Shock Uncut Version

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SHOCK

ANESTHETIC

IMPLICATIONS ANDMANAGEMENT: AN

OVERVIEW

MODERATOR : DR J S DALI

PRESENTER : PRASHANTH



56 yr old natha, a farmer by occupation is brought tothe emergency with altered consciousness.

He is occasionally responding to commands and hasfeeble pulses with gross tachycardia.Accompanying attendant gives a history of reducedappetite and abdominal pain since 1 week. Natha givesa history of non passage of flatus or faeces since 3

daysHeart rate- 130/min. BP 70 systolic, rapid shallowbreathing evident.Physical examination shows a grossly distended

abdomen with diffuse tenderness, reduced air entry inboth lower lobes of lungs with normal heart sounds.



“A momentary pause in the act of death.”

-John Collins Warren, 1800s



Syndrome in which tissue perfusion is reduced suchthat blood flow is inadequate to meet cellular metabolic requirements.

Alterations in one or more components of thecirculatory system that regulate cardiovascular performance- intravascular volume,cardiac

function,arteriolar resistance,capillarycirculation,venules, venous capacitance circuit andmainstream patency

DEFINITION





CIRCULATORY PARAMETERS



Inflammatory mediators

Mitochondrial abnormalities

Accumulation of tissue CO2

C



VO2- Oxygen uptake or consumption

DO2- Oxygen supply

ERO2- Extraction ratio

Increase in VRO2:

1) Redistribution

2) Capillary recruitment













FLUID

HOMEOSTASIS



35 yr old Natha from mukhya pradesh presentingwith h/o vomiting and diarrhoea X 2 days and

altered sensorium since 1 day.On examination, peripheral pulses were feeble,tachycardia present, bp systolic 70 mm hg,tachypnoea present. Eyes are sunken, skin dryto feel.

Identify the disorder affecting his cardiovascular status

Hypovolemic shock







HOW CAN YOU ASSESS FLUID BALANCE IN

THE POST OPERATIVE PERIOD??

















FLUID RESUSCITATION

Crystalloids• Lactated Ringer’s solution• Normal saline

Colloids• Hetastarch• Albumin

Packed red blood cells

Infuse to physiologic endpoints



Cardiogenic Shock

• Cardiogenic shock (CS) is a state of inadequate tissue perfusion due to cardiac

dysfunction, and complicates 7-10% of casesof acute myocardial infarction

• Without treatment,associated with a 70-80%mortality rate, and is the leading cause

of death in patients hospitalized for an acutemyocardial infarction









Natha after 6 days of admission in thehospital suddenly develops a spike of fever

associated with tachycardia and warmextremities. Pulses are well palpable.he haspersistent hypotension despite adequate fluidresuscitation. Body fluids for appropriate

biochemiacal investigations are being sent.

Septic shock

SEPTIC SHOCK- pathophysiology











John is wheeled into the emergency after aroad traffic accident. The paramedics give an

alleged history of multiple puncture wounds onthe chest and dipping vitals. On examination,his vitals are not recordable and breath soundsare diminished on the right side. He has agonal

respiratory pattern in obvious distress





Chest Trauma

• Second leading cause of trauma deaths

after head injury

• About 20% of all trauma deaths

• Initial exam directed toward:

– Open pneumothorax

– Flail chest

– Tension pneumothorax

– Massive hemothorax

– Cardiac tamponade



Tension Pneumothorax

•

One-way valve forms in lung or chest wall• Collapse of lung tissue

• Cardiac output falls

•

Signs and Symptoms – Extreme dyspnea

– Restlessness, anxiety, agitation

– Decreased breath sounds

– Hyperresonance to percussion

– Cyanosis

– Subcutaneous emphysema



Tension Pneumothorax

• Management

– Secure airway

– High concentration O2 with NRB

– If available, request ALS intercept for pleuraldecompression



Hemothorax• Blood in pleura space

• Most common result of major chest wall trauma

• Present in 70 to 80% of penetrating, major non-

penetrating chest trauma

• Signs and Symptoms

– Rapid, weak pulse

– Cool, clammy skin

– Restlessness, anxiety

– Thirst

– Chills

– Hypotension

– Collapsed neck veins



Hemothorax

• Management – Secure airway

– Assist breathing with high concentration O2

–

Rapid transport



Abraham is involved in a motorbike collisionand is rushed to the emergency unconscious.

His vitals are not recordable and his breathingis irregular. Neck veins seem distended.Multiple rib injuries and fracture of the sternumis suspected on examination. The paramedics

have already inserted chest tubes B/L prior toshifting suspectiong hemothorax.



