SHOCK

Introduction

• Septic shock mortality 40-60%
  • 30-45% within 1 month of presentation
• Cardiogenic shock mortality 36-56%
  • 60-90% within 1 month of presentation
• Definition
  • Circulatory insufficiency with resultant imbalance between tissue oxygen delivery and consumption leading to end-organ dysfunction
• Categories
  • Distributive
  • Cardiogenic
  • Hypovolaemic
  • Obstructive

Cardiac output

• HR x SV
• Dependent on:
  • Inotropy (speed and shortening capacity of myocardium)
    • Autonomic, short-lived increases in afterload (Anrep effect) or HR (Bowditch effect)
    • Acidotic milieu inhibits contractility and BP
  • Chronotropy (rate of contraction)
    • Sympathetic
  • Lusitropy (ability to relax and fill)
    • Sympathetic
  • NA increases cardiac cAMP levels to increase chronotropy and sequester calcium leading to myocardial relaxation
• Up to 40% of patients with sepsis have transient cardiomyopathy manifested by reduced contractility and increased mortality

Equations

• MAP = CO x SVR
• DO2 = CO x CaO2
  • = CO x [(1.39xHbxSaO2) + (PaO2 x 0.0031)]
  • Normal = 1000mL O2/min
• Oxygen consumption = CO x (CaO2 – CvO2)
  • = CO x Hb x 1.39 x (SaO2 – SmvO2)
  • 250mL O2/min
• Shock index = HR / SBP
  • Normal 0.5-0.7
  • Persistent elevation >1.0 indicates impaired LV function (due to blood loss or cardiac depression) and carries high mortality rate)

Lactic acid

• Lactic acid rapidly buffered to lactate
• Rises in settings of anaerobic metabolism from:
  • Inadequate oxygen delivery
  • Increased oxygen demand from sympathetic stimulation (i.e. status epilepticus)
  • Impaired oxygen utilisation (septic shock or post-resuscitation phase)
  • Correlates with short-term prognosis of critically ill patients in ED
  • Normal <2.0

Compensatory mechanisms

• Carotid baroreceptor stretch reflex activates SNS
  • Arteriolar vasoconstriction (redistribution away from skin/splanchnic/renal/skeletal muscle)
    • Subsequent cellular ATP depletion leads to ion-pump dysfunction, sodium influx, efflux of potassium and reducing in membrane resting potential
    • Leads to hyperkalaemia, hyponatraemia, azotaemia, hyper/hypoglycaemia and lactic acidosis
  • Increased HR and contractility
  • Constriction of venous capacitance vessels to increase venous return
  • Release of adrenaline, noradrenaline, dopamine, cortisol to increase arteriolar and venous tone
  • Release of ADH and activation of RAS to enhance water and sodium conservation

SIRS (no longer widespread use)

• 2 or more of the following:
  • Temp >38 or <36
  • HR >90/min
  • RR >20 or CO2 <32
  • WCC >12, <4 or >10% immature forms or band

Shock categories

Venous access

Peripheral IVC

• Phlebitis: Hypertonic solutions, potassium, phenytoin, vancomycin, antibiotics reconstituted from powder
• Infection
  • Skin infection especially common if left in >48 hours
  • Leg > arm
  • Hand > wrist/arm
  • Similar risk to IA line
  • Systemic infection in 1/2500
• Accidental arterial insertion
  • 10% of patients have superficial arteries at cub fossa
• Catheter shear
• Air embolism – Risk if catheter above heart, large catheter size or infusion under pressure

Infusion rates

Flow is proportional to 4^th power of the radius and inversely proportional to length

2 moderate sized cannulae provide more flow than one large cannula

Pressure bag increases flow by 80% (vs. 40% manual compression)

RIC line

• 17G introducer
• 16G dilator
• 8.9cm total length infusion sheath
• Can use any superficial vein with 5-7cm of usable straight length
• Femoral and subclavian not suitable as RIC too short
• Insert guidewire through any cannula already sited (20G preferred)
• Use 11 blade scalpel to make 3mm incision at wire insertion point then advance RIC and introducer together

