ShockDr SAM GEORGE

CONSULTANT ANAESTHESIA & INTENSIVE CARE

OverviewDefinitions

Initial Assessment – ABC

Stages of Shock

Physiologic Determinants of Shock

Types of Shock

Common Features of Shock

Work-up

Generic Approach to Management

Case scenarios and Management

Take Home Points

Definition of Shock Inadequate perfusion and oxygenation of cells

Hypotension is not a requirement

Why should you care?

High mortality - 20-90%

Early on the effects of O2 deprivation on the cell are REVERSIBLE

Early intervention reduces mortality

Remember!Assessment Intervention and Monitoring

happens together in acute scenarios.

Initial Assesment - ABCAirway:

Does pt have mental status to protect airway? GCS less than “eight” means “intubate” Airway is compromised in anaphylaxis

Breathing: If pt is conversing with you, A & B are fine Place patient on oxygen

Circulation: Vitals (HR, BP) 2 large bore (#16g) IV, start fluids (careful if cardiogenic shock),

put on continuous monitor

ABC “DE”

In a trauma, perform ABCDE, not just ABC

Deficit or Disability Assess for obvious neurologic deficit Moving all four extremities? Pupils? Glascow Coma Scale (M6, V5, E4)

Exposure Remove all clothing on trauma patients

TYPES OF SHOCKType of Shock Insult Physiologic

EffectCompensation

Cardiogenic Heart fails to pump blood out•MI, arrhythmia, aortic stenosis, mitral regurg,

↓CO BaroRc↑SVR

Obstructive Heart pumps well, but the outflow is obstructed•Extracardiac obstructive causes such as PE, tension pneumothorax, tamponade

↓CO BaroRc↑SVR

Hypovolemic Heart pumps well, but not enough blood volume to pump•Hemorrhage•Fluid Loss (Vomiting, Diarrhea, Burns)

↓CO BaroRc↑SVR

Distributive Heart pumps well, but there is peripheral vasodilation•Septic, anaphylactic, and neurogenic shock•Pancreatitis, burns, multi-trauma via activation of the inflammatory response

↓SVR ↑CO

Stages of Shock

Timeline and progression will depend on:

-Cause

-Patient Characteristics

-Intervention

Insult

Preshock(Compensation)

Shock(CompensationOverwhelmed)

End organDamage

Death

Stages of Shock: ExampleStage Pathophysiology Clinical Findings

Insult Splenic Rupture -- Blood Loss Abdominal tenderness and girth

Preshock Hemostatic compensationMAP =↓CO(HR x↓SV) x ↑ SVR Decreased CO is compensated by increase in HR and SVR

MAP is maintainedHR will be increasedExtremities will be cool due to vasoconstriction

Shock Compensatory mechanisms fail

MAP is reducedTachycardia, dyspnea, restlessness

End organ dysfunction

Cell death and organ failure Decreased renal functionLiver failureDisseminated Intravascular CoagulopathyDeath

Common Features of ShockHypotension (not an absolute requirement)

SBP < 90mm Hg, not seen in “preshock”

Cool, clammy skin Vasoconstrictive mechanisms to redirect blood from periphery to

vital organs Exception is warm skin in early distrib. shock

Oliguria (↓kidney perfusion)

Altered mental status (↓brain perfusion)

Metabolic acidosis

Hypovolemic Shock

Distributive Shock

Cardiogenic Shock

ObstructiveShock

HR Increased Increased(Normal in Neurogenic shock)

May be increased or decreased

Increased

JVP Low Low High High

BP Low Low Low Low

SKIN Cold Warm (Cold in severe shock)

Cold Cold

CAPREFILL

Slow Slow Slow Slow

Type of Shock

Insult Physiologic Effect

Compensation

CompensationHeart Rate

CompensationContractility

Cardiogenic Heart fails to pump blood out

↓CO BaroRc↑SVR

↑ ↑

Obstructive Heart pumps well, but the outflow is obstructed

↓CO BaroRc↑SVR

↑ ↑

Hemorrhagic Heart pumps well, but not enough blood volume to pump

↓CO BaroRc↑SVR

↑ ↑

Distributive Heart pumps well, but there is peripheral vasodilation

↓SVR ↑CO ↑

No Change - in neurogenic shock

↑

No Change - in neurogenic shock

Compensatory Mechanisms

Additional Compensatory Mechanisms

Renin-Angiotensin-Aldosterone Mechanism AII components lead to vasoconstriction Aldosterone leads to water conservation