Cardiovascular Trauma

Any patient with significant blunt or

penetrating trauma to chest has

heart/great vessel injury until provenotherwise



Cardiac Tamponade

• Rapid accumulation of blood in space between heart,

pericardium

• Heart compressed

• Blood entering heart decreases

• Cardiac output falls

• Signs and Symptoms

– Hypotension unresponsive to treatment

– Increased central venous pressure (distended

neck/arm veins in presence of decreased arterial BP)

– Small quiet heart (decreased heart sounds)

Figure 60-37 Echocardiogram showing pericardial effusion causingcardiac tamponade A subcostal view in early diastole shows a large



cardiac tamponade. A subcostal view in early diastole shows a largecircumferential pericardial effusion compressing the heart, with theright ventricle completely collapsed. (From Roy CL, Minor MA,

Brookhart MA, et al: Does this patient with a pericardial effusion havecardiac tamponade? JAMA 297:1810-1818, 2007.)

Cardiac Tamponade



Cardiac Tamponade

• Management – Secure airway

– High concentration O2

–

Rapid transport – Definitive treatment is pericardiocentesis

followed by surgery

T ti A ti A



Traumatic Aortic Aneurysm

• Caused by sudden decelerations, massive blunt force:

– Vehicle collisions

– Falls from heights

– Crushing chest trauma

– Blunt chest trauma

– Animal kicks

• Rupture usually occurs just beyond left subclavian artery

•Attachment of aorta to pulmonary artery at this point producesshearing force on aortic arch





• Signs and Symptoms – Increased BP in arms in absence of head injury

– Decreased femoral pulses with full arm pulses

–

Respiratory distress – Ache in chest, shoulders, lower back,

abdomen. (Only 25% of patients)

Detection requires high index of suspicion

Tra matic Aortic Ane r sm




• Management

– High concentration oxygen

– Assist ventilation

– Suspect spinal injury – Rapid transport

A i t d Abd i l T



Associated Abdominal Trauma

• Diaphragm forms dome that extends up

into rib cage

• Trauma to chest below 4th rib =

Abdominal injury until proven otherwise



TAKE A BREAK!



Anaphylaxis during anesthesia

• Definition

Anaphylaxis : rapid, generalized immunologically

mediated events involving an antigen-specific IgE-

mediated mechanism that occur after exposure toforeign substances in previously sensitized persons

Anaphylactoid reaction : not mediated by way of

the IgE antibody and prior exposure is not necessary



The incidence of anaphylaxis in GA is about

1:5000 to 1: 20000 and with a mortality rate

of up to 6%

Mechanism :1.Specific IgE cross-linked by allergen (drug)

2. Complement activation by specific IgG or IgM

binding to antigen (drug)

3. Direct complement activation by way of thealternate pathway

4. Direct activation of mast cells or basophils

CAUSES OF ANAPHYLAXIS AND ANAPHYLACTOID REACTIONS DURING ANESTHESIA



Causes Rate of Reaction (%)

Muscle relaxants 61.6

Latex 16.6

Antibiotics 8.3

Hypnotics 5.1

Colloids 3.1

Opioids 2.7

Other (aprotinin, ethylene oxide, local anesthetics)

2.6

Data from French survey by Perioperative Anaphylactoid Reactions Study Group; 1648 patients, July 1994 to December 1996.



T t t (2)



Treatment (2)

• Initial therapy

1. Stop administration of antigen

2. Maintain airway with 100% oxygen

3. Discontinue all anesthetic agents4. Start intravascular volume expansion (2–4 L of

crystalloid with hypotension)

5. Administer epinephrine (5–10 μg intravenous

initial bolus with hypotension, titrated as needed;0.1–0.5 mg intravenously with cardiovascular collapse)

Treatment (3)



( )

Secondary treatment1. Antihistamines (0.5–1 mg/kg diphenhydramine)

2. Catecholamine infusions (starting doses: epinephrine,5–10 μg/min; norepinephrine, 5–10 μg/min, as aninfusion, titrated as needed)

3. Bronchodilators (inhaled albuterol or terbutaline withbronchospasm)

4. Corticosteroids (0.25–1 g hydrocortisone; alternating1–2 g methylprednisolone)

5. Sodium bicarbonate rarely needed (0.5–1 mEq/kg with

persistent hypotension and acidosis refractory tovolume repletion and epinephrine)

6. Airway evaluation (before extubation)



THE ROLE OF AN ANAESTHESIOLOGIST??