USS-guided peripheral access

• 50% higher first-pass success rate in patients with expected difficult access
• Moderately superior in those with expected moderately difficult access
• Inferior in patients with expected easy access
• Likelihood of failing within 72 hours is inversely related to proportion of catheter in vein
  • 100% if <30% of cannula in vein
  • 30% if 30-65%
  • 0% if >65%

IO labs

• Discard first 2-6mL of marrow
• CO2 and platelet counts significantly lower than venous
• WCC significantly higher than venous
• Group and X-match possible
• Poor correlation for K, Mg, Ca, PO4 and glucose
• Flow rates
  • Humeral IO 83mL/min
  • Tibial IO 15mL/min
• Can inject up to 3mg/kg lignocaine through IO once inserted to alleviate pain

MAC line

• Multiple lumen access catheter
• Short double lumen catheter with sheath introducer
• 14F overall diameter
• 9F large lumen for rapid infusions (500mL/min under gravity alone)
• 12G line for other infusions
• May not be safe for contrast injections (while traditional CVL’s are)
• Residual defect in vein wall can cause significant haemorrhage if site not compressible e.g. subclavian
• Dilator, catheter and sheath introduced into vessel together
• Sheat introducer needs to be capped once inserted to prevent haemorrhage and air embolism

CVL

• Risk factors for complications
  • Inexperienced operatore
  • <2% if one attempt made; 7% with 2 attempts and 12% with 3 attempts
  • Previous surgery
  • BMI >30 or <20
  • Previous catheterisation
  • Children
  • Short neck
• Complications
  • Pneumothorax
    • 3% of subclavian insertions vs. 0.1% of IJ insertions
  • Arterial puncture
    • 4% subclavian, 8% IJ, 12% femoral
    • Leave in situ and get vascular consult if 7Fr or larger/6Fr or larger if anticoagulated
    • If smaller than this, remove and compress site
  • Malpositioning – 3%
  • Venous thrombosis
    • 2-3% of subclavian catheters
    • 20% of femoral catheters
  • Infection
    • 11% overall– highest if catheter moves the most (IJ, femoral)
    • 12.8% for multilumen catheters
    • 1-2% incidence of BSI
    • Decreased by chlorhex/sulphadiazine impregnation (cost-effective if >2% infection rate across institution)
  • Vascular erosions
    • Left-sided CVL responsible for 70% of SVC erosions
    • Usually within first 7 days
    • Almost always fatal. Can confirm by thoracocentesis (fluid from pleura same constituents as IV fluid being delivered), CXR and contrast study with contrast entering mediastinum)
    • Rx: Removal (does not increase bleeding) and vascular consult
  • Air embolism
    • Prevent by occluding lumen whenever open to air
• Insertion technique
  • Do not insert dilator into vein itself (it is a skin dilator)
  • Close clip on central (brown) lumen and put caps on the others
  • When wire coming up brown lumen, open clip and then when you remove the wire, put thumb over brown lumen end (never leave open to air AT ALL)
• Tip position
  • 1-2cm above carina (ensures outside pericardial reflection)
  • Tip should run parallel to SVC wall
  • Avoid atrial placement as atrial puncture is a possibility
• Biopatch disc of chlorhexidine prevents catheter-related infection

Internal Jugular

• Insert at apex of clavicular and sternal heads of SCM aiming towards ipsilateral nipple
• Insertion length in adults
  • Right side = Height/10
  • Left side = Height/10 + 4

Subclavian

• Most anatomically consistent site
• Largest diameter in shock state as traction opens
• Right-side preferred but left side easier for right-handed operators
  • Left side associated with abutment on SVC and damage to thoracic duct
• Rotate patients head 30 degrees towards side of insertion
• Insertion point 1/3 from suprasternal notch
• Start thumb breadth down and out from this and go superficially until hit clavicle then push entire needle/syringe down until get under clavicle and aim towards sternal notch
• Length of insertion
  • Right side = height/10 – 2cm
  • Left side = Height/10 +2cm

