in tissue perfusion, resulting
in decreased tissue oxygen delivery
Hypotension is not a requirement
Shock can occur with a normal blood pressure
and hypotension can occur without shock
Poor tissue perfusion
Results in multiple organ failure and death
Basic Physiology
Tissue perfusion is dependent on SVR and CO
Imbalance between oxygen delivery and oxygen
consumption which leads to cell death, end
organ damage, multi-system organ failure, and
death.
Basic Physiology
Oxygen Delivery = CO x arterial content of O2
Cardiac Output = HR x Stroke Volume
Stroke Volume is a function
Preload
Afterload
Myocardial Contractility
Basic Physiology
Understanding Shock
• Inadequate systemic oxygen delivery activates
autonomic responses to maintain systemic
oxygen delivery
• Sympathetic nervous system
• NE, epinephrine, dopamine, and cortisol release
• Causes vasoconstriction, increase in HR, and increase of
cardiac contractility (cardiac output)
• Renin-angiotensin axis
• Water and sodium conservation and vasoconstriction
• Increase in blood volume and blood pressure
Understanding Shock
• Cellular responses to decreased systemic oxygen
delivery
• ATP depletion → ion pump dysfunction
• Cellular edema
• Hydrolysis of cellular membranes and cellular death
• Goal is to maintain cerebral and cardiac
perfusion
• Vasoconstriction of splanchnic, musculoskeletal, and renal
blood flow
• Leads to systemic metabolic lactic acidosis that
overcomes the body’s compensatory mechanisms
Global Tissue Hypoxia
• Endothelial inflammation and disruption
• Inability of O2 delivery to meet demand
• Result:
• Lactic acidosis
• Cardiovascular insufficiency
• Increased metabolic demands
Multi organ Dysfunction
Syndrome (MODS)
• Progression of physiologic effects as shock ensues
•
•
•
•
Cardiac depression
Respiratory distress
Renal failure
DIC
• Result is end organ failure
Initial Patient Assessment
Recognition of Shock
Clinical signs and symptoms depends on
the severity of the shock
Early manifestations include tachycardia
and cutaneous vasoconstriction
Clinical Pathophysiology of Shock
General / Vital signs
Cardiovascular- tachycardia
Skin- vasoconstriction vs. vasodilation
Respiratory- increased RR
Urinary- decrease urine output
Neurologic- confusion, agitation
Extremities- cold vs. warm
Clinical Endpoints of Shock
DECREASED BLOOD FLOW TO BRAIN AND HEART
Restless, agitated, confused, lethargy
Hypotension
Tachycardia
Tachypnea
END-STAGE SHOCK
Bradycardia
Arrhythmias
Death
Types of shock and differential
diagnosis
1.Hypovolemic shock
2.Cardiogenic shock
3.Obstructive shock
4.Distributive shock
Common Causes
1.Hypovolemic shock
Due to decreased circulating blood volume in
relation to the total vascular capacity and
characterized by a reduction of diastolic filling
pressures
1. Hypovolemic shock
Loss of blood (hemorrhagic shock)
Loss of plasma
Loos of fluid and electrolytes
Loss of blood (hemorrhagic shock)
External hemorrhage
Trauma
Gastrointestinal tract bleeding
Internal hemorrhage
Hematoma
Hemothorax or hemoperitoneum
Loss of plasma
Burns
Exfoliative dermatitis
Loos of fluid and electrolytes
External
Vomiting
Diarrhea
Excessive sweating
Hyperosmolar states (diabetic ketoacidosis, hyperosmolar
nonketotic coma)
Internal (third-spacing)
Pancreatitis
Ascites
Bowel obstruction
2. Cardiogenic shock
Due to cardiac pump failure related to loss of myocardial
contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and
characterized by elevations of diastolic filling pressures
and volumes
2. Cardiogenic shock
Dysrhythmia
Tachyarrhythmia
Bradyarrhythmia
Pump failure (secondary to myocardial infarction or
other cardiomyopathy)
Acute valvular dysfunction (especially regurgitant
lesions)
Rupture of ventricular septum or free ventricular wall
3. Obstructive shock
Due to obstruction to flow in the cardiovascular
circuit and characterized by either impairment of
diastolic filling or excessive afterload
3. Obstructive shock
Tension pneumothorax
Pericardial disease (tamponade, construction)
Disease of pulmonary vasculature (massive pulmonary emboli,
pulmonary hypertension)
Cardiac tumor (atrial myxoma)
Left atrial mural thrombus
Obstructive valvular disease (aortic or mitral stenosis)
4. Distributive shock
Caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized
(after fluid resuscitation) by increased cardiac
output and decreased SVR
4. Distributive shock
Septic shock
Anaphylactic shock
Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency
Clinical classification of shock
Mild (<20% of blood volume lost)
Moderate (20-40% of blood volume lost)
Severe (>40% of blood volume lost)
Mild (<20% of blood volume lost)
Pathophysiology
Decreased peripheral perfusion only of organs able to
withstand prolonged ischemia (skin, fat, muscle, and bone).
Arterial pH normal
Clinical Manifestations
Patient complains of feeling cold.
Postural hypotension and tachycardia.
Cool, pale, moist skin; collapsed neck veins; concentrated
urine.
Moderate (20-40% of blood volume lost)
Pathophysiology
Decreased central perfusion of organs able to tolerate
only brief ischemia (liver, gut, kidneys).
Metabolic acidosis present
Clinical Manifestations
Thirst
Supine hypotension and tachycardia (variable)
Oliguria and anuria.
