2Vicken Y. Totten Shock lecture Thanks to David Cheng MD And all who taught me
3DefinitionSHOCK: inadequate organ perfusion to meet the tissue’s oxygenation demand
4PATHOPHYSIOLOGY OF SHOCK SYNDROME Cells switch from aerobic to anaerobic metabolismlactic acid productionCell function ceases & cells swellmembranes becomes more permeableelectrolytes & fluids seep in & out of cellCells Die in Many Organs Death
5Stages of shock Compensated /Early Shock Vasoconstriction (renin & carotid sinus baroceptorIncrease in HR and RR <- sympthatic activation)Normotensive usually <- (aldosterone/ADH Na+/h20 retention)Decompensated / late ShockCool, clammy , hypotenisve.Vital organ preservationWorsening LOCContinued increase in HR and RR <-----(Chemreceptor respose to metabolic acidosis)Irreversible-HR and RR drop Multi Organ Failure Impending death)Compensated (early shock)-Body recognizes problem and triggers mechanisms to correct BP (autotransfusion)Vasoconstriction < (renin & carotid sinus baroceptorIncrease in HR and RR < sympthatic activation)Normotensive usually <------(aldosterone/ADH Na+/h20 retention)Decompensated (late shock)-Compensatory mechanisms can not keep up and begin to fail (bld moves to vital organs)Signs and symptoms more profound (pale cool clammy hypoBP)Worsening LOCContinued increase in HR and RR <-----(Chemreceptor respose tometabolic acidosis)Irreversible-no longer be helped by compensatory mechanisms (HR and RR dropMOFImpending death)
6Symptoms of Shock Fevers / Rigors (sepsis) SSCP (cardiogenic) General SymptomsSpecific SymptomsFevers / Rigors (sepsis)SSCP (cardiogenic)Wheezing (anaphylaxis)Trauma pain (hypovolemia)AnxiousDizzinessWeaknessFaintnessThirsty“I am sick”
7Early Signs of Shock in Non Complicated Patients WARM EARLY STAGE / PRESHOCKNeed high index of suspicion b/c lack of signs+/- tachycardia+/- orthostatics (HR more sensitive than BP)+/- pulse pressure narrowing+/-restless
8“Hypoperfusion can be present in the absence of significant hypotension.” (Don’t only relay on BP for diagnosisng shock)-fccs course
9Signs of Late Shock Hypotension COLD LATE STAGECold, clammy and pale skinRapid, weak, thready pulseRapid breathing (blow off CO2 met acidosis)CyanoticAMS->ComaAnuria
18Remember History and Physical often limited by patient’s condition Patient presentation can be variable secondary toSeverity of the perfusion defectUnderlying causePrior organ dysfunctionExam should be tailored to be performed quickly with highest yield for uncovering the cause of shock.
22Adequate circulating blood volume depends on 3 components; A minor impairment in one can be compensated for by the other 2 for a limited time. Prolonged or severe impairments will lead to SHOCK.
23An Approach to Shock – Know this! BP = SVR x COBP = blood pressureCO = cardiac output (pump & fluids)SVR = systemic vascular resistance (pipes)
24If the blood pressure is low, then either the: An Approach to ShockIf the blood pressure is low, then either the:CO is loworSVR is lowBOTH
25Low SVR There are only a few causes of low SVR. They ALL cause vasodilation:Septic shockNeurogenic (spinal cord injury) shockAnaphylaxis ShockVasodilator (antihypertensive) Posioning
26Look at and feel the patient! How do you assess SVR?Look at and feel the patient!Low SVR has the features:warm !!!pinkBounding pulseshyperdynamic heart (fast and pounding)
27Cause of shock (low BP) is then: What if the SVR is high?PalePoor cap refill (>2 seconds)Cool arms/legs (>2 degree C difference)Thready pulses (narrow pulse pressure (incr DBP))Cause of shock (low BP) is then:low CO
28CO = HR x SV What are factors of CO? CO = cardiac output HR = heart rateSV = stroke volume
29HR Problems Heart Rate problems are easy to diagnose Rate: bradycardia versus tachycardia
30Most difficult to diagnose and manage Low SV (stroke volume)Most difficult to diagnose and manage
31Stroke Volume depends on Preload--is the ventricle full?Hypovolemic ShockObstructive Shock (ie Tension PTX, Tamponade)Cardiac functionSqueezeContractility– can the ventricle contract?Can blood get out? Valve function:normal?regurgitation?stenosis?
