Shock and Resuscitation Flashcards
what is shock?
– 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
is shock a disease?
no its a syndrome associated with many disease conditions
will you always see increased HR in cats that are in shock?
not always, they suck at compensating
what are some clinical signs of shock? (10)
- 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
what are some aspects of shock that are specific to cats?
- Bradycardia (HR < 160 bpm)
- Hypothermia
- Hypotension; Hypothermia decreases ability to cope with fluid load, Begin resuscitation but do not ‘blast’ a cat with fluids until you determine their response to rewarming
what is the physiologic response to shock and what does it lead to an increase in?
– Increased sympathetic output; Epinephrine (adrenaline) & NE released from adrenal glands
Increase in:
– Heart rate
– Cardiac contractility
– Vasoconstriction
what are three endocrine responses 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
how is vasoconstriction organ selective (3)
– 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)
what are the 3 stages of shock and what defines them?
- Early compensatory shock
– Physiologic responses maintain blood pressure - Early decompensatory shock
– Associated with clinical signs of shock - Decompensatory / terminal shock
– Irreversible shock
what are the clinical signs of early compensatory shock? what is the key sign?
- Clinical signs: Tachycardia, normal or elevated BP, normal or increased pulses, hyperemic mm, CRT< 1 sec
-heart rate is key
for early compensatory shock; what is happening by the patient? is it easy to diagnose? what is it a result of? what is the outcome?
- Appropriate cardiovascular compensation
- Easily missed, animal essentially normal
- Result of baroreceptor mediated release of catecholamines; successful increase in CO
- Good response noted to volume replacement, good outcome
what is the second stage of shock
early decompensatory shock
early decompensatory shock; what happens to blood flow, what are the clinical signs, what is the prognosis
- 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
what is tiring in the second stage of shock
compensatory mechanisms
what stage is late decompensatory shock
terminal shock
can a patient suffer from more thn one category of shock
yerrrrr
late decompensatory shock; clinical signs, is it reversible, what damage has been done
- 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
what is exhausted in late decompensatory shock
compensatory mechanisms
4 categories to classify shock
- Hypovolemic
- Obstructive
- Distributive = vasodilatory = hyperdynamic
- Cardiogenic
what is cardiogenic shock?
- Inadequate ventricular pump function
- Inadequate delivery of oxygenated blood to vital organs->Hypoperfusion
what can cardiogenic shock be due due?
May be due to:
– Myocardial failure (ie. Cardiomyopathy)
– Valvular dysfunction (ie. Severe mitral valve disease)
– Arrhythmias
what is hypovolemic shock? what happens regarding blood volume?
- 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
phase 1 of hemorrhage; what shifts? time range, what is attempted, what else adjusts
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
etiology of hypovolemic shock (2)
- Blood loss / hemorrhage
* External
* Internal - Dehydration
* Polyuria
* GI loss
* Burns
* 3rd space losses (eg. ascites)
what happens within minutes of fluid shift
-splenic contracture in dogs (not cats)
-release of sequestered RBCs; PCV falling but is boosted, total solids drops
what can happens with continued hemorrhage related to PCV
With continued hemorrhage; PCV may drop rapidly due to depletion of
hepatic / splenic reserves
phase 2 of hypovolemic shock; what happens to water, what is activated
- Phase 2 – Water retention
- Activation of the renin – angiotensin - aldosterone (RAAS) system
what happens when the RAAS system is activated
– Promotes Na + and H 2O 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 happens with distributive (vasodilatory) shock and common causes
- 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
etiology of non-cardiogenic obstructive shock and examples
– 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
in distributive shock, where is 70% of the blood volume
70% of blood volume is in the venous system
massive vasodilation leads to relative hypovolemia
what aspects of patient assessment need to be considered? (7)
- Heart rate & rhythm
- MM colour & CRT
- Pulse quality & Blood Pressure
- Urine output
- PCV / TS
- Lactate production
- Blood gases
what do we see in the initially hyperdynamic phase of distributive shock
- Normal to increased CO
- Brick red mucous membranes
- Rapid (<1 sec) CRT
- Tachycardia
- Bounding pulses
- Warm extremities
what happens/what do we see with decompensation
- Decreased cardiac contractility
- Decreased CO
- Poor peripheral pulses
- Hypotension
- Pale mm
- Prolonged CRT > 2-3 seconds
how often should parameters be monitored with shock patients
every 5-15 minutes
two things to assess related to heart and rhythm
- Auscultate the heart
* Heart sounds – are they there?
* Heart rate
* Arrhythmias - Feel a pulse
* Pulse rate
* Rhythm – note pulse deficits
* Pulse pressure
what is pulse quality dependent on?
Dependent on difference palpated between systolic & diastolic pressures = pressure difference
what does MM assess? what is normal? what type of shock do we not see changes in CRT?