Central venous pressure

• Classically (if no cardiorespiratory disease)
  • <5cmH20 = Hypovolaemia
  • 5-12cmH20 = Normal
  • >12cH20 = Hypervolaemic

Arterial lines

• Radial art line
  • 20% transient occlusion rate
  • 15% haematoma rate
  • 0.1% permanent ischaemic injury rate
  • 0.1% sepsis rate
• US guidance
  • 85% first-time placement vs. 50%
  • Fewer placement attempts

Arterial waveform

• Slope of upstroke reflects myocardial contractility (dP/dt)
• Waveform analysis can determine
  • Systolic respiratory variability
  • MAP respiratory variability

SvO2 and O2 extraction ratio

• Normally >70% overall
• 77% in IVC due to lower O2 extraction by kidney vs. 71% in SVC
• According to tissue type
  • Heart 60%
  • Brain 33%
  • Liver 15%
  • Kidney 7.5%
  • Skeletal muscle (at rest) 5%

Blood flow to organs

• Kidney 400mL/100g tissue/min
• Heart 80
• Brain 50
• Liver 20
• Skeletal muscle 5
• Tissues with the highest blood flows are the most prone to damage in hypovolaemia

SBP and mortality

Common pitfalls

The elderly and the young

Falsely reassured by HR and BP and not measuring perfusion

Not considering adrenal crisis

Delayed initiation of vasopressors

Inadequate volume resuscitation

Not considering alternative explanations e.g. occult bleeding

Aims of treatment

• Improved tissue oxygenation is the primary goal
• Improving blood flow has increased priority if tissues with high blood flow (e.g. kidneys, heart) are diseased or more severely affected (e.g. improving perfusion is better for AKI than improving oxygenation)
• Improving oxygenation has increased priority if tissues with high oxygen extraction ratios (e.g. brain, heart) are diseased or more severely affected

Fluid challenge

• 250mL of crystalloid or passive leg raise
• If minimal rise in pressure, additional fluid boluses may continue to improve CO
• CVP rise >3cmH20 suggests right heart reaching peak of Frank-Starling curve and further fluid may worsen CO

Assessment of intravascular volume

• Palpable pulses
  • Radial = 80mmHg
  • Femoral = 70mmHg
  • Carotid = 60mmHg
• Risk of mortality following trauma increases as ED SBP drops below 110mmHg
  • Increases by 5% for every 10mmHg drop below 110
  • 25% mortality for SBP 60mmHg
• Capillary refill
  • <2sec in adult males (3-4 seconds in elderly and females)
  • Temperature dependent
  • Compress distal phalanx of middle/ring finger for 5 seconds
• Dry mucous membranes 70% sensitive for hypovolaemia
• US IVC >33% inspiratory collapse 90% sensitive and specific (best
• Orthostatic vital signs
  • Postural increase in HR >30
    • 22% sensitive for 500mL blood loss, 95% specific
    • 97% sensitive for 1000mL blood loss, 98% specific
  • Postural drop in SBP >20mmHg
    • 10% sensitive for 500mL blood loss if <65yo
    • 30% sensitive and 80% specific for moderate hypovolaemia (LR+ 1.5)
  • Also seen in autonomic neuropathy, diabetes, alcoholic state (acute or chronic), Shy-Drager syndrome, fever, vasodilation

IVC in spontaneous ventilation

• If IVC <12mm diameter, 95% specific for CVP <10 and 90% will respond to fluids
• >75% collapse with inspiration has high correlation with improved CO after fluid challenge
• If inspiratory collapse >40% (or >15% with PPV)
  • 75% will respond to fluid challenge (LR+ 5.3)
• In PPV
  • Significantly reduced inspiratory collapse and in reality often causes distension
  • Must be supine
• CVP measurement correlates poorly with fluid responsiveness
  • Particularly if cardiac or respiratory disease present
  • 75% of shocked patients with CVP <8 will respond to fluid (LR+ 2.6)

