Surgery Lecture 7 Shock, Fluids And Electrolytes

Front 1

What is the definition of shock?

Back 1

Shock is the CLINICAL STATE that develops when tissue OXYGEN DELIVERY, or utilization, is compromised

Front 2

What does the amount of oxygen delivered depend on?

Back 2

Cardiac output
Concentration of oxygen

Front 3

What does cardiac output depend on ?

Back 3

HR x SV

Front 4

What do oxygen concentrations depend on?

Back 4

hemoglobin and hemoglobin saturation of oxygen

Front 5

What are the 4 categories of shock?

Back 5

1) Hypovolemic
2) Cardiogenic
3) Distributive
4) Hypoxic

Front 6

What are the 2 causes of hypovolemic shock?

Back 6

1) Hemorrhagic
2) Nonhemorrhagic (e.g. third space losses, severe dehydration, urinary losses, severe vomiting/ diarrhea

Hint 6

Wh

Front 7

What are the two types of cardiogenic shock?

Back 7

1) Systolic failure
-e.g. CHF, DCM, mechanical defects)
2) Diastolic failure
-HCM, tamponade, tension, pneumothorax

Front 8

What are 4 causes of distributive shock?

Back 8

1) Sepsis
2) Anaphylaxis
3) Drugs
4) Neurogenic

Front 9

What are 4 causes of hypoxic shock?

Back 9

1) Hypoxemia
2) Anemia
3) Methemoglobinemia
4) Carbon monoxide poisoning

Front 10

Overall, why is shock so bad?

Back 10

Hypoxia---> altered cell membrane ---> organ fail---> death

Front 11

Hypoxia -----> __________-----> ANAEROBIC METABOLISM

Back 11

Blocks pyruvate entry into Kreb's cycle

Front 12

Why does HYPERLACTEMIA develop during shock?

Back 12

Lactate produced by anaerobic glycolysis can't be recycled into pyruvate or glucose without oxygen

Front 13

Why does METABOLIC ACIDOSIS develop in patients in shock?

Back 13

H+ is produced as a result of ATP---> ADP and can't be used by the mitochondria w/o oxygen

Front 14

What happens to the cell in response to a lack of ATP within the cell?

Back 14

Loss of electrical and chemical gradients---> CELL SWELLING, INFLAMMATION, DEATH

Front 15

What do dangerous associated molecular patterns (DAMPs) result in during shock?

Back 15

INFLAMMATORY RESPONSE

Front 16

Why do coagulopathies develop early in the course of shock?

Back 16

Endothelial damage and exposure of collagen--> endothelial release of tPA, protein C etc.

Front 17

What happens when oxygen returns in shock patients?

Back 17

REPERFUSION INJURY
-reactive oxygen and nitrogen species
-"no reflow" phenomenon

Front 18

What detects the decreased blood pressure in shock patients?

Back 18

Baroreceptors (carotid body & aortic arch)
Low pressure stretch receptors (atrial & pulmonary artery)
Chemoreceptors

Front 19

What happens when the baroreceptors and low pressure stretch receptors detect low vascular pressure?

Back 19

Sends signal up the sympathetic nerve causing:
-Constrict arterioles--> increased SVR --> redirects blood to vital organs
-Constrict the veins/venules---> increased venous return ---< increased CO & increased HR

Front 20

What will be the clinical signs of shock in response to the sympathetic stimulation?

Back 20

Pale mucous membranes
Increased CRT
Cool extremities

Front 21

What do the carotid and aortic bodies sense in the periphery? In the medulla?

Back 21

Periphery: sense decreased O2
Medulla: sense increased H+ in CSF and Increased CO2

Front 22

What happens when the chemoreceptors detect decreased oxygen or acidosis?

Back 22

sympathetic nerve causes:
-increased ventilation---> decreased CO2 and decreased H+ (blows off CO2)
**Leads to altered respiratory pattern (tachypnea)

Front 23

What are the 4 neurohormonal responses from the sympathetic nerve stimulation during shock?

