Shock and Resuscitation Flashcards
what is shock? Definition:
– Inadequate oxygen delivery to the tissues
– A condition of severe hemodynamic & metabolic dysfunction characterized by reduced tissue perfusion, impaired oxygen delivery & inadequate cellular energy production
Clinical Signs of Shock
- Reduced level of mentation
- Hypothermia / Cool extremities
- Tachycardia (bradycardia in cats)
- Increased respiratory rate & effort
- Poor peripheral pulses
- Decreased blood pressure
- Pale mucous membranes
- Prolonged capillary refill time
- Decreased urine production
- Decreased GI blood flow/ GI ulceration
Shock - Physiologic Response
– Increased sympathetic output
* Epinephrine (adrenaline) & Norepinephrine released from adrenal glands
- Increase in
– Heart rate
– Cardiac contractility
– Vasoconstriction
how does vasoconstriction occur during shock? what parts of the body are more affected and why?
- Organ selective
– Affects organs with large numbers of a–adrenoreceptors * Skin, Skeletal mm, splanchnic organs, kidneys
– Perfusion maintained to - Carotid, coronary & hepatic arteries
– Allows preservation of blood flow to vital organs, but can result in ischemia of less vital tissues - Ie. Renal ischemia / failure
endocrine response to shock?
- Epinephrine & norepinephrine
– Released from adrenal glands & vasomotor endplates
– Immediate response - Antidiuretic hormone
– Released from the pituitary
– To conserve water
– Response within minutes - Renin–Angiotensin–Aldosterone (RAAS) system
– At the level of the kidneys
– Stimulated to conserve Na+ & water
– Response within hours
3 Stages of Shock
- Early compensatory shock
– Physiologic responses maintain blood pressure - Early decompensatory shock
– Associated with clinical signs of shock - Decompensatory / terminal shock
– Irreversible shock
Early Compensatory Shock; what is it, what are clinical signs? how is it created by the body?
- Appropriate cardiovascular compensation
- Clinical signs:
– Tachycardia, normal or elevated BP, normal or increased pulses, hyperemic mm, CRT< 1 sec - Easily missed, animal essentially normal
- Result of baroreceptor mediated release of catecholamines
– successful increase in CO - Heart rate is KEY
- Good response noted to volume replacement, good outcome
Early Decompensatory Shock; what is it? why does it occur and what do we see? clinical signs? prognosis?
- The 2nd stage of shock
- Compensatory mechanisms tiring
- Redistribution of blood flow:
– decreased blood flow to the kidneys, gut, skin & muscles - Clinical signs:
– Tachycardia, tachypnea, poor peripheral pulses, hypotension, prolonged CRT, pale mm, hypothermia, depressed mentation - Prognosis
– Fair to good with immediate intervention
Late Decompensatory Shock; what is it, when does it occur? what are the clinical signs? prognosis?
- Terminal Shock
- Compensatory mechanisms exhausted
- Clinical signs:
– Slowed heart rate (relative), pale cyanotic mm, absent CRT, weak / absent pulses, severe hypotension, hypothermia, mentally unresponsive / coma, no urine production - Generally irreversible
– Not responsive to aggressive fluid resuscitation - Damage has overwhelmed the body’s natural protective mechanisms
– Multiple organ dysfunction / failure
four broad categories of shock, based on pathophysiologic mechanisms:
- Hypovolemic
- Obstructive
- Distributive = vasodilatory = hyperdynamic
- Cardiogenic
- Patient can suffer from more than one category
what is cardiogenic shock?
- Inadequate ventricular pump function
- Inadequate delivery of oxygenated blood to vital organs
> Hypoperfusion - Maybe due to:
– Myocardial failure (ie. Cardiomyopathy)
– Valvular dysfunction (ie. Severe mitral valve disease) – Arrhythmias - To be dealt with outside of this lecture
what is Hypovolemic Shock?
- Profound decrease in intravascular (blood) volume
– Loss of ≥ 30-40% of circulating blood volume OR
– 10-15% dehydration - Inadequate blood volume to deliver to vital organs
>Hypoperfusion
Etiology of hypovolemic shock
- Blood loss / hemorrhage
* External
* Internal - Dehydration
* Polyuria
* GI loss
* Burns
* 3rd space losses (eg. ascites)
signs of shock suggest how much blood loss?
> 30%
as you become dehydrated, where will your body draw water from?
interstitial fluid,
then intracellular fluid,
then intravascular fluid
-body will spare intravascular compartment via fluid shifts until profound dehydration is encountered
phases of hemorrhage
- interstitial fluid shifts
- water retention
what is phase 1 of hemorrhage? when and why does it occur? what are the observable signs?
- Phase 1 – Interstitial fluid shifts
– Within 1 hour
– Attempt to restore intravascular volume & organ perfusion
– Fluid shift dilutes - Red cell mass (PCV)
- Total solids (TS)
– Splenic contracture in the dog & horse - Spleen can sequester up to 30% of the RBCs
what are the immediate effects of fluid shifts in dogs (vs cats) during hemorrhage?
Within minutes
Splenic contracture in dogs (not cats):
Release of sequestered RBCs
*PCV falling but is boosted
*TS - falls
what is phase 2 of hemorrhage/hypovolemic shock? what happens and what can we observe?
- Phase 2– Water retention
- Activation of the renin – angiotensin-aldosterone (RAAS) system
– Promotes Na+ and H2O retention by the kidneys
– Further drop in PCV noted - Within 8 hours – 36-50% of ultimate change in PCV
- Within 24 hours – 70%
– Administration of crystalloids or colloids will cause a more rapid decrease in PCV & Total Solids
what is the etiology of non-cardiogenic, obstructive shock?
– Diminished cardiac output secondary to compression on the vascular system or obstruction to blood flow
– Blood can’t get to the heart!
– Blood can’t be ejected from the heart!
– Examples
* Gastric dilation volvolus
* Tension pneumothorax
* Pericardial tamponade
* Pulmonary embolism
what are the causes of distributive (vasodilatory) shock?
- Maldistribution of blood flow
– Microvascular circulation
– Failure of the vascular smooth muscle to constrict
> Vasodilatory shock - Most common causes:
– Sepsis, anaphylaxis, a hypoadrenocorticism, drug reactions
& massive trauma
Normally 70% of blood volume is in the venous system
>Massive vasodilation leads to ….. Relative hypovolemia
“Relative Hypovolemia” - vessels dilate
1. Underfilled venous system… Poor venous return…..decreased arterial blood pressure
2. Decreased systemic vascular resistance (SVR)
3. Initially improved cardiac output
what do we observe clinically in the initial phase of distributive shock?
Initially Hyperdynamic Phase
* Normal to increased CO
* Brick red mucous membranes
* Rapid (<1 sec) CRT
* Tachycardia
* Bounding pulses
* Warm extremities
how do the clinical signs of distributive/septic shock differ from those of other types of shock (eg. hypovolemic)?
- Reduced level of mentation
- Hypothermia / Cool extremities (warm extremities)
- Tachycardia (bradycardia in cats)
- Increased respiratory rate & effort
- Poor peripheral pulses (bounding peripheral pulses)
- Decreased blood pressure
- Pale mucous membranes (injected mucous membranes)
- Prolonged capillary refill time (rapid)
- Decreased urine production
- Decreased GI blood flow/ GI ulceration
=> Distributive/Septic shock in parentheses
….Final common pathway for shock of any cause:
Decompensation
* Decreased cardiac contractility
* Decreased CO
* Poor peripheral pulses
* Hypotension
* Pale mm
* Prolonged CRT > 2-3 seconds