Pulse pressure variation

• In ventilated patients only!!
• If reduction in pulse pressure >10% during inspiration
  • 85% will respond to fluid bolus
• Passive leg raise
  • Increase in AUC of pulse volume >10-15% suggests fluid responsive
    • 92% of patients will respond to fluid challenge (LR+ 11)
    • Only 12% of patients without this will respond to fluid

Early treatment of shock

• ABCDE approach to shock resuscitation
  • Establishing airway
    • Often optimally controlled by intubation
    • Preload with fluids and vasoactive agents prior to PPV
  • Controlling the work of breathing
    • Crucial if significant tachypnoea exists (significant consumers of O2)
    • If mechanical ventilation utilised, match to pre-intubation rate/volume if possible
    • Consider neuromuscular blockade, especially if severely hypoxaemic

• Optimising circulation
  • Trendelenburg position does not improve cardiopulmonary performance compared to supine (may worsen gas exchange and predispose to aspiration)
  • Passive leg raise may be effective and if BP or CO improve, warrants fluid resuscitation
  • N/S 10-20mL/kg boluses with reassessment. Consider Hartmann’s if large volumes to prevent hyperCl acidosis
  • Target MAP 65-70 (possibly higher if chronic HTN)
  • Vasopressors if inadequate response to fluid resuscitation (NA, then adrenaline if inotropy required)
• Assuring adequate oxygen delivery
  • Target SpO2 >91%, consider transfusion if Hb <70 (<90 if cerebral/coronary ischaemia risk)
• Achieving end points of resuscitation
  • HR, BP, UO may underestimate defree of hypoperfusion and oxygen debt
  • Target MAP >65 (or higher if chronic HTN), CVP 8-12, ScvO2 >70% and UO >0.5mL/kg/hr
  • Source control is crucial

Colloids

• IV half-life of albumin 16 hours vs. 30-60min for N/S
• Resuscitation with colloids requires 2-4x less volume
• Crystalloids generally preferred in ED as cheaper, easier and no clear mortality benefit for colloids
  • Some trend towards benefit for albumin in sepsis
  • Worse outcomes in head injury for colloids
  • Avoid HES in sepsis. Can cause renal impairment and worsened mortality, impairs platelet function and reduced Factor VIII and vWF

Bicarbonate use

• Shifts O2-dissociation curve to the left (higher SpO2 for given PaO2 = less oxygen delivery to tissues)
• May worsen intracellular acidosis through this + release of CO2
• If pH <7.1, can consider use if acidaemia deemed to be impairing vascular tone or myocardial contractility/dysrhythmia
• Consider use in situations such as ESRD and RTA where bicarbonate cannot be reclaimed normally

Persistent shock

• Are there issues with equipment, vasopressor delivery?
• Has the patient been adequately volume resuscitated?
• Is there occult bleeding i.e. bullet hole, stab wound, ectopic pregnancy, AAA
• Does the patient have a pneumothorax after CVL/intubation?
• Does the patient have adrenal insufficiency (up to 30% prevalence)
• Is the patient allergic to the medications provided?
• Is there cardiac tamponade (esp. dialysis or cancer patient)?
• Is there an associated acute MI, aortic dissection or PE?

