Shock Flashcards
Fluid Composition
• The 60-40‐20 Rule:
– 60 % of body weight is water
– 40% of body weight is intracellular fluids
– 20% of body weight is extracellular fluid
Stroke Volume
Stroke Volume is the amount of blood released from the heart per beat (Beat Volume)
Cardiac Output
The amount of blood circulated from the heart in a minute
3 Principle factors that affect Cardiac Output
– Preload
– Afterload
– Myocardial contractility
Preload
• Blood delivered to the heart during diastole
• Measured as LVEDV
– via PCWP (Pulmonary capillary wedge pressure) or CVP
• Is dependant on venous return
• Decreased venous return can reduce preload
• Increased preload = increased stroke volume
Afterload
- Pressure at which the ventricle pumps against
- Blood is ejected only after the resistance is overcome
- Dependant on the degree of peripheral arterial vasoconstriction
- Vasoconstriction = increased resistance = increased aX\fterload = decreased stroke volume
Myocardial Contractility
The force generated by the myocardium on contraction
Blood Pressure
The resistance of blood flow by the force of friction between the blood and walls of the vessels
PVR (Peripheral Vascular Resistance)
may also be seen as Systemic Vascular Resistance (SVR)
Blood Flow
- PVR is dependent on internal diameter of vessels and viscosity of blood
- Aorta and arteries do not significantly change diameter
- Arterioles can change lumen to a factor of 5
Blood pressure Afterload
- Increased aXerload = ↑ BP
* Decreased aXerload = ↓ BP
Baroreceptors
Sensory fibers located in the aortic and carotid tissues
Baroreceptors
Help control BP by two negative feedback mechanisms:
– Lower BP in response to increased arterial pressure
– Increase BP in response to decreased arterial pressure
Chemoreceptor Reflexes
• Low arterial pressure stimulates peripheral chemoreceptor cells in
carotid and aortic bodies
• If oxygen or pH decreases, stimulate vasomotor center of medulla
Venous Systemic pressures
Venous system constricLon increases preload and SV
Arterial Systemic pressures
Arterial system constriction increases afterload and BP
Microcirculation
- Capillary network
- Responsive to needs of local tissues
- Will adjust to supply/bypass tissues in need/or without need
- Utilizes the pre and post capillary sphincters to facilitate these needs
Affects on microcirculation:
– Local control by tissues – Nervous control of blood flow – Baroreceptors – Chemoreceptors – CNS Ischemia response – Hormonal response – Adrenal-medullary response – Renin-angiotensin-aldosterone mechanism – Vasopressin – Reabsorption of tissue fluid
Oxygen
- Binds to hemoglobin and diffuses across capillary membrane
- 97 -‐ 100 % of hemoglobin are saturated in normal setting
Fick’s principle
– Adequate FiO2 – Appropriate O2diffusion from blood to capillaries – Adequate #’s of RBC’s – Proper tissue perfusion – Effective tissue off loading
Inadequate Tissue Perfusion (Three basic causes)
– Inadequate cardiac output
– Inadequate volume
– Inadequate container
Inadequate cardiac output
- Inadequate preload
- Inadequate stroke volume
- Excessive afterload
- Inadequate heart rate
Inadequate volume
Hypovolemia
– Hemorrhagic
– Fluid loss
Inadequate container
- Over-‐dilation
* Excessive increase in SVR
Three true classifications of shock
– Anaphylactic
– Distributive
– Obstructive
Types of shock
- Psychogenic D
- Neurogenic D
- Respiratory D
- Hypovolemic D
- Hemorrhagic D
- Cardiogenic O / D
- Metabolic D
- Septic D
- Anaphylactic A
Psychogenic shock
• Relative hypovolemia due to severe vasodilation
– Vasal vagal type response
• Caused by sudden and temporary sympathetic nervous system failure.
Neurogenic shock
- Also know as Spinal Shock
- Massive Relative hypovolemia due to severe vasodilation
- Damage caused to the nervous system inhibiting its involuntary/voluntary control of homeostasis
- Sudden loss of sympathetic tone to the smooth muscles of the vessels below the point of injury
- Without constant stimulation widespread relaxation of these muscles causes a decrease in PVR and a drop in BP
Respiratory shock
- Airway obstruction
- Hypoventilation
- Toxic inhalation
- Severe pulmonary edema
- Exacerbation COPD
- Multi-lobe bilateral pneumonia (septic also)
Hypovolemic Shock
• Inadequate perfusion of tissues caused by a volume deficiency other than blood. • AKA third space loss • Severe dehydration – diarrhea / vomiting – peritonitis – heat exhaustion – severe burns
Cardiogenic Shock
- Failure of the pump to supply O2tissues
- Potentially a combination shock ( like anaphylaxis ) depending on the etiology i.e.
