shock shawn dowling, pgy-5. objectives briefly discuss general pathophysiology classification of...

Shock

Shawn Dowling, PGY-5

Objectives

Briefly discuss general pathophysiology Classification of shockReview of vasopressorsLots of casesWe will not talk about septic shock - this will be discussed in a future set of rounds

Intro35M. Pulled from an industrial fire.

Brought in by EMS.

Pt is awake, but clearly altered. Only complaint is a HA. Prev well.

T37, HR 110, BP 160/70, RR 20/100% c/s 7

The nurses have already drawn a venous gasCO is 18%, lactate is 13

Is this patient in shock?

What do you think is going on?Lactate > 10 is highly predictive of cyanide toxicity with inhalational exposure regardless of CO levelBaud FJ, et al: Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med 2001; 325:1761–1766.

How do you want to treat this patient other than with O2 +/- hyperbarics? Why?

Only give the sodium thiosulfate portion of the Cyanide Antidote Kit – if you give them the nitrite component you induce more of a functional anemia which they will not tolerate because of the other functional anemia – the CO

Definition of shock

Rude unhinging of the machinery of lifeOr

The inability of the circulatory system to adequately supply tissues with 02 & nutrients and remove cellular waste

Diagnosis of Shock – Rosen’s Need 4 of 6 Ill appearance or decreased LOC (as a general rule MAP< 50 before AMS)HR > 100RR > 22 or PC02 < 32Base deficit <-5 or lactate >4Urine output < 0.5 ml/kg/hrHypotension > 20 minute duration

NOTE - ↓BP not required for Dx

Diagnosing ShockThe more advanced the shock state, the easier the Dx, but…

Significant tissue hypoxia appears to exist prior to development of significant signs & symptoms

THE BETTER WE CAN RECOGNIZE SHOCK, THE EARLIER WE CAN INSTITUTE Tx

TIME IS TISSUE (see RIVERS STUDY)

Can be is shock with “normal” vitalsNormal BP in face of hypovolemia means some organs are hypoperfused to maintain systemic BP

Shock is the transition between life and death

Shock unifying features:

Imbalance between cellular O2 demand and supply

Disrupted cellular homeostasis

Failed aerobic metabolism –> anaerobic metabolism –> lactic acidosis

Calcium shifts - impairs cardiac contractility

Failed ion gradients and cellular pumps

Cell edema and death

How does our body compensate?

Counter-regulatory mediatorsCatecholamines, glucocorticoids, angiotensin, vasopressin, insulin

Increased substratesglucose, TG and FFA

Anaerobic metabolismincr CO2:02 ratio

Pertinent Critical Care formulas

CO = HR x SV

BP = CO x SVR

O2 content = 1.34 x hgb x O2 saturation + 0.003 x Po2

(02 bound to hgb) (02 in plasma)

Oxygen delivery is the CO x O2 contentWhy is this equation so important to a shock talk?In which shock scenario do we target the O2 in plasma for treatment?

CO poisoning

What are some different shock classifications?

Classification of Shock

Many different waysMnemonics

Physiologic

Clinical

It doesn’t matter which you use as long asYou know it cold

It’s exhaustive

Shock

BP = ↓CO x ↓SVR

HypovolemicCardiogenicObstructive

Distributive

ShockShock

Hypovolemic Cardiogenic Obstructive Distributive

Bleeding or Fluid Loss•Overt•Occult•Excessive Losses

•Vessels•Rhythm•Valvular•Myocardium•Pericardium

•Intravascular •Extravascular

NASTENeurogenicAnaphylacticSepticToxicologicEndocrine

Hypovolemic

Overt/Occult losses of blood5 sources of life threatening hemorrhage in trauma?Chest, Abdo, Pelvis, Long bones, Street (from skin)

Excessive Fluid loss3rd spacing (burns, pancreatitis, dermatologic, ascites)Excessive sweating/vomiting/diarrhea/urine output(diuretics, DI)

Cardiogenic

VesselsAMI or acute or chronic– usually need to infarct 40% to cause shockAoD

RhythmBradyTachydysthrythmias

ValvularStenosisRegurgitation

MyocardiumRupture (FW or VSD)MyocarditisCardiomyopathyRV involvement

PericardiumTamponade

Obstructive

IntravascularPEAmniotic Fluid EmbolismAir embolismFat embolism

ExtravascularTension PTXCardiac tamponadeSVC syndrome

Distributive

NeurogenicAnaphylacticSepticToxicologic

(CaCB, BB), CO, cyanide, iron, ASA, etc

EndocrineAdrenal insufficiency, thyroid storm, electrolytes (hyperK)