Fluid and blood resuscitation

• Severe haemorrhage after injury has 30-40% mortality rate
  • Responsible for 50% of deaths occurring within 24 hours of injury
• Trauma-induced coagulopathy
  • Loss of coagulation factors from haemorrhage
  • Haemodilution from crystalloid resuscitation
  • Exacerbated by acidosis and hypothermia
    • Acidosis itself only impairs coagulation directly once <7.0
  • Exacerbated by platelet consumption/dysfunction, hyperfibinolysis and clotting factor consumption
    • Related to degree of injury and haemorrhage
  • Early on characterised by anticoagulation and hyperfibrinolysis
  • Endothelial damage stimulates increase in thrombomodulin expression on endothelium that complexes with thrombin and in turn activates protein C
    • Complexed thrombin is then not available to cleave fibrinogen to fibrin
    • Subsequent consumption of plasminogen-activator inhibitor-1 by activated protein C contributes to hyperfibinolysis

Clinical features

• Classification of haemorrhage severity based on percent blood volume loss is not accurate and should not be used to guide ED resuscitation
• Bradycardia or lack of tachycardia can occur in 30% of patients with intra-abdominal haemorrhage due to increased vagal tone in setting of haemoperitoneum
• Diagnosis
  • Vital signs offer little unless significantly deranged
  • Metabolic information, MOI and appropriate imaging offer best chance of early recognition of seere haemorrhage and guiding treatment
  • Oxygen debt is the only physiological measure clearly linked to both mortality and morbidity. Clearly linked to inflammation.
  • Lactate and/or base deficit and subsequent clearance/normalisation as an endpoint is prudent and associated with improved survival
  • These are late findings however, and more sensitive indicator early on is increased oxygen consumption (low ScvO2 <60-70% – or >25% extraction)

Resuscitation

• Targets
  • Restore intravascular volume
  • Maintain oxygen-carrying capacity
  • Limit ongoing blood loss
  • Prevent develop of coagulopathy
  • Prevent and treat hypothermia aggressively

Haemostatic hypotensive resuscitation

• In traumatic shock, goal is deliberate hypotensive resuscitation to limit intravascular expansion and blood pressure
• Goals are SBP 80-90mmHg (90-95 in head injury)
  • 110 if <50 or >69 and 100mmHg if 50-69 once haemorrhage controlled for head injury
• Aim is to limit bleeding until immediately prior to operative intervention to control bleeding site
• Fluid resuscitation thus indicated if SBP <70-80mmHg and/or evidence of reduced cerebral perfusion
  • Improved early and 30-day survival in civilian setting
• Problematic in those with cerebral or coronary ischaemia risk, baseline hypertension and traumatic brain injury

Hypotensive resuscitation

• Distinguishing ‘controlled’ from ‘uncontrolled’ haemorrhage
  • Penetrating usually uncontrolled vs. blunt may be either
  • Normal haemostatic mechanisms suggest controlled
  • If response to resuscitation is maintained – suggests controlled
  • If no response or ongoing deterioration – suggests uncontrolled
• Standard treatment for:
  • Ruptured AAA
  • Aortic dissection
  • Penetrating trauma
  • Epistaxis
• Role unclear for
  • Non-penetrating thoracic trauma, GI haemorrhage, ectopic and PPH

Hypotensive resuscitation

• Contraindications
  • Blast injuries (increased mortality in animal studies)
  • Controlled haemorrhage
  • Evidence of serious end-organ hypoperfusion
    • Neurotrauma
    • Renal impairment
    • Myocardial ischaemia

Crystalloids

• Large volumes of N/S or lactated Ringer’s/Hartmann’s can cause neutrophil activation
• Lactated Ringer’s/Hartmann’s can increase cytokine release and may increase lactic acidosis
• N/S can exacerbate intracellular potassium depletion and cause hyperchloraemic acidosis
• 30% of infused fluid remains in intravacular compartment at best
• No more than 2L should be administered before giving blood products, especially if ongoing haemorrhage is expected
• Optimally, blood product only resuscitation is preferred
• Ringers Lactate/Hartmann’s can buffer acidosis (lactate can take on H+ ion to form lactic acid and thus is not adding metabolic acid to body system)

Colloids

• No proven benefits
• Albumin showed trend towards improved outcome in sepsis
• Worse outcomes in traumatic brain injury
• Theoretically remain in intravascular compartment for longer, but capillary permeability in severe illness limits this
• More costly and higher risk of allergic reaction