1) ANESTHESIA FOR A CRITICALLY ILL PATIENT

2) PERIOPERATIVE CONCERNS ABOUT SHOCK ANDCARDIAC EVENTS.......

DO WE NEED TO EDUCATE OURSELVES???

ENTRY OF CRITICALLY ILL PATIENTS



ENTRY OF CRITICALLY ILL PATIENTS.

1. The Emergency DepartmentVictims ofmajor trauma requiring immediate operativeintervention fall into two categories:

* Major hemorrhage of any source that cannot becontrolled by simple resuscitative measures

* Patients with traumatic intracranial hemorrhage* Patients presenting with acute general surgicalpathology of a nontraumatic nature

2. The general hospital* Inpatients may deteriorate during the course of Rx

3. The Intensive Care Unit* most likely to have all resuscitative measures in

place. Mechanical ventilation, invasive lines..

POLYTRAUMA



POLYTRAUMA

* leading cause of death under the age of 40 and thethird leading cause overall.* Many patients are intoxicated.* Injuries are often multi-system in nature.

Deaths from trauma follow a trimodal distribution.

* Immediate deaths- 1st few minutes – massiveHemorrhage or crush injuries, massive CNS traumaor (potentially avoidable) airway obstruction.

* Early deaths - hemorrhage or hypoxia, preventable.* Late deaths are chiefly due to sepsis and organ

failures.

Assessment of the trauma patient



* The Advanced Trauma Life Support system, as promoted bythe American College of Surgeons since 1979

* Assessment, diagnosis and initial treatment carried outsimultaneously.

* This is facilitated by a team approach with a “team leader”.* The patient needs to be examined thoroughly.* The first priority- detect and treat immediately life

threatening conditions , second priority-detect other injuries.* Radiological investigations* Relevant senior specialists should be involved .* The abdomen should be evaluated...Peritoneal lavage.* Administer appropriate antibiotics and tetanus toxoid.* All dislocations and fractures should be splinted and

reduced.

Airway and cervical spine protection



* The cervical spine - assumed to be at risk andprotected from further damage , hard cervical collarmandatory.

* Unless immediate intubation is required, the cervicalspine should be assessed by radiological inv.

* If intubation is required, preoxygenation followed by oral intubation with manual in-line stabilization of the

cervical spine by an assistant.* Neurological signs should be documented before

intubation, if possible.* If the patient cannot be intubated then a surgical

airway should be created.

Breathing/ventilation



Breathing/ventilation* High-flow O2.* Clinically obvious pneumothoraces to be drained.* low threshold for immediate tracheal intubation –

even before the result of arterial blood gases.* Indications for immediate intubation and ventilation

-gross respiratory distress, obvious hypoventilationand severe shock.

Circulation* External hemorrhage to be controlled.* Large bore catheters inserted and volume infused.

* Blood should be sent for blood gases andcrossmatching.

Patient transfer to and from the OR



* The patient’s airway must be adequately secured.

* Ventilation must be adequate, either spontaneous ormechanical. Manual ventilation unpredictable andunreliable.* Lifting of patients on and off stretchers is a cause of inadvertant extubation.

* Blood pressure must be maintained with a combinationof fluids and inotropic agents.* Patient monitoring must be appropriate to ensure safetransfer.* Consideration should be given to pharmacologicalsedation and muscle relaxation.* Communication between transferring and receivingstaff .

* Planning to minimize delays and waiting in ORreception areas



reception areas. .* Appropriate equipment required during the transfer-

portable ventilator,full oxygen cylinder,equipment for reintubation,drugs – e.g. sedation, paralysis, cardiac resuscitation,self-inflating bag or equivalentbattery-powered syringe pumps if required.

* There is no excuse for battery-powered equipmentbecoming exhausted, oxygen cylinders emptying ordrug syringes running out.





Patient positioning



* Lines, tubes and bags- Every piece of equipment insertedinto the patient is there for a reason.

* Patients may not have had a full primaryand secondary survey.. the cervical spine should stay fixed* Patient should not be moved without a formal log-rollingtechnique being used.* Edematous , weakened skin prone to tearing, bruising andvulnerable to pressure injury.

Perioperative hypothermia



* Acute blood loss .* Central mechanisms of thermoregulation disrupted.

* reduced metabolic rate associated with anesthesia,* vasodilation under anesthesia,* abolished subclinical shivering,* exposure,* cold fluids used for skin preparation ,

* inadequately warmed IV fluids.