- Massive AMI
- Valvular insufficiency
- Lethal dysrhythmia
- Cardiac arrest
- 60 -‐ 90 % mortality rate
Metabolic Shock
Shock as the result of a change in the chemistry of the endocrine system of the body. – Insulin shock – Diabetic ketoacidosis – Adrenal gland failure – Thyroid gland failure – Pituitary gland failure – Renal failure – Toxic ingestion
Septic Shock
- Massive infection and toxin production resulting in inability of the cell to exchange O2/CO2 resulting in cellular death
- Relative hypovolemia due to pool of blood in extremities
- 1 month mortality rate 35 -‐ 45 %
Hemorrhagic Shock
- Internal/external hemorrhage resulting in hypovolemia and a systemic reduction in tissue perfusion.
- Mortality rate dependent on etiology, early recognition, and aggressive intervention
Progression of shock
- Follows a sequence of stages related to changes in capillary perfusion and cellular necrosis
- The following examples given are for hemorrhagic shock (blood loss)
Classifications of hemorrhage • Class I (Vasoconstriction)
– 15 % blood loss (500 -750 mls)
• Healthy body can easily accommodate for the loss
• No effect on BP, Pulse pressure or renal output
Classifications of hemorrhage • Class I (Vasoconstriction)
Compensation
• Catecholamine release
• RR
– Normal ranges (may show slight increase to maintain O2 supplies with increased HR)
• HR
– Mild tachycardia to maintain CO due to reduced SV
• B/P
– Possible orthostatic hypotension (should appear within normal limits since CO is maintained)
• Cap Refill
– Normal
• CNS
– Mild anxiety
ClassificaLons of hemorrhage • Class II (Capillary and Venule Opening)
– 15 -25 % blood loss (750 -1250 mls)
Classifications of hemorrhage Class II (Capillary and Venule Opening)
Compensation
– First line compensatory mechanisms can no longer maintain BP • Secondary mechanisms now employed – Early decompensation • RR – Tachypnea • HR – Tachycardia • B/P – Hypotension may be prevalent (decreased pulse pressures) • CR – Delayed • CNS – Anxiety • Other – Pale, Cool and Clammy Skin (due to peripheral shutdown and catecholamine releases)
Capillary Washout
• Accumulated cellular waste products cause post-capillary sphincter to relax
• Waste products, cellular contents, and coagulated cells dumped into venous circulation
– Profound metabolic acidosis
– Release of microscopic emboli
• Body moves quickly towards death
Classifications of hemorrhage
• Class III (Disseminated Intravascular Coagulation)
– 25 -‐ 35 % blood loss (1250 -‐ 1750 mls)
Classifications of hemorrhage
• Class III (Disseminated Intravascular Coagulation)
Compensation
– Compensatory mechanisms unable to cope – Late decompensation • Without intervention, patient survival unlikely • RR – Tachypnea • HR – Tachycardia • B/P – Moderate/severe hypotension (narrowing pulse pressures) • CR – Delayed • CNS – Anxiety / confusion
What is DIC ?
• DisseminaLng Intravascular Coagulopathy
– Phospholipids released due to injured/lysed cells
– Prolonged low CO also triggers phospholipids release due to endothelium injury
What is the result of DIC
– Systemic coagulation
– Diffuse fibrin formation (results in multiple microscopic emboli)
– Exhaustion of clotting factors
– Fibrinolytic system activate due to coagulation activation
Classifications of hemorrhage
• Class IV (Multiorgan Dysfunction Syndrome)
– >35% blood loss (>1750 mls)
Classifications of hemorrhage
• Class IV (Multiorgan Dysfunction Syndrome)
Irreversible Shock
• Survival unlikely • RR – Tachypnea • HR – Thready, rapid pulse • B/P – Severe hypotension • CR – Delayed • CNS – Unresponsive • Other – Decreased to absent urine output
Why dose this sequale occur?
