Shock, vascular access and fluid therapy 1.2 Flashcards
Define respiratory acidosis
The result of hypoventilation and accumulation of CO2
Define stroke volume
The volume of blood pumped out of the left ventricle with every heart beat
Define systolic blood pressure
The force exerted on the walls of arteries as blood is pumped from the ventricles
Define diastolic blood pressure
The force of blood on the walls of arteries when the ventricles are relaxed (filling)
Provide multiple definitions of shock
- Where oxygen delivery to cells/tissues is insufficient for demand
- Inadequate cellular energy production or decreased cellular oxygen utilisation related to decreased blood flow that leads to cell death and organ failure
- Failure of circulatory system to maintain effective circulation, resulting in decreased oxygen delivery to cells
Define bacteraemia
The presence of viable bacteria in the blood
Define septic shock
Severe sepsis associated with hypotension that is unresponsive to appropriate fluid resuscitation
Define multiple organ dysfunction syndrome (MODS)
Dysfunction of the endothelial, cardiopulmonary, renal, nervous, endocrine and gastrointestinal systems associated with the progression of systemic inflammation
Define crystalloids
Solutions of electrolytes and/or glucose in water
Define colloids
Macromolecules in a solution
Because of their size they are retained intravascularly and exert colloid osmotic pressure
Why is anaerobic metabolism considered a temporary fix during low oxygen delivery?
Results in lactate accumulation and metabolic acidosis
How can a reduced DO2 lead to death?
Forced to utilise anaerobic metabolism
Insufficient energy produced = cells unable to function normally
Abnormal cell function = cell death = Organ dysfunction = organ failure = death
What are potential causes of hypovolaemic shock?
Haemorrhage
GI losses
What are potential causes of distributive/septic shock?
Septic peritonitis
Pyometra
Pyothorax
What are potential causes of obstructive shock?
Pericardial effusion (could also be considered cardiogenic)
GDV
Pulmonary thromboembolism
What are potential causes of cardiogenic shock?
End stage cardiomyopathy
Severe arrhythmias
What impacts blood pressure?
Cardiac output
Total peripheral resistance
Blood viscosity
In sequence, describe how haemorrhage impacts stroke volume
Haemorrhage -> decreased blood volume -> decreased venous return/cardiac preload to right atrium -> decreased volume from left ventricle (stroke volume)
Neuroendocrine compensatory mechanisms are mediated by what?
HPA axis - Sympatho-adrenal response
What are the aims of compensatory mechanisms during shock?
Increase cardiac output and blood vessel tone to increase cell perfusion
Describe/define acute compensatory mechanisms for shock
Immediate onset
Focus on increasing venous return and blood supply to myocardium -> allows to function effectively under increased demands
Triggered by sympathetic nervous system
If reliance if prolonged, mechanisms fail = decompensated shock
Explain how decrease blood volume leads to acute compensatory mechanisms being activated and what are these?
Decreased blood volume = decreased baroreceptor impulses
Stimulates SNS = increased activity
Catecholamine release
Peripheral vasoconstriction
tachycardia
Increased cardiac contractility
Explain how hypoxaemia leads to acute compensatory mechanisms being activated and what are these?
Hypoxaemia detected by chemoreceptors -> aorta and carotid artery
Increase in SNS activity and catecholamine release
Also cortisol release
Cortisol provides immediate glucose source
What are the vital roles of cortisol, including during shock?
Normal maintenance of vascular tone and endothelial integrity
Regulation of fluid within extravascular compartments
Potentiates impact of catecholamines on vasoconstriction
Describe the chronological sequence of RAAS
Decreased real perfusion stimulates baroreceptors in kidney
Stimalates RENIN release
RENIN converts Angiotensinogen to Angiotension I and II
Immediate response of angiotensin II = peripheral vasoconstruction & reabsorption of some salts and water
Delayed response of angiotensin II - Aldosterone release from adrenal cortex = increase sodium, chloride and water reabsorption from distal convoluted tubules in the kidney (v2 receptors) = increased blood volume
Where/when is ADH released during hypovolaemia and what is it’s role?
Released from posterior pituitary gland when osmolarity of blood increases and volume decreases
Binds to V1 receptors on peripheral arterioles = peripheral vasoconstriction
Define cardiogenic shock
Major failure of forward flow such that CO is insufficient to allow perfusion of the whole body
Briefly, how can DCM lead to cardiogenic shock?
