SHOCK

DAKOTA HORTON

SHOCK

Critical condition characterized by sudden drop in blood flow throughout the body
Circulatory system fails to maintain adequate blood flow
Fails to deliver oxygen and nutrients.

Decreased tissue perfusion

Impaired cellular metabolism
Imbalance between supply and demand for oxygen and nutrients

CLASSIFICATION OF SHOCK
Low Blood Flow
Cardiogenic shock
Hypovolemic shock
Absolute hypovolemia
Relative hypovolemia

Maldistribution of Blood Flow

Neurogenic shock
Anaphylactic shock
Septic shock

CARDIOGENIC SHOCK
Decreased blood flow from compromised cardiac output
Systolic dysfunction
Inability of the heart to pump blood forward
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension

Diastolic dysfunction
Inability of the heart to fill during diastole
Pericardial tamponade

Dysrhythmias
Structural factors
Valvular abnormality: stenosis, regurgitation
Ventricular septal rupture

CARDIOGENIC SHOCK- CLINICAL PRESENTATION

Decreased capillary refill time
Chest pain may or may not be present
Tachypnea, crackles, wheezes
Increased sodium and water retention, decreased renal blood blow, decreased urine output
Pallor, cool and clammy skin
Decreased cerebral perfusions, confusion, anxiety, agitation
Decreased bowel sounds, nausea, vomiting

HYPOVOLEMIC SHOCK
Loss of intravascular fluid
Absolute hypovolemia
External loss of whole blood
Hemorrhage, trauma, surgery, GI bleeding

Loss of other body fluids

Vomiting, diarrhea, diuresis,

Causes: severe trauma with massive tissue injury or hemorrhage

Relative Hypovolemia
Pooling of blood or fluids
Bowel obstruction

Fluid shifts
Burn injuries, ascites

Internal bleeding
Fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis

Massive vasodilation
From sepsis

HYPOVOLEMIC SHOCK- CLINICAL PRESENTATION

Decreased preload, stroke volume and capillary refill time
Tachypnea that later progresses to bradypnea
Decreased urine output
Pallor, cool clammy skin
Anxiety, confusion, agitation
Absence of bowel sounds

NEUROGENIC SHOCK
Hemodynamic consequence of spinal cord injury, disease or opioid overdose
massive vasodilation without compensation
caused by the loss of SNS vasoconstrictor tone
Or depression of the vasomotor center (from opioids, benzodiazepines)

Leads to a pooling of blood in the blood vessels, tissue hypoperfusion and impairment of

cellular metabolism
Can occur within 30 minutes of a spinal cord injury to T5 vertebrae or above and can last

up to 6 weeks
Important clinical manifestations
Hypotension
bradycardia
Inability to regulate temperature

ANAPHYLACTIC SHOCK
Life threatening hypersensitivity reaction to a substance
Immediate reaction
Massive vasodilation
Release of vasoactive mediators
Increase in capillary permeability
Fluid leaks from the vascular space into the interstitial space

Airway swelling, breathing and circulation problems

Untreated anaphylactic shock can lead to respiratory or cardiac arrest

ANAPHYLACTIC SHOCK- CLINICAL PRESENTATION

Chest pain
Third spacing of fluid
Swelling of lips and tongue, larynx and epiglottis
SOB, wheezing, rhinitis, stridor
Flushed skin, pruritus, angioedema
Anxiety, confusion, decreased level of consciousness, metallic taste
Cramping, abdominal pain, nausea, vomiting, diarrhea

SEPTIC SHOCK
Sepsis septic shock
Systemic inflammatory response to an infection
Infection stimulates extreme or exagerrated immune response

Patient experiences hypotension that cannot be reversed with fluid resuscitation, and

tissue perfusion abnormalities

Primary organisms that cause sepsis are gram-negative and gram-positive bacteria,

parasites, fungi and viruses

Clinical presentation is complex, no single specific symptom to diagnose
At risk patients: older adults, infants <1 year, immunosuppressed/immunocompromised

patients, malnourished patients, patients with diabetes mellitus, cancers, chronic kidney
disease and heart failure