-assessment of tissue perfusion
-normal is <2 seconds
-Shock causes a prolongation of the CRT; Except vasodilatory shock – CRT is shortened
when are femoral vs peripheral pulses absent
- Femoral pulses
– Absent once systolic BP < 40 mmHg - Peripheral pulses (dorsal pedal, radial)
– Absent when systolic BP < 60–70 mmHg
what does BP do in compensatory shock vs decompensation
compensatory shock; may be normal or increased
decompensation; decreased BP
what is urine output a measure of
organ perfusion
what does PVC and TS not help us assess
do not help assess degree of acute hemorrhage
what is lactic acid a biproduct of
anaerobic metabolism
what is the best and most current way to note response to therapy
Trending an improvement in lactate is the best & most current way to note response to therapy
what does increased lactase mean
means poor oxygen delivery to tissues
why is shock associated with metabolic acidosis (2)
- Decreased perfusion & oxygen delivery
- Lactic acid production
what is delivery of oxygen to the tissues dependent on (2)
– Cardiac output of the animal
– Oxygen content of arterial blood
what does tissue perfusion necessitate (5)
– Efficient cardiac pump
– Adequate intravascular volume
– Vasomotor tone
– Adequate hemoglobin / red cell mass
– Good lung function
5 steps on your to do list for resuscitation
- Ensure patent airway & patient ventilating; Intubate & ventilate if necessary
- Supplement O2
- Provide intravascular volume support; Crystalloids, colloids, blood products (Not appropriate for cardiogenic shock)
- Administer pain medication
- Treat primary problem; Correct GDV, thoracocentesis for tension pneumothorax, address hemoabdomen, etc
what is the goal of resuscitation
normalization of vital parameters
what is the most common mismanagement for patients
Inadequate fluid resuscitation is the most common mismanagement for patients who die from trauma
what compartment needs resuscitation in dehydration cases
interstitial/intracellular compartment
what compartment needs resuscitation in shock cases
intravascular compartment
what is considered first line for fluid selection
crystalloids (BES)
4 options for fluid selection for the intravascular compartment
– Crystalloids
– Colloids
– Hypertonic saline
– Blood components
examples of balanced electrolyte solutions (4)
- Lactated Ringers Solution (LRS)
- Plasmalyte A , Plasmalyte 148
- Normosol R
- 0.9% NaCl
what is the volume of crystalloid administration to blood loss
3:1
composition of crystalloids
– Water, electrolytes (concentrations similar to blood)
– Solutions containing small molecules that may easily pass through blood vessels
blood volume for dog vs cat vs horse vs ruminant
– 80-90 ml/kg (Dog)
– 60 ml/kg (Cat)
– 100 ml/kg (Horse)
– 60 ml/kg (Ruminant)
crystalloid rate
- As fast as necessary
- Conceptualize shock rate delivered over 1 hour
- Administer ¼ dose in 15-minute increments & reassess
synthetic colloids dose
MAX daily dose
– 20 ml/kg/day (dog)
– 10 ml/kg/day (cat)
* Administer in ¼ aliquots over 5-10 minutes
* Repeat up to 4X as necessary
hypertonic saline; features, how it works
- Hyperosmolar solution
- Many Na + molecules draw water into the intravascular space
- Very rapid intravascular volume expansion
- Short duration of action; As Na+ molecules are redistributed
colloids; what do they contain, what support do they provide, volumes required
- Solutions containing large molecules that are trapped & stay within the blood vessels
- Provide oncotic support
- As they stay in the vessel, smaller volumes required for intravascular volume expansion
how to address shock related to fluid replacement with anesthesia vs without?
With Anesthesia
* Replace ½ deficits prior to induction
Without Anesthesia
* Replace remaining deficits over next 12-24 hours
* Rehydration of interstitial compartment to occur over longer time
natural vs synthetic colloids
natural
* Plasma, Blood
* Remain in the vessel
* Require collection
* May need to be thawed
synthetic
* Examples; Pentastarch (Canada), Hetastarch (US), Tetrastarch (Voluven), Dextrans
* Remain in the vessel + draw fluid into the vessel
* Readily available
when colloids, hypertonic saline or blood are used for fluid resuscitation, what is reduced
Crystalloid requirements are reduced (~50%)
what can happen with over aggressive fluid administration (3)
- Dislodge early clots
- Aggravate fluid extravasation into damaged tissues
– Lungs – pulmonary edema
– Brain – increased intracranial pressures - Contribute to excessive hemodilution
– General rule of thumb: aggressive fluid administration drops PCV and TS by 1/3
– Transfusion suggested if –> PCV acutely < 25% , TS < 3.5- 4.0 g/L
examples of corticosteroids that can be used and 3 adverse effects
Examples :
– Dexamethasone
– Prednisolone sodium succinate (Solu-delta-cortef)
– Methylprednisolone sodium succinate (Solu Medrol)
Adverse effects:
– Increased risk of infection
– GI ulceration
– No improvement in outcome!
when should we administer antibiotics
- Administer if
– Open wounds
– Bacteremia /sepsis strong differential diagnosis
– Immunocompromised patient
what happens if you delay resuscitation of a previously healthy patient
Delays in resuscitation of a previously
healthy patient may render them
unresponsive to aggressive therapy later on –> decompensatory shock
what are some possible consequences of shock? (7)
– GI hemorrhage / ulceration
– Acute renal failure
– Bacterial translocation
– Endotoxemia / sepsis
– DIC (Blood clotting abnormalities)
– Respiratory failure (ARDS)
– Multiple organ failure
