Shock Flashcards
Types of shock
Hypovolemic
Cardiogenic
Circulatory Shock (Distributive)
Septic Shock
Neurogenic Shock
Anaphylactic Shock
Obstructive
Shock
is a condition where the blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cell function.
Hypovolemic shock
- decrease in intravascular volume S/S Hypotension Tachycardia Rapid, shallow respirations; cracks Decreased peripheral pulses Pale, cool extremities Decreased urinary output/oliguria Irritability, restlessness, lethargy
Cardiogenic shock
- impaired heart pumping
Circulatory shock
- maldistribution or mismatch of blood flow to the cells
Distributive shock
is defined as a change in vascular capacitance resulting in peripheral vasodilation and abnormal redistribution of blood flow.
Obstructive shock
is due to an obstruction of blood flow in the cardiovascular system. Caused by either
impairment of diastolic filling (decreased ventricular preload) excessive afterload (increased ventricular afterload)
Causes of obstructive shock
Impaired diastolic filling
- Cardiac (pericardial) tamponade
- Tension pneumothorax
- Hemothorax
- Mechanical ventilation
- Asthma
- Intrathoracic obstructive tumours
Impaired systolic contraction
- Right ventricle
Pulmonary embolus (massive)
Acute pulmonary hypertension
- Left ventricle
Saddle embolus
Aortic dissectionDescribe the hemodynamics of the hypovolemic, distributive and cardiogenic shock.
http://postimg.org/image/c9erlz78x/
Causes of cardiogenic shock
1) Coronary
- More common, seen most often in patients with an MI
- Occurs when a significant amount of left ventricular myocardium has been destroyed
2) Noncoronary
- Severe metabolic problems - severe hypoxemia, acidosis, hypoglycemia, and hypocalcemia
- Tension pneumothorax
Pharm. for cardiogenic shock
Vasoactive med therapy consists of using multiple drug therapies to restore and maintain adequate CO. The aim is to improve cardiac contractility, decrease preload and afterload, or a stable heart
1) Dobutamine (Dobutrex) - inotropic effects by stimulating myocardial beta receptors improving CO. Alpha-adrenergic receptors are also stimulated, decreasing pulmonary and systemic vascular resistance.
2) Nitroglycerin - by IV, venous vasodilator reducing preload. At high doses, causes arterial vasodilation and reduces afterload also.
3) Dopamine - vasoactive effects dependent on dosage
May be used with dobutamine and nitroglycerin to improve tissue perfusion
Low-dose dopamine (0.5-3.0 mcg/kg/min) increased renal perfusion and mesenteric flow. Does not affect cardiac output
Medium-dose dopamine (4-8 mcg/kg/min) has sympathomimetic properties and improves contractility and slightly increases heart rate
High-dose dopamine (8-10 mcg/kg/min) predominantly causes vasoconstriction, which increases afterload and thus increases cardiac workload. This is NOT DESIRED!
Central venous pressure (CVP)
Normal CVP is 3 to 8 mm Hg: pressure within the superior vena cava,
a) elevated indicates an increase in blood volume ie sodium and water retention, excessive IV fluids,alteration in fluid balance, or kidney failure
b) Decrease indicates a decrease in circulating blood volume ie fluid imbalance, hemorrhage, severe vasodilation, pooling of blood in extremities
Septic Shock
Type of circulatory (distributive shock), when the blood volume is abnormally displaced in the vasculature, causing relative hypovolemia, leading to inadequate tissue perfusion
Pathophysiology of septic shock
Microorganism invades body tissues and the patient exhibits an immune response
Activation of inflammatory response, producing increased capillary permeability and vasodilation
Phases of septic shock
1) Hyperdynamic, progressive phase - High cardiac output with systemic vasodilation;
2) Hypodynamic, irreversible phase - Low cardiac output with vasoconstriction - Reflects the body trying to compensate for the hypovolemia cause by the loss of intravascular volume through the capillaries
Hyperdynamic, progressive phase OF SEPTIC SHOCK
HR increases, progressing to tachycardia
Blood pressure usually within normal limits
Hyperthermic and febrile
Warm, flushed skin
Bounding pulses
RR is increased
Urinary output at normal or decreased
Nausea, vomiting, diarrhea, or decreased bowel sounds
Subtle mental status change - confusion or agitation
Hypodynamic, irreversible phase of SEPTIC SHOCK
Reflects the body trying to compensate for the hypovolemia cause by the loss of intravascular volume through the capillaries