Severe (>40% of blood volume lost)
Pathophysiology
Decreased perfusion of heart and brain.
Severe metabolic acidosis.
Respiratory acidosis possibly present.
Clinical Manifestations
Agitation, confusion or obtundation.
Supine hypotension and tachycardia invariably present.
Rapid, deep respiration.
Evaluation
Airway: includes brief evaluation of mental status
Breathing: If patient is conversing with you, A & B
are fine.
Circulation: Vitals (HR, BP). Includes placement of
adequate IV access,
Disability: identification of gross neurologic injury
Exposure: ensures complete exam
Evaluation
Laboratory
Hgb, WBC, platelets
PT/PTT
Electrolytes, arterial blood gases
BUN, Cr
Ca, Mg
Serum lactate, mixed venous oxygen saturation (SVO2)
ECG
Evaluation
Invazive monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter
Mixed or central venous oxygen
saturation (SvO2/ScvO2)
Oxygen delivery(DO2) and
oxygen consumption(VO2)
As indicated
o Chest x-ray
o Pelvic x-ray
o Abd/pelvis CT
o Chest CT
o GI endoscopy
o Bronchoscopy
o Vascular radiology
Treatment
Identify & reverse the cause
Restore tissue perfusion
Restore organ function
Treatment of Shock
General Management
• ABCDE
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation
Airway
• Determine need for intubation but remember:
intubation can worsen hypotension
• Sedatives can lower blood pressure
• Positive pressure ventilation decreases preload
• May need volume resuscitation prior to
intubation to avoid hemodynamic collapse
Control Work of Breathing
• Respiratory muscles consume a significant amount of oxygen
• Resting ventilatory muscles will permit diversion of cardiac
output to other hypo perfused organs
• Tachypnea can contribute to lactic acidosis
• Mechanical ventilation and sedation decrease WOB and
improves survival
Optimizing Circulation
• Unless there are signs of intravascular volume overload
initial resuscitation with IV fluids is generally indicated.
• Isotonic crystalloids
• Titrated to:
• CVP 8-12 mm Hg
• Urine output 0.5 ml/kg/hr. (30 ml/hr.)
• Improving heart rate
• May require 4-6 L of fluids
• No outcome benefit from colloids
• Vasopressor medications should be selected based on
the cause of shock
Maintaining Oxygen Delivery
• Decrease oxygen demands
• Provide analgesia and anxiolytics to relax muscles and avoid
shivering
• Maintain arterial oxygen saturation/content
• Give supplemental oxygen
• Maintain Hemoglobin > 10 g/dL
• Serial lactate levels or central venous oxygen
saturations to assess tissue oxygen extraction
End Points of Resuscitation
• Goal of resuscitation is to maximize survival and
minimize morbidity
• Use objective hemodynamic and physiologic
values to guide therapy
• Goal directed approach
•
•
•
•
Urine output > 0.5 mL/kg/hr.
CVP 8-12 mmHg
MAP 65 to 90 mmHg
Central venous oxygen concentration > 70%
Persistent Hypotension
• Inadequate volume resuscitation
• Pneumothorax
• Cardiac tamponade
• Hidden bleeding
• Adrenal insufficiency
• Medication allergy
Resuscitation Fluids
Blood
Lactated Ringers
Normal Saline
Colloids
Hypertonic Saline
Blood Substitutes
Evaluation of Treatment
Assess organ perfusion
Urinary output
Mental Status
Skin exam
Vitals
Which Pressor should I choose?
Hypovolemic shock
Fluids and Blood
Cardiogenic shock
Dobutamine - 1 agonist
Increases squeeze and heart
rate
Neurogenic shock
Fluids, phenylephrine,
norepinephrine, look for
another type of shock if it is
persistent
Anaphylactic shock
Fluids and epinephrine
Septic shock
Phenylephrine- alpha agonist
Increases SVR by arteriolar
constriction
Norepinephrine - alpha and beta
agonists
Dopamine
Low Dose - increases renal blood
supply
Medium Dose - beta effects
(increases heart rate and squeeze)
High Dose - alpha effects (arteriolar
constriction)
Early versus delayed administration of
norepinephrine in patients with septic shock.
The 28-day mortality was 37.6% overall.
Among the 213 patients, a strong relationship between delayed initial norepinephrine administration
and 28-day mortality was noted.
The average time to initial norepinephrine administration was 3.1¿±¿2.5 hours.
Every 1-hour delay in norepinephrine initiation during the first 6 hours after septic shock onset was
associated with a 5.3% increase in mortality.
Twenty-eight day mortality rates were significantly higher when norepinephrine administration was
started more than or equal to 2 hours after septic shock onset (Late-NE) compared to less than 2
hours (Early-NE).
Mean arterial pressures at 1, 2, 4, and 6 hours after septic shock onset were significantly higher and
serum lactate levels at 2, 4, 6, and 8 hours were significantly lower in the Early-NE than the Late-NE
group.
The duration of hypotension and norepinephrine administration was significantly shorter and the
quantity of norepinephrine administered in a 24-hour period was significantly less for the Early-NE
group compared to the Late-NE group.
The time to initial antimicrobial treatment was not significantly different between the Early-NE and
Late-NE groups.
Conclusion: Early administration of norepinephrine in
septic shock patients is associated with an increased
survival rate.
Crit Care. 2014 Oct 3;18(5):532.
Bai X, Yu W, Ji W, Lin Z, Tan S, Duan K, Dong Y, Xu L, Li N.
Survival and outcomes improve with
early perfusion, adequate oxygenation,
and identification with appropriate
treatment of the cause of shock.