ADH leads to water retention and thirst

Inflammatory cascade

Work-upHistory to determine etiology

Bleeding (recent surgery, trauma, GI bleed) Allergies or prior anaphylaxis Sx consistent with pancreatitis, EtOH history Hx of CAD, MI, current chest pain/diaphoresis

Examination Mucous membranes, JVD, lung sounds, cardiac exam, abdomen,

rectal (blood), neuro exam, skin (cold & clammy or warm)

Investigations: Labs/Tests directed toward suspected dx’s

GENERIC APPROACH TO MANAGEMENT OF SHOCK

OPTIMISE OXYGEN CONTENT

OPTIMISE CARDIAC OUTPUT

OPTIMISE BLOOD PRESSURE

OPTIMISE REGIONAL BLOOD FLOW

In Short

The oxygenated blood carried forward by the cardiac output has to reach the Vital organs,

this is only possible if there is a good pressure gradient

and the organ vascular resistance is low;

try to maintain the Blood pressure within the regional Auto regulation range,

I prefer to target the kidneys as they are a filter and require higher mean arterial pressures, essentially ensures all other organs are also perfused

OPTIMISE OXYGEN CONTENT

HbCheck if appears pale or anaemicCheck Hb and coagulation status

Sao2 just a pulse oximeter tells you the SpO2Check SaO2 on ABG

OPTIMISE CARDIAC OUTPUTCO = Stroke volume (SV) x Heart rate (HR)

STROKE VOLUME depends on

Preload

Contractility

Afterload

Check each component of Cardiac Output

Stroke Volume (depends on 3 factors) Preload

Look at response to fluid bolus If improves BP could be suggestive of

decreased preload (volume) and a reasonable contractility.

If no improvement or worsening BP could be suggestive of a Contractility problem or excess preload (volume) situation

Look at CVP

Check each component of Cardiac Output

Contractility Check any history suggestive of Ischaemic

disease or CCF Check ECHO and ECG results A high systolic pressure could be suggestive of

good contractility

Check each component of Cardiac Output

Afterload Check Echo if suggestive of any obstructive

features If peripheries cold could indicate increased

vascular resistance If peripheries warm could indicate vasodilation

and decreased vascular resistance a low diastolic Blood pressure could indicate low

vascular resistance a high diastolic Blood pressure could indicate

increased vascular resistance

Check each component of Cardiac Output

HR If low, 2 possible interventions

electric pacing

pharmacological intervention if high, 2 possible interventions

electric cardioversion Defibrillation

pharmacological intervention

OPTIMISE BLOOD PRESSUREProduct of Cardiac output and peripheral

resitance.

BP=CO X PR

OPTIMISE REGIONAL BLOOD FLOW

Improve Blood pressure, which is a product of Cardiac Output peripheral resistance (squeeze)

Improve, Regional Blood Flow = (p1-p2) / R, i.e. by increasing Mean Arterial pressure decreasing venous or the compartment pressure whichever is higher, and also decreasing the organ vascular resistance

Auto regulation range

try to match Renal auto regulation range Kidneys

MAP 80-180 mmHg Brain

MAP 65-130 mmHg Heart

MAP 50-150 mmHg If hypertensive Autoregulation values could shift to

right, essentially you will need Higher MAP (mean arterial pressure) to perfuse the vital organs.

Case 155yo male otherwise healthy who is fresh post-

op from a colon resection for CA

Called for tachycardia, hypotension, altered mental status, and abd distension

On exam: pale, dry mucous membranes, disoriented, abdomen is tender and tense

UOP is 15mL over past hour

What else do you want to know?

What is the most likely diagnosis?

Case 1The one thing you want to know: Hct (Hgb)

Dx: Hemorrhagic (hypovolemic) shock

Management ABC (need intubation? IV access?) Wide open fluids and T&C 6 units PRBC Send coags when sending for CBC Make sure it’s not an MI (chest pain, EKG) Give blood & prepare for re-exploration in OR

Case 275yo male PMH CAD, PVD, DM who is post-op

from AAA repair complains of crushing substernal chest pain

Stat 12-lead EKG shows ST elevation in 2 contiguous leads

What do you do?

