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3/4/2015 1 Circulatory shock Circulatory shock Types Etiology Pathophysiology Types Etiology Pathophysiology Types, Etiology, Pathophysiology Types, Etiology, Pathophysiology Blagoi Marinov, MD, PhD Blagoi Marinov, MD, PhD Pathophysiology Dept. Pathophysiology Dept. Physiology of Circulation: Physiology of Circulation: The Vessels The Vessels 600 000 miles of vessels containing 5 600 000 miles of vessels containing 5-6 liters of blood 6 liters of blood 600,000 miles of vessels containing 5 600,000 miles of vessels containing 5 6 liters of blood 6 liters of blood Vessel tone is controlled by the sympathetic and Vessel tone is controlled by the sympathetic and parasympathetic nervous system. parasympathetic nervous system. Pre Pre-capillary sphincters control blood flow through the capillary sphincters control blood flow through the capillaries in response to O capillaries in response to O2 demand of the tissue. demand of the tissue. Preload is dependant on constant peripheral vascular Preload is dependant on constant peripheral vascular resistance. resistance.

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Page 1: Types Etiology PathophysiologyTypes, Etiology, Pathophysiology - Shock... · 3/4/2015 1 Circulatory shock Types Etiology PathophysiologyTypes, Etiology, Pathophysiology Blagoi Marinov,

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Circulatory shockCirculatory shockTypes Etiology PathophysiologyTypes Etiology PathophysiologyTypes, Etiology, PathophysiologyTypes, Etiology, Pathophysiology

Blagoi Marinov, MD, PhDBlagoi Marinov, MD, PhDPathophysiology Dept.Pathophysiology Dept.

Physiology of Circulation:Physiology of Circulation:The VesselsThe Vessels

600 000 miles of vessels containing 5600 000 miles of vessels containing 5--6 liters of blood6 liters of blood 600,000 miles of vessels containing 5600,000 miles of vessels containing 5 6 liters of blood6 liters of blood

Vessel tone is controlled by the sympathetic and Vessel tone is controlled by the sympathetic and parasympathetic nervous system.parasympathetic nervous system.

PrePre--capillary sphincters control blood flow through the capillary sphincters control blood flow through the capillaries in response to Ocapillaries in response to O22 demand of the tissue.demand of the tissue.

Preload is dependant on constant peripheral vascular Preload is dependant on constant peripheral vascular resistance. resistance.

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MicrocirculationMicrocirculation

Responsive to local tissue needsResponsive to local tissue needsResponsive to local tissue needsResponsive to local tissue needs

Capillary beds can adjust size to supply Capillary beds can adjust size to supply undernourished tissue and bypass tissue undernourished tissue and bypass tissue with no immediate needwith no immediate need

PrePre--capillary sphincters and post capillary capillary sphincters and post capillary ee cap a y sp c e s a d pos cap a ycap a y sp c e s a d pos cap a ysphincters open and close to feed or sphincters open and close to feed or bypass tissuesbypass tissues

Causes of Inadequate PerfusionCauses of Inadequate Perfusion

Inadequate pumpInadequate pumpInadeq ate preloadInadeq ate preloadInadequate preloadInadequate preloadPoor contractilityPoor contractilityExcessive afterloadExcessive afterloadInadequate heart rateInadequate heart rate

Inadequate fluid volumeInadequate fluid volumeHypovolemiaHypovolemiaHypovolemiaHypovolemia

Inadequate containerInadequate containerExcessive dilationExcessive dilationInadequate systemic vascular resistanceInadequate systemic vascular resistance

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Hemodynamic ParametersHemodynamic Parameters

Systemic Vascular Resistance (SVR)Systemic Vascular Resistance (SVR) Systemic Vascular Resistance (SVR)Systemic Vascular Resistance (SVR)

Cardiac Output (CO)Cardiac Output (CO)

Mixed Venous Oxygen Saturation (SvO2)Mixed Venous Oxygen Saturation (SvO2)

Central Venous Pressure (CVP)Central Venous Pressure (CVP)

SyncopeSyncope

FaintingFainting -- lack of blood flow to the brainlack of blood flow to the brainFainting Fainting lack of blood flow to the brainlack of blood flow to the brainCan be confused with a neurological Can be confused with a neurological

condition (seizure)condition (seizure)DifferenceDifferenceEpisode begins in a standing positionEpisode begins in a standing positionPatient remembers feeling faint or lightheadedPatient remembers feeling faint or lightheadedPatient becomes responsive almost Patient becomes responsive almost

immediately after becoming supineimmediately after becoming supineSkin is usually pale and moistSkin is usually pale and moist

