Ch.1 Shock: Pathophysiology, Diagnosis, Treatment and Physiologic Response to Trauma Flashcards
Major factors affecting blood flow
1 - Circulating volume
2 - Cardiac pump function
3 - Vasomotor tone/peripheral resistance.
Stroke volume is the result of?
1 - Ventricular preload
2 - Myocardial contractility
3 - Ventricular afterload.
Myocardial contractility is defined as
The rate of cross-bridge cycling between actin and myosin filaments within cardiomyocytes.
Causes of decreased preload
1 - Hypovolemia
2 - Decreased ventricular filling time
3 - Impaired ventricular relaxation
4 - Decrease in vasomotor tone
5 - Vasodilation
Clinically how is myocardial contractility assessed?
Echocardiographic measures of global systolic function
like left ventricular ejection fraction
and fraction shortening
The fundamentals of treatment of shock
Restoration and maintenance of CO through
1- Manipulation of preload
2 - After load
3 - Myocardial contractility
4 - Heart rate
Ventricular after load is directly affected by what?
Vasomotor tone or peripheral vascular resistance
What is the outcome of hypertension on ventricular after load
Afterload rises with a resultant fall in CO and tissue perfusion
The three classifications of shock
1 - Hypovolemic
2 - Cardiogenic
3 - Distributive
Define cariogenic shock
Cardiac m cannot pump out adequate SV to maintain perfusion
Define distributive shock
Vasomotor tone is lost resulting in decrease in BP and venous return
Common causes of distributive shock
1 - Neurogenic shock
2 - Septic shock
3 - Anaphylactic shock
What is relative hypoxia or dysoxia
Increased metabolic demand resulting in relative tissue deficits or
Oxygen uptake is impaired because of mitochondrial failure
What is the mechanism of obstructive shock?
Obstruction of ventilation or of CO
Examples of obstructive shock
1 - Pneumothorax
2 - Pericardial tamponade
3 - Diaphragmatic hernia
4 - Severe abdominal distension causing vena cava obstruction
Autonomic traffic
Interplay btw parasympathetic and sympathetic nervous system
How do the baroreceptors in the carotid sinus, aortic arch and right atrium respond to a fall in pressure within the vessels
Decrease inhibition of sympathetic tone
while increasing inhibition of vagal activity
and decreasing the release of atrial natriuretic peptide (ANP) by cardiac myocytes.
Resulting in vasoconstriction and an increase in peripheral resistance and BP
What occurs in hyperdynamic stage of shock
Tachycardia
Increased SV
Shortened CRT
What does renin stimulate the production of
Angiotensin I (Converts to angiotensin ii - acts directly on blood vessels causing contraction - vasoconstriction)
What results from a decrease in renal perfusion
Secretion of renin - stimulates production of angiotensin I which converts to angiotensin II
This increases sympathetic tone on peripheral vasculature and promotes aldosterone release
Effect of aldosterone on BP
Restores circulating volume by increasing renal tubular sodium and water reabsorption
How does AVP (ADH) act to augment low BP
Potent vasoconstrictor
Stimulates increased water reabsorption in the renal collecting tubules
What is seen clinically in decompensated shock
1 - Tachycardia
2 - Tachypnea
3 - Poor peripheral pulses
4 - Cool extremities
5 - Mild anxiety
6 - Sweating
What occurs at a cellular level during decompensated shock
Decreased oxygen delivery and accumulation of waste products results in loss of critical energy-dependent functions
ie enzymatic activities, membrane pumps and mitochondrial activity leading to cell swelling and release of intracellular calcium stores.
Cytotoxic lipids, enzymes and ROS released from damaged cells further damage cells, triggering inflammation
Exposure of sub endothelial tissue factor activates what?
Coagulation and complement cascades
What are the end results of decompensated shock
Pooling of blood in peripheral tissue beds
Decrease in in BP
Decrease in venous return
Decrease in CO
Decrease in perfusion
Resulting in organ failure
Class 1 shock
Blood loss of <15% total blood volume
Class 2 shock
Blood loss of 15-30% - is the inset of hyper dynamic shock
Clinical signs - tachycardia, tachypnea, increased CO and peripheral resistance, anxiety, sweating.
Increased lactate and high anion gap
Class 3 shock
Hypodynamic shock
Profound tachycardia, tachypnea, anxiety, prolonged CRT, decreased urine output, cold extremities, lactic acidosis
Hypotensive
Class 4 uncompensated shock
Bradycardai
Obtundation
Anuria
Profound hypotension
Circulatory collapse
Death
Define delivery of oxygen (DO2)
DO2 = CO X CAO2
(CAO2 = content of oxygen in the arterial blood)
(CO = amount of blood perfusing the tissue)
The amount of oxygen per volume of blood is determined by
The amount of haemoglobin or red cell mass and the saturation of that Hamoglobin
What is the first vital step to restoring oxygen delivery in shock?
Fluid therapy
The ideal fluid should produce what?
A predictable and lasting increase in intravascular volume
with an electrolyte composition as close as possible to that of extracellular fluid
being metabolised and excreted without any accumulation in the tissues
without producing adverse metabolic or systemic effects
and remain cost effective
What % of rapidly infused crystalloids will diffuse out of the vascular space into the interstitial and intercellular space
80%
Why are crystalloids alone not suitable for total volume loss replacement
80% will diffuse out, therefore will need to use 4-5 times the vol of fluid lost
results in excess total body water
extreme excess of sodium and chloride
Cellular swelling can occur triggering/potentiating inflammatory responses
Large vol infusions can cause
1 - abdominal compartment syndrome,
2 - acute respiratory distress syndrome,
3 - congestive heart failure,
4 - dilution coagulopathy
“A balanced fluid therapy approach of administering crystalloids for hypovolemic shock is currently recommended” - how should this be delivered?