- Glycogen and fat metabolized anaerobically
- Cell membrane permeability increases
- Na+& H2O enter the cell causing overhydration
- K++ leaks out and Ca+enters cell
- Lactic acid and CO2 levels increase and cell ruptures
Physiological Response to Shock
Variations and determining factors – Age and relative health – Older adults – Children – General physical condition – Preexisting disease – Ability to activate compensatory mechanisms – Medications – Specific organ system affected
Assessing Shock
- Early recognition is a key to patient survival
- Look for subtle signs both initially and ongoing
- Frequent ongoing assessments and trending
Shock Assessment
- Scene assessment
- Primary assessment
- Focused history and secondary
- Detailed secondary assessment
- Ongoing assessment
Shock Management
- Airway and breathing
- Hemorrhage control
- Fluid resuscitation
- Temperature control
- Pharmacological intervention
Differential Shock Assessment Findings
Assumed to be Hypovolemic until proven otherwise
Differential Shock Assessment Findings
Cardiogenic shock
– Differentiate from Hypovolemic shock by:
• Chief complaint – Chest pain – Dyspnea – Tachycardia • Heart rate • Signs of congestive heart failure • Dysrhythmias
Differential Shock Assessment Findings
• Distributive shock
– Differentiate from Hypovolemic shock by:
• Mechanism suggesting vasodilatation – Spinal cord injury – Drug overdose – Sepsis – Anaphylaxis • Warm, flushed skin • Lack of tachycardia response (not reliable)
Differential Shock Assessment Findings
• Obstructive shock
– Differentiate from hypovolemic shock by signs and symptoms of:
- Cardiac tamponade
- Tension pneumothorax
- Pulmonary embolism
Detailed Physical Examination
• Vital signs – Pulse – Blood pressure – Orthostatic vital signs • Evaluate patient’s ECG
Resuscitation
Restore adequate tissue oxygenation by:
– Ensuring adequate oxygenation
– Maintaining effective volume-to-container size ratio
– Rapid transport to appropriate medical facility
Red Blood Cell Oxygenation
• Need adequate tissue oxygenation
• For red blood cell oxygenation:
– Patent airway
– Support ventilation with high FiO2
• If necessary, positive-pressure ventilation
– Correct airway abnormalities that interfere with adequate ventilation
Ratio of Volume to Container Size
• Container must be full of fluid to carry oxygen
• Accomplish by:
– Decreasing size of container
• Especially in shock states not associated with hemorrhage
– Vasoactive medications in some distributive shock (Sepsis and Cardiogenic)
– Volume replacement may be needed
Fluid Resuscitation
• What solutions to use?
– Crystalloid
– Colloid
Key Principles in Managing Shock
- Open airway
- High‐concentration oxygen
- Assist ventilation as needed
- Control external bleeding (if present)
- IV fluid replacement if appropriate
- Consider PASG (if protocols allow)
- Maintain body temperature
- Monitor ECG and oxygen saturation
- Reassess vital signs
Hypovolemic Shock
Correct circulatory deficit and its causes
– Crystalloid fluid replacement for dehydration
– Volume replacement for hemorrhage (controversial)
– Definitive surgery
– Critical care support
– Postoperative rehabilitation
Hypovolemic Shock
• Fluid volume replacement
• Large volume fluid replacement if:
– Systolic BP >100 mmHg AND
– Isolated head or extremity injuries
– Not for penetrating trauma in urban center
• Blunt or penetrating trauma in rural area:
– IV Fluids to maintain systolic BP>90 mm Hg
Cardiogenic Shock
• Improve pumping action of heart and manage dysrhythmias
– Fluid replacement
– Drug therapy (if needed)
– Cardiogenic shock due to myocardial ischemia or infarction requires:
• Reperfusion strategies
• Possible circulatory support
– Manage tension pneumothorax and cardiac tamponade
Neurogenic Shock
• Treatment similar to hypovolemia
– Avoid circulatory overload
– Monitor lung sounds for pulmonary congestion
• Vasopressors may be indicated
Anaphylactic Shock
• Subcutaneous epinephrine in acute anaphylactic reactions • Other therapy – Oral, IV, or IM antihistamines – Bronchodilators – Steroids reduce inflammatory response – Crystalloid volume replacement – Airway management
Septic Shock Treatment
• Management of hypovolemia (if present)
• Correction of metabolic acid-‐base imbalance
• Prehospital care
– Fluid resuscitation
– Respiratory support
– Vasopressors to improve cardiac output
– Thorough history to find source of sepsis
Integration of Patient Assessment and the Treatment Plan
• For severe hemorrhage or shock:
– Rapid recognition
– Initiation of treatment
– Prevention of additional injury
– Rapid transport to appropriate hospital
– Advance notification to receiving facility
Shock Definition
• Shock is a state of inadequate perfusion of the tissues.
– Transitional stage between homeostasis and death
– Underlying killer of all trauma patients
• Often presents with subtle signs and symptoms