Shock / Ischemia / CPR / Trauma Flashcards
Define shock
Inadequate cellular energy production.
Which conditions is hypovolemic shock commonly associated with?
Internal or external blood loss or excessive loss of other body fluids (e.g., severe vomiting, diarrhea, polyuria, burns).
Why is CO reduced in hypovolemic shock?
Due to decreased venous return
Compensatory mechanisms for hypovolemic shock?
o They are mechanisms that attempt to raise the circulating blood volume.
o An increase in sympathetic activity causes vasoconstriction, increased cardiac contractility, and tachycardia, with a resultant rise in cardiac output.
o Extreme vasoconstriction and microvascular alterations induce mobilization of fluid from the interstitial and extracellular spaces to the intravascular space.
o Additionally, a reduction in renal blood flow activates the renin-angiotensin-aldosterone system, which further up-regulates the sympathetic nervous system and causes sodium and water retention via the production of both aldosterone and antidiuretic hormone, respectively.
Clinical signs of a compensated hypovolemic shock?
Because the net effect of these responses is to increase intravascular volume, clinical signs of shock may be subtle initially:
Mild to moderate mental depression, tachycardia with normal or prolonged CRT, cool extremities, tachypnea, and a normal blood pressure.
Pulse quality is often normal, and this stage is generally referred to as “compensated shock.”
Clinical signs of decompensated hypovolemic shock?
o With ongoing compromise of systemic perfusion, compensatory mechanisms are no longer adequate and often begin to fail.
o Pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent as the animal progresses to decompensated shock.
o If left untreated, reduced organ perfusion results in signs of end organ failure (e.g., oliguria) and ultimately death.
What is a distributive shock? Examples?
A maldistribution of blood flow, result in distributive shock.
Sepsis, anaphylaxis
Phases of sepsis/SIRS?
o Initial hyperdynamic phase of sepsis or SIRS is characterized by tachycardia, fever, bounding peripheral pulse quality, and hyperemic mucous membranes secondary to cytokine (NO) mediated peripheral vasodilation (vasodilatory shock).
o If septic shock or SIRS progresses unchecked, a decreased cardiac output and signs of hypoperfusion often ensue as a result of cytokine effects on the myocardium or myocardial ischemia.
o Clinical changes may then include tachycardia, pale (and possibly icteric) mucous membranes with a prolonged capillary refill time, hypothermia, poor pulse quality, and a dull mentation.
o Hypodynamic septic shock is the decompensatory stage of sepsis and without intervention will result in organ damage and death.
How are cats different than dogs in shock manifestations?
o The hyperdynamic phase of shock is rarely recognized in cats.
o In contrast to dogs, changes in heart rate in cats with shock are unpredictable; they may exhibit tachycardia or bradycardia.
o In general, cats typically present with pale mucous membranes (and possibly icterus), weak pulses, cool extremities, hypothermia, and generalized weakness or collapse.
o In cats the lungs are vulnerable to damage during shock or sepsis, and signs of respiratory dysfunction are common in this species.
Functional classifications and examples of shock
T/F Gradual resolution of tachycardia (and hypotension) often signals successful return of cardiovascular stability, whereas persistent tachycardia indicates ongoing cardiovascular instability.
TRUE
What is the main goal when treating shock?
Optimizing oxygen delivery to the tissues.
How are the following characteristics in a well-perfused patient?
CVP - normal value?
UOP - normal value?
MAP - normal value?
Body temperature, HR, heart rhythm, RR, MM color and CRT (normal/abnormal)
CVP between 0 and 5 cm H2O
UOP at least 1 ml/kg/hr
MAP between 70 and 120 mmHg
Normal body temperature, heart rate, heart rhythm, and respiratory rate; and moist, pink mucous membranes with a CRT of less than 2 seconds
Why would shock patients develop hyperactatemia?
Critically ill patients with inadequate oxygen delivery, oxygen uptake, or tissue perfusion often develop hyperlactatemia and acidemia that are reflective of the severity of cellular hypoxia.
A lactic acidosis in human patients carries a ________ risk for developing multiple organ failure, and these people demonstrate a ________ mortality rate than those without an elevated lactate concentration.
Greater
Higher
T/F Normal neonatal and pediatric patients may have higher lactate concentrations
TRUE
Who much value has one single measurement of lactate?
o Serial lactate measurements taken during the resuscitation period help to gauge response to treatment and evaluate resuscitation end points.
o The changes in lactate concentrations are a better predictor of survival than are single measurements.
What is a pulmonary artery catheter (PAC) and what can we measure with it?
o A right-sided cardiac catheter or pulmonary artery catheter (PAC, also termed Swan-Ganz catheter or balloon-directed thermodilution catheter) is typically used to monitor systemic oxygen transport parameters.
o The PAC enables the measurement of central venous and pulmonary arterial pressure, mixed venous blood gases (PvO2 and SvO2), pulmonary capillary wedge pressure (PCWP), and cardiac output.
o With this information, further parameters of circulatory and respiratory function can be derived (SV, EDV, SVR index, PVR index, arterial oxygen content, mixed-venous oxygen content, DO2 index, VO2 index, and oxygen extraction ratio).
o A PAC allows the clinician to assess the cardiovascular and pulmonary function of shock patients. The response to treatment and titration of fluid therapy, vasopressors, and inotropic agents can also be monitored.
Cardiac output and systemic DO2 should be optimized using intravascular volume loading until the PCWP approaches ___ to ___ mm Hg. A PCWP higher than___ to ____ mm Hg will promote the formation of pulmonary edema, further impairing oxygenation and overall oxygen transport.
10 to 12mmHg
15 to 20mmHg
I we assume a constant VO2, what does affect SvO2?
SvO2 is determined by cardiac output, hemoglobin concentration, and SaO2.
What conditions can alter SvO2
Where should ideally be SvO2 measured?
In the pulmonary artery.
In animals that do not have a PAC, venous oxygen saturation can be measured from the central circulation, using a central venous catheter in the cranial or proximal caudal vena cava. SvO2 is then termed ScvO2 (central venous oxygen saturation).
A maintenance of a continuously measured ScvO2 above ____ (in addition to maintaining central venous pressure above ___ to ____ mmHg, MAP pressure above ____mmHg and urine output above _____ ml/kg/h) resulted in a ____ reduction in mortality compared with the same treatment without ScvO2 monitoring.
70%
8 to 12mmHg
65 mmHg
0.5mL/kg/h
15%
T/F The mainstay of therapy for all forms of shock except cardiogenic shock is based on rapid administration of large volumes of intravenous fluids to restore an effective circulating volume and tissue perfusion.
TRUE