Hypertonic solutions

• No clinically significant benefit seen in RCT’s when hypertonic saline compared to N/S

PRBC

• If haemorrhage definitely controlled, do not transfuse if Hb >100
• Consensus recommendations are for transfusion <60-70 for those without cardiopulmonary, cerebral or peripheral vascular disease
• For Hb 60-100, use clinical judgement
• Lower thresholds if ongoing haemorrhage
• Can be stored for 45 days
• Lose deformability, limiting their ability to pass through capillary beds and potentially causing capillary plugging
• Lose 2,3-DPG, shifting O2-dissociation curve to the left (reduced tissue oxygen offloading)
• No harms shown in outcomes from older PRBC vs. new

FFP

• Contains all the coagulation factors of whole blood
• Can be stored for 1 year
• Takes 15-20 minutes to thaw
• Can be kept thawed for up to 5 days
• ABO compatibility is required, but because there are no red cells, Rh compatibility is not important
• Universal donor is AB+ (as lack antibodies to ABO and rhesus antigens)

Platelets

• 6 units of pooled random-donor platelet concentrate (or one apheresis donation) should raise platelet count by 50

Massive transfusion protocols

• Definition: Requirement for >10U PRBC within first 24 hours of injury
• Variable predictive of MTP requirement:
  • Penetrating mechanism of injury
  • Positive FAST
  • BP <90; HR >120
  • If haemorrhage is evident and haemostasis not immediately achievable, switch from crystalloid to plasma-based MTP immediately
• 3-5% of civilian trauma patients receive MTP
• Higher ratios approaching PRBC:FFP 1:1 have shown improved survival in combat and civilian settings and reduced incidence of trauma-induced coagulopathy
  • Seems to provide survival benefit independent of coagulopathy (may improve endothelial function and repair vascular permeability)
• Many centres also include early platelet supplementation in MTP as declined function/consumption occurs early
• The precise best ratio of PRBC:FFP:Platelets is controversial
• Benefits of adjuncts (calcium, cryoprecipitate, fibrinogen concentrate, desmopressin and prothrombin concentrates) are not known

Tranexamic acid

• 1g IV in 100mL N/S if within first 3 hours then 1g over 8 hours
• CRASH 2 study
  • 1.5% improvement in mortality with unselected use in trauma
  • Subgroup analysis suggested worse mortality if given >3 hours after trauma
• Meta-analysis
  • 10% loss of benefit for every 15 minute delay in administration
  • Beneficial role most evidence-based in PPH and TEG-based hyperfibrinolysis

Calcium

• PRBC and FFP contain citrate leading to hypocalcaemia through chelation
• Target iCa > 0.9 (Tintinalli); >1.3 elsewhere
• Calcium chloride is preferred as a well-perfused liver is required to release calcium from calcium gluconate

Thromboelastography (TEG) and thromboelastometry (ROTEM)

• Take into account cellular and non-cellular pathways
• Can be used to guide treatment of trauma-induced coagulopathy
• Impact on clinical case is uncertain at this time

Component-based targets

Non-product adjuncts

• Tranexamic acid
• Heparin reversal
  • Protamine 1mg IV /100 IU Heparin
• Warfarin reversal
  • 10mg IV vitamin K; consider prothrombin complex concentrate
• NOAC reversal
  • Specific agent OR prothrombin complex concentrate
• Desmopressin
  • 0.3mcg/kg IV
  • Releases Factor VIII and vWF from platelets
  • Indicated in renal failure, Haemophilia A and vWillebrand disease

Cardiogenic shock

• Leading cause of in-hospital death in acute MI
• 4-8% of STEMI patients
• 2.5% of NSTEMI
• 10% of AMI patients overall develop cardiogenic shock in the ED with median time to onset of 6 hours
• ¼ of cardiogenic shock cases present in shock, ¼ within 6 hours and ¼ later on first day
• 50% mortality (half in first 48 hours)
• Early recognition of cardiogenic shock or ongoing ischaemia are key
• Prompt and successful revascularisation is the cornerstone of therapy