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Shock Shock definitiondefinition

Profound and widespread failure ofProfound and widespread failure ofProfound and widespread failure of Profound and widespread failure of the circulation leading to the circulation leading to

inadequate tissue perfusioninadequate tissue perfusion(e.g. cellular hypoxia and injury and vital organ (e.g. cellular hypoxia and injury and vital organ

dysfunction)dysfunction)y )y )

Leads to Multiple Organ Dysfunction Leads to Multiple Organ Dysfunction Syndrome (Syndrome (MODSMODS))

Shock Shock –– OverviewOverview

The effects of tissue hypoperfusion areThe effects of tissue hypoperfusion areThe effects of tissue hypoperfusion are The effects of tissue hypoperfusion are initally reversible, but lead to cellular initally reversible, but lead to cellular hypoxia which can cause:hypoxia which can cause:Cell membrane and ion pump dysfuctionCell membrane and ion pump dysfuction

Intracelluar edemaIntracelluar edema

Leakage of intracellular contents into the Leakage of intracellular contents into the extracelluar spaceextracelluar space

Inadequate regulation of intracelluar pHInadequate regulation of intracelluar pH

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General Pathophysiology of General Pathophysiology of Shock StatesShock States

Classifications of ShockClassifications of Shock

11.. Hypovolemic shock; (classic shock)Hypovolemic shock; (classic shock)11. . Hypovolemic shock; (classic shock)Hypovolemic shock; (classic shock) The most common form. It is a standard used to The most common form. It is a standard used to

compare other forms of shock in differential compare other forms of shock in differential diagnosis.diagnosis. Hemorrhagic / Blood lossHemorrhagic / Blood loss Dehydration / Fluid lossDehydration / Fluid loss

22.. Extracardiac Obstructive Shock:Extracardiac Obstructive Shock: Pulmonary Embolism / Blocked pulmonary circulationPulmonary Embolism / Blocked pulmonary circulation

Tension Pneumothorax / Increased intrathoracic Tension Pneumothorax / Increased intrathoracic pressure pressure

Cardiac Tamponade / Pressure on myocardium. Cardiac Tamponade / Pressure on myocardium. Decreased preload.Decreased preload.

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33. . Cardiogenic Shock:Cardiogenic Shock: ::

Classifications of ShockClassifications of Shock

Heart (pump) Failure (40% of Myocardium damaged by AMI)Heart (pump) Failure (40% of Myocardium damaged by AMI)

44.. Distributive ShockDistributive Shock::

NeurogenicNeurogenic // Spinal cord injury , drug overdose or poisoning Spinal cord injury , drug overdose or poisoning which affects nervous systems ability to maintain vascular tone which affects nervous systems ability to maintain vascular tone leading to vasodilation.leading to vasodilation.

AnaphylacticAnaphylactic / Vasodilation and fluid shifting from capillary to cell. / Vasodilation and fluid shifting from capillary to cell. Leads to micro clotting (hives) and smooth muscle contraction Leads to micro clotting (hives) and smooth muscle contraction (brochospasm)(brochospasm)

SepticSeptic / vasodilation and fluid shifting due to / vasodilation and fluid shifting due to overwhelming infection.overwhelming infection.

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HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

Shock due to loss of intravascular fluid volumeShock due to loss of intravascular fluid volume Shock due to loss of intravascular fluid volumeShock due to loss of intravascular fluid volume

Possible causesPossible causes

Internal or external hemorrhageInternal or external hemorrhage

Traumatic hemorrhageTraumatic hemorrhage

Long bone or open fracturesLong bone or open fractures

Severe dehydration from GI lossesSevere dehydration from GI losses

Plasma losses from burnsPlasma losses from burns

Diabetic ketoacidosisDiabetic ketoacidosis

Excessive sweatingExcessive sweating

HYPOVOLEMIC SHOCKHYPOVOLEMIC SHOCK

Also can result from internal thirdAlso can result from internal third--space lossspace loss Also can result from internal thirdAlso can result from internal third--space lossspace loss

Possible causesPossible causes

Bowel obstructionBowel obstruction

PeritonitisPeritonitis

PacreatitisPacreatitis

Liver failure resulting in ascitesLiver failure resulting in ascites

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CARDIOGENIC SHOCKCARDIOGENIC SHOCK

Inability to pump enough blood to supply allInability to pump enough blood to supply all Inability to pump enough blood to supply all Inability to pump enough blood to supply all body partsbody parts

