SHOCKSHOCKPhil Ukrainetz, MD, PGY5Phil Ukrainetz, MD, PGY5

Jeff Plant, MD, FRCPCJeff Plant, MD, FRCPCCore Rounds, August 9, 2002Core Rounds, August 9, 2002

Shock talk outlineShock talk outline

In the trenches approachIn the trenches approach What’s the evidenceWhat’s the evidence What is on the horizonWhat is on the horizon

Shock definitionShock definition

A condition of the circulatory system A condition of the circulatory system whereby there is inadequate tissue whereby there is inadequate tissue nourishment and removal of toxic nourishment and removal of toxic

metabolitesmetabolites

Better shock definitionBetter shock definition

Inadequate blood flow secondary to Inadequate blood flow secondary to decreased cardiac output or mal-decreased cardiac output or mal-distributed output that results in distributed output that results in

irreversible tissue damageirreversible tissue damage

Why is my sphincter tone so Why is my sphincter tone so high?high?

Shock is the transition between life and Shock is the transition between life and deathdeath

Cornerstone of emergency medicineCornerstone of emergency medicine You need to know it coldYou need to know it cold

Shock:assert yourself and know Shock:assert yourself and know your teamyour team

Preparation:Preparation: Who’s the bossWho’s the boss Know names of staffKnow names of staff Assign tasks including reinforcing that you Assign tasks including reinforcing that you

are running the code (AKA: shut-up or are running the code (AKA: shut-up or leave)leave)

Shock: the set upShock: the set up

T: TriageT: Triage V: Vitals including C/S and O2 satV: Vitals including C/S and O2 sat M: Pulse-ox, ACF IV x 2, cardiac monitor, M: Pulse-ox, ACF IV x 2, cardiac monitor,

O2 NRBO2 NRB

Your role as code leaderYour role as code leader

Your position is at the foot of the bed with Your position is at the foot of the bed with your hand on the pts femoral artery and your your hand on the pts femoral artery and your eyes on the monitoreyes on the monitor

Do not get roped into proceduresDo not get roped into procedures Direct specific people for specific tasksDirect specific people for specific tasks Close the loop - “Please intubate the patient Close the loop - “Please intubate the patient

and let me know when it is done” - then and let me know when it is done” - then check that tasks have been completed.check that tasks have been completed.

Shock: it is as simple as ABC’sShock: it is as simple as ABC’s

C: quick look because early defibrillation C: quick look because early defibrillation makes such a differencemakes such a difference

A: if they will take a tube give it (have sux A: if they will take a tube give it (have sux on hand), confirm tubeon hand), confirm tube

B: adequate vent and oxB: adequate vent and ox C: fluids then pressorsC: fluids then pressors S: sugar and tempS: sugar and temp

Shock: you want a directed Shock: you want a directed historyhistory

Do not wait for the info - ask these questions:Do not wait for the info - ask these questions: A: AllergiesA: Allergies M: Medications - cardiac CCB/BB/DigM: Medications - cardiac CCB/BB/Dig P: PMHX - surgery?P: PMHX - surgery? L: Last meal - who cares but it makes L: Last meal - who cares but it makes

AMPLE a wordAMPLE a word E: Events leading upE: Events leading up

Shock: how do I know they are in Shock: how do I know they are in shock?shock?

Confirm shockConfirm shock Encephalopathic - MAP of 50 before decr Encephalopathic - MAP of 50 before decr

CBF - do not rely ALOC to diagnose shockCBF - do not rely ALOC to diagnose shock HypotenseHypotense TachypneaTachypnea Oliguria - sensitive at < 0.5cc/kg/hrOliguria - sensitive at < 0.5cc/kg/hr Cold skinCold skin

Shock:how do I diagnose the Shock:how do I diagnose the etiologyetiology

Head to toe etiologic clues:Head to toe etiologic clues: Head: pupils, neck stiffness, JVDHead: pupils, neck stiffness, JVD Chest: muffled HS, S3, murmur, cracklesChest: muffled HS, S3, murmur, crackles Abdo: peritonitis, tenseAbdo: peritonitis, tense Skin: warm, cold, purpura fulminansSkin: warm, cold, purpura fulminans

Shock:how should I remember it?Shock:how should I remember it?

S: Sepsis/distributive - warm skin?S: Sepsis/distributive - warm skin? H: Hypovolemic - hemorrhage/third spaceH: Hypovolemic - hemorrhage/third space O: ObstructiveO: Obstructive C: Cardiogenic - pump, rhythm, valveC: Cardiogenic - pump, rhythm, valve K: Anaphylactic - red, laryngospasm or K: Anaphylactic - red, laryngospasm or

wheeze?wheeze?

Shock: when can I call the codeShock: when can I call the code

Have I done everything?Have I done everything? Confirm ABC’s Confirm ABC’s ACLS and fluid / pressor resuscitation)ACLS and fluid / pressor resuscitation)

When can I call a code? - When can I call a code? - confirm 5 H’s and their treatmentconfirm 5 H’s and their treatment

H: HypovolemicH: Hypovolemic H: HypoxiaH: Hypoxia H: H+ ions/acidosisH: H+ ions/acidosis H: HyperkalemiaH: Hyperkalemia H: HypothemiaH: Hypothemia

Fluids and pressorsFluids and pressors Tube / ox / ventTube / ox / vent HCO3 crapolaHCO3 crapola Get I stat K+ Get I stat K+

Peaked T’s, sine Peaked T’s, sine wave?wave?

Rectal tempRectal temp

When can I call a code? - When can I call a code? - confirm 5 T’s and their treatmentconfirm 5 T’s and their treatment

T: TabletsT: Tablets T: Tension ptxT: Tension ptx T: TamponadeT: Tamponade T: Thrombo T: Thrombo

coronarycoronary T: Thrombo pulmoT: Thrombo pulmo

Digibind, glucagonDigibind, glucagon Needle, tubeNeedle, tube PericardiocentesisPericardiocentesis PTCA, lysePTCA, lyse TPA 100mg?TPA 100mg?

