SASH : Shock by Dr Erin Mooney

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


EDV - ESV



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


EDV - ESV



• 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


EDV - ESV



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


EDV - ESV



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!

SASH : Shock by Dr Erin Mooney

Health & Medicine

Transcript of SASH : Shock by Dr Erin Mooney