Ch. 1: Shock (pathophysiology, diagnosis, treatment, and physiologic response to trauma) Flashcards

1
Q

Define shock

A

Shock is the progression of cascade of events that begins when cells or tissues are deprived of an adequate energy source because of oxygen deprivation.

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1
Q

Define cardiac output

A

Cardiac output is the amount of blood pumped out from the left and right ventricle in 1 minute. It is defined by the stroke volume and the heart rate.

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2
Q

Define classes of shock based on blood loss

A

a. Class I: mild <15% blood loss of the total blood volume
b. Class II: 15-30% blood loss, when hyperdynamic shock begins
c. Class III: >30% blood loss,
d. Class IV: uncompensated life-threatening hypovolemia

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3
Q

Primary disturbances causing shock

A

a. Hypovolemic shock: blood loss, third space sequestration, severe dehydration
b. Cardiogenic shock: pump failure, failure of the cardiac muscle
c. Distributive shock: microcirculatory failure
d. Obstructive shock: combination of the hypovolemic, cardiogenic and distributive shock. Caused by tension pneumothorax, pericardial tamponade, diaphragmatic hernia, severe abdominal distension putting pressure on the caudal vena cava.

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4
Q

Fill in the figure for determinants of cardiac output and blood pressure.

A
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5
Q

Explain hyperdynamic stage of shock

A

Hyperdynamic shock occurs when >15% of the total blood volume is lost. Baroreceptors and stretch receptors in the carotid sinus, right atrium, and aortic arch sense a drop in intravascular pressure, and respond with decreasing inhibition of the sympathetic tone, increase inhibition of vagal tone, and decrease release atrial natriuretic peptide (ANP) release from the cardiomyocytes. This results in tachycardia, increased stroke volume (SV), andshortened CRT. This stage occurs if blood loss continues past the compensated stage of shock.

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6
Q

Clinical signs of shock

A

a. Class I: the body is capable of restoring volume deficits via compensatory responses and there may be little to no change in the physical findings other than drop in urine output.
b.Class II: tachycardia, tachypnea, bounding pulse (increased CO and peripheral vascular resistance. Mental agitation may be present. Dilated pupils and sweating due to increased sympathetic tone. Increased lactate and high anion gap metabolic acidosis
c.Class III: profound tachycardia and tachypnea, anxiety, and agitation. Urine output cease, jugular filling and CRT are prolonged, pulse pressure is weak, and extremity temperatures are decreased. Lactic acidosis, decreased blood pressure
d.Class IV: severe tachycardia turns to bradycardia. Obtundation, anuria, profound hypotension, circulatory collapse, and death. Increased cardiac troponin I. Potentially arrhythmias

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7
Q

Define oxygen delivery

A

DO2 is defined by content of oxygen in the arterial blood (CaO2) as well as theamount of blood perfusing the tissue (CO).DO2= CO X CaO2

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8
Q

Composition and benefits of balanced electrolyte solutions

A

Commercially available fluids. The common BES available for horses include lactated ringer, normosol-R, Plasma-Lyte, and are composed of sodium and chloride with varying amounts of calcium, potassium and magnesium. Physiological saline solution (0.9% NaCl) differs in that it contains only sodium and chloride. BES are designed as replacement fluids, meaning that the electrolyte composition is designed to closely approximate the electrolyte composition ofthe extracellular fluid. Because of their accessibility and low viscosity, crystalloids can be administered fast and quickly restore the circulating volume.

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9
Q

What are adverse effects of aggressive fluid therapy with isotonic crystalloids?

