Ch.1 Shock: Pathophysiology, Diagnosis, Treatment and Physiologic Response to Trauma Flashcards by Denise Mc Sweeney

Major factors affecting blood flow

1 - Circulating volume
2 - Cardiac pump function
3 - Vasomotor tone/peripheral resistance.

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Stroke volume is the result of?

1 - Ventricular preload
2 - Myocardial contractility
3 - Ventricular afterload.

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Myocardial contractility is defined as

The rate of cross-bridge cycling between actin and myosin filaments within cardiomyocytes.

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Causes of decreased preload

1 - Hypovolemia
2 - Decreased ventricular filling time
3 - Impaired ventricular relaxation
4 - Decrease in vasomotor tone
5 - Vasodilation

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Clinically how is myocardial contractility assessed?

Echocardiographic measures of global systolic function
like left ventricular ejection fraction
and fraction shortening

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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

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Ventricular after load is directly affected by what?

Vasomotor tone or peripheral vascular resistance

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What is the outcome of hypertension on ventricular after load

Afterload rises with a resultant fall in CO and tissue perfusion

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The three classifications of shock

1 - Hypovolemic
2 - Cardiogenic
3 - Distributive

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Define cariogenic shock

Cardiac m cannot pump out adequate SV to maintain perfusion

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Define distributive shock

Vasomotor tone is lost resulting in decrease in BP and venous return

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Common causes of distributive shock

1 - Neurogenic shock
2 - Septic shock
3 - Anaphylactic shock

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What is relative hypoxia or dysoxia

Increased metabolic demand resulting in relative tissue deficits or
Oxygen uptake is impaired because of mitochondrial failure

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What is the mechanism of obstructive shock?

Obstruction of ventilation or of CO

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Examples of obstructive shock

1 - Pneumothorax
2 - Pericardial tamponade
3 - Diaphragmatic hernia
4 - Severe abdominal distension causing vena cava obstruction

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Autonomic traffic

Interplay btw parasympathetic and sympathetic nervous system

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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

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What occurs in hyperdynamic stage of shock

Tachycardia
Increased SV
Shortened CRT

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What does renin stimulate the production of

Angiotensin I (Converts to angiotensin ii - acts directly on blood vessels causing contraction - vasoconstriction)

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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

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Effect of aldosterone on BP

Restores circulating volume by increasing renal tubular sodium and water reabsorption

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How does AVP (ADH) act to augment low BP

Potent vasoconstrictor
Stimulates increased water reabsorption in the renal collecting tubules

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What is seen clinically in decompensated shock

1 - Tachycardia
2 - Tachypnea
3 - Poor peripheral pulses
4 - Cool extremities
5 - Mild anxiety
6 - Sweating

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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

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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