Thin myocardial walls
Insufficient contractile strength
Inadequate stroke volume
Define distributive shock
Abnormal distribution of blood due to peripheral vasodilation
Blood pools in peripheral vessels and capillaries
Decreased CIRCULATING blood
During treatment, how may hypovolaemic and distributive shock respond differently?
Hypovolaemic = lack of circulating volume = Clinical signs improve with IVFT
Distributive = Inadequate circulation, not a volume issue = no response to IVFT
What abnormality causes peripheral vasodilation in distributive shock?
Vasoplegia due to exaggerated inflammatory response (inflammatory mediators)
What is the most common cause of sepsis?
Bacteria - E.coli
What diagnostic is highly suggestive of anaphylaxis?
Oedema in the wall of the gall bladder (halo sign) on ultrasound
What are the initial clinical signs of distributive shock
Pyrexia
Brick-red mucous membranes
Bounding pulses
Rapid CRT
Due to vasoplegia, peripheral vasodilation and initial hyperdynamic response (dogs)
What causes distributive shock to later mimic hypovolaemic shock in its clinical signs?
Ongoing cell death
Fluid loss
How might cats present differently with sepsis?
Not likely to have a hyperdynamic response
Will present similarly to hypovolaemic, alongside icterus and abdominal pain
How can pericardial effusion lead to obstructive shock?
Fluid in pericardial sac = insuffcient pre-load = reduced CO (aka tamponade)
Give examples of clinical signs associated with decompensated shock
Increasingly stuporous/comatose
Mucous membranes grey/brown
Increasing hypotension
Bradycardia
Ventricular arrhythmias
List 9 clinical signs associated with shock (not including early distributive)
Impaired mentation - decreased oxygen delivery to neurons
Tachycardia (cats may have normal HR or be bradycardic)
Tachypnoea
Pale MM
Prolonged CRT
Weak/absent peripheral pulses
Cold extremities
Decreased peripheral temperature
Decreased rectal/core temperature
Why do skin tents occur?
Loss of interstitial fluid leads to loss of tissue pliability and lubrication
Why might retropulsion of the eye be used to assess feline dehydration and what would the findings be?
In normal hydration, nicitating membrane should immediately reduce to normal position following retropulsion
When dehydrated, nicitating membrane more likely to stick to the globe and slowly slide back
Which area of a patient is the best to assess skin tenting and why?
Subcutaneous fat provides greater lubrication than lean tissue
Cranium and axillary region
Why can PCV allow for assess of dehydration?
PCV & TP increased due to overall loss of free water leading to haemoconcentration
Why do sighthounds usually have a higher PCV?
Large muscle mass
Low body fat
Why do young animals (<6 months) have a lower PCV?
Larger amount of free water present
How can severe dehydration lead to hypovolaemia?
As cells and interstitial spaces become progressively dehydrated, fluid is drawn from the intravascular space due to osmosis
Briefly explain the pathogenesis of SIRS
Excessive response to inciting insult
Normal response causes localised pro-inflammatory response
If insult severe enough, systemic pro-inflammatory response develops
Describe what happens during inflammation
Increased blood supply to the area (vasodilation)
increased capillary permability
Fluid exudate
Leucocyte delivery
Aside from an excessive inflammatory response, what else is excessive during SIRS? and what does this cause?
Anti-inflammatory response
Immunosuppression
Immunoparalysis
What factors affect the likelihood of SIRS developing?
The severity and duration of the insult
What is LPS and what is it’s role in distributive shock?
Lipopolysaccharide
Key component of cell wall of gram-negative bacteria
Potent initiator of septic inflammatory cascade
What are common sources of gram-negative bacteria in sepsis? Give examples of how these may occur
GI and urogenital
GI leakage into abdomen i.e. penetrating FB, GI neoplasia, perforated ulcers
What components of the cell wall of gram-positive bacteria can activate the inflammatory cascade? and explain potential sources
peptidoglycan
lipoteichoic acid
Wounds and IV catheters
Give two examples that a Streptococcus Canis infection can cause?
Toxic shock syndrome
Necrotizing fasciitis
How can vasodilation lead to MODS?
Hypotension and decreased organ perfusion
Define vasoplegia
Loss of vasoconstrictor response to catecholamines
Describe how increased vascular permeability can lead to MODS/MOF
Leads to interstitial oedema and decreased plasma volume and hypoalbuminaemia
What other disease process is commonly associated with SIRS?
DIC
Describe covert DIC
Inflammation leads to activation of haemostatic mechanisms inducing a prothombotic state - hypercoagulable
What issue does covert DIC pose?