Remember shock is a spectrum - Remember shock is a spectrum - recognize its early symptomsrecognize its early symptoms

ConfusedConfused TachypneaTachypnea Pulse pressure Pulse pressure

changechange OliguriaOliguria Anion gapAnion gap CoagulopathyCoagulopathy

ComaComa ARDSARDS HypotensionHypotension AnuriaAnuria Metabo;ic acidosisMetabo;ic acidosis DICDIC

Shock classifications: how to Shock classifications: how to rally in an examrally in an exam

Simplest: vasogenic, cardiogenic, Simplest: vasogenic, cardiogenic, hypovolemichypovolemic

Quantitative vs qualitativeQuantitative vs qualitative SHOCK mnemonicSHOCK mnemonic It doesn’t matter how you do it just be It doesn’t matter how you do it just be

comprehensive and be able to rattle it offcomprehensive and be able to rattle it off

Shock classifications: how to Shock classifications: how to rally in an examrally in an exam

Pre - heartPre - heart– hypovolemia, venous poolinghypovolemia, venous pooling

HeartHeart– contractility, arrythmias, mech obstructioncontractility, arrythmias, mech obstruction

Post - heartPost - heart– loss of vascular tone, inability to deliver to loss of vascular tone, inability to deliver to

tissues, inability of tissues to utilizetissues, inability of tissues to utilize

Quantitative shock: circulatory Quantitative shock: circulatory defectdefect

Quantitative: large area of decreased tissue Quantitative: large area of decreased tissue perfusion secondary to a circulatory defectperfusion secondary to a circulatory defect

Vasogenic, hypovolemic and cardiogenic in Vasogenic, hypovolemic and cardiogenic in originorigin

Compensate with hyperdynamic state; HR, Compensate with hyperdynamic state; HR, CO increased and clamp downCO increased and clamp down

Correct the circulatory defectCorrect the circulatory defect

Qualitative shock: altered milieauQualitative shock: altered milieau

Affects the metabolic milieau from the get-Affects the metabolic milieau from the get-gogo

Sepsis, hemoglobinopathies, crush, heat, cell Sepsis, hemoglobinopathies, crush, heat, cell poisonspoisons

Do not necessarily have a compensatory Do not necessarily have a compensatory periodperiod

Identify the toxin and customize Identify the toxin and customize management management

Shock unifying features:Shock unifying features:

Disrupted cellular homeostasisDisrupted cellular homeostasis Think failed anaerobic metabolismThink failed anaerobic metabolism AcidosisAcidosis Calcium influx, SR pukesCalcium influx, SR pukes Failed ion gradients and cellular pumpsFailed ion gradients and cellular pumps Cell edema and deathCell edema and death

Some other $25 cent words to Some other $25 cent words to throw aroundthrow around

Membrane lipid peroxidationMembrane lipid peroxidation Free radicalsFree radicals Nitric oxide damageNitric oxide damage Enzymatic denaturationEnzymatic denaturation ““Inflammatory mediators”Inflammatory mediators”

How does our body compensate?How does our body compensate?

Counter-regulatory mediatorsCounter-regulatory mediators Catecholamines, glucocorticoids, Catecholamines, glucocorticoids,

angiotensin, vasopressin, insulinangiotensin, vasopressin, insulin Increased substrates: glucose, TG and FFAIncreased substrates: glucose, TG and FFA Anaerobic metabolism: incr CO2:02 ratioAnaerobic metabolism: incr CO2:02 ratio

Oxygen metabolismOxygen metabolism

Shock is a state of oxidative Shock is a state of oxidative phosphorylative failurephosphorylative failure

Loss of autoregulationLoss of autoregulation Inability to match demandInability to match demand Paralyze paradoxers: 50-100% increase in Paralyze paradoxers: 50-100% increase in

02 demands, 50% decrease in CBF02 demands, 50% decrease in CBF DELIVER 02!!!!!!!!!!!!!DELIVER 02!!!!!!!!!!!!!

Hemorrhagic shockHemorrhagic shock

CaseCase

50 year old male MVA victim, HR is 120, 50 year old male MVA victim, HR is 120, BP is 100/75, RR is 20 complaining of BP is 100/75, RR is 20 complaining of abdominal and chest pain. What is the abdominal and chest pain. What is the likely blood loss?likely blood loss?

What is the utility of the What is the utility of the Hemorrhagic Shock Classification?Hemorrhagic Shock Classification?

Class I Class II Class III Class IV

Volume <750ml 750 – 1500 1500-2000 > 2000

% < 15% 15-30% 30-40% > 40%

HR < 100 100 - 120 120 – 140 > 140

PP N or incrd decreased decreased decreased

BP normal normal decreased decreased

LOC anxious anxious confused lethargic

Classification utilityClassification utility

It makes you consider the signs of shockIt makes you consider the signs of shock It makes you aware that you can have It makes you aware that you can have

significant blood loss with very little signs significant blood loss with very little signs or symptomsor symptoms

It tells you that patients become It tells you that patients become hypotensive late so don’t waithypotensive late so don’t wait

Compensatory mechanisms for Compensatory mechanisms for blood lossblood loss

Cardiac: increase rate to 150 then Cardiac: increase rate to 150 then diminished returnsdiminished returns

Resistance: catecholamines increase Resistance: catecholamines increase diastolic pressure, narrowed pulse pressurediastolic pressure, narrowed pulse pressure

Capacitance: shunt from catechol receptor Capacitance: shunt from catechol receptor rich gut and skin, decreased renal function rich gut and skin, decreased renal function means increased vascular columemeans increased vascular colume

CaseCase

14 year old male MVA victim, weighing 50 14 year old male MVA victim, weighing 50 kg has a fractured femur, seat belt sign and kg has a fractured femur, seat belt sign and a GCS of 14. The accident happened right a GCS of 14. The accident happened right outside ACH only minutes ago. His heart outside ACH only minutes ago. His heart rate is 95, BP is 95/65, RR is 20. Do these rate is 95, BP is 95/65, RR is 20. Do these vitals make you sweat?vitals make you sweat?

Supine vitals sensitivitySupine vitals sensitivity

I would sweat, supine vitals are:I would sweat, supine vitals are: Not very sensitiveNot very sensitive 15% loss has no change in vitals15% loss has no change in vitals 30% loss before hypotense30% loss before hypotense Act early and aggressively - especially in Act early and aggressively - especially in

kids. They crump late and fast.kids. They crump late and fast.

CaseCase

Nurse comes to you saying “The girl Nurse comes to you saying “The girl involved in the slow speed (5km/hr) rear involved in the slow speed (5km/hr) rear end MVC, the one who is complaining of end MVC, the one who is complaining of abdominal pain has an orthostatic increase abdominal pain has an orthostatic increase of 20 BPM”. Is this useful information? of 20 BPM”. Is this useful information?

Orthostatic vitalsOrthostatic vitals Consider the context, however in the absence of Consider the context, however in the absence of

concerning trauma they are not sensitiveconcerning trauma they are not sensitive Normal euvolemic patients average an orthostatic Normal euvolemic patients average an orthostatic

increase of 15 BPM, therefore an orthostatic increase of 15 BPM, therefore an orthostatic increase of 20 BPM is not helpfulincrease of 20 BPM is not helpful

A meaningful orthostatic increase is 30 BPM and A meaningful orthostatic increase is 30 BPM and this requires a 20% loss of blood volume. this requires a 20% loss of blood volume.

