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Pharm Test 4 > Shock and Resuscitation > Flashcards

Shock and Resuscitation Flashcards

1
Q

what is shock? Definition:

A

– 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

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2
Q

Clinical Signs of Shock

A
  • 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
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3
Q

Shock - Physiologic Response

A

– Increased sympathetic output
* Epinephrine (adrenaline) & Norepinephrine released from adrenal glands

  • Increase in
    – Heart rate
    – Cardiac contractility
    – Vasoconstriction
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4
Q

how does vasoconstriction occur during shock? what parts of the body are more affected and why?

A
  • 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
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5
Q

endocrine response to shock?

A
  1. Epinephrine & norepinephrine
    – Released from adrenal glands & vasomotor endplates
    – Immediate response
  2. Antidiuretic hormone
    – Released from the pituitary
    – To conserve water
    – Response within minutes
  3. Renin–Angiotensin–Aldosterone (RAAS) system
    – At the level of the kidneys
    – Stimulated to conserve Na+ & water
    – Response within hours
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6
Q

3 Stages of Shock

A
  1. Early compensatory shock
    – Physiologic responses maintain blood pressure
  2. Early decompensatory shock
    – Associated with clinical signs of shock
  3. Decompensatory / terminal shock
    – Irreversible shock
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7
Q

Early Compensatory Shock; what is it, what are clinical signs? how is it created by the body?

A
  • 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
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8
Q

Early Decompensatory Shock; what is it? why does it occur and what do we see? clinical signs? prognosis?

A
  • 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
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9
Q

Late Decompensatory Shock; what is it, when does it occur? what are the clinical signs? prognosis?

A
  • 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
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10
Q

four broad categories of shock, based on pathophysiologic mechanisms:

A
  1. Hypovolemic
  2. Obstructive
  3. Distributive = vasodilatory = hyperdynamic
  4. Cardiogenic
  • Patient can suffer from more than one category
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11
Q

what is cardiogenic shock?

A
  • 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
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12
Q

what is Hypovolemic Shock?

A
  • 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
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13
Q

Etiology of hypovolemic shock

A
  1. Blood loss / hemorrhage
    * External
    * Internal
  2. Dehydration
    * Polyuria
    * GI loss
    * Burns
    * 3rd space losses (eg. ascites)
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14
Q

signs of shock suggest how much blood loss?

A

> 30%

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15
Q

as you become dehydrated, where will your body draw water from?

A

interstitial fluid,
then intracellular fluid,
then intravascular fluid

-body will spare intravascular compartment via fluid shifts until profound dehydration is encountered

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16
Q

phases of hemorrhage

A
  1. interstitial fluid shifts
  2. water retention
17
Q

what is phase 1 of hemorrhage? when and why does it occur? what are the observable signs?

A
  • 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
18
Q

what are the immediate effects of fluid shifts in dogs (vs cats) during hemorrhage?

A

Within minutes
Splenic contracture in dogs (not cats):
Release of sequestered RBCs
*PCV falling but is boosted
*TS - falls

19
Q

what is phase 2 of hemorrhage/hypovolemic shock? what happens and what can we observe?

A
  • 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
20
Q

what is the etiology of non-cardiogenic, obstructive shock?

A

– 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

21
Q

what are the causes of distributive (vasodilatory) shock?

A
  • 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

22
Q

what do we observe clinically in the initial phase of distributive shock?

A

Initially Hyperdynamic Phase
* Normal to increased CO
* Brick red mucous membranes
* Rapid (<1 sec) CRT
* Tachycardia
* Bounding pulses
* Warm extremities

23
Q

how do the clinical signs of distributive/septic shock differ from those of other types of shock (eg. hypovolemic)?

A
  • 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

24
Q

….Final common pathway for shock of any cause:

A

Decompensation
* Decreased cardiac contractility
* Decreased CO
* Poor peripheral pulses
* Hypotension
* Pale mm
* Prolonged CRT > 2-3 seconds

25
Q

Patient Assessment for shock; what do we look at

A
  • Heart rate & rhythm
  • MM colour & CRT
  • Pulse quality & Blood Pressure
  • Urine output
  • PCV/TS
  • Lactate production
  • Blood gases
26
Q

how often should we re-evaluate parameters when monitoring for shock?

A

– Every 5 – 15 minutes

27
Q

heart rate and rhythm during shock; what do we expect, what do we look for and how?

A
  • Shock is associated with tachycardia
    1. Auscultate the heart
  • Heart sounds – are they there?
  • Heart rate
  • Arrhythmias
    2. Feel a pulse
  • Pulse rate
  • Rhythm – note pulse deficits
  • Pulse pressure
  • Recommend ECG if available
28
Q

MM Colour & CRT during shock; what are we looking for?

A
  • Assessment of tissue perfusion
  • CRT is evaluated by blanching the mm & noting the time to return of colour
  • Normal is < 2 seconds (1-1.5 seconds)
  • Shock causes a prolongation of the CRT
    – Except vasodilatory shock – CRT is shortened
29
Q

what does blood pressure have to fall to for us to consider it hypotension?

A
  • Normal:
    ~ Systolic 120 mmHg ; MAP 100 mmHg ; Diastolic 80 mmHG
  • Hypotension
    – Systolic < 90 mmHg
    – MAP <60 mmHg
    – Severe hypotension is the hallmark of shock!
30
Q

what blood pressure does cerebral, renal, and muscle perfusion require?

A
  • Cerebral perfusion requires MAP > 40mmHg
  • Renal perfusion requires MAP > 60 mmHg
  • Muscle perfusion requires MAP >70mmHG
31
Q

what does pulse quality depend on? what pulses are normally most prominent and when will they be absent? when will peripheral pulse generally be absent?

A
  • Dependent on difference palpated between systolic & diastolic pressures = pressure difference
  • But, pressure difference;
    – 120/80 mmHg = 40 mmHg
    – 90/50 mmHg = 40 mmHg > thready
  • Femoral pulses
    – Most prominent
    – Absent once systolic BP < 40 mmHg
  • Peripheral pulses (dorsal pedal, radial)
    – Absent when systolic BP < 60 – 70 mmHg
32
Q
  • Arterial blood pressure (BP) product of:
A

– BP = CO x SVR
– BP = (HR x SV) x SVR

33
Q

in compensatory shock, BP may be;

A

normal or increased

34
Q

how will BP change with decompensation

A

decrease

35
Q

what is urine output a measure of? what is a normal value? how can we monitor this easily?

A
  • Measure of organ perfusion
  • If there is pee, the kidneys are being perfused
  • Normal urine production – 1-2 ml/kg/hr
  • Palpate & monitor the size of the bladder routinely
36
Q

how should we monitor PCV and total solids during a shock case? how often?

A
  • Establish at admission (baseline)
    – May be normal on admission as fluid shifts have not had time to occur
    – Do not help assess degree of acute hemorrhage
  • Repeat in:
    – 15 minutes
    – 30-60 minutes
37
Q

why is lactate production useful to measure during a shock case? what is the normal value? how valuable is this measurement for checking response to therapy?

A
  • Lactic acid is a by-product of anearobic metabolism
  • With hypoperfusion of organs, anearobic metabolism prevails
    >increased production of lactate
  • Normal lactate <2 mmol/L
  • Trending an improvement in lactate is the best & most current way to note response to therapy

Pharm Test 4 (10 decks)

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