Back 23

1) Renin-angiotensin-aldosterone system
-resorbs H2O & Na from kidney
2) Vasopressin
3) Hypothalamic-pituitary-adrenal axis
-CRH---> ACTH--> cortisol
-Also epinephrine, glucagon &GH
-catabolic state increases glucose for fight or flight
4) Splenic contraction
-increases RBCs

Front 24

What are 2 causes of activation of the renin-angiotensin-aldosterone system?

Back 24

1) Decreased stretch in the glomerular afferent a. & decreased [Na] in macula densa
2) Directly by sympathetic n.

Front 25

What are the 2 affects of vasopressin release in shock patients?

Back 25

1) Aquaporin-2 channels resorb water
2) Direct vasoconstriction

Front 26

What is the "passive response" of the body to shock (in response to decreased MAP)?

Back 26

Decreased MAP--> decreased hydrostatic pressure in capillaries
-fluid shifts from interstitial--> intravascular space

Front 27

What drives oxygen diffusion?

Back 27

Reduced cellular PO2 tension

Front 28

What are the 3 clinical stages of shock?

Back 28

1) Compensatory phase
2) Early decompensatory phase
3) Late decompensatory phase

Front 29

What is the compensatory stage of shock?

Back 29

Hemodynamic parameters are stable
Hypermetabolic state and high energy expenditure

Front 30

What is the early decompensatory phase of shock?

Back 30

Compensatory mechanisms begin to fail
-Blood flow is preferentially redistributed to vital organs

Front 31

What are the 5 things occurring during the late decompensatory phase of shock?

Back 31

1) Autoregulatory escape
2) Vasodilation prevails over sympathetic -mediated vasoconstriction
3) Cardiovascular collapse
4) Cardiopulmonary arrest imminent
5) Poorly responsive
-body has just given up

Front 32

What compensates during class I of acute blood loss? What are the clinical signs of class I acute blood loss?

Back 32

Transcapillary refill from interstitial fluid
Clinical signs or manifestations are minimal or absent

Front 33

What are the 4 clinical signs of class II acute blood loss?

Back 33

1) Resting tachycardia
2) orthostatic changes in HR, BP
3) decreased urine output
4) agitated mental state

Front 34

The Class II correlates to the "________ phase" and maybe entering the "_________ phase".

Back 34

Compensatory phase
Early decompensatory phase

Front 35

Class III of acute blood loss marks the onset of what?

Back 35

Hypovolemic shock

Front 36

What are the clinical signs present with class III acute blood loss?

Back 36

Worsening decrease in BP, decrease urine output and possibly anuria
-Tachycardia- vasoconstrictor response may be lost at this stage

Front 37

Class III of acute blood loss correlates with the _________ phase.

Back 37

Early decompensatory phase

Front 38

Class IV of acute blood loss foreshadows what?

Back 38

Circulatory collapse, severe and immediately life-threatening

Front 39

Class IV of acute blood loss correlates with the _______ phase.

Back 39

Late decompensatory phase

Front 40

What is the total blood volume in a dog and cat?

Back 40

TBV= 90 m/kg in dogs and 60 mL/kg in cats

Front 41

What are 3 causes of septic shock?

Back 41

1) gram negative bacteria endotoxins (LPS)
2) Gram positive--> exotoxins
3) Systemic or severe fungal infections

Front 42

What is the definition of endotoxemia?

Back 42

Presence of endotoxins in the blood---> Cytokine activation and secondary free radical formation, histamine release, complement, platelet activating factor, kinins, etc
-can lead to other 3 forms of shock

Front 43

What is SIRS?

Back 43

Systemic inflammatory response syndrome- the criteria that a patient has to meet to conclude they have sepsis
-every specie has a different response to shock
-temperature, HR, RR, WBC

Front 44

What are the 5 easy steps to treating shock?

Back 44

1. Brief history, PE and measure BP
2) Simultaneously:
-Place IV catheter, get sample for initial labs (big 4, lstat, CBC, chem, UA +/- coags, +/- blood gas etc
-Start immediate and aggressive supportive case (most likely IV fluid therapy, except if cardiac)
3) More history and PE
4) Focused diagnostics
-Aus, CT, CSR, echocardiogram, serum titers, etc.
5) Treat underlying cause

Front 45

True or false. Shock is a primary condition.