Hemorrhagic shock managementHemorrhagic shock management

ManagementManagement– ABCs, vascular access, crystalloid bolus X 2, blood ABCs, vascular access, crystalloid bolus X 2, blood

transfusion prntransfusion prn– Search for the cause of blood loss: CXR, abdo and Search for the cause of blood loss: CXR, abdo and

pelvispelvis– controversiescontroversies

crystalloid versus colloidcrystalloid versus colloid immediate versus delayed immediate versus delayed small versus large volume resuscitationsmall versus large volume resuscitation Optimal endpoints of resuscitationOptimal endpoints of resuscitation

CaseCase

An ICU nurse gawks at you when you ask An ICU nurse gawks at you when you ask to give the hemorrhagic shock patient NS. to give the hemorrhagic shock patient NS. She remarks you should pull up your She remarks you should pull up your MAST pants and start giving pentaspan, MAST pants and start giving pentaspan, albumin or something useful - is she right?albumin or something useful - is she right?

ColloidsColloids

Albumin, protoplasm protein fraction, Albumin, protoplasm protein fraction, hydroxyethylstarch, gelatin, dextranhydroxyethylstarch, gelatin, dextran

AdvantagesAdvantages– less fluid required, more volume in vascular less fluid required, more volume in vascular

space, potential to draw fluid in from tissuesspace, potential to draw fluid in from tissues DisadvantagesDisadvantages

– expensive, allergic reactions, coagulopathiesexpensive, allergic reactions, coagulopathies

ColloidsColloids

Cochrane Database of Systematic Reviews. Cochrane Database of Systematic Reviews. BMJ 1998: 317:235-40.BMJ 1998: 317:235-40.– Objective: effect of albumin on mortalityObjective: effect of albumin on mortality– Study: 30 RCTs total 1419 patientsStudy: 30 RCTs total 1419 patients– Results: RR of death 1.46 hypovolemia, 2.40 Results: RR of death 1.46 hypovolemia, 2.40

burns, 1.69 hypoalbuminemiaburns, 1.69 hypoalbuminemia– Pooled RR of death 1.68 (1.26,2.23)Pooled RR of death 1.68 (1.26,2.23)– Conclusion: albumin increases mortalityConclusion: albumin increases mortality

ColloidsColloids

Cochrane Database 2000. Colloids versus Cochrane Database 2000. Colloids versus crystalloids for fluid resuscitation.crystalloids for fluid resuscitation.– Albumin: Albumin: 18RCTs18RCTs RR1.52 (1.08,2.13)RR1.52 (1.08,2.13)– HES:HES: 7 RCTs7 RCTs RR 1.16 (0.68,1.96)RR 1.16 (0.68,1.96)– Gelatin: Gelatin: 4 RCTs4 RCTs RR 0.50(.08,3.03)RR 0.50(.08,3.03)– Dextran: Dextran: 8 RCTs8 RCTs RR 1.24 (.94,1.65)RR 1.24 (.94,1.65)– Conclusion: No evidence that albumins reduce Conclusion: No evidence that albumins reduce

risk of death in trauma, burns, or surgeryrisk of death in trauma, burns, or surgery

Colloid summaryColloid summary

There is NO evidence that colloids decrease There is NO evidence that colloids decrease mortality in the resuscitation of critically ill mortality in the resuscitation of critically ill patients.patients.

There IS evidence that colloids increase There IS evidence that colloids increase mortality in the resuscitation of critically ill mortality in the resuscitation of critically ill patients.patients.

Hypertonic salineHypertonic saline

AdvantagesAdvantages– less volume, stays in vascular space, draws less volume, stays in vascular space, draws

fluidfluid DisadvantagesDisadvantages

– hypernatremia, hyperosmolarity, seizures, hypernatremia, hyperosmolarity, seizures, coagulopathy, anaphylactoid rxns with dextrancoagulopathy, anaphylactoid rxns with dextran

Hypertonic salineHypertonic saline

Animal evidence Animal evidence – improved hemodynamics and mortalityimproved hemodynamics and mortality

Human evidenceHuman evidence– Wade et al 1997: HS and HSD in traumaWade et al 1997: HS and HSD in trauma– Metanalysis of 8 RCTS of HSD and 6 HSMetanalysis of 8 RCTS of HSD and 6 HS– HS (7.5% saline): no difference in mortalityHS (7.5% saline): no difference in mortality– HSD (+6%dextran): decreased mortality in 7/8 HSD (+6%dextran): decreased mortality in 7/8

trials overall 3.5%; trend only ---> Not stat signtrials overall 3.5%; trend only ---> Not stat sign

Hypertonic salineHypertonic saline

Cochrane Database 2001. Alderson P.Cochrane Database 2001. Alderson P.– Objective: effect on mortalityObjective: effect on mortality– Study: metanalysis of 8 RCTsStudy: metanalysis of 8 RCTs– Results: pooled RR of 0.88 (0.74, 1.95)Results: pooled RR of 0.88 (0.74, 1.95)– Conclusion: there is a trend toward reduction Conclusion: there is a trend toward reduction

in mortality with HSD although not statistically in mortality with HSD although not statistically significantsignificant

Hypertonic saline summaryHypertonic saline summary

There is evidence of TRENDS toward There is evidence of TRENDS toward lower mortality in resuscitation with lower mortality in resuscitation with hypertonic saline but statistical significance hypertonic saline but statistical significance has not been demonstrated …………has not been demonstrated …………

More RCTs are needed………..More RCTs are needed………..

CaseCase

A 20 year old male comes in with a knife A 20 year old male comes in with a knife wound to his abdomen. He is bleeding wound to his abdomen. He is bleeding profusely. The trauma surgeon will be here profusely. The trauma surgeon will be here in 10 minutes. The patients systolic is 70. in 10 minutes. The patients systolic is 70. How much and what fluid would you like How much and what fluid would you like Doctor?Doctor?

Controlled fluid resuscitationControlled fluid resuscitation

ATLS recommends 2 litres then switch to O ATLS recommends 2 litres then switch to O negative blood.negative blood.

Newer research suggests minimal fluids if Newer research suggests minimal fluids if there is a short time to the ORthere is a short time to the OR

Rationale: early, aggressive fluid Rationale: early, aggressive fluid resuscitation with large volume dislodges resuscitation with large volume dislodges soft clots and dilutes clotting factors leading soft clots and dilutes clotting factors leading to increased hemorrhage and mortalityto increased hemorrhage and mortality

Bickell et al 1990Bickell et al 1990The Detrimental Effects of Intravenous Crystalloid after The Detrimental Effects of Intravenous Crystalloid after

Aortotomy in Swine. Surgery 110: 529-36.Aortotomy in Swine. Surgery 110: 529-36.