A

Approximately 80% of volume will rapidly diffuse out of the vascular space into the interstitial and intrercellular space, needing 4-5 times greater volume to be infused than volume lost. This may exceed total body water and extreme excesses of sodium and chloride.
If the electrolyte constituents of isotonic crystalloids differ from those in the intracellular space, this will cause cellular swelling. Cellular swelling affects the activity of various protein kinases; increases intracellular calcium concentrations; alters ion pump activity, membrane potential, and cytoskeletal structure, and activates phospholipase A. Consequently, high volumes of crystalloids can trigger or potentiate an inflammatory response and have a negative impact in the face of ischemia and reperfusion. Large volume infusions may cause abdominal compartment syndrome, acute respiratory distress syndrome, congestive heart failure, gastrointestinal motility disturbances and dilutional coagulopathy.

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10
Q

What are the benefits of hypertonic crystalloids?

A

Hypertonic saline, 7.2%, is the most commonly used. One infusion of hypertonic saline will expand the intravascular space by approximately twice the volume infused, pulling fluid from the intracellular and interstitial spaces. This expansion is however short lived, and eventually the fluid will diffuse into the interstitial space. Because of the variation in reflection coefficients for sodium, hypertonic saline pulls fluid from the intracellular space. In case of shock patients where endothelial cells swell, this is beneficial as an infusion with HSS will decrease cellular swelling, thus increasing the capillary diameter and improve perfusion. It has a low viscosity allowing for rapid infusion. Dose 2-4ml/kg IV.

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11
Q

What are colloids and their benefit?

A

a. Colloids can be natural or synthetic in origin. Colloids are solutions containing large molecule that, because of their size and charge, are principally retained within the vascular space. Colloid concentrations are higher in the intravascular space, exerting an oncotic pressure that opposes the hydrostaticpressure and helps retain water in or draw it into the intravascular space.
b.Natural colloids: plasma, whole blood, and bovine albuminProviding protein such as albumin, antibodies, critical clotting factors, antithrombin 3, and other plasma constituents.Whole blood is the ideal replacement fluid in patients with hypovolemic shockas a severe blood loss. Providing red blood cells and protein helps to retain fluid within the intravascular space and improves oxygen carrying capacity of the blood.
c. Synthetic colloids hydroxyethyl starch and dextrans. 10ml/kg significantly increases oncotic pressure in some patients for longer than 120hours. Easier to use, and more readily available compared to natural colloids.

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12
Q

What are the vasopressors used in horses and their mode of action?

A

a. Dobutamine: strong beta1-adrenergic agonist, weaker affinity for beta2- and alpha- adrenergic agonist
b.Norepinephrine: beta1- and alpha-adrenergic affinity
c. Vasopressin: binds V2 receptors on the cell surface of tubular cells, initiating an intracellular cascade which results in the generation of the water channel, aquaporin-2. Antidiuretic action on the collecting ducts of the kidney.

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13
Q

What to measure in hypovolemic patients?

A

a.Heart rate
b.CRT: indicate level of peripheral perfusion
c.Jugular fill: gives indication for central venous pressure, should be less than 5 seconds
d. Extremity temperature: indicating regional perfusion.
e. Pulse pressure
f. Urine output: decreased output of less than 1ml/kg/hr indicate continued hypovolemia
g.Mentation
h. Arterial blood pressure: indirect or direct measuring
i.Oxygen extraction
j.Mixed venous partial pressure of oxygen
k.Cardiac output

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14
Q

How to predict outcome in case of hypovolemic shock?

A

a.Good prognosis: rapid control of hemorrhage, restoration of perfusion, normalization of blood gas values, and prevention of dilutional coagulopathy b.Poor prognosis: decreased lactate clearance and prolonged uncontrolled bleeding.

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15
Q

Define the two phases of metabolic response to trauma

A

a. The ebb phase: first several hours after injury. This phase is characterized byhypovolemia and low flow or perfusion to the injured site.
b.The flow phase: once perfusion is restored. Divided into two period
i. Catabolic period: vital signs will change similar to that of hyperdynamic response (tachycardia, tachypnea, sweating, agitation). Decreased appetite
ii. Anabolic period: the return to homeostasis. Cortisol levels fall during this final period and normalization of physiology occurs.