32Perfusion (blood pressure) depends on: BP = CO x SVRCO = HR x SVSV = preload & cardiac contractility-valve
36Diagnosis of Shock MAP < 60 or decrease of 20 from baseline systolic BP 90 systolic BP > 40 mm Hg from the patient’s baseline pressureShock index (HR>SBP)Clinical s/s of hypoperfusion of vital organs
37Mean Arterial Pressure MAP is the mean perfusion pressure for the tissuesMost require a MAP of 60 or greater!Dependent only on the elastic properties of the arterial walls and the mean blood volume in the arterial treeMAP = (2 x DBP) + SBP3
38Pulse Pressure=SBP-DBP Pulse Pressure=SBP-DBP The difference between the systolic (fxn of ejection fraction) and diastolic pressures (function of SVR and distensibility (elastic recoil) of the aortaWideNormal mmHgCommonly seen with fever, anemia, exercise and hyperthyroidismAR (aortic regurgitation) is also a causeNarrowMay indicate an increase in vascular resistance with decreased stroke volume (ie aortic stenosis or decreased intravascular volume)
39Invasive Markers Global Markers Regional Markers Base Deficit Lactate Gastric pHSublingual CO2
40Base Deficit Inadequate tissue perfusion leads to tissue acidosis Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4Normal range +3 to –3 mmol per LElevated base deficit correlates with the presence and severity of shock
41Base Deficit Inadequate tissue perfusion leads to tissue acidosis Amount of base required to titrate 1 L of whole arterial blood to a pH of 7.4Normal range +3 to –3 mmol per LElevated base deficit correlates with the presence and severity of shock
42Initial Lactate Weil and Afifi. (Circulation 1970)
43Lactate and Outcomes Adult Patients A peak blood lactate levelof >4.0 mmol/Lwas identified as astrong independentpredictor of mortalityand morbidityand suggests that tissue hypoperfusionDemmers Ann Thorac Surg 70:2082-6:2000
45Gastric Intramucosal pH Blood flow is not uniformly distributed to all tissue bedsRegions with inadequate tissue perfusion may exist while global markers are ‘normal’Gut mucosa among the first to be affected during shock and the last to be restored to normalIntramucosal pH falls when perfusion becomes inadequate
46Sublingual capnometry: A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shockhypercarbia is a universal indicator of critically reduced tissue perfusion.
47Sublingual CO2 Decrease gut perfusion Non-invasive, hand held monitor Gastric tissue = esophagus = sublingual tissueNon-invasive, hand held monitorRapid measurementSensitive marker of decreased blood flow
48Sublingual capnometry: A new noninvasive measurement for diagnosis and quantitation of severity of circulatory shockP SL CO2 provides a prompt indication of the reversal of tissue hypercarbia when circulatory shock is reversed
53Correct PA-C PositionFrom the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.
70Goals of Shock Resuscitation Restore blood pressureNormalize systemic perfusionPreserve organ function
71Parameters of Adequate Resuscitation Urine output ( ml/kg/hr)acceptable renal perfusionReversal of lactic acidosis (nl. pH)improved perfusionNormal mental statusadequate cerebral perfusion
72Goal RAPIDLY RESTORE TISSUE PERFUSION SHOCK: an EMERGENCY !!!Goal RAPIDLY RESTORE TISSUE PERFUSIONRecognize it !!!Immediate stabilization: ABC……. SHOTGUN approachNormalization of BP, pulse, UOPHemodynamic parametersRestoration of aerobic metabolism, elimination of tissue acidosis, repayment of O2 debtTreat the cause
75Management Re-assess every 5-15 minutes ABC’sMaintain airwayDecrease work of breathing & Optimize 02Circulation & Control Hemorrhage includes:Direct pressurePressure pointsFluids & DrugsMust address and treat:PRELOADAFTERLOADPUMPRe-assess every 5-15 minutes(the sicker the patient, the shorter the interval
76Management priorities in hypoperfused states BP potency: Dopamine...NE…Vasopressin/PhenylephrineWhen in doubt, try a little more volume
82Treatment - Hypovolemic Reverse hypovolemia & hemorrhage controlCrystalloid vs. Colloid1 L crystalloid 250 ml colloidWatch for fluid overload by reassessing lung sounds3:1 Rule (3cc crystalloid for 1cc bld loss)Watch for hyperchloremic metabolic acidosis when large volumes of NaCl are infusedBest to give in 250 mL boluses in CHF followed by reassessment for another 250 cc bolusColloids: (ex: albumin)Will increase osmotic pressure, watch for pulm edemaRemain in vascular space longer (several hrs)NOT increase survivalprbc sooner than later500 ml whole blood increases Hct 2-3%, 250ml PRBC’s increases Hct 3-4%Increases oxygen carrying capacityUsed with acute hemorrhaging (mntn Hct 24% and Hgb 8g/dL)NOT FOR VOLUMEFFP for coagulopathy (all factors)Factor viiPLT for thrombocytopeniaPressors?
83ResuscitationTransport times < 15 minutes showed pre-hospital fluids were ineffective, however, if transport time > 100 minutes fluid was beneficial.Penetrating torso trauma benefited from limited resuscitation prior to bleeding control. Not applicable to BLUNT victims.