Micro-thombi in organs - widespread clot formation, organ ischaemia due to flow being reduced
Describe over DIC
Consumption of coagulation factors and platelets - hypocoagulable state, leads to bleeding tendencies
Explain why SIRS can lead to renal dysfunction
Prolonged hypotension
Which pulmonary dysfunctions are associated with SIRS and why do they happen?
Acute lung injury (ALI)
Acute Respiratory Distress Syndrome
Secdonary to systemic inflammation leads to loss of normal pulmonary surfactant and accumulation of protein-rich fluids in the lungs
Which large organ system is not considered vital during shock and what impact does this have?
GIT - Vasoconstriction = reduced perfusion
List GIT complications associated with SIRS and what clinical signs may be seen
Hypotension, micro thombi and deregulation of rregional blood flow impact GI perfusion
Increased epithelial permeability, due to hypoperfusion, can result in bacterial translocation into the lymphatics and blood stream
Bowel oedema due to hypoalbuminaemia
Vomiting, diarrhoea, haematochezia and ileus
List clinical signs associated with SIRS
Depression
Fever (dogs) Hypothermia (cats and late stage dogs)
Red mm/Rapid CRT
Bounding pulses (dogs only)
Tachycardia (dogs) Bradycardia (cats)
Tachypnoea
V/D
Define C-reactive proteins (CRP)
Released by hepatocytes in response to tissue injury
Measured in dogs as marker for systemic inflammation
Can be used to identify improvement/deterioration
Describe the role of lactate measurements in shock patients
Expected increased lactate due to anaerobic metabolism (normal <2.5mmol/L)
Best to use as a trend rather than evaluating one-off value which is snapshot of that moment
Why are septic patients often hypoglycaemic?
Increased glucose utilisation
What are two parameters to measure which would be highly indicative of sepsis?
Low BG
Increased lactate
Why might patients with SIRS become hypoalbuminaemic?
Associated vasculitis leads to protein loss from vasculature
What may be seen regarding the leukocytes in a septic patient?
Leucocytosis or leucopaenia
What unique change may a septic cat show on bloods?
Hyperbilirubinaemia - Alongside clinically icteric
Describe/list monitoring requirements for a SIRS patient
Frequent assessment of perfusion parameters
Frequent assessment for complications i.e. petechiation, prolonged bleeding
Serial BP reading
Monitoring delivery/response to IVFT
Collecting samples for BG, electrolytes, PCV, WBC, platelets, lactate, clotting times, urinalysis
Monitor ECG for arrhythmias
Monitoring urine output - ongoing oliguria/anuria is significant
Pain scoring/monitoring - monitor response/need for analgesia
Pulse oximetry
Describe/list nursing care requirements for a SIRS patient
Maintain vascular access/delivery of IVFT
Pain assessment, administer analgesia, decreased stress/pain
Deliver medication
Nutritional management - feeding tubes
Oxygen provisions - ensure correct, not distressing
Describe/list nursing care requirements for recumbent patients
Bladder/urinary cath care
Regular turning (q2-4h) to prevent decutis ulcers
Prevention of aspiration pneumonia
oral/ocular care
Prevent of soiling - management of rectal foley systems
PROM/massage/coupage/physio
Name three things an IV catheter can be placed/used for
Infusion of fluids (inc blood products)
Sampling
Medication administration
List reasons a central venous catheter may be placed
> 5 days IVFT administration
Hypertonic medications/fluids
Multiple necessary medications
Serial sampling
total parenteral nutrition
Measuring CVP
List unique properties of catheters that make them safe for use
Most made of silicone/polyurethane
Inert so less likely to stimulate inflammatory reaction/clot formation
Flexibility useful for IV/central lines
Radiopaque
What type of catheter is best suited for large volume of fluids for a hypovolaemic patient
Short length
Wide gauge
List different types of IV catheters
Over-the-needle
Through-the-needle
Butterfly/winged
Peel-away
Over-the-wire/guide wire
What is the most commonly type of catheter used?
Over the needle
What type of catheters are often used for central lines and what makes them different?
Through the needle
Longer and wider bore
Multi-lumen option - bloods/meds/fluids
What is the main vein which central catheters are placed and what other alternative placements are there?
Jugular - Main
Medial saphenous - cats
Lateral/medial saphenous - dogs
Known as PICC line - peripherally inserted central catheter
How often should syringe drivers and infusion pumps be serviced and calibrated?
Yearly
