Shock Flashcards
What is the definition of shock?
Shock is defined as - inadequate cellular energy production and most commonly occurs secondary to poor tissue perfusion from low or unevenly distributed blood flow. This leads to a critical decrease in oxygen delivery (DO2) compared with oxygen consumption (VO2) in the tissues.
Source - CCM
What are the three mechanisms stated to commonly result in a reduced DO2?
Loss of intravascular volume, maldistribution of vascular volume, failure of the cardiac pump?
Source - CCM
What does the term compensated shock denote?
Mild to moderate mental depression, tachycardia with normal or prolonged capillary refill time, cool extremities, tachypnea, and a normal blood pressure. Pulse quality is often normal – when sympathetic stimuli compensates for losses.
Source - CCM
What is decompensated shock?
Pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent as the animal progresses to decompensated shock. Ultimately, if left untreated, reduced organ perfusion results in signs of end organ failure (e.g., oliguria) and ultimately death.
Source - CCM
What are the classifications of Shock
Hypovolaemic, Cardiogenic, Distributive, Metabolic, Hypoxaemic
Source - CCM
What is the initial hyperdynamic phase of SIRS/Sepsis?
tachycardia, fever, bounding peripheral pulses, hyperaemic Mm – secondary to cytokine mediate vasodilation –> if this progresses signs of decreased cardiac output may predominate –> pale mms, tachycardia, prolonged crt, hypothermia
Source - CCM
How do feline shock presentations differ to canine?
less predictable – may be brady or tachycardic, pale mms, weak pulses, hypothermic.
Source - CCM
What testing is recommended in patients exhibiting shock states?
venous or arterial blood gas with
lactate measurement, a complete blood cell count, blood chemistry
panel, coagulation panel, blood typing, and urine analysis should
be performed. Thoracic and abdominal radiographs, abdominal
ultrasound, and echocardiography may be indicated once the patient
is stabilized
Source - CCM
What is a normal pulmonary capillary edge pressure and how is it measured?
10-12mmHG –> swann-Ganz in floated into branch of the pulmonary artery
When is mixed venous O2 decreased?
if DO2 decreases or if VO2 increases
Source CMM
What is the mainstay of treatment of shock?
Re-establishing DO2 – usually with rapid administration of intravascular volume except in cardiogenic.
Source CCM
What volume of crystalloids remains in the intravascular space after 30 mins
25%
Source - CCM
In what situation is hypotensive resuscitation advantageous?
Poorly controlled haemorrhage
Source CCM
What does the administration of hypertonic saline cause?
A transient shift of fluid into the intravascular space.
May also reduce endothelial swelling, modulate inflammation, increase contractility, produce mild vasodilation.
Source - CCM
What are the characteristics of cardiogenic shock?
a systolic or diastolic cardiac dysfunction resulting in hemodynamic abnormalities such as increased heart rate; decreased stroke volume; decreased cardiac output; decreased blood pressure; increased peripheral vascular resistance; and increases in the right atrial, pulmonary arterial, and pulmonary capillary wedge pressures. These pathologic changes result in diminished tissue perfusion and increased pulmonary venous pressures, resulting in pulmonary oedema and dyspnoea.
Source - CCM
Next Questions from - Cellular Metabolic Changes in Shock PDF MDR 2020 - Corrin Boyd
Next Questions from - Cellular Metabolic Changes in Shock PDF MDR 2020 - Corrin Boyd
List some effects of ATP depletion
intracellular acidosis
ion flux
oxidative stress
adenosine release
altered gene expression
How much ATP is produced per molecule of glucose in aerobic metabolism?
36 ATP
What happens to glycolysis in shock?
Initially upregulated however ox-phos cannot occur, pyruvate accumulates and NAD is depleted.
Pyruvate is converted to lactate to allow replenishment of NAD –> allowing glycolysis to continue.
How does intracellular acidosis occur in shock?
Normally hydrolysis of ATP produces one H+ and oxidative production of ATP consumes H+
In shock ATP continues to be used and hydrolysed however glycolysis does not consume H+ therefore an intracellular acidosis results.
CO2 production from small amounts of remaining oxidative metabolism contributes
What is the cellular response to intracellular acidosis
Activation of multiple acid extruders - these often require ATP and therefore fail during shock
Discuss the action of Monocarboxylate transporter (MCT) in shock?
An acid extrusion transmembrane protein - carry one H+ and a monocarboxylate out of the cell. The most abundant monocarboxylate in shock is lactate.
Beta-hydroxybutyrate and acetate are also transported out.
Which explains why lactate isn’t solely responsible for base deficit in shock
What percentage of ATP in the normal cell is used by Na+/K+ atpase pumps?
25-50%
Discuss ion change ion flux in shock?
- No ATP for maintenance of Na+/K+ pumps –> influx of Na and efflux of K+
- As cell depolarises more Na+/K+ channels open - makes it worse
- in an attempt to combat intracellular acidosis Na/H+ pumps result in an even worse accumulation of Na+
- cell depolarisation also opens Ca2+ channels, while Na+/Ca2+ channels cause an increase in Ca2+ while trying to get Na+ out
- This increase in Ca2+ results in activation of ryanodine receptors (calcium-induced-calcium release) worsening intracellular Ca2+