Objective: does rapid volume replacement inc mortality?Objective: does rapid volume replacement inc mortality? Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg )Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg ) ResultsResults MortalityMortality HemorrhageHemorrhage ControlsControls 0/80/8 783 ml783 ml RL tx grpRL tx grp 8/88/8 2142ml2142ml

Bickell et al 1992. HSD vs RL after AortotomyBickell et al 1992. HSD vs RL after Aortotomy HSD tx grpHSD tx grp 5/85/8 1340ml1340ml

Bickell et al. NEJM 1994.Bickell et al. NEJM 1994.Immediate versus Delayed Fluid Resuscitation for Immediate versus Delayed Fluid Resuscitation for

Hypotensive Patients with Penetrating Torso TraumaHypotensive Patients with Penetrating Torso Trauma

Study: 598 patients SBP<90, odd/even day Study: 598 patients SBP<90, odd/even day randomization, immediate fluids vs none until ORrandomization, immediate fluids vs none until OR

Immediate fluids - Immediate fluids - mortality 110/303 (38%)mortality 110/303 (38%) Delayed fluids -Delayed fluids - mortality 86/289 (30%)mortality 86/289 (30%) ARR 8%, NNTT 12ARR 8%, NNTT 12 Statistically significant p = 0.04Statistically significant p = 0.04 Conclusion: delayed fluid resuscitation reduces Conclusion: delayed fluid resuscitation reduces

mortality in hypotensive patients with penetrating mortality in hypotensive patients with penetrating traumatrauma

Controlled Fluid ResuscitationControlled Fluid Resuscitation

Cochrane Database 2001. Kwan I. Timing Cochrane Database 2001. Kwan I. Timing and volume of fluid administration for and volume of fluid administration for patients with bleeding following trauma.patients with bleeding following trauma.– 3 RCTs for early vs delayed fluids3 RCTs for early vs delayed fluids– 3 RCTs for large vs small volume3 RCTs for large vs small volume– NO evidence for early or large volume fluid NO evidence for early or large volume fluid

replacement and trends toward increased replacement and trends toward increased mortalitymortality

Controlled Fluid Resuscitation - Controlled Fluid Resuscitation - ConclusionsConclusions

There is evidence (limited) that early, large There is evidence (limited) that early, large volume aggressive fluid resuscitation volume aggressive fluid resuscitation increases mortality in penetrating trauma.increases mortality in penetrating trauma.

Further study needed on penetrating trauma Further study needed on penetrating trauma without immediate access to OR and for without immediate access to OR and for blunt trauma and CHIblunt trauma and CHI

CaseCase

You can’t get an IV in your exsanguinating You can’t get an IV in your exsanguinating patient. A med student whips out a sternal patient. A med student whips out a sternal intraosseus infuser - Is it safe? Does it intraosseus infuser - Is it safe? Does it work? Do people use these?work? Do people use these?

Sternal Intraosseus Infusion Sternal Intraosseus Infusion

Rationale:Rationale: Average IV times are 1.5 to 10 minAverage IV times are 1.5 to 10 min Too many outright failures to start IV’sToo many outright failures to start IV’s Sternum easy to locate and accessSternum easy to locate and access High red marrow contentHigh red marrow content

Sternal Intraosseus InfusionSternal Intraosseus Infusion

FAST system (First Access for Shock and FAST system (First Access for Shock and trauma, Pyng Medical Corp., Vancouver, trauma, Pyng Medical Corp., Vancouver, BC)BC)

Intraosseus infusion system with depth Intraosseus infusion system with depth control control

A new system for sternal A new system for sternal inraosseus infusion in adultsinraosseus infusion in adultsMacnab et al, Prehospital Emerg Care 2000;4Macnab et al, Prehospital Emerg Care 2000;4

Report the first 50 uses of the new systemReport the first 50 uses of the new system Adult patients, urgent need for fluids or meds, Adult patients, urgent need for fluids or meds,

unacceptable delay or inability to achieve IV unacceptable delay or inability to achieve IV accessaccess

Mean time to IV access was 77 secondsMean time to IV access was 77 seconds Overall success rate 84%Overall success rate 84% First time users 74%First time users 74% Experienced 95%Experienced 95%

Macnab et al, Prehospital Emerg Macnab et al, Prehospital Emerg Care 2000;4, 173-177Care 2000;4, 173-177

Only 44% success in obese patientsOnly 44% success in obese patients Flow rates of 80ml/min IV and 150 ml/min Flow rates of 80ml/min IV and 150 ml/min

by syringeby syringe No complications or complaints at 2 month No complications or complaints at 2 month

follow upfollow up Rapid and safe alternativeRapid and safe alternative

Macnab et al, Prehospital Emerg Macnab et al, Prehospital Emerg Care 2000;4, 173-177Care 2000;4, 173-177

Still misses our hardest to start group - Still misses our hardest to start group - obese, shocky patientobese, shocky patient

Will it make a difference in outcome?Will it make a difference in outcome? Shouldn’t you compare to IM Shouldn’t you compare to IM

administration of drugs or central access in administration of drugs or central access in the ED?the ED?

What about a pediatric unit?What about a pediatric unit?

CaseCase

80 yr old male comes in with a leg cellulitis, 80 yr old male comes in with a leg cellulitis, you start him on IV ancef and go to see you start him on IV ancef and go to see more patients. Two hours later you are more patients. Two hours later you are called back. The patient pressure is 70/50 called back. The patient pressure is 70/50 he is stuporous, has paradoxical breathing he is stuporous, has paradoxical breathing and his cellulitis is now up to his groin. and his cellulitis is now up to his groin. What has happened and what are you going What has happened and what are you going to do?to do?

SepsisSepsis

Microbiologic cause of shock. Typically Microbiologic cause of shock. Typically secondary to gram negative endotoxins but secondary to gram negative endotoxins but also due to gram positive, parasitic and also due to gram positive, parasitic and fungal infectionsfungal infections

Gram positive infxn ~ 35 – 40%Gram positive infxn ~ 35 – 40% Gram negative infxn ~ 55 – 60%Gram negative infxn ~ 55 – 60% Most common sitesMost common sites

– Lung, abdomen, urinary tractLung, abdomen, urinary tract

Hemodynamic changes with Hemodynamic changes with sepsissepsis

Compensating:Compensating: Endotoxin decreased SVR with Endotoxin decreased SVR with Compensatory increase in cardiac output. Compensatory increase in cardiac output. Presents as hyperdynamic, warm patient.Presents as hyperdynamic, warm patient.