Primary cause is severe left ventricular failure Primary cause is severe left ventricular failure (AMI, CHF)(AMI, CHF) Accompanying hypotension decreases coronary Accompanying hypotension decreases coronary

artery perfusion, worsening the situationartery perfusion, worsening the situationy p , gy p , g

Other compensatory mechanismsOther compensatory mechanisms--increased increased peripheral resistance, increased myocardial O2 peripheral resistance, increased myocardial O2 demand demand --worsen situationworsen situation

CARDIOGENIC SHOCKCARDIOGENIC SHOCK

Other causesOther causes Other causesOther causes

Chronic progressive heart diseaseChronic progressive heart disease

Rupture of papillary heart muscles or Rupture of papillary heart muscles or intraventricular septumintraventricular septum

EndEnd--stage valvular diseasestage valvular disease

Patients may be normovolemic or hypovolemicPatients may be normovolemic or hypovolemic

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COCOR.A.S.R.A.S. CatecholamineCatecholamine

CARDIOGENIC SHOCKCARDIOGENIC SHOCK

COCOActivationActivation

OO22

Volume/Volume/PreloadPreload

SVRSVRMyocardialMyocardialOO22 demanddemand

ReleaseRelease

DyspneaDyspnea

22

supplysupply

PeripheralPeripheral& pulmonary& pulmonary

edemaedemaImpairedImpaired

myocardial functionmyocardial function

DISTRIBUTIVE SHOCKDISTRIBUTIVE SHOCK

Shock resulting from inadequate peripheral Shock resulting from inadequate peripheral resistance due to widespread vasodilationresistance due to widespread vasodilation

Common causesCommon causes SepsisSepsis

AnaphylaxisAnaphylaxis

Spinal cord injurySpinal cord injury

Central nervous system injuriesCentral nervous system injuries

Insulin overdoseInsulin overdose

Addisonian crisisAddisonian crisis

No sympathetic responseNo sympathetic response

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Sympathetic ToneSympathetic Tone Vascular ToneVascular Tone

DISTRIBUTIVE SHOCKDISTRIBUTIVE SHOCK

Sympathetic ToneSympathetic ToneOrOr

Parasympathetic ToneParasympathetic Tone

Vascular ToneVascular Tone

Massive VasodilationMassive VasodilationTissueTissueperfusionperfusion

SVR & PreloadSVR & Preload Cardiac OutputCardiac Output

Distributive ShockDistributive ShockVariantsVariants

Anaphylactic ShockAnaphylactic ShockAnaphylactic ShockAnaphylactic ShockMechanism: severe allergic reactionMechanism: severe allergic reaction

Skin: hives, possible petechia. Urticaria, pallor, Skin: hives, possible petechia. Urticaria, pallor, cyanosiscyanosis

Blood pressure: abrupt fall in cardiac outputBlood pressure: abrupt fall in cardiac output

Respiration: rapid shallow, dyspnea with stridor, Respiration: rapid shallow, dyspnea with stridor, wheezes, crackles, leading to respiratory arrestwheezes, crackles, leading to respiratory arrest

Other: swelling of mucus membranes/pulmonary Other: swelling of mucus membranes/pulmonary edemaedema

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Septic shockSeptic shock

Distributive ShockDistributive ShockVariantsVariants

Septic shockSeptic shockMechanism: overwhelming infectionMechanism: overwhelming infection

Skin: varies form flushed pink (if fever is present) to Skin: varies form flushed pink (if fever is present) to pale and cyanotic. Purple blotches possible, peeling pale and cyanotic. Purple blotches possible, peeling skin, general or on palms and soles of feetskin, general or on palms and soles of feet

Blood pressure: earlyBlood pressure: early——cardiac output increases but cardiac output increases but toxins prevent increase in BP. Late toxins prevent increase in BP. Late ------ drop in BP, drop in BP, hypotensionhypotension

Respiratory: dyspnea with altered lung soundsRespiratory: dyspnea with altered lung sounds

Other: high fever, (except in elderly and very young), Other: high fever, (except in elderly and very young), Late sign is pulmonary edemaLate sign is pulmonary edema

Neurogenic ShockNeurogenic Shock

Distributive ShockDistributive ShockVariantsVariants

ggMechanism: vasodilationMechanism: vasodilation

Skin: areas of vasodilation, at first become warm, pink Skin: areas of vasodilation, at first become warm, pink and dry. Later with pooling: pallor and cyanosis to the and dry. Later with pooling: pallor and cyanosis to the upper surfacesupper surfaces

Pulse: highly variable depending on injury or action of Pulse: highly variable depending on injury or action of drug/poison: May be abnormally slow or abnormallydrug/poison: May be abnormally slow or abnormallydrug/poison: May be abnormally slow or abnormally drug/poison: May be abnormally slow or abnormally fast, fast,

Respiration: severely compromised: becoming slow, Respiration: severely compromised: becoming slow, shallow, with abnormal patterns. Patient may loose shallow, with abnormal patterns. Patient may loose stimulus to breathstimulus to breath

Other: hypothermia. Other: hypothermia.