SEPTIC SHOCK- CLINICAL PRESENTATION

Significant increase or decrease in temperature
Decreased ejection fraction
Hyperventilation
Respiratory alkalosis progressing to respiratory acidosis
Hypoxemia
Respiratory failure
Acute respiratory distress syndrome
Pulmonary hypertension
Crackles
Decreased urine output
Warm and flushed skin progressing to cool and mottled skin
Alteration in mental status: confusion
Agitation
Coma(late)
GI bleeding paralytic ileus

STAGES OF SHOCK

Compensatory
Progressive
Refractory

COMPENSATORY STAGE OF SHOCK

Body activates neural, hormonal and biochemical compensatory mechanisms
Attempt to maintain homeostasis
First sign of shock: hypotension d/t decreased Cardiac output, decreased pulse pressure

Neurological Compensation
Baroreceptors in the carotid and aortic bodies activate the sympathetic nervous system
Stimulate the release of epinephrine and norepinephrine
Vasoconstriction
Blood flow to vital organs such as heart and brain is maintained
Blood flow to non vital organs and peripheries is reduced (kidneys, GI tract, skin, lungs)

Endocrine compensation
Decreased blood flow to the kidneys activates the renin-angiotension system

COMPENSATORY STAGE CONT.

Renin-angiotension system
Stimulates the release of aldosterone which results in sodium and water reabsorption
Sodium reabsorption raises the serum osmolality stimulating the release of ADH which further

reabsorbs water from the kidneys to increase blood volume

increased absorption of fluids leads to increase circulating blood volume
Increased blood volume and vasoconstriction leads to increased blood pressure and cardiac output

Shunting blood from nonvital organs

Decreased blood flow to GI tract leads to slowing of peristalsis
Decreased blood flow to the skin leads to cool and clammy skin (disregarding early stages of septic

shock)
Decreased blood flow to the lungs results in physiological dead space. This dead space results in a

mismatch between ventilation and perfusion

Arterial oxygen levels decrease
Rate and depth of respirations increase to compensate

PROGRESSIVE STAGE
Progressive stage of shock begins as compensatory mechanism fail
Condition deteriorates, Blood pressure progressively falls
Aggressive interventions are necessary to prevent development of Multi Organ Dysfunction

Syndrome
Distinguishing features of this stage
Continued decreased cellular perfusion
Altered capillary permeability causing fluid to shift from vascular space into the interstitial space

Hypoperfusion
Pulmonary system first to display signs of dysfunction
Pulmonary vasoconstriction
Fluid shifts causing pulmonary interstitial edema

PROGRESSIVE STAGE- CONT

Cardiovascular system
Decrease in CO, BP, coronary, artery and cerebral perfusion
Changes in patients mental status

Impaired renal function

Mucosal barrier of the GI tract dies
Decreased function of the liver

REFRACTORY STAGE (IRREVERSIBLE)

Final stage
Decreased perfusion from peripheral vasoconstriction and decreased CO
Accumulation of lactic acid
Loss of intravascular volume worsens
Clinical manifestations
Unresponsive
Loss of reflexes
Pupils unreactive and dilated
Profound hypertension, decreased CO, bradycardia, Blood pressure inadequate to perfuse vital organs
Severe refractory hypoxemia
Respiratory failure
Ischemic gut
Anuria
DIC

NURSING INTERVENTIONS
Early recognition and prompt interventions are required for successful management of

shock
Identify and treat underlying cause
Oxygen and ventilation as needed
Fluid resuscitation
Drug therapy
Sympathomimetic drugs
Vasodilators

Ongoing monitoring of:

LOC
VS

SEPSIS SIX
What you can do within the first hour for atleast 6

hours
1) Give 100% oxygen
2) Take blood cultures to determine antibiotic therapy
3) IV antibiotics
4) IV fluid therapy
5) measure lactate and hemoglobin
6) Insert catheter and monitor urine output
Robson, W. P., & daniels, R. (2008). The sepsis six: Helping patient to survive sepsis. British Journal of Nursing, 17(1), 20.

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