Hemodynamic changes with Hemodynamic changes with sepsissepsis

Decompensating: Decompensating: Can appear like cardiogenic shock Can appear like cardiogenic shock Bacterial myocardial depressantBacterial myocardial depressant Increased pulmonary pressures (ARDS) Increased pulmonary pressures (ARDS) Pump failure and decreased forward flow Pump failure and decreased forward flow Presents as cold patient in failure. Poor Presents as cold patient in failure. Poor

prognosisprognosis

Sepsis general treatmentSepsis general treatment

TVMTVM ABC’SABC’S 2 litres crystalloid2 litres crystalloid Pressors Levo>dopaminePressors Levo>dopamine Early empiric antibioticsEarly empiric antibiotics

Fluid resuscitationFluid resuscitation

Important in septic shockImportant in septic shock Initially relative hypovolemia/fluid defecitsInitially relative hypovolemia/fluid defecits Low CO and filling pressures which may Low CO and filling pressures which may

respond to volumerespond to volume Increased blood and plasma volumes Increased blood and plasma volumes

associated with enhanced survival and associated with enhanced survival and increased COincreased CO– Weil MH et al., AM J Med 1978Weil MH et al., AM J Med 1978

Vincent J-L, et al., Intensive Care Vincent J-L, et al., Intensive Care Medicine (2001) Medicine (2001)

Colloids and Crystalloid each work wellColloids and Crystalloid each work well Colloids in Europe, Crystalloids in NAColloids in Europe, Crystalloids in NA Uncertain if one superiorUncertain if one superior Need 2-4 x more volume with crystalloid Need 2-4 x more volume with crystalloid

for same filling pressuresfor same filling pressures

Fluids and sepsis summaryFluids and sepsis summary

Aggressive fluid challenge importantAggressive fluid challenge important– Dx clueDx clue– Important physiologicallyImportant physiologically

Will improve myocardial performance and Will improve myocardial performance and O2 deliveryO2 delivery

VasopressorsVasopressors

Cornerstone of Rx together with fluids and Cornerstone of Rx together with fluids and antibioticsantibiotics

Goal: increase MAP and therefore end Goal: increase MAP and therefore end organ perfusion organ perfusion

First line agents:First line agents:– Dopamine or levophedDopamine or levophed

Most common choicesMost common choices

Dopamine: Dopamine: – 1-5 ug/kg/min ~ dopaminergic1-5 ug/kg/min ~ dopaminergic– 5-10 ug/kg/min ~ beta activity5-10 ug/kg/min ~ beta activity– >10 ug/kg/min ~ alpha activity>10 ug/kg/min ~ alpha activity

Levophed:Levophed:– Potent alpha agonistPotent alpha agonist– Some beta propertiesSome beta properties

Structurally very similarStructurally very similar

DopamineDopamine

In past/and still with many, dopamine In past/and still with many, dopamine preferred agentpreferred agent

Effects well establishedEffects well established Physicians comfortable with usePhysicians comfortable with use

NorepinephrineNorepinephrine

Concern with levophed worsening end Concern with levophed worsening end organ hypoperfusionorgan hypoperfusion

Based on limited evidenceBased on limited evidence Older studies on pressors, levophed used as Older studies on pressors, levophed used as

last resort and thus poor outcomeslast resort and thus poor outcomes– Hesselvik JF, et al., Crit Care Med 1989Hesselvik JF, et al., Crit Care Med 1989

NorepinephrineNorepinephrine

Norepinephrine improves renal blood flow Norepinephrine improves renal blood flow and tissue oxygenation in patients with and tissue oxygenation in patients with septic shock:septic shock:– Desjars et al., Crit Care Med 1989Desjars et al., Crit Care Med 1989– Rendl-Wenzel et al., Intensive Care Med Rendl-Wenzel et al., Intensive Care Med

1993.1993.– Meadows et al., Crit Care Med 1988Meadows et al., Crit Care Med 1988– Martin C., et al., Crit Care Medicine 2000Martin C., et al., Crit Care Medicine 2000

Dopamine versus norepinephrineDopamine versus norepinephrine

Martin et al., Chest 1993Martin et al., Chest 1993 Marik et al., JAMA 1994Marik et al., JAMA 1994 Small studies (n=20), surrogate markersSmall studies (n=20), surrogate markers Levophed has favourable effect on Levophed has favourable effect on

hemodynamics and end organ perfusion as hemodynamics and end organ perfusion as compared to dopaminecompared to dopamine

Pressor summaryPressor summary

Dopamine/Levophed first line agentsDopamine/Levophed first line agents Levophed may be the superior agent in Levophed may be the superior agent in

septic shockseptic shock Make sure the pump is full firstMake sure the pump is full first Avoid supranormal restoration of MAPAvoid supranormal restoration of MAP Invasive monitoring req’dInvasive monitoring req’d

Bochud et al., Intensive Care Bochud et al., Intensive Care Medicine 2001Medicine 2001

4 retrospective studies of gram neg 4 retrospective studies of gram neg bacteremiabacteremia– McCabe et al., Arch Intern Med 1962.McCabe et al., Arch Intern Med 1962.– Bryant et al., Arch Intern Med 1971.Bryant et al., Arch Intern Med 1971.– Freid et al., Arch Intern Med 1968.Freid et al., Arch Intern Med 1968.– Young et al., Ann Intern Med 1977.Young et al., Ann Intern Med 1977.

Four studies combinedFour studies combined

N=1190N=1190 Appropriate Abx mort rate~28%Appropriate Abx mort rate~28% Inappropriate Abx mot rate~49%Inappropriate Abx mot rate~49% P<0.001P<0.001

Intensive Care Medicine 2001Intensive Care Medicine 2001

Early appropriate antimicrobial Rx Early appropriate antimicrobial Rx improves the outcome of patients with improves the outcome of patients with blood borne infections and severe sepsis or blood borne infections and severe sepsis or septic shock..in patients with both gram septic shock..in patients with both gram negative and positive bacteremianegative and positive bacteremia

Empirical antibiotic choicesEmpirical antibiotic choices

CarbapenemCarbapenem B-lactam + aminoglycosideB-lactam + aminoglycoside 33rdrd/4/4thth generation cephalosporin generation cephalosporin ? Extended spectrum penicillin? Extended spectrum penicillin

La messageLa message

Initial rapid appropriate antibiotics in Initial rapid appropriate antibiotics in patients with severe sepsis/septic shock can patients with severe sepsis/septic shock can be life savingbe life saving

CaseCase

Despite Dop at 20 u/min/kg and Levo at Despite Dop at 20 u/min/kg and Levo at 4ug/min the cellulitic patient still only has a 4ug/min the cellulitic patient still only has a pressure of 80 systolic. He is tubed and has pressure of 80 systolic. He is tubed and has no urine output by foley. What else is in no urine output by foley. What else is in your arsenal?your arsenal?