What is the diagnosis?

Case 2

ABC, get good access, continuous monitor

Dx: Acute ST elevation MI

Treatment: “MONA” Oxygen, Aspirin, Nitroglycerin, Morphine Beta-blockade (no heparin or tPA due to surg) Plavix & GP IIb/IIIa inhibitor (i.e. eptifibatide) Stat cardiology consult for cardiac cath

Case 2, continuedCath reveals critical stenosis of left main s/p

balloon angioplasty

24 hrs later, in ICU intubated

Vitals: 80/50

On exam: cool, clammy extremities

Echocardiogram: severe LV dysfunction

What is the diagnosis & management?

Case 2, continuedDx: Cardiogenic shock 2ndary to STEMI

Management

RESUSCITATIVE CARE (remember, ABC)

SUPPORTIVE CARE Ventilator support Inotropes and Vasopressors Cardiac output monitoring to optimize volume status and cardiac function

May need intra-aortic balloon pump

DEFINITIVE CARE PCI Thrombolysis, Aspirin, Heparin (maintain

coronary patency)

Case 360yo male heavy drinker brought in by EMS with nausea,

vomiting, severe epigastric pain radiating to the back

Tachycardic, hypotensive

Altered mentation, dry mucous membranes, minimal UOP after Foley

What is the most likely diagnosis? Differential diagnosis?

How do you manage this patient?

Case 3Acute pancreatitis

DDx of acute abdomen: Perforated viscus, acute mesenteric ischemia, cholecystitis, SBO, Ruptured AAA, MI

Hypovolemic shock from vomiting and Distributive shock from the inflammation: vasodilation, vasopermeability (3rd-space)

Management

RESUSCITATIVE CARE (remember, ABC) These pts require heavy, heavy fluid resus

SUPPORTIVE CARE NPO, NGT feed post-pyloric, consider CT scan

DEFINITIVE CARE

Case 455yo male also post-op from colon resection

for CA, epidural placed for post-operative pain control

Called by nurse for hypotension and bradycardia

Abdomen soft, no pallor, altered mentation

Hct is 38

Most likely diagnosis?

Case 4Neurogenic shock 2ndary to epidural

Differentiated from hypovolemic due to bradycardia

Management

RESUSCITATIVE CARE (remember, ABC) IVF

SUPPORTIVE CARE If BP does not respond, then alpha-agonist such as phenylephrine until above measures stabilize patient, then wean the vasopressor

DEFINITIVE CARE Turn down or turn off epidural,

Case 525yo male presents with diffuse abdominal

pain of 1day duration, started initially as epigastric pain after a meal. Takes ibuprofen 3x a day.

Vitals: hypotensive, tachycardic

Tense abdomen, involuntary guarding, altered mental status, oliguric

What is the diagnosis & management?

Case 5Septic shock 2ndary to perf duodenal ulcer

This patient has diffuse peritonitis

Management:

Management

RESUSCITATIVE CARE (remember, ABC) IV & resuscitation (requires heavy fluids)

SUPPORTIVE CARE If pt, does not respond to fluids, may need vasopressors (norepinephrine)

Have beta-agonist effects to help pump function as well as alpha-agonist for periph vasoconstriction

DEFINITIVE CARE Broad-spectrum IV antibiotics Emergent OR for ex-lap, washout & repair

Take Home PointsShock = poor tissue perfusion/oxygenation

Know difference btw compensated/uncomp shock

3 types are based on physiology of shockHypovolemic due to decreased preloadCardiogenic due to decreased SV or CODistributive due to decreased SVR

Know the common signs a/w shockOliguria, AMS, cool/clammy skin, acidosis

Work-up & management starts with ABC

Aggressive resuscitation except if cardiogenic

Vasopressors if hypotensive despite fluids

Thanks

MAPDiastolic + 1/3 Pulse pressure

REGIONAL BLOOD FLOWFLOW= P1-P2 / R

P1= MAP

P2= VENOUS PRESSURE

REGIONAL BLOOD FLOWCORONARY BLOOD FLOW=

AORTIC ROOT DIASTOLIC PRESSURE-LVEDP

---------------------------------------------------CORONARY VASCULAR RESISTANCE

CEREBRAL BLOOD FLOW=MAP-CVP/ICP

-----------------

C.VASC.RESISTANCE