Top three causes of shock in infantsSepsisHypovolemicCardiac

SHOCK in a neonateSepsisCardiacnon-Accidental TraumaMetabolicSurgical

Physical Exam

Two purposes1. Try to determine if the patients is in shock

– Look for evidence of end organ damage

2. Determine the cause of the shock– JVP & perfusion status is VERY helpful

Thanks to ICU Crash Course

Match the shock with the appropriate vasopressor and why

Sepsis

Neurogenic Shock

Anaphylactic Shock

Epinephrine

Ephedrine

Phenylephrine

Norepinephrine

Dopamine

Milrinone

Direct vs indirect vasopressors

Direct agents stimulate the receptor directly

Indirect agents have their effect by stimulating the adrenals to release catecholamines

:. If stressor has been ongoing for a period of time -> body’s catecholamine reserve is likely deplete and the indirect agents will have less effect

DirectNorepiEpiPhenylephrine

IndirectDopamineDobutamineEphedrine

αα

ßß11

ßß22

DD

D=Dopaminergic

Receptor Primary location Primary fx

α Vessel walls Peripheral Arterial Constriction

ß1 Heart Inotropy/Chronotropy

ß2 Lungs/Skeletal muscle Dilatation of smooth muscle (skeletal and bronchial)

D Kidneys Increase renal blood flow

D=Dopaminergic

Receptor Primary location Primary fx

Cochrane Review:(updated) Feb. 11, 2005.

For all kinds of shock RCTs

Levo vs Dop (3 studies, N=62) RR death 0.88 (0.57,1.36)

Levo + dob vs epi (2 studies, N=52) RR death 0.98 (0.57,1.67)

Unfortunately, these studies are too small to definitively answer the question but better data to support that norepi achieves HD endpoints better and since it’s a direct agent likely better for septic patients

Case 1

PP: 8yo F with known allergy to wasps

PMHx: Healthy and no meds

HPI:

At day camp and “forgot” her epi-pen

Stung by 2 hornets after accidentally running into a nest

Presents by personal vehicle to ED

Given PO Benadryl by family member

Case 1

GenerallyAppears unwell and flushedHR=128, RR=38, T=37.8, BP=85/40, Sat 89% RA

CVSTachy, warm extremities

RespSignificant indrawingAudible wheeze throughoutNo stridor noted

Derm Urticarial rash and diffuse flushing

ENTLip swelling noted and uvula swollen on exam

Case 1

1) Name the general category of shock

2) Describe the pathophysiology

3) Name the management goals

4) Define the best interventions to obtain the above goals

5) Name potential pitfalls

Case 1

The pediatric nurse is panicked…..

He wants to know how much Epinephrine you want to give this child and by what route…..

Case 1

The patient is not responding to your IM epinephrine

The pressure is 60 systolic and the patient has become obtunded…..

Case 2

PP:58yo Male with known shrimp allergy

PMHXMI 2 years agoNIDDMHTN

HPI:Ate the “egg roll special” at a Thai restaurantImmediate throat swellingEMS called and IM epinephrine given on route

Case 2

GenerallyAppears flushed and unwell with marked work of breathing and distressHR 62, RR 28, BP 80/46, Sat 89% on mask, T37.4

CVSNormal heart sounds, normal cap refill

Resp Diffuse wheeze throughout

AbdomenSoft but mildly tender

Neuro Starting to appear somnolent

Case 2

You repeat another IM injection of 0.3cc of 1:1000 epi and give H1 and H2 blockers intravenously

There is no improvement and the patient remains hypotensive and relatively bradycardic…..

Case 2

1) Name the general category of shock2) Describe the pathophysiology• Difference between anaphylaxis and

anaphylactoid?

3) Name the management goals4) Define the best interventions to obtain

the above goals5) Name potential pitfalls

Management

FluidsMeds

Epi is the first line Tx for anaphylaxis IV (1:10,000)

1 mL (100ug) aliquot – repeat q60sec until desired effect

Infusion - 1ug/min-4ug/minIf pt not in shock – IM (why not SC?)

Ventolin nebsBenadryl 50mg IVZantac 50mg IVSolu-medrol 125mg IV

Glucagon (for pts on ßß, ?ACE-I)1-2mg IV Then 5-15mcg/min infusion Inotropic/chronotropic/vasoactive properties beyond the b-receptor

Case 3

80M. Hx of COPD.

Presents with productive cough and feels unwell.

T-40, RR28, sats 85% on NRB, HR-120, BP 90/50

Working Dx – Pneumonia + Sepsis

You decide you going to intubate this patient because of failure to oxygenate

Any concerns? How are you going to prepare? Induction agent? Other meds?