• Definition:
  • Persistent SBP <90
  • CI <2.2L/min/m2 and 
  • Elevated filling pressure (PCWP >18)
• Pathophysiology
  • Pump failure
  • Diastolic BP also drops (absent a rise in SVR) resulting in reduced coronary artery perfusion and vicious cycle
  • It is the diastolic dysfunction that occurs early and seems to be the dominant mechanism behind cardiogenic shock
  • Lactic acidosis from poor tissue perfusion contributes to vicious cycle
  • pH <7.25 inhibits response to endogenous and exogenous catecholamines
  • LV failure constitutes 80% with remainder acute severe MR, ventricular septal rupture, predominant RV failure, free wall rupture and tamponade

• Risk factors
  • Elderly
  • Female
  • Acute or prior ischaemic event associated with:
    • Impaired EF
    • Extensive infarct
    • Proximal LAD occlusion
    • Anterior MI (>50%)
    • Multivessels CAD
  • Prior MI
  • Congestive heart failure
  • Diabetes
  • Shock associated with first MI should prompt search for mechanical cause
  • Reinfarction soon after MI
  • 2/3 have flow-limiting stenosis in all 3 major coronary arteries
  • 20% have left main stenosis

Clinical assessment

• If apex beat is in normal position, likely acute shock vs. CHF
• 10% of cardiogenic shock in AMI is due to mechanical complications
  • New murmur may be the only physical finding
  • Acute MR
    • Chordae tendinae rupture or papillary muscle failure
    • Soft holosystolic murmur at apex
    • With papillary muscle dysfunction, murmur starts after S1 and finishes before S2
  • Acute ventral septal defect
    • New loud holosystolic murmur at left parasternum, often with palpable thrill
  • Acute aortic insufficiency
    • Soft diastolic murmur and soft S1

• Shock secondary to RV infarction
  • IV fluids to optimise RA pressure (10-15)
  • Avoidance of excess fluids (as shifts interventricular septum into LV)
  • Vasopressors
  • Intra-aortic balloon pump
  • Reestablishment of infarct-artery flow
• Mitral regurgitation
  • Most often on first day, with second peak several days later
  • Intra-aortic balloon pump is ideal with dobutamine to raise cardiac output
  • Reducing afterload reduces the volume of regurgitant flow
  • Early mitral valve surgery
• Ventricular septal rupture
  • Similar to MR management with IABP and early surgery for viable candidates
• Free wall rupture
  • Most likely in first week
  • Frequent increases with age, first infarction, history of HTN, no history of angina and large Q-wave infarct
  • Typically sudden loss of pulse, BP and consciousness by sinus rhythm on eCG (PEA)
  • Cardiac tamponade ensues and CPR is ineffective
  • Urgent pericardiocentesis with surgical repair is curative but most cases die immeidiately

• Treatment
  • I&V often required but reduces preload and may lead to catastrophic deterioration. Be prepared
  • Correct any hypoxaemia, hypovolaemia, rhythm disturbances, electrolytes and acid-base disturbance
  • Aspirin early
  • Relieve chest pain with nitrates/morphine if SBP >90
  • Crystalloid boluses for hypotension 250-500mL if suspected RV infarct with hypotension
  • Inotropes
    • Do not change outcome but temporise while awaiting revascularisation or repair of mechanical disruption
    • Dobutamine preferred if not profoundly hypotensive
      • Can cause vasodilation so avoid use alone if SBP <90
    • Dopamine may increased cardiac work by increased HR
      • May be combined with dobutamine for more effective therapy
    • Noradrenaline
      • Preferred if SBP <70
      • Can be combined with dobutamine as more potent vasoconstrictor
    • Adrenaline
      • Alternative to NA/dobutamine but associated with tachycardia, dysrhythmias and systemic acidosis
    • Dobutamine 2-5mcg/kg/min up to 20
      • Inotrope and potent vasodilator
    • Dopamine 3-5mcg/kg/min up to 20-50
      • Inotrope and vasoconstrictor
    • Noradrenaline 2mcg/min titrated to 30 as required
      • Vasoconstrictor and inotrope
      • Preferred as single agent over dobutamine if SBP <70
    • Adrenaline 0.1-0.5mcg/kg/min
      • Inotrope and vasoconstrictor; Second-tier due to dysrhythmias and acidosis
    • Milrinone 0.5mcg/kg/min
      • Inotrope and vasodilator. Second-tier to dobutamine