Back 45

False, that's why history is so important so can identify the underlying cause of shock

Front 46

How should you approach doing physical exam for shock patients?

Back 46

Do an abbreviated exam initially, then keep re-visiting
-Signs may be subtle: mild tachycardia, pulses may feel particular "strong" (wide pulse pressure)
-May be alert, appropriate, ambulatory
-If decompensating signs are more classic

Front 47

Dysfunction of "shock organs" means dysfunction of what 2 things?

Back 47

GI tract, lungs

Front 48

What should you do if you suspect cardiogenic shock?

Back 48

Check for jugular vein distension

Front 49

Are cats in shock bradycardic or tachycardic? Hyperthermic or hypothermic?

Back 49

Tachycardic
Hypothermic

Front 50

What are 2 ways to assess hemodynamics?

Back 50

1) Blood pressure
2) Central venous pressure

Front 51

What are 2 non-invasive methods used to measure BP?

Back 51

1) Doppler
2) Oscilometric
-unreliable if < 5 kg

Front 52

What is the gold standard to measuring BP?

Back 52

Invasive BP: arterial catheter

Front 53

What is the goal mean arterial pressure for small animals? Systolic arterial pressure?

Back 53

MAP >60 mm Hg
SAP > 90 mm Hg

Front 54

What do you want to look at when evaluating the central venous pressure?

Back 54

Trends are helpful, absolute values less helpful

Front 55

What is considered cardiogenic shock when evaluating CVP?

Back 55

> 10 cm H20 drop

Front 56

Fluid overload is rare in what animal?

Back 56

Horses

Front 57

What are 4 ways to perform metabolic assessment?

Back 57

1) CBC/chem
2) Big4 (PCV/TS/BG/Azo stick)
3) Istat8+ (lytes & acid base)
-can run arterial blood gas
4) Lactate

Front 58

What are 2 ways to assess oxygenation?

Back 58

1) Arterial blood gas
2) Pulse oximetry (SpO2-saturation of hemoglobin)

Front 59

Pulse oximetry may be inaccurate so you should correlate the results with what 3 things?

Back 59

HR, RR, MM color
-Just because saturation is good doesn't mean high PaO2

Front 60

What should you do if SpO2 is low or borderline?

Back 60

Administering flow of O2 will never hurt and may be life-saving especially if cardiogenic shock

Front 61

How should fluids be administered?

Back 61

IV or interosseous- never SQ or IM or oral

Front 62

What are the 3 general principles of fluid therapy?

Back 62

1) Determine volume, type, rate of administration
2) Determine reason(s) for therapy
3) Determine route of administration

Front 63

What are 4 reasons for fluid therapy?

Back 63

1) Shock treatment
-60-90 mL/kg depending on species
2) Deficit replacement
-estimate % loss x BW (kg)
3) Provide maintenance
-~60 mL/kg/day in dogs & cats
4) Ongoing losses: estimated by monitoring
-TPR, PCV/TS, urine output, vomiting and/or diarrhea, lactate, blood gas analyses

Front 64

What are 4 examples of isotonic crystalloids?

Back 64

1) LRS
2) Normosol-R
3) 0.9% NaCl
4) Plasmalyte -A

Front 65

How is 0.9% NaCl different from the other 3 isotonic crystalloids?

Back 65

Lacks a buffer and is acidifying

Front 66

True or false. Do not use isotonic crystalloids for maintenance fluids.

Back 66

True

Front 67

What is the shock dose of fluids for dogs? Cats?

Back 67

Dogs: 60-90 mL/kg
Cats: 40-60 mL/kg

Front 68

How should you administer isotonic crystalloids for a shock patient?