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Obstructive ShockObstructive Shock(Extracardiac)(Extracardiac)

Decreased diastolic fillingDecreased diastolic fillingDecreased diastolic fillingDecreased diastolic fillingTension pneumothoraxTension pneumothorax

Pericardial tamponadePericardial tamponade

Increased ventricular afterloadIncreased ventricular afterloadMassive PEMassive PE

Differentiating Types of Differentiating Types of ShockShock

(hemodynamic profiles)(hemodynamic profiles)

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SummarySummarySHOCK= Inadequate Tissue PerfusionSHOCK= Inadequate Tissue Perfusion

Mechanisms:Mechanisms: Mechanisms:Mechanisms: Inadequate oxygen delivery Inadequate oxygen delivery

Release of inflammatory mediatorsRelease of inflammatory mediators

Further microvascular changes, compromised Further microvascular changes, compromised blood flow and further cellular hypoperfusionblood flow and further cellular hypoperfusion

Inadequate elimination of metabolic wasteInadequate elimination of metabolic waste..

Clinical Manifestations:Clinical Manifestations:Multiple organ failureMultiple organ failure

HypotensionHypotension

METABOLISM METABOLISM OF POOR PERFUSION STATESOF POOR PERFUSION STATES

Metabolism isMetabolism is anaerobicanaerobic Metabolism is Metabolism is anaerobicanaerobic

Glucose breaks down into pyruvic acid, but not enough Glucose breaks down into pyruvic acid, but not enough oxygen is present to enter into the Krebs oxygen is present to enter into the Krebs cyclecycle

Pyruvic acid accumulates, degrades into lactic acid, Pyruvic acid accumulates, degrades into lactic acid, which also accumulates along with other metabolic acids which also accumulates along with other metabolic acids

Cells die; tissues die; organs fail; organ systems fail; Cells die; tissues die; organs fail; organ systems fail; death ultimately ensuesdeath ultimately ensues

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Cellular Response to ShockCellular Response to Shock

TissueTissue Impaired cellularImpaired cellularOO22

perfusionperfusion

AnaerobicAnaerobicmetabolismmetabolism

metabolismmetabolism22

useuse

Impaired Impaired glucose glucose usageusage

Stimulation of Stimulation of clotting cascade & clotting cascade &

inflammatoryinflammatoryresponseresponse

NaNa++ PumpPumpFunctionFunction

ATPATPsynthesissynthesis

Cellular edemaCellular edema Vascular volumeVascular volume

Intracellular NaIntracellular Na++

& water& water

Stages of Shock: Stages of Shock: Classic Shock SyndromeClassic Shock Syndrome

11 CompensatedCompensated -- body is able to compensate andbody is able to compensate and1.1. CompensatedCompensated body is able to compensate and body is able to compensate and maintain tissue perfusion.maintain tissue perfusion.

2.2. ProgressiveProgressive ((uncompensateduncompensated) ) -- body begins to loss body begins to loss its ability to compensate its ability to compensate -- inadequate perfusion inadequate perfusion begins.begins.

3.3. IrreversibleIrreversible -- Cell and tissue damage result in Cell and tissue damage result in multimulti--system organ failure leading to death. system organ failure leading to death.

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Body defense mechanisms attempt to preserve majorBody defense mechanisms attempt to preserve major

COMPENSATED SHOCKCOMPENSATED SHOCK

Body defense mechanisms attempt to preserve major Body defense mechanisms attempt to preserve major organsorgansPrecapillary sphincters close, blood is shuntedPrecapillary sphincters close, blood is shunted

Increased heart rate and strength of contractionsIncreased heart rate and strength of contractions

Increased respiratory function bronchodilationIncreased respiratory function bronchodilation Increased respiratory function, bronchodilationIncreased respiratory function, bronchodilation

Decreased skin perfusionDecreased skin perfusion

Altered mental statusAltered mental status

COMPENSATED SHOCKCOMPENSATED SHOCK

Will continue until problem solved or shock progresses toWill continue until problem solved or shock progresses to Will continue until problem solved or shock progresses to Will continue until problem solved or shock progresses to next next stagestage

