SHOCK
ERIN MOONEY, BVSC DACVECC7TH MAY, 2014
shock is common, but under-recognised
• early recognition is important to prevent progression of the shock state• dramatic impact on survival
SHOCK
• Inadequate cellular energy production • oxygen or glucose
• Usually due to inadequate oxygen delivery (DO2)• cardiovascular dysfunction
ENERGY PRODUCTION
glycolysis
tricarboxylic acid cycle
oxidative phosphorylation
anaerobic metabolism yields 2 moles ATP
aerobic metabolismyields 36 moles ATP
WHAT’S BAD ABOUT SHOCK?• Preferential shunting of blood away from splanchnic
circulation, skin and muscle• GI translocation sepsis
• Sluggish blood flow through capillary beds• renal• cerebral• myocardial
• Further anaerobic metabolism• cellular energy deficit MOF
OXYGEN DELIVERY (DO2)DO2 = CO x CaO2
HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
EDV - ESV
venous return and diastolic function systolic function and SVR
blood volume and SVR
TYPES OF SHOCK
• Hypovolaemic• Maldistributive• Cardiogenic • Obstructive• Metabolic • Hypoxic
HYPOVOLAEMIC SHOCK
blood volume is too low to maintain DO2
DO2 = CO x CaO2
HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
EDV - ESV
venous return and diastolic function systolic function and SVR
blood volume and SVR
CAUSES OF HYPOVOLAEMIC SHOCK• Haemorrhage
• disruption of vessels• trauma• neoplasia
• coagulopathy
• Severe dehydration leading to hypovolaemia • prolonged v/d• massive polyuria• burns• third spacing• inadequate access to water
DEHYDRATION ≠ HYPOVOLAEMIA
• Dehydration is a decrease in extracellular fluid volume, i.e- the interstitial and intravascular spaces
• Because blood volume is spared at the expense of interstitial volume, “hydration” generally refers the interstitial fluid volume
• Dehydrated patients may or may not be hypovolaemic
• Hypovolaemic patients may or may not be dehydrated
HYDRATION
• MM moistness
• Skin turgor
• Globe position
VOLUME
• Heart rate
• MM colour, CRT
• Pulse quality
• Temperature
PCV/TS AND HAEMORRHAGE
Hypovolaemia Euvolaemia
Acute bleeding
PCV: 50TS: 60
PCV: 25TS: 30
Improving hypovolaemia
PCV: 40TS: 45
Normal patient: PCV/TS 50/60
MALDISTRIBUTIVE SHOCK
• Maldistribution is a loss of vascular tone (SVR)
• Leads to sluggish blood flow and DO2, particularly in capillaries, and decreased venous return, with knock-on effects for cardiac output
DO2 = CO x CaO2
HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
EDV - ESV
venous return and diastolic function systolic function and SVR
blood volume and SVR
• Sepsis• abdominal sepsis• urosepsis – pyelonephritis/lower urinary tract infection• pneumonia• pyometra• pyothorax• deep pyoderma• hepatic/pancreatic abscess
• SIRS• pancreatitis• polytrauma• burns• major surgery
• Anaphylaxis
• Addisonian Crisis
SEPSISThe pathogenesis of maldistributive shock in sepsis is multi-factorial:• increased production of nitric oxide• over-activation of K+/ATP channels• deficiency of vasopressin• critical illness-related corticosteroid insufficiency
CARDIOGENIC SHOCK
Shock related to failure of the pump mechanism of the heart• failure to fill during diastole• failure to eject adequate stroke volume during systole
CHF adds hypoxia to the mix
DO2 = CO x CaO2
HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
EDV - ESV
venous return and diastolic function systolic function and SVR
blood volume and SVR
CAUSES OF CARDIOGENIC SHOCK• Diastolic failure
• HCM• severe mitral insufficiency• pericardial effusion
• Systolic failure• DCM• sepsis-induced myocardial dysfunction
• Tachyarrhythmias• Bradyarrhythmias
both
OBSTRUCTIVE SHOCK
• Physical obstruction to arterial or venous blood flow
• Examples:• GDV• PTE• heartworm disease• +/- pericardial effusion
METABOLIC SHOCK• Deranged intracellular metabolic activity
• DO2 is normal
• Examples:• hypoglycaemia• toxicities that cause uncoupling of ox phos:
• cyanide• arsenic• 1080• bromethalin
• mitochondrial dysfunction in sepsis and SIRS
HYPOXIC SHOCK
• Decrease in arterial blood oxygen content• i.e- not related to blood flow
• Examples:• severe anaemia (PCV < 10%)• CO toxicity• methaemoglobinaemia• severe pulmonary disease
IDENTIFYING SHOCK
Mixture of history, physical exam and laboratory evidence
Physical exam is your most important tool
IDENTIFYING SHOCKPerfusion parameters:• MM colour*• CRT• HR• pulse quality• temperature (particularly of extremities)• mentation• urine output• blood pressure
* may be injected with maldistribution
LABORATORY EVIDENCE OF SHOCKLess fancy:• metabolic acidosis
• decreased SBE• decreased HCO3• +/- acidaemia (depends on compensation)