Back 68

Give 1/4 to 1/3 IV rapidly over ~ 5 minutes, re-assess +/- repeat bolus +/- finish dose over 45-60 minutes
-KEEP REASSESSING PATIENT

Front 69

****Within 30 minutes how much of the infused crystalloids are still present within the intravascular space?

Back 69

25% of dose

Front 70

Is hypertonic saline usually used in LA or SA medicine?

Back 70

LA

Front 71

What is the hypertonic saline used for fluids? What is the max dose?

Back 71

7.5% NaCl max dose 4 mL/kg

Front 72

What are the effects of hypertonic saline on the vascular system?

Back 72

-Increases circulating volume by 2-4 x the amount given
-Raises BP, improves CO, lowers SVR, improves O2 delivery

Hint 72

Hy

Front 73

Hypertonic saline may decrease _________ and therefore subsequent multiple organ failure.

Back 73

Ischemia/ reperfusion injury

Front 74

Where does water shift when an animal is given hypertonic saline?

Back 74

Shifts water into plasma from RBCs and endothelium, then from interstitial space and cells

Front 75

How do you administer hypertonic saline?

Back 75

MUST give crystalloids to replace the resultant fluid deficit
-Give 10 x the amount of hypertonic saline in crystalloids
e.g. 10 L of isotonic fluid w/ 1L of hypertonic saline

Front 76

What are 3 examples of synthetic colloids?

Back 76

1) Hetastarch
2) Voluven
3) Dextran-70

Front 77

**How do you administer synthetic colloids?

Back 77

NEVER ALONE-always w/ crystalloids
-5-10 mL/kg IV bolus and repeat as needed

Front 78

What patients do you use synthetic colloids on?

Back 78

Hypoproteinemic patients w/ low cardiac output

Front 79

What is the max dose of synthetic colloids per 24 hour period?

Back 79

20-30 mL/kg / 24 hours in dogs and cats
-except voluven

Front 80

What is the half life of synthetic colloids?

Back 80

~25 hours
-last longer than crystalloids

Front 81

What animal is more sensitive to fluid overload via synthetic colloids?

Back 81

Cats
-Be more conservative in total volume used

Front 82

What are 3 blood products that can be used in small animal medicine?

Back 82

1) Fresh frozen plasma (FFP)
2) Packed RBC (pRBC)
3) Whole blood

Front 83

What does fresh frozen plasma provide the patient with?

Back 83

Coagulation factors
Increases cardiac output

Front 84

How should fresh frozen plasma be administered? How much?

Back 84

10-20 mL/kg given IV over 4 hours

Front 85

What is the difference b/w fresh frozen plasma and frozen plasma?

Back 85

Frozen plasma has been thawed and re-frozen and lacks most of the coagulation factors FFP contains

Front 86

What are packed RBCs used for?

Back 86

To replenish oxygen carrying capacity of the blood by increasing RBC mass (PCV)

Front 87

When should you recheck the PCV when using packed RBCs?

Back 87

~1 hour post-transfusion

Front 88

When is whole blood the best choice?

Back 88

If available, when the patient needs both packed RBCs and fresh frozen plasma (coagulation factors and oncotic pressure)

Front 89

Electrolyte and acid-base imbalances should be treated based on what?

Back 89

Results of metabolic monitoring and repeat tests frequently to assess response to treatment

Front 90

Should you recheck electrolyte and acid-base status before or after fluid treatment?

Back 90

recheck after because fluid treatment almost always will have corrected many if not all of the initial derangments

Front 91

When do you administer vasopressors IF they're needed?

Back 91

AFTER adequate volume re-expansion: CVP and/or full shock dose of crystalloids and maxxed out colloids

Front 92

When should you administer antibiotics to shock patients?

Back 92

If suspect septic, once stabilized--> get C & S and start empirical antibiotics
-Consider gram-stain

Front 93

When are steroids used for shock?

Back 93

Low-dose glucocorticoids controversial
-even in addisonian hypovolemic shock, steroids are not immediately life saving
High-dose glucocorticoids for tx of shock is ineffective or even harmful and strongly contraindicated

Front 94

What is the only type of shock that fluids should NOT be used for?

Back 94

Cardiogenic shock