BP drops
Skin is cool and pale
Temp is normal or below normal
HR and RR remain high
No urinary output
Multiple organ dysfunction progresses to failure
Pharm of septic shock
a) Broad-spectrum antibiotics are started until culture and sensitivity reports are received
b) Vasopressors
- Norepinephrine (NE) - first choice
- Epinephrine - Additional agent to norepi
- Vasopressin - can be added to norepi to raise MAP or decrease NE dosage
- Dopamine - alternative in highly selected patients (low risk of tachyarrythmias, and absolute or relative bradycardia)
Vasopressors
- Norepinephrine (NE) - first choice
- Epinephrine - Additional agent to norepi
- Vasopressin - can be added to norepi to raise MAP or decrease NE dosage
- Dopamine - alternative in highly selected patients (low risk of tachyarrythmias, and absolute or relative bradycardia)
Patients at risk for shock
Elderly Immunosuppressed Extensive trauma Burns Diabetes
Really good resource about sepsis
http://www.survivingsepsis.org/sitecollectiondocuments/implement-pocketguide.pdf
Describe the pathophysiology of distributive shock
- Massive arterial and venous dilation allows blood to pool peripherally
- Arterial dilation reduces systemic vascular resistance
Initial cardiac output is high, due to reduction in afterload and heart using increased effort to maintain perfusion - Pooling of blood in the peripheral causes a decrease in venous return
- This decrease in venous return causes a decreased stroke volume and decreased cardiac output
- This causes the blood pressure to decrease and thus decreased tissue perfusion
Risk Factors for Septic Shock
Immunosuppression Extremes of age (65yr) Malnourishment Chronic illness Invasive procedures
Risk Factors for Neurogenic Shock
Spinal cord injury
Spinal anesthesia
Depressant action of meds
Glucose deficiency
Risk Factors for Anaphylactic Shock
Penicillin sensitivity
Transfusion reaction
Bee sting allergy
Latex sensitivity
Describe Neurogenic Shock
- Vasodilation occurs as a result of a loss of sympathetic tone
- May have a long duration (from spinal cord injury) or a short one (syncope or fainting)
- Spinal shock is a type of neurogenic shock (see spinal cord injuries for info on it)
- Characterized by
Dry, warm skin (hypovolemic shock has cool, moist skin)
Bradycardia (other types of shock have tachycardia)
Causes of Neurogenic Shock
Spinal cord injury Spinal anesthesia Nervous system damage Depressant action of meds Hypoglycemia - insulin reaction/insulin shock
Management of Neurogenic Shock
Restore sympathetic tone either through
Stabilization of the spinal cord injury
Positioning the patient properly (in spinal anesthesia cases)
Treatment of neurogenic shock depends on the cause
If hypoglycemia (insulin shock) is the cause, glucose in rapidly given
What’s the diff between neurogenic shock and spinal shock? -from Life in the Fast Lane
Neurogenic shock is classically characterised by hypotension, bradycardia and peripheral vasodilatation. Neurogenic shock is due to loss of sympathetic vascular tone and happens only after a significant proportion of the sympathetic nervous system has been damaged – as may occur with lesions at the T6 level or higher.
Spinal shock is not a true form of shock. It refers to the flaccid areflexia that may occur after spinal cord injury, and may last hours to weeks. It may be thought of as ‘concussion’ of the spinal cord and resolves as soft tissue swelling improves. Priapism may be present.
Describe anaphylactic shock
Caused by severe allergic reaction when a patient who has already produced antibodies to an antigen, develops a systemic antigen-antibody reaction
Since they have already produced antibodies, this patient has been previously been exposed to the substance
This can be prevented by avoiding subsequent exposure, such as with a medication allergy
Mast cells release vasoactive substances, ie histamine or bradykinin, which causes widespread vasodilation and capillary permeability
Occurs rapidly and is life threatening
Managing anaphylactic shock
Remove the causative antigen
Administer meds to restore vascular tone
Provide emergency life support
Epinephrine for vasoconstriction
Diphenhydramine (Benadryl) to reverse the effects of histamine (reduces capillary permeability)
Albuterol to reverse bronchospasm
May need to perform CPR, ET intubation or tracheostomy