• hyperlactataemia• pre-renal azotaemia• oliguria/anuria• estimate volume status and CO via echocardiography
LACTATE• Produced from pyruvate, a waste product of glycolysis
• During anaerobic metabolism, there is increased production of pyruvate increased lactate production
• The most common cause of hyperlactataemia is anaerobic metabolism during shock (“Type A hyperlactataemia”)
• Production also increases with SIRS/sepsis, administration of steroids and some types of neoplasia (“Type B hyperlactataemia”)
LABORATORY EVIDENCE OF SHOCKFancy:• direct CO monitoring via PAC (gold standard)• mixed venous oxygen via PAC• combined CVP and direct BP• central venous oxygen via CVC
CLASSIFYING SHOCK
compensated shock
early, decompensated shock
late, decompensated shock
COMPENSATED SHOCK
• Catecholamine surge to maintain perfusion/DO2 causes tachycardia and vasoconstriction
• Can be hard to identify; tachycardia in a patient that’s not boisterous or stressed
• HR 130 - 160• tall, narrow pulses
• pink/pale pink MM (+/- “injected” in sepsis/SIRS) • CRT 0.5 – 1.5 sec• normal body temperature (+/- elevated in sepsis/SIRS)• extremities may be cool• quiet mentation• normal BP • normal UOP• normal mild hyperlactataemia
Hypovolaemia
Sepsis
EARLY DECOMPENSATED SHOCK
Compensatory mechanisms become overwhelmed and DO2 starts to fall
• HR 160 – 200• reduced femoral pulse quality, absent metatarsal pulses
• pale pink MM (+/- injected in SIRS/sepsis)• CRT (1.5 – 2 sec)• mild hypothermia with cool extremities• quiet mentation• mild moderate hypotension• decreased UOP• mild moderate hyperlactataemia
LATE DECOMPENSATED SHOCK• During this phase, DO2 is inadequate to maintain organ
function.
• Death is imminent
• HR >200• ** bradycardia may develop shortly before death.• weak to absent femoral pulses
• grey/patchy MM• CRT > 2 sec or undetectable• hypothermia and cold extremities• obtundation• severe hypotension• decreased absent urine output• severe hyperlactataemia
CATS ARE NOT SMALL DOGS• Cats tend to become bradycardic and hypothermic earlier
in shock, particularly in sepsis
• A sick bradycardic cat is a very sick cat indeed
TREATING SHOCKDO2 = CO x CaO2
HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
EDV - ESV
venous return and diastolic function systolic function and SVR
blood volume and SVR
FLUID THERAPY IN SHOCK• Fluid “resusc” is usually performed with isotonic
crystalloids
• Shock dose:• 90ml/kg in dogs • 60ml/kg cats
• How do we give it?• Fast!
respective blood volumes
• Administer ¼ shock dose over 10 – 15 min then re-assess your patient.
• If your goals of resusc have not been met, keep going
• Goals of resusc:• HR 80 – 120• pink MM, CRT 1 – 2 s• normal pulse quality• warm extremities, normothermia• normal mentation• SBP 100 – 140• normal UOP
FAST?
http://www.impactednurse.com/pics5/notstatH.jpg
OTHER FLUID TYPES• Hypertonic saline (7%)
• hypertonic crystalloid• dose: 3 – 5ml/kg once
• Artificial colloids• use in shock is controversial• renal failure, coagulopathies
• NEVER bolus hypotonic fluids• 0.45% saline• 0.45% saline + 2.5% glucose• 5% glucose in water• plasmalyte-56• normosol-M
I’VE GIVEN SHOCK FLUIDS … NOW WHAT?• In cases of uncomplicated hypovolaemia, your work is
done
• In most cases, shock will continue unless you address the the underlying cause, because only 25% of your crystalloids will still be in IV space 30 min after infusion
• Must diagnose and address the underlying cause ASAP
• Sepsis• volume first• vasopressors if needed, once resusc• treat the septic focus
• Active haemorrhage• need to stop the haemorrhage• large amounts of fluids can exacerbate bleeding
• patients may benefit from a low-volume resusc strategy until haemostasis can be achieved
• blood products early
• GDV• hypovolaemia plays a role• need to also relieve the obstruction
• Concurrent shock and head trauma• treat the CV system first!
• essential for adequate cerebral DO2• once perfusion is restored, administer hyperosmolar
agents
OTHER TYPES OF SHOCK• Cardiogenic shock
• NO FLUIDS• pulmonary oedema
• oxygen, furosemide• nitroprusside
• pleural effusion• thoracocentesis
• dobutamine/pimobendan for systolic failure• anti-arrhythmics for tachycardias• pacemaker for bradycardias• pericardial effusion
• pericardiocentesis STAT!
• Severe anaemia• red cells!
• usually pRBC
STEROIDS IN SHOCK
Don’t use them
…except in anaphylaxis and addisonian crisis
IN SUMMARY…
• Shock is common! Particularly after trauma
• Treating shock is relatively straight-forward
• Treating shock is a life-saving move!
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