Steroids in septic shockSteroids in septic shock

Rationale: Rationale: Anti-inflammatoryAnti-inflammatory Relative adrenal insufficiency in many of Relative adrenal insufficiency in many of

cases of refractory shockcases of refractory shock Upregulates catecholamine receptorsUpregulates catecholamine receptors Hopefully immunosuppression and bleed Hopefully immunosuppression and bleed

risk did not counter benefitsrisk did not counter benefits

Interest in RoidsInterest in Roids

Interest since the 1940’sInterest since the 1940’s Known beneficial inKnown beneficial in

– Pediatric bacterial meningitisPediatric bacterial meningitis– Typhoid feverTyphoid fever– PCP pneumoniaPCP pneumonia

Early mega-dose steroid trialsEarly mega-dose steroid trials

1930s mega-dose steroids 1930s mega-dose steroids (methylprednisolone 30/mg/kg x 3-4 doses)(methylprednisolone 30/mg/kg x 3-4 doses)

Trend towards increased mortality with Trend towards increased mortality with corticosteroidscorticosteroids

No beneficial effect in septic shock patientsNo beneficial effect in septic shock patients Increase incidence of GI bleedingIncrease incidence of GI bleeding Trend towards increased mortality from Trend towards increased mortality from

secondary infectionssecondary infections

Newer steroid trials in the 1990’sNewer steroid trials in the 1990’s

Revisited the steroid issue except at small Revisited the steroid issue except at small dosesdoses

They aimed to replace steroids for a They aimed to replace steroids for a “Relative adrenal insufficiency”“Relative adrenal insufficiency”

Researchers hoped get catecholamine Researchers hoped get catecholamine sensitivity and anti-inflammatory effects sensitivity and anti-inflammatory effects stillstill

Bollaert et al.,Critical Care Medicine Bollaert et al.,Critical Care Medicine 19981998

Double-blind, placebo controlled Double-blind, placebo controlled Septic shock pts according to ACCP criteria Septic shock pts according to ACCP criteria

or pressors >48hrsor pressors >48hrs Solu-cortef 100mg IV q 8hrs x 5days vs. Solu-cortef 100mg IV q 8hrs x 5days vs.

placebo with taperingplacebo with tapering Baseline pt characteristics similarBaseline pt characteristics similar

ResultsResults

Shock reversal by day 7:Shock reversal by day 7:– 15/22 (68% Rx group)15/22 (68% Rx group)– 4/19 (21% placebo group)4/19 (21% placebo group)– P=0.007P=0.007

Trend in Rx group of decrease mortalityTrend in Rx group of decrease mortality– 63% vs 32% p=0.0963% vs 32% p=0.09

No increase adverse outcomesNo increase adverse outcomes

Briegel et al., Crit Care Med Briegel et al., Crit Care Med 1999.1999.

Double blind, randomized, placebo controlled Double blind, randomized, placebo controlled (n=40)(n=40)

Pts in septic shockPts in septic shock Pts included if on vasopressors less than 72 Pts included if on vasopressors less than 72

hrshrs Randomized to solu-cortef 100mg IV then Randomized to solu-cortef 100mg IV then

low dose infusion low dose infusion Primary end point = time to shock reversalPrimary end point = time to shock reversal

ResultsResults

Shock reversal 2 days in Rx group vs. 7 Shock reversal 2 days in Rx group vs. 7 days in placebo (p=0.005)days in placebo (p=0.005)

Mortality unaffected by RxMortality unaffected by Rx 1 GI bleed in Rx group1 GI bleed in Rx group

Annane et al., Crit Care Med, Annane et al., Crit Care Med, 2001 2001

Review of the steroid literatureReview of the steroid literature ConclusionsConclusions

– NO ROLE FOR HIGH DOSE STEROIDSNO ROLE FOR HIGH DOSE STEROIDS– Growing evidence for replacement steroids Growing evidence for replacement steroids

in pressor dependent septic shockin pressor dependent septic shock

CaseCase

A 10 year old tubed patient comes into A 10 year old tubed patient comes into PICU with febrile status epilepticus.. You PICU with febrile status epilepticus.. You astutely start him empirically on vanco and astutely start him empirically on vanco and cefotaxime. Two hours later the child is cefotaxime. Two hours later the child is coughing up blood, hypoxemic despite your coughing up blood, hypoxemic despite your best efforts and has a BP of 70/40 on best efforts and has a BP of 70/40 on maximum pressors? What is the latest maximum pressors? What is the latest agent for septic shock?agent for septic shock?

Activated Protein CActivated Protein C

Rationale:Rationale: Pro-fibrinolyticPro-fibrinolytic Anti-thromboticAnti-thrombotic Anti-inflammatoryAnti-inflammatory

Bernard et al., NEJM 2001Bernard et al., NEJM 2001

Randomized, double blind(phase 3 trial)Randomized, double blind(phase 3 trial) N=1690 severe sepsisN=1690 severe sepsis Placebo vs. APCPlacebo vs. APC End point 28 day mortalityEnd point 28 day mortality

Bernard et al., NEJM 2001Bernard et al., NEJM 2001

Mort rate;Mort rate;– 30.8% placebo30.8% placebo– 24.7% Rx group24.7% Rx group

Absolute risk reduction 6.1% (p=0.005)Absolute risk reduction 6.1% (p=0.005) NNTT 16 (CI NNTT 10-50)NNTT 16 (CI NNTT 10-50) Serious bleeding 3.5% vs 2%(p=0.06)Serious bleeding 3.5% vs 2%(p=0.06) NNTH 67NNTH 67

CommentaryCommentary

Study results have been criticizedStudy results have been criticized Some of the investigators have left the Some of the investigators have left the

groupgroup Cost-effectiveness study of APC in CHR Cost-effectiveness study of APC in CHR

hopefully to make it in Lancet … we ain’t hopefully to make it in Lancet … we ain’t going to be using itgoing to be using it

CaseCase

A 28 year old women is found at home by A 28 year old women is found at home by friends she is obtunded, hypotensive and friends she is obtunded, hypotensive and has purpura fulminans. After maximal has purpura fulminans. After maximal pressor support and the ravages of pressor support and the ravages of meningococcemia her toes and fingers are meningococcemia her toes and fingers are black. Your staff intensivist is at a loss. black. Your staff intensivist is at a loss. Because you went to Phil’s talk you are Because you went to Phil’s talk you are going to suggest?going to suggest?