Initially a rapid 20ml/kg(10L fro 500kg) bolus over 30-60mins - assessing cardiovascular system regularly
BES (Balanced electrolyte solutions) are designed to be what sort of fluids in equine medicine
Replacement fluids not maintenance fluids.
Most common concentration used of hypertonic saline solution
7.2%
What is the tonicity of HSS compared to plasma?
HSS has 8 times the tonicity of plasma
in IV infusion of HSS will expand the intravascular space by how much
Approximately twice the volume infused
Where does HSS principally pull volume from?
Intracellular space
Effect of HSS on neutrophils
Blunts neutrophil activation and may alter balance btw inflammatory and antiiflammatory cytokine responses
Recommended dose of HSS?
2-4ml/kg or 1-2L for a 500kg horse
How do colloids work?
Retained within the vascular space, exert oncotic pressure that helps draw water in
Normal equine plasma has a colloid oncotic pressure of?
20mmHg
What is the oncotic pressure of HES (Hydroxyethyl Starch)?
30mmHg
Benefits of colloids over HSS?
Prolonged action
Advantages of natural colloids
Provide protein such as albumin, antibodies, clotting factors, antithrombin 3
Cons of natural colloids such as plasma
Hypersensitivity rxns in up to 10% of horses
Also need to defrost so not good in emergency
HES products should be used cautiously in what patients
Preexisting renal disease
What dose of HES is recommended
10ml/kg
What % and kDa HES is currently used
6% HES,130kDa/0.4:tetrastarch
Higher molecular weight has been associated with coagulopathies in human med
A 10ml/kg dose of HES has been shown to increase oncotic pressures for how long?
120hours
At what dose of HES has evidence of spontaneous bleeding been reported
20-40ml/kg
Why is whole blood indicate in severe cases of hypovolemia
Provide oxygen carrying capacity
Colloid oncotic support
Platelets
Coagulation factors
What is the circulating blood volume in an adult horse?
7-9% of body weight (35-45L in a 500kg horse)
When will clinical signs of blood loss be seen?
After the loss of 15% of circulating blood volume or (approx 6L during an acute bleed)
What does Dobutamine act on?
Strong Beta 1 adrenoreceptor agonist
Weaker Beta2 and Alpha adrenoreceptor affinity
Primary use of dobutamine?
Deliver oxygen to tissues via its positive inotropic activity
Dose of dobutamine
1-5ug/kg/min
What does norepinephrine act on?
Strong B1 and Alpha adrenergic affinity resulting in vasoconstriction and increased cardiac contractility
What does CVP asses
Cardiac function
Blood volume
Vascular resistance
Holding off the jugular vein should result in visible filing within how long
5 seconds
What is the normal CVP in a standing horse
7-12mmHg
How is CVP measured in a standing horse
Catheter in cranial vena cava/right atrium
If measured in jugular vein with standard ivc will get false elevated CVP but can be used to track changes
What is normal urine output
1ml/kg/hr
Fluid therapy to prevent renal ischemia is indicated when urine output is how much?
0.5ml/kg/hr
Arterial blood pressure is a reflection of?
CO and total vascular resistance
Because of the compensatory increase in peripheral resistance, blood pressure does not consistently fall until blood volume has decreased by what %
30% or more
A MAP of what is necessary to maintain adequate perfusion of the brain
65mmHg
Normal MAPs in healthy awake horses using indirect coccygeal artery are..
105-135mmHg
Aerobic metabolism of glucose results in
36 moles of ATP per molecule of glucose
Anaerobic metabolism of glucose results in
2 moles of ATP per molecule of glucose
and L-lactate
Type B hyperlactatemia can occur as a result of
hepatic dysfunction, pyruvate dehydrogenase inhibition, catecholamine surges, sepsis or SIRS
Oxygen extraction is determined by
The difference btw the oxygen saturation of arterial blood (SaO2) and oxygen saturation of venous blood (SvO2)
O2ER = (SaO2-SvO2)/SaO2
Can be determined by measuring central venous saturation and arterial oxygen saturation
In a healthy horse the O2ER ranges from
20-30%
The O2ER can be useful in evaluating what
Response to resuscitative strategies
In low-perfusion states PvO2 will increase or decrease?
Decrease
Mixed venous blood is obtained from where to asses mixed PvO2
Catheterise the pulmonary artery
Normal PjvO2 (Jugular venous pressure of oxygen)
40-50mmHg
Normal SjvO2 (Jugular venous oxygen saturation)
65-75%
Increased venous partial pressure of oxygen in the presence of significant perfusion or supply deficits can signify what
Impaired oxygen consumption caused by mitochondrial or cellular dysfunction
- recognised in septic shock or after cardiopulmonary resuscitation
What is the gold standard for CO monitoring?
Pulmonary thermodilution method which requires catheterisation of the pulmonary artery
What techniques are used to monitor CO in equine medicine
1 - Lithium dilution - lithium injected into venous system - lithium concentration-time curve which is used to calculate CO
Repeated sampling can lead to lithium toxicity
2 - Transcutaneous echocardiography - volumetric better results than Doppler
In what cases is measuring CO most beneficial
Cases failing to respond to initial resuscitation efforts
Cases with complex disease involving multiple organ systems
Cases with cardia disease
What is the MAP and systolic pressure desired in controlled resuscitation
MAP 40-60mmHg
Systolic 80-90mHg
What is the ebb phase of metabolic response to trauma characterised by?
Hypovolemia and low flow or perfusion to the injured sit
Occurs during first several hours after injury