Sepsis and airway management

Sepsis significantly increases you O2 requirements – therefore these patients can desaturate quite rapidly – :. Optimize the conditions (i.e. positioning, pre-oxygenate, best-intubator, etc)

Use of accessory muscles can ↑O2 consumption by 50-100%!Another reason to manage their airway early or if you are not meeting your physiologic end points

Any other concerns

Post-intubation hypotension

Septic patients are very catecholamine driven – intubating can remove that stimuli and they can drop their pressures precipitouslyAlso, the agents we give for intubation may play a role ↑ intra-thoracic pressure (from mechanical ventilation) can drop the preload :. causing hypotension)

Intubating a septic patientPre-oxygenate as much as possiblePretreat with fluids +/- bicarb if you thing they are really acidotic (no evidence)Careful choice of induction agent

Ketamine or ½ dose etomidate (0.15mg/kg) are likely best options, AVOID propofol

Have some pressors drawn up (phenyl/norepi)Why not dopamine or ephedrine?phenylephrineHow do you mix this?10mg in 100mL bag – draw up 10cc and give 1cc(100Ug)/dose

RSI if no CI (gives you the best look)

http://ca.youtube.com/watch?v=pY8jaGs7xJ0





Case 3

PP: 38yo Male transfer by STARSPmHx: Asthma but otherwise healthyMeds: Ventolin and Flovent PRNHPI:

Patient riding QUAD in kananaskis country and flipped+ Helmet and no LOCTrapped under bike for 10 minutes extrication by friendsSTARS scene callNo major blood loss noted on scene

Case 3Generally

GCS 12/15 patient confused and aggitatedHR 120, BP 81/40, RR 15, Temp 37.2, Sats 92%

CVSTachycardic, normal HS, Cap refill 4 seconds, weak thready pulse

RespClear bilaterally but poor inspiratory effort

AbdomenDiffusely tender to palpationSoft and not distended

MSKPelvis is grossly unstable to palpationPerineal hematoma notedFemurs and hips normal to exam

NeuroPEARL, No signs of depressed skull or basal skull injuryNo signs of head trauma

Case 3






Case 3

You do a ED FAST and it is negative for free fluid in the abdomen

What do you want to do now?

Case 4

68yo Male with known small cell lung CaMeds:

Undergoing outpatient chemotherapy and radiotherapy at TBCC for last 2 months

HPI:3 day history of dyspnea, apprehension and mild chest painPresents today feeling very unwell, presyncopal and markedly short of breath on minimal exertion

Case 4

Generally Appears unwell and dyspneic, markedly diphoreticHR 119, RR 24, BP 90/55, Sat 98% RA, Temp 36.9

CVSFaint HS appreciated, normal S1S2 and no EHSExtremities cool and cap refill 3-4 seconds, +mottledPeripheral edema is noted JVP = 6cm above sternal angle and pulsus paradoxus = 22mmHg

Resp Chest clear throughout but shallow breaths

AbdSoft but tender to palpation diffusely

Neuro Alert but confused and disorientated

DDX of pulsus paradoxus

Cardiac:pericardial effusionTamponadePECardiogenic shock

Pulmonary:AsthmaCOPDTension pneumothorax

Other:AnaphylaxisSVC syndrome

Case 4






Management of Tamponade

Maximize preloadFluids to ↑ filling pressure

Pressors

(dialysis)Uremic pce is an indication

PericardiocentesisSee remergs.com for how to

(thoracotomy)If post-traumatic

Temporizing Measures

Definitive Measures

Case 5

PP: 26yo FemalePMHx: HealthyHPI:

Involved in motorcycle accident at highway speeds + Helmet+ LOC on scene and now GCS 9STARS transfer and advised hypotensive on route unresponsive to fluids

Case 5Generally

GCS 6, collared, not responding to painNo obvious sites of external bleedingHR 57, RR 16, BP 79/40, Sats 98% 3L NP, T37.8

CVSHeart sounds normal, no pedal edema, JVP normalWarm and dry skin

RespNormal

AbdomenSoft and non-distended

MSKPelvis stable

NeuroPEARL, no signs of depressed or basal skull fractureReflexes absentPoor rectal tone

C-spine xray

Case 5

What is the difference between spinal shock and neurogenic shock?

Spinal Shock

Concussive injury to the spinal cordCauses total neurological dysfunction distal to the site of injuryUsually lasts <24hrs

May persist for several days

The end of spinal shock is heralded by the return of…..