VasopressinVasopressin

Known to be potent vasoconstrictor via V1 Known to be potent vasoconstrictor via V1 receptor smooth musclereceptor smooth muscle

Evidence that in septic shock there is a Evidence that in septic shock there is a relative lack of vasopressinrelative lack of vasopressin

VasopressinVasopressin

Malay et al., J Trauma 1999Malay et al., J Trauma 1999 Tsuneyoshi et al., Crit Care Medicine 2001Tsuneyoshi et al., Crit Care Medicine 2001 Studies limited by design and small Studies limited by design and small

numbers (N=10)numbers (N=10) Surrogate markers not mortality used as Surrogate markers not mortality used as

end-pointsend-points

VasopressinVasopressin

Vasopressin does increase MAP in pts with Vasopressin does increase MAP in pts with septic shockseptic shock

? Improved mortality? Improved mortality Larger studies requiredLarger studies required ? Consider in ED as alternative to high dose ? Consider in ED as alternative to high dose

pressorspressors

Sepsis management summarySepsis management summary

Don’t forget fluidsDon’t forget fluids Levophed works better than dopamineLevophed works better than dopamine Don’t delay giving appropriate ABXDon’t delay giving appropriate ABX Increasing evidence for steroids in Increasing evidence for steroids in

refractory septic shockrefractory septic shock ? Activated protein C/vasopressin in future? Activated protein C/vasopressin in future

Obstructive shockObstructive shock

CaseCase

28 year old female, known breast cancer 28 year old female, known breast cancer comes in in extremis. She is cyanotic, has a comes in in extremis. She is cyanotic, has a JVD to her ear, lungs are dry and she is JVD to her ear, lungs are dry and she is hypotense with a systolic BP of 70. You hypotense with a systolic BP of 70. You are positive she has a PE and you have TPA are positive she has a PE and you have TPA in hand - are you going to lyse her? in hand - are you going to lyse her?

PE and shockPE and shock

Needs to take out 50% of lung surface areaNeeds to take out 50% of lung surface area Increase pulmonary pressures to 40mmHGIncrease pulmonary pressures to 40mmHG Cause backflow and septal shiftCause backflow and septal shift Hypotense, JVD +/- cyanosisHypotense, JVD +/- cyanosis

Lysis and massive PELysis and massive PE

Not been studied enough to prove lysis improves Not been studied enough to prove lysis improves survival in PE induced shocksurvival in PE induced shock

Lysis does improve RV dilation, tricuspid Lysis does improve RV dilation, tricuspid regurgitation and cardiac output in sub-massive regurgitation and cardiac output in sub-massive PEPE

I would treat with 02, fluids and pressors and get I would treat with 02, fluids and pressors and get a CT or echoa CT or echo

If TPA is to be given: 100mg bolus? Over If TPA is to be given: 100mg bolus? Over 30min? 2 hours? - no consensus30min? 2 hours? - no consensus

CaseCase

25 yr old male, left sided anterior chest 25 yr old male, left sided anterior chest wound. Two hypotensive episodes where wound. Two hypotensive episodes where patient almost passes out. In between he is patient almost passes out. In between he is alert and talking and says his chest just alert and talking and says his chest just hurts. There is no Beck’s triad - he has two hurts. There is no Beck’s triad - he has two IV’s in. What do you want to do?IV’s in. What do you want to do?

Pericardial tamponade statsPericardial tamponade stats

2% of penetrating chest trauma2% of penetrating chest trauma Stab > GSWStab > GSW Beck’s triad only in 1/3Beck’s triad only in 1/3 CXR will often reveal a globular heart, ED CXR will often reveal a globular heart, ED

ultrasound will typically confirm clinically ultrasound will typically confirm clinically significant tamponadesignificant tamponade

CaseCase

42 year old male comes in c/o crushing 42 year old male comes in c/o crushing retrosternal chest pain and is hypotensive at retrosternal chest pain and is hypotensive at 80/60. The patient is having an 80/60. The patient is having an anterolateral infarct by EKG. How would anterolateral infarct by EKG. How would you manage the patient?you manage the patient?

Cardiogenic shockCardiogenic shock

ManagementManagement– small fluid bolusessmall fluid boluses– invasive monitoringinvasive monitoring– vasopressorsvasopressors

norepinephrinenorepinephrine dopaminedopamine dobutaminedobutamine

Cardiogenic shock approachCardiogenic shock approach

AMI +shock?AMI +shock?

||

RV infarct?RV infarct?

YES /YES / \ NO \ NO

Volume resuscitate<<<----------------------Pulmonary congestion present?Volume resuscitate<<<----------------------Pulmonary congestion present?

|| NO | YES NO | YES

|| | |

Response adrquate---------------------->>>>Response adrquate---------------------->>>> PressorPressor

| YES NO| YES NO | |

|| | |

Revascularize<<<----------------------------Response adequateRevascularize<<<----------------------------Response adequate

YESYES | NO | NO

||

IABC and PTCAIABC and PTCA

Cardiogenic shockCardiogenic shock

DefinitionDefinition– decreased cardiac output and evidence of tissue decreased cardiac output and evidence of tissue

hypoxia in presence of adequate intravascular volumehypoxia in presence of adequate intravascular volume CriteriaCriteria

– hypotension (SBP < 90) x 30 min, or 30mmHG hypotension (SBP < 90) x 30 min, or 30mmHG below baseline, cardiac index < 2.2 L/min/m2, PCWP below baseline, cardiac index < 2.2 L/min/m2, PCWP > 15 mmHg> 15 mmHg

PathologicallyPathologically– Will have lost 40% of myocardiumWill have lost 40% of myocardium

Cardiogenic shock - pressor Cardiogenic shock - pressor choiceschoices

Dobutamine: beta adrenergic Dobutamine: beta adrenergic – positive B1 ionotrope; may drop BP b/c of positive B1 ionotrope; may drop BP b/c of

vasodilationvasodilation– SBP 70 - 100 without signs of hypoperfusion a/f SBP 70 - 100 without signs of hypoperfusion a/f

fluidsfluids Dopamine: dopaminergic, beta , alpha adrenergicDopamine: dopaminergic, beta , alpha adrenergic

– SBP 70 - 100 with signs of hypoperfusion after fluidsSBP 70 - 100 with signs of hypoperfusion after fluids Norepinephrine: alpha agonistNorepinephrine: alpha agonist

– SBP < 70 after fluidsSBP < 70 after fluids

Why use pressors in cardiogenic Why use pressors in cardiogenic shock?shock?

Increase your diastolic pressure or coronary Increase your diastolic pressure or coronary artery filling pressureartery filling pressure

They do however increase your LVEDP They do however increase your LVEDP which decreases coronary perfusionwhich decreases coronary perfusion

Dobutamine and IABP will increase Dobutamine and IABP will increase diastolic pressure and drop LVEDPdiastolic pressure and drop LVEDP

What is mortality in patient who What is mortality in patient who present with AMI andpump present with AMI andpump

dysfunction?dysfunction?

Killip Classification of Pump Dysfunction and Killip Classification of Pump Dysfunction and

Mortality in AMIMortality in AMI Class ExamClass Exam MortalityMortality I I No crackles, clearNo crackles, clear 5%5% II Crackles, S3II Crackles, S3 20%20% III Pulmonary edemaIII Pulmonary edema 30%30% IV Cardiogenic shockIV Cardiogenic shock 80%80%

So what should I do with my So what should I do with my patients in cardiogenic shock?patients in cardiogenic shock?

