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SHOCK
Sevgi Bilgen
2014-2015
Students should learn;
The definition of shock
Types of shock
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
Results in multiple organ failure and death
Inadequate oxygen delivery leading to shock can
occur despite the patient being hypertensive or
normotensive
Clinicians should not wait for the presence of
hypotension before aggressively attempting to
reverse shock and restore adequate tissue
perfusion.
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
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.0031)
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
Goal is to maintain cerebral and cardiac perfusion
Understanding Shock
Prolonged oxygen deprivation leads to cellular hypoxia,
derangement of critical biochemical processes at the
cellular level,
which can progress to the systemic level
Understanding Shock
Cellular effects include cell membrane ion pump
dysfunction,
intracellular edema,
leakage of intracellular contents into the extracellular space,
inadequate regulation of intracellular pH
Understanding Shock
Systemic effects include alterations in the serum pH,
endothelial dysfunction,
redox state,
further stimulation of inflammatory and
anti-inflammatory cascades.
Understanding Shock
The effects of oxygen deprivation are initially
reversible, but rapidly become irreversible.
The result is sequential cell death,
end-organ dysfunction.
Progressive end-organ dysfunction leads to irreversible
organ damage and patient death.
Clinical Endpoints of Shock
DECREASED BLOOD FLOW TO BRAIN AND HEART
Restless, agitated, confused, lethargy
Hypotension
Tachycardia
Tachypnea
END-STAGE SHOCK
Bradycardia
Arrhythmia
Death
Initial Patient Assessment
Recognition of Shock
Clinical signs and symptoms depends on
the severity of the shock
Early manifestations include tachycardia
and cutaneous vasoconstriction
Cardinal features
Cardinal features of shock include;
hypotension,
oliguria,
abnormal mental status,
metabolic acidosis, and,
in some patients, cool and clammy skin.
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
Characterized by a reduction of diastolic filling
pressures.
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
Internal (third-spacing)
Vomiting
Pancreatitis
Diarrhea
Ascites
Excessive sweating
Bowel obstruction
Hyperosmolar states (diabetic
ketoacidosis, hyperosmolar
nonketotic coma)
Hypovolemic shock
Depending upon the cause of the hypovolemic shock,
patients may report;
hematemesis, hematochezia, melena,
vomiting, diarrhea,
abdominal pain.
There may be evidence of blunt or penetrating trauma,
or the patient may be postoperative.
Hypovolemic shock
Physical manifestations may include;
decreased skin turgor (in younger patients),
dry skin,
dry axillae,
dry tongue,
dry oral mucosa.
Hypovolemic shock
Patients may have postural hypotension,
decreased jugular venous pressure,
diminished central venous pressure.
There may be anemia, or the amylase and lipase may be
elevated
2. Cardiogenic shock
Due to cardiac pump failure related to loss of
myocardial contractility or structural/mechanical
failure of the cardiac anatomy
characterized by elevations of diastolic filling
pressures and volumes
Cardiogenic shock
Pump failure (secondary to myocardial infarction or
other cardiomyopathy) Acute myocardial ischemia is
most common cause
Arrhythmia
Tachyarrhythmia
Bradyarrhythmia
Acute valvular dysfunction
Rupture of ventricular septum or free ventricular wall
Cardiogenic shock
Depending upon the cause of the cardiogenic shock,
patients may report;
dyspnea,
chest pain,
palpitations.
Many patients have a history of cardiovascular disease.
Cardiogenic shock
Lung examination may reveal diffuse crackles
cardiac examination may reveal a new murmur, gallops,
or soft heart sounds.
The jugular venous pressure and central venous
pressure may be increased,
the distal arterial pulses may be diminished.
Cardiogenic shock
There may be evidence of pulmonary congestion or
pulmonary edema on a chest radiograph,
recent or current ischemia on an electrocardiogram.
Cardiac enzymes may be elevated.
An echocardiogram may demonstrate the etiology.
3. Obstructive shock
Due to obstruction to flow in the cardiovascular
circuit
Characterized by either impairment of diastolic
filling or excessive afterload
Obstructive shock
Tension pneumothorax
Pericardial disease (tamponade)
Disease of pulmonary vasculature (massive pulmonary emboli,
pulmonary hypertension)
Cardiac tumor (atrial myxoma)
Left atrial mural thrombus
Obstructive valvular disease (aortic or mitral stenosis)
Tension pneumothorax/exam
absent unilateral breath sounds on the affected side;
trachea deviated to the opposite side;
hyper-resonance to percussion on affected side
Cardiac tamponade/exam
muffled hearts sounds
low BP
jugular venous distention
pulsus paradoxus
Pulmonary emboli/exam
possible cyanosis
respiratory distress with use of accessory muscles
lung auscultation normal
jugular venous distention if large embolism
calf tenderness
tachycardia
low oxygen saturations
4. Distributive shock
Caused by loss of vasomotor control resulting in
arteriolar/venular dilatation
characterized (after fluid resuscitation) by
increased cardiac output and decreased SVR
Distributive shock
Septic shock
Anaphylactic shock
Neurogenic shock
Vasodilator drugs
Acute adrenal insufficiency
Depending upon the cause of the
distributive shock; patients may report
dyspnea
fatigue
productive cough
malaise
dysuria, hematuria
headache
chills
photophobia
myalgias
pain
rashes
recent ingestion
Distributive shock
There may be fever
tachypnea
tachycardia
leukocytosis
abnormal mental status
flushing
Clinical classification of
hemorrhagic 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.
DIAGNOSTIC APPROACH
When a patient is suspected of having shock,
diagnostic evaluation should occur at the same time as
resuscitation.
Resuscitative efforts should NOT be delayed for
history, physical examination, laboratory testing, or
imaging.
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
Goals of Shock Resuscitation
Restore blood pressure
Normalize systemic perfusion
Preserve 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
Norepinephrine – (alpha+beta
agonists) Epinephrine+ vasopressin
Increases SVR by arteriolar
constriction
Dopamine
Low Dose - increases renal blood
supply
Medium Dose - beta effects
(increases heart rate and squeeze)
High Dose - alpha effects (arteriolar
constriction)
Survival and outcomes improve with early
perfusion, adequate oxygenation, and
identification with appropriate treatment of
the cause of shock.