Can be difficult to detect with subtle indicatorsCan be difficult to detect with subtle indicators

TachycardiaTachycardia

Decreased skin perfusionDecreased skin perfusion

Alterations in mental Alterations in mental statusstatus

Some medications such as Some medications such as --blockersblockers can hide signs can hide signs and symptomsand symptoms

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UNCOMPENSATED SHOCKUNCOMPENSATED SHOCK

Physiological responsePhysiological response

Precapillary sphincters open, blood pressure fallsPrecapillary sphincters open, blood pressure falls

Cardiac output fallsCardiac output falls

Marked increase in heart rateMarked increase in heart rate

Rapid, thready pulseRapid, thready pulsep , y pp , y p

Blood surges into tissue beds, blood flow stagnatesBlood surges into tissue beds, blood flow stagnates

Red cells stack up in rouleauxRed cells stack up in rouleaux

Agitation, restlessness, confusionAgitation, restlessness, confusion

Easier to detect than compensated shockEasier to detect than compensated shock

UNCOMPENSATED SHOCKUNCOMPENSATED SHOCK

Easier to detect than compensated shockEasier to detect than compensated shock

Prolonged capillary refill timeProlonged capillary refill time

Marked increase in heart rateMarked increase in heart rate

Rapid thready pulseRapid thready pulse

Agitation, restlessness, confusionAgitation, restlessness, confusion

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IRREVERSIBLE SHOCKIRREVERSIBLE SHOCK

Compensatory mechanisms fail cell deathCompensatory mechanisms fail cell death Compensatory mechanisms fail, cell death Compensatory mechanisms fail, cell death begins, vital organs falterbegins, vital organs falter

Patient may be resusitated but will die later of Patient may be resusitated but will die later of ARDS, renal and liver failure, sepsisARDS, renal and liver failure, sepsis

Shock Shock -- MortalityMortality

Despite extensive research mortality ratesDespite extensive research mortality ratesDespite extensive research, mortality rates Despite extensive research, mortality rates remain highremain high

HypovolemicHypovolemic: variable, depends on etiology and time : variable, depends on etiology and time to treatmentto treatment

CardiogenicCardiogenic: 60: 60--90%90%

DistributiveDistributive (Septic): 35(Septic): 35--40%40%

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Shock Shock -- ManagementManagement

Systemic Inflammatory Response Systemic Inflammatory Response Syndrome (SIRS)Syndrome (SIRS)

Defined as when generalized inflammation occurs andDefined as when generalized inflammation occurs and Defined as when generalized inflammation occurs and Defined as when generalized inflammation occurs and threatens vital organsthreatens vital organs

Causes: massive tissue injury, burns, and pancreatitis, Causes: massive tissue injury, burns, and pancreatitis, severe infections or sepsissevere infections or sepsis

Effects: endothelium is damaged and allows fluid to leak Effects: endothelium is damaged and allows fluid to leak into the body tissues, results in poor perfusion of blood into the body tissues, results in poor perfusion of blood to organsto organs

Body is in a hypermetabolic stateBody is in a hypermetabolic state

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Multiply Organ Dysfunction Multiply Organ Dysfunction Syndrome (MODS)Syndrome (MODS)

Defined: when 2 or more organ systems are failing at one Defined: when 2 or more organ systems are failing at one g y gg y gtimetime

Is caused by the immune system’s uncontrolled response to Is caused by the immune system’s uncontrolled response to severe illness or injurysevere illness or injury

Common cause of death of patients in the ICU, with mortality Common cause of death of patients in the ICU, with mortality of 50%of 50%of 50%of 50%

Identifying and acting quickly can help survivalIdentifying and acting quickly can help survival

Can develop quickly following surgery, trauma, or severe Can develop quickly following surgery, trauma, or severe burns or slowly in the case of an infectionburns or slowly in the case of an infection

Treatment for SIRS/MODSTreatment for SIRS/MODS

Critical careCritical careCritical careCritical care

GoalsGoals Prevent and treat infectionsPrevent and treat infections

Maintain tissue oxygenationMaintain tissue oxygenation

Provide nutritional and metabolic responseProvide nutritional and metabolic response

Support failing organsSupport failing organs

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Hemodynamic MonitoringHemodynamic Monitoring

Goal is to optimize tissue oxygenationGoal is to optimize tissue oxygenation Goal is to optimize tissue oxygenationGoal is to optimize tissue oxygenation

LactateLactate

CVPCVP

Arterial pressureArterial pressure

Urine outputUrine output Urine outputUrine output

Pulse oximetryPulse oximetry

Thank you !