Ideally PTCAIdeally PTCA If there is a CCU with IABP capabilities - get If there is a CCU with IABP capabilities - get

them therethem there Second line would be to get systolic BP to 90 and Second line would be to get systolic BP to 90 and

lyselyse If you cannot get BP to 90 then treat If you cannot get BP to 90 then treat

conservatively or lyse (the evidence would say conservatively or lyse (the evidence would say there is no difference between the two - but a there is no difference between the two - but a bleeding risk with TPA)bleeding risk with TPA)

PTCA indications: CATHD’PTCA indications: CATHD’JACC 1996; 28:1328-1428JACC 1996; 28:1328-1428

C: Cardiogenic shockC: Cardiogenic shock A: Anterior MI (STE >= 4 leads)A: Anterior MI (STE >= 4 leads) T: Thrombolytic contra-indicationsT: Thrombolytic contra-indications H: Hemodynamic instability/dysrhythmiasH: Hemodynamic instability/dysrhythmias D: Duration less than 60 minutesD: Duration less than 60 minutes

Don’t lyse in cardiogenic shockDon’t lyse in cardiogenic shock

Thrombolysis in cardiogenic shockThrombolysis in cardiogenic shock– GISSI (N=280)GISSI (N=280) 30day mortality30day mortality– streptokinasestreptokinase 70.1%70.1%– medical mxmedical mx 69.6%69.6%

– NO trial has shown reduction mortality with NO trial has shown reduction mortality with cardiogenic shock with thrombolysiscardiogenic shock with thrombolysis

Temporize with IABC and then Temporize with IABC and then lyse or preferably do PTCAlyse or preferably do PTCA

Intra-Aortic Balloon PumpIntra-Aortic Balloon Pump– Gusto I: early IABP + lysis showed trend Gusto I: early IABP + lysis showed trend

towards lowered 30d and one year mortalitytowards lowered 30d and one year mortality– SHOCK trial: IABP + lysis mortality 17% SHOCK trial: IABP + lysis mortality 17%

versus medical mx alone 32%versus medical mx alone 32%– ongoing researchongoing research

Cardiogenic: the SHOCK trial Cardiogenic: the SHOCK trial Hochman JS et al. Early revascularizationin AMI + Hochman JS et al. Early revascularizationin AMI + cardiogenic shock: NEJM 1999; vol 341 (9): 625-34.cardiogenic shock: NEJM 1999; vol 341 (9): 625-34.

RCT of AMI + cardiogenic shockRCT of AMI + cardiogenic shock– 152 early revascularization (PTCA or CABG) 152 early revascularization (PTCA or CABG)

or 150 initial medical mx only (lysis initially, or 150 initial medical mx only (lysis initially, some had PTCA/CABG after 52hrs)some had PTCA/CABG after 52hrs)

– End Point early revasc. Med Mx statsEnd Point early revasc. Med Mx stats– 30d mort30d mort 46.7%46.7% 56%56% p=.11p=.11– 6mo mort6mo mort 50.3%50.3% 63.1%63.1% p=.027p=.027

Cardiogenic Shock:Cardiogenic Shock:the SHOCK trialthe SHOCK trial

Hochman JS. One year survival following Hochman JS. One year survival following early revascularization for cardiogenic early revascularization for cardiogenic shock. JAMA 2001.shock. JAMA 2001.– Early revascularization survival Early revascularization survival 46.7%46.7%– Initial medical mx survivalInitial medical mx survival 33.6%33.6%– Statistically significant p<0.03Statistically significant p<0.03– NOTE: sub group analysis only shows NOTE: sub group analysis only shows

mortality difference in age < 75yomortality difference in age < 75yo

CaseCase

76 year old female had an inferior MI 3 76 year old female had an inferior MI 3 days ago. You are called to assess her in days ago. You are called to assess her in CCU. She is hypotense, c/o of new chest CCU. She is hypotense, c/o of new chest pain and has an impressive holosystolic pain and has an impressive holosystolic murmur. What is on your differential and murmur. What is on your differential and how are you going to manage her?how are you going to manage her?

Holosystolic murmurHolosystolic murmur

Loss of mechanical cardiac functionLoss of mechanical cardiac function Anteroseptal MI: acute VSD - thrillAnteroseptal MI: acute VSD - thrill Inferior MI: papillary muscle rupture - no Inferior MI: papillary muscle rupture - no

thrillthrill Both need urgent echoBoth need urgent echo Cardiac surgical consultation - “Like Cardiac surgical consultation - “Like

sewing moonbeams to flatus”sewing moonbeams to flatus”

CaseCase

A 20 year old male roofer comes in within A 20 year old male roofer comes in within 30 minutes of his accident. He cannot 30 minutes of his accident. He cannot move or feel anything below his shoulders. move or feel anything below his shoulders. He is arreflexic, hypotense and bradycardic. He is arreflexic, hypotense and bradycardic. Is this spinal shock or neurogenic shock? Is this spinal shock or neurogenic shock? How are you going to treat him?How are you going to treat him?

Neurogenic shockNeurogenic shock

Cervical spine transections that result in Cervical spine transections that result in transection of sympathetic fibrestransection of sympathetic fibres

Loss of sympathetic tone and unopposed Loss of sympathetic tone and unopposed vagal tonevagal tone

Patients present bradycardic and Patients present bradycardic and hypotensivehypotensive

Spinal shock can present identicallySpinal shock can present identically

Neurogenic shockNeurogenic shock

Still give fluidsStill give fluids Give dopamine, phenylephrine or ephedrineGive dopamine, phenylephrine or ephedrine Use atropine for bradycardia and intubationUse atropine for bradycardia and intubation T4 transections are the lowest lesions that T4 transections are the lowest lesions that

will give you neurogenic shockwill give you neurogenic shock

CaseCase

28 year old female comes in post bee sting. 28 year old female comes in post bee sting. She is glowing red, hypotense and She is glowing red, hypotense and stridorous. How are you going to manage stridorous. How are you going to manage her? What is your epi approach?her? What is your epi approach?

Anaphylaxis - only take homeAnaphylaxis - only take home

ABC IV’SABC IV’S A: AdrenalineA: Adrenaline B: BenadrylB: Benadryl C: CorticosteroidsC: Corticosteroids I: IV fluidsI: IV fluids V: VentolinV: Ventolin Severe: epinephrine IVSevere: epinephrine IV

– 1ml of 1:10,000 q 30seconds to effect1ml of 1:10,000 q 30seconds to effect

ThanksThanks

Simon BartleySimon Bartley Idan KhanIdan Khan Rob HallRob Hall Jeff PlantJeff Plant Morad HameedMorad Hameed

Keep the dream alive….Keep the dream alive….