Bulbocavernousus reflex

Neurogenic Shock

Disruption of sympathetic autonomic ganglia resulting in loss of vasomotor tone and lack of reflex tachycardia

Results in hypotension (low SVR)

Bradycardia: can be absolute or relativeDue to unopposed vagal tone to heart

Usually only occurs is lesion is at/above T4

DDx for hypotension & bradycardiaMedications (CaCB, BB, digoxin)

Neurogenic Shock

Adrenal insufficiency

++ vagal tone (yng, intra-abdominal issue)

Case 5






Management of neurogenic shock

Fluids – they have relative hypovolemiaAtropine 0.5 mg – 1.0 mg iv

Can try to help with their pressure transientlyHave ready for intubation as they may brady down 2ndary to the vagal response

PressorsPhenylephrine: 100mcg aliquots is a good temporizerEphedrine is an alternative

Case 6

53yo M

1400 golfing and severe central CP radiating to R shoulder and SOB

Within minutes was unresponsive and EMS called

Nitro given and BP ↓↓

Palpable pressure on route

Case 6

Generally Appears very unwell, pale diaphoretic and cool periphery. Minimally responsiveHR 108, BP 88/65, Sats 84% non-rebreather, RR 30

CVSTachy with no obvious murmurCool peripheries and thready pulse

Resp Diffuse crackles throughoutPink froth at the mouthSignificant respiratory distress

Case 6





5) Name potential pitfall

Shock Post-MI

DDxMyocardium: pump failure,VSD, FWR, RV infarct

Valvular: acute MR

Rhythm: brady/tachycardia

Other (later): PE, pericardial effusion, stroke, bleed (from a/c)

Cardiogenic shock approach

AMI +shock?

RV infarct? YES NO

Volume resuscitate Pulmonary congestion present? NO YES

Response adequate Pressor

Revascularize Response adequate YES

IABP and PTCA

Thanks Phil

YESNO

NO

How does a IABP work?

Cardiogenic Shock:Approach

Stabilize the ABCsIdentify etiology of cardiogenic shockSmall fluid bolus (250cc)Don’t be shy on fluids if RV infarctIonotropic/vasopressor supportManage infarct (avoid ßß & nitrates)

Cath vs lytics

MI + Cardiogenic shock:How to manage the MI?

OptionsThrombolysis

Get BP up with ionotropes then thrombolyse

Stabilize with IABP then thrombolyse

Early Revascularization (PTCA or CABG)

What does the literature tell us?


Thrombolysis in cardiogenic shockGISSI (N=280) 30 day MR

streptokinase 70.1%

medical mx 69.6%

NO trial has shown reduction mortality with cardiogenic shock with thrombolysis

Thanks Rob

SHOCK trial

RCT of AMI + cardiogenic shock152 early revascularization (PTCA or CABG) or 150 initial medical mx only (lysis initially, some had PTCA/CABG after 52hrs)

End Point early revasc. Med Mx stats

30d MR 46.7% 56% p=.11

6mth MR 50.3% 63.1% p=.027

Cardiogenic Shock:the SHOCK trial

Hochman JS. One year survival following early revascularization for cardiogenic shock. JAMA 2001.

End Point early revasc. Med Mx stats

1yr survival 46.7% 33.6% p=.03


Conclusions …….Patients with AMI complicated by cardiogenic shock, especially those < 75yo, should undergo emergent revascularization (PTCA or CABG)

Bonus Case78F.

Presents with SOB, hypoxia + hypotensionPMHX: CAD, CHF

VS:HR 110 BP 80/50, RR28, sats 88%RAJVP up, lungs are clear, no peripheral edema – poorly perfused

You order a portable CXR

What do you think?

What do you want to do?

Which can help you make the Dx?

STAT ECHO

CT

– but this patient is not stable enough for CT

Empiric heparinwhile investigating(if no CI)

As the pCXR is being done the patient finally stops pestering you with questions about what you think is going on.

You’re enjoying the silence until you see the monitor…

What do you want to do know?

Jerjes-Sanchez C. et al. Streptokinase and Heparin versus Heparin Alone in Massive Pulmonary Embolism: A Randomised Controlled Trial. Journal of Thrombosis and

Thrombolysis. 1995.

Prospective and randomised trial, N=8all had “massive” PE and in cardiogenic shockhigh prob. V/Q, with abnormal RH on echo or >9 obstructed segments on V/Q100% survival in streptokinase plus heparin group 100% mortality in heparin group

Small study, lots of limitations BUT one of the few studies on this

tPA in PE

The role for tPA in submassive PE is debatable – not a decision for us to makeIf the patient is in shock & they have a PE – give tPA (likely in consultation with ICU)

In the mean time intubate, heparinize + fluids PRN +/- pressors

If the patient has a cardiac arrest – give it tPA dosing

1mg/kg over 2-5 mins if in CAOver 30mins if perfusingIf stable 100mg over 2 H & ask yourself why you’re giving it in emerg

shock shawn dowling, pgy-5. objectives briefly discuss general pathophysiology classification of...

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