Shock
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Transcript of Shock
Shock
Shawn Dowling, PGY-5
ObjectivesBriefly 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 7The nurses have already drawn a venous gas
CO 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 shockRude unhinging of the machinery of life
OrThe 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 supplyDisrupted cellular homeostasisFailed aerobic metabolism –> anaerobic metabolism –> lactic acidosisCalcium shifts - impairs cardiac contractilityFailed ion gradients and cellular pumpsCell 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 ShockMany different ways
MnemonicsPhysiologicClinical
It doesn’t matter which you use as long asYou know it coldIt’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
HypovolemicOvert/Occult losses of blood
5 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)
CardiogenicVessels
AMI or acute or chronic– usually need to infarct 40% to cause shockAoD
RhythmBradyTachydysthrythmias
ValvularStenosisRegurgitation
MyocardiumRupture (FW or VSD)MyocarditisCardiomyopathyRV involvement
PericardiumTamponade
ObstructiveIntravascular
PEAmniotic Fluid EmbolismAir embolismFat embolism
ExtravascularTension PTXCardiac tamponadeSVC syndrome
DistributiveNeurogenicAnaphylacticSepticToxicologic
(CaCB, BB), CO, cyanide, iron, ASA, etcEndocrine
Adrenal 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
EpinephrineEphedrinePhenylephrineNorepinephrineDopamineMilrinone
Direct vs indirect vasopressors
Direct agents stimulate the receptor directlyIndirect 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 1PP: 8yo F with known allergy to waspsPMHx: Healthy and no medsHPI:
At day camp and “forgot” her epi-penStung by 2 hornets after accidentally running into a nestPresents by personal vehicle to ED Given PO Benadryl by family member
Case 1Generally
Appears 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 shock2) Describe the pathophysiology3) Name the management goals4) Define the best interventions to obtain
the above goals5) 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 epinephrineThe 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 2Generally
Appears 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 intravenouslyThere is no improvement and the patient remains hypotensive and relatively bradycardic…..
Case 21) 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
ManagementFluidsMeds
Epi is the first line Tx for anaphylaxis IV (1:10,000)
1 mL (100ug) aliquot – repeat q60sec until desired effectInfusion - 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 380M. Hx of COPD. Presents with productive cough and feels unwell.T-40, RR28, sats 85% on NRB, HR-120, BP 90/50Working Dx – Pneumonia + SepsisYou decide you going to intubate this patient because of failure to oxygenateAny 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 hypotensionSeptic 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 3PP: 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
1) Name the general category of shock2) Describe the pathophysiology3) Name the management goals4) Define the best interventions to obtain
the above goals5) Name potential pitfalls
Case 3
You do a ED FAST and it is negative for free fluid in the abdomenWhat do you want to do now?
Case 468yo 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 4Generally
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 paradoxusCardiac:
pericardial effusionTamponadePECardiogenic shock
Pulmonary:AsthmaCOPDTension pneumothorax
Other:AnaphylaxisSVC syndrome
EKG
EDUS
Case 4
1) Name the general category of shock2) Describe the pathophysiology3) Name the management goals4) Define the best interventions to obtain
the above goals5) Name potential pitfalls
Management of TamponadeMaximize preload
Fluids 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 5PP: 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 ShockConcussive 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 heartUsually only occurs is lesion is at/above T4
DDx for hypotension & bradycardiaMedications (CaCB, BB, digoxin)Neurogenic ShockAdrenal insufficiency++ vagal tone (yng, intra-abdominal issue)
Case 5
1) Name the general category of shock2) Describe the pathophysiology3) Name the management goals4) Define the best interventions to obtain
the above goals5) Name potential pitfalls
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 M1400 golfing and severe central CP radiating to R shoulder and SOBWithin minutes was unresponsive and EMS called
Nitro given and BP ↓↓Palpable pressure on route
Case 6Generally
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
EKG
Case 6
1) Name the general category of shock2) Describe the pathophysiology3) Name the management goals4) Define the best interventions to obtain
the above goals5) Name potential pitfall
Shock Post-MI
DDxMyocardium: pump failure,VSD, FWR, RV infarctValvular: acute MRRhythm: brady/tachycardiaOther (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?
OptionsThrombolysisGet BP up with ionotropes then thrombolyseStabilize with IABP then thrombolyseEarly Revascularization (PTCA or CABG)
What does the literature tell us?
MI + Cardiogenic shock:How to manage the MI?
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 trialRCT of AMI + cardiogenic shock
152 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
MI + Cardiogenic shock:How to manage the MI?
Conclusions …….Patients with AMI complicated by cardiogenic shock, especially those < 75yo, should undergo emergent revascularization (PTCA or CABG)
Bonus Case78F. Presents with SOB, hypoxia + hypotension
PMHX: 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
N CXR
What do you think?
What do you want to do?
Which can help you make the Dx?
STAT ECHOCT
– 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 PEThe 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