84Role of PASG?Higher mortality rate in penetrating thoracic, cardiac traumaRole undefined in rural, blunt traumaSplinting role
85Cardiogenic Shock Mech Signs defect in cardiac function (lost > 40% Fxn)Signs cardiac output PAOP/CVP SVR left ventricular stroke work (LVSW)
86Cardiogenic Shock Myocardial failure (MI) Severe Arrhythmia Severe Valvular dysfunctionReduction in cardiac output:>Decreased oxygen delivery
87Symptoms of Cardiogenic Shock Skin: progressive peripheral vasoconstriction results in cool, moist, pale skin with mottlingCHF SxJVD, HJR, APE, pedal edemaHeart:Sounds: d/t enlargement and congestion you can hear murmurs or S3 or S4Pulse: rapid rate and thready/weak pulseBP: decreased BP and MAPUO: decreases early d/t decreased renal perfusion
88Cardiogenic Shock Assess for: Signs of heart failure Signs of tamponadeCardiac dysrrhythmiaMyocardial infarctionTachycardiaMuffled heart sounds or third heart soundEngorged neck veins with hypotensionDyspneaEdema in feet and ankles
89Coronary Perfusion Pressure Coronary PP = DBP - PAOPcoronary perfusion = P across coronary a.GOAL - Coronary PP > 50 mm Hg
90Treatment of Cardiogenic Shock Increase oxygen supply to the heartDecrease O2 consumption (pain meds/sedation)Increase O2 delivery (Mech vent, reperfusion of the coronary arteries)Maximize the cardiac outputMntn normal rhythm (dysrhythmics, pacing, cardioversion)Diastolic Vasopressors (dopamine, epi, norepi, vasopressin)Improve myocardial contractility--Inotropesdobut and amrinoneDecrease the afterload (workload of the LV)IABPLVAD
91The Failing HeartImprove myocardial function, C.I. < 3.5 is a risk factor, 2.5 may be sufficient.Fluids first, then cautious pressorsRemember aortic DIASTOLIC pressures drives coronary perfusion (DBP-PAOP = Coronary Perfusion Pressure)If inotropes and vasopressors fail, intra-aortic balloon pump & LV assist devices
95Anaphylactic Shock Rapid onset Diffuse vasodilation mechanism from histamine & bradykininEdema from increased capillary permeabilityBronchoconstriction
96Symptoms Onset within seconds and progression to death in minutes Cutaneous manifestationsurticaria, erythema, pruritis, angioedemaRespiratory compromisestridor, wheezing, bronchorrhea, resp. distressCirculatory collapsetachycardia, vasodilation, hypotensionCNSapprehension->ams->coma
97Diagnosis History and physical alone make the diagnosis Lab values serve no roleHistamine levels are elevated for about 30 min, tryptase for several hours.
98Treatment Remove the antigen ABC’s IV Fluids, O2, cardiac monitor, pulse oxFirst line Rx:EpinephrineFor severe bronchospasm, laryngeal edema, signs of upper airway obstruction, respiratory arrest or shock: IV epi100 micrograms of 1:100,000 (place 0.1 mL of 1:1000 in 10 mL of NS, give over 5-10 min)If less severe, can give mL 1:1000 SC
99Treatment 2nd line: H1 blocker: Diphenhydramine 25-50 mg IV H2 blocker: Ranitidine 50 mg or Famotidine 20 mg IV.)Steroids (Methylprednisolone 125 mg IV or Prednisone mg po)AlbuterolFor patients taking Beta-blockers with refractory hypotension, think about glucagon
101SEPSISSystemic Inflammatory Response (SIRS) manifested by two or > of following:Temp > 38 or < 36 centigradeHR > 90RR > 20 or PaCO2 < 32WBC > 12,000/cu mm or > 10% Bands (immature wbc)
102Risk factors of Sepsis Extreme age: <1 and >65 years Surgical / invasive proceduresMalnutritionChronic illnessDM, CRF, HepatitisCompromised immune statusAIDS, immunosuppressives, EtOH, malignanciesDrug resistant organisms
103What is Sepsis? SIRS Sepsis Severe Sepsis Septic Shock Sepsis is the combination of the Systemic Inflammatory Response Syndrome (SIRS) & a confirmed or presumed infectious etiology.Severe Sepsis: SIRS criteria, source of infection and infection-induced organ dysfunction or hypoperfusion abnormalities (sepsis + lactic acidosis/oliguria/AMS/etc.)Septic Shock: SIRS criteria, source of infection, and hypotension not reversed with fluid resuscitation and associated with organ dysfunction or hypoperfusion abnormalitiesA long line sepsis trials…but first, what is sepsis? SIRS, or Systemic Inflammatory Response Syndrome, is the overall inflammatory response of a host. We often think that “sepsis” implies that someone is close to death. This isn’t true. But they may be…Someone with sepsis can be as benign as a strep pharyngitis with a fever of 102.2, HR of 125, and WBC=16 or it can be a hypotensive patient with meningococcemia who will die in the next several hours.