• Mechanical assist devies
  • Intra-aortic balloon pump
    • Improves diastolic perfusion pressure and unloads the LV, improves coronary perfusion, increases diastolic flow (double wave form pulse), decreases afterload, decreases degree of mitral regurgitation
    • Proven benefit if under 50 and going for PCI/CABG
    • Improves survival after thrombolytic therapy
    • Outside of those receiving reperfusion therapy, benefit is not clear
    • Resolution of instability has positive prognostic value
    • Inflation immediately after T wave at start of diastole then deflation at beginning of systole just before QRS
    • CI: Severe AR, aortic disease, sepsis, irreversible disease
    • Augments CO by 20-40% at most
    • Complications: Limb ischaemia, haemorrhage, infection, thrombocytopaenia, aortic rupture, spinal ischaemia, thromboembolism, gas embolism, anticoagulation complications
  • Cardiac impeller
    • Impeller catheter inserted intra-arterially through AV into LV
    • Blood is drawn into device at apex and ejected into aorta
    • Maximum cardiac output 2.5-5L/min
  • VAD
    • Approved for bridge to cardiac transplant
    • No mortality benefit vs. intra-aortic balloon pumps in patient with refractory cardiogenic shock
    • Can support LV/RV or both
    • Continuous flow LVAD’s reduce preload
    • Cardiac output is very preload dependent and afterload sensitive
    • Pulse pressure 5-15mmHg
    • Complications
      • Arrhythmias
      • Thromboembolism
      • Haemorrhage (40%)
        • Mostly in first month after insertion
      • Infection
        • 40% of patients within 1 year
        • Gram-positives mostly (S. epidermidis, S. aureus)
      • Stroke
        • 25% of patients suffer cerebrovascular event
        • MAP <85 and INR 2-3 help reduce this risk
        • Right cerebral hemisphere much more common
      • Device failure
    • Pump thrombus – Low CO with falsely elevated pump flow measures
    • Suction events
      • Large negative pressures in left heart
      • Can cause catheter collapse and marked leftward displacement of the IV septum
      • Caused by RV failure, hypovolaemia, tamponade, arrhythmias and inflow cannula malposition
      • Results in low CO, MAP, low VAD flow
    • Cannula malposition

• VAD assessment
  • NIV BP impossible and no pulses
  • MAP is indicative of perfusion
    Measure HR by ECG
  • NIV BP with doppler defines MAP
  • Invasive arterial line requires USS-guidance
  • Pulse oximetry unobtainable
  • Pump speed usually 2200-2800/min (HVAD) or 8000-10 000 (HeartMate II)
    • Suction events reduce speed
  • Pump power usually 4-6 watts

• VAD Management
  • Early referral to service
  • Treat MAP >85 aggressively
  • Treat haemorrhage as per usual
  • Broad-spectrum bacterial and anti-fungal cover if infection suspected
  • Management of AF is the same
  • Ventricular arrhythmias
    • May be well tolerated with VAD in place
    • Amiodarone is first-line
    • Electrical cardioversion often required
  • Suction events
    • Fluid load

ECMO

• Indications in the ED
  • Severe poisoning
  • Myocarditis
  • Refractory VF/VT
  • PE
• Less likely of benefit if
  • Increasing age, myocardial ischaemia, chronic cardiomyopathy, renal disease, smoker

Cardiogenic shock

Last Updated on November 5, 2021 by Andrew Crofton