104Septic Shock Bacterial, viral, fungal infection “Warm shock” is early stageFever, tachycardia, tachypnoea, leucocytosis,inadequate oxygen extraction (High SvO2, Metabolic acidosis) in infected tissues“Cold shock” is late stage
105Septic/Inflammatory Shock Signs: Early– warm w/ vasodilation, often adequate urineoutput, febrile, tachypneic.Late-- vasoconstriction, hypotension, oliguria,altered mental status.Monitor/findings: Early—hyperglycemia, respiratoryalkylosis, hemoconcentration,WBC typically normal or low.Late – Leukocytosis, lactic acidosisVery Late– Disseminated IntravascularCoagulation & Multi-OrganSystem Failure.
106Septic Shock TX Prompt volume replacement - fill the tank Early antibiotic administration - treat the causeIf MAP < 60Dopamine = g/kg/minNorepinephrine = titrate (1-100 g/min)
108Neurogenic ShockEssential derangement: paralysis of the sympathetic chain which controls vascular tone from injury to thoracic or cervical level spinal cord injury.Produces decreased SVR from loss of vascular tone and bradycardia from unopposed parasympathetic input to SA node.
109Neurogenic (Vasogenic) Shock Caused by:Spinal cord injury loss of SNSMassive venous pooling & arteriolar dilatationSigns and Symptoms:Hypotension without tachycardiaWarm pink skin from cutaneous vasodilationLow BP w/ minimal response to fluidsAccompanying Neurologic deficitSpinal shock is not Neurogenic shockSpinal Shock: the temporary loss of spinal reflex activity that occurs below a total or near total spinal cord injury
110Treatment of Neurogenic Shock Increase vascular tone and improve COIncrease preload with fluidsCVPPAWPIncrease vascular toneVasopressorsMaintain heart rateTreat bradycardia if symptomaticMaintain adequate oxygenationWatch with SCI because of the disruption of O2 to the medullaInitiate therapy to prevent DVTSluggish venous flow will increase risk factorsSteroids (Methylprednisolone 30mg/kg over 15 min in first hour, then 5.4 mg/kg/hr x 23 hours)There are contradicting studies, all of which have flawThe symptoms of neurogenic shock typically last 1-3 weeks
112Adrenal Crisis Distributive Shock CausesAutoimmune adrenalitisAdrenal apoplexy = B hemorrhage or infarctThis is suspected when patient is non-responsive to fluids, vasopressors and antibiotics.Electrolytes may reveal hypoNa+ & hyperK+Steroids may be lifesaving in patient who is unresponsive to fluids-inotropic-vasopressor (hydrocortisone 100mg IV)
113Vasopressor Agents?Augments contractility, after preload established, thus improving cardiac output.Risk tachycardia and increased myocardial oxygen consumption if used too soonRationale, increased C.I. improves global perfusion
116Dobutamine -agonist 5 - 20 g/kg/min potent inotrope, variable chronotropecaution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
117Norepinephrine Potent -adrenergic vasopressor Some -adrenergic, inotropic, chronotropicDose g/minUnproven effect with low-dose dopamine to protect renal and mesenteric flow.
118Epinephrine - and -adrenergic effects potent inotrope and chronotropedose g/minincreases myocardial oxygen consumption particularly in coronary heart disease
119AmrinonePhosphodiesterase inhibitor, positive inotropic and vasodilatory effectsincreased cardiac stroke output without an increase in cardiac stroke workmost often added with dobutamine as a second agentload dose = mg/kg g/kg/min dripmain side-effect - thrombocytopenia
121Calcium Sensitisation by Levosimendan Enhanced contractility of myocardial cell by amplifying trigger for contraction with no change in total intracellular Ca2+Clinical trials statusUltimately, the binding of levosimendan to troponin C evokes a stabilising, prolonged conformational change that occurs when calcium binds to troponin C. This is an enhancement of calcium's effects, and it thus increases the force of contraction. Sensitising the filaments to calcium rather than increasing calcium levels means that there is less potential for arrhythmia and increased contractile force with less energy consumption (i.e., myocardial oxygen demand is not increased).
122Endpoints?ACS / ATLS - restoration of vital signs and evidence of end-organ perfusionSwan-guided resuscitationC.I. 4.5, DO2I 670, VO2I 166Lactic Acid clearanceGastric pH
123Shock: “rude unhinging of the machinery of life.” Don’t forget...Shock: “rude unhinging of the machinery of life.”-Samuel D. Gross, 1872