Adverse effects of perioperative hypothermia* Delayed awakening.* Organ function depressed H

* Hemodynamic instability during rewarming** Oxygen consumption* Wound infection* Coagulopathy .* Myocardial ischemia

Prevention of hypothermia

* Ci l il i i h b di id b b



* Circle system ventilation with carbon dioxide absorberand heat and moisture exchanger.

* Fluid warmer for all intravenous fluids.* Warmed patient mattress.* Insulation of all areas of the patient .* Use of a forced air warming system.* Use of heat-retaining insulating materials less effective

VENTILLATION AND AIRWAY MANAGEMENT

* Si ifi t t l i j



* Significant acute lung injury.* Shallow breathing can increase PVR leading to hypoxia

and acidosis* Increased work of breathing -- myocardial ischemia* In severe shock, the reduced blood flow to the

diaphragm coupled with the increasedminute volumeand respiratory energy expenditure causes respiratory

failure-- Controlled ventilation.** Lung protective strategies (e.g. PEEP, low tidal

volumes, low peak and plateau airway pressures,permissive hypercapnia)

* Decreased venous return,cardiac output

* Deteriorationat the end of surgery- extubation vselective ventillation



ANAESTHETIC AGENTS

C O G S



INDUCTION AGENTS:Thiopentone

EtomidatePropofolKetamine

OPIOIDS:

MorphineFentanylRemifentanyl

MUSCLE RELAXANTS:

Succinyl choline vs NDMR

Inhalational agents



1. Enflurane – greatest degree of myocardial depression

for equivalent MAC amongst all.2. Sevoflurane – less increase in cerebral blood volume.Rapid onset and rapid recovery.

3. Halothane – rarely used nowadays.4. Isoflurane – impressive safety profile, Hypotension

chiefly by vasodilation.5. Desflurane - specialized delivery systems required.Very short-acting.6. Nitrous oxide (N2O) – due to low blood gas solubility

has very fast uptake and onset.Second gas effect

Practical conduct of anesthesia* Conventional assessments of fitness not helpful.* Many of these patients require ongoing resuscitation



* Many of these patients require ongoing resuscitation.The ABC system is widely followed:

A =airway including cervical spine protection,B =breathing,C =circulation.

* inotropes and vasopressors* Intraoperative control of blood sugar .

* Portable monitors with full invasive monitoring* Ruptured aneurysms and other cases of massive

hemorrhage should be “prepped” on the table prior toinduction.

* Communication and timing with theater staff,

surgeons, porters, etc., to eliminate delays inpotentially difficult circumstances and environments.

Intraoperative monitoring

Full monitoring according to local and national protocols



Full monitoring according to local and national protocols

In addition:Indwelling arterial line for:* beat-to-beat monitoring of blood pressure,* sampling of blood for blood gas measurement,* control of inotrope and vasopressor infusions,

Central venous catheter for:* measurement of filling pressure, i.e. preload of theright ventricle,* guide to fluid requirements, and

* infusion of irritant drugs, e.g. inotropes, vasopressorsand IV nutrition.

End points of fluid therapy

Reduction in tachycardia and improvement in blood



Reduction in tachycardia and improvement in bloodpressure and urine volumes are important, albeit crude

Both CVP and PCWP have limitations.

More recent, dynamic approaches:* Central venous saturation. Saturation of the central

venous blood (ScvO2) .* Pulse pressure variation (PPV).* Additionally and importantly, it is suggested that if there is no PPV there will be no increase in CO no matterhow much fluid is given (in the patient undergoing IPPV)

The role of the anesthetist in outcomes

* Obvious clinical errors



Obvious clinical errors.* Choice of anesthetic agents.

* Hemodynamic control* Ischemia. Volatile agents (and probably opiates) in

Preconditioning.

Adapting ACLS to the PerioperativePeriod



Anesthesiology Centric ACLS by AndreaGabrielli, Michael F. O’Connor, and Gerald A. Maccioli.

Approved work product of the

ASA’s Committee on Critical Care

http://www.asahq.org/clinical/Anesthesiology-CentricACLS.pdf

Common Causes of ACLS events inthe perioperative setting:



the perioperative setting:

Anesthetico Intravenous anesthetic overdoseo Inhalation anesthetic overdoseo Neuraxial block with high level sympathectomyo Local anesthetic systemic toxicityo Malignant hyperthermiao Drug administration errors

Respiratoryo Hypoxemia

o Auto PEEPo Acute Bronchospasm

Cardiovascular

V l fl



o Vasovagal reflexo Hypovolemic and/or hemorrhagic shocko Tension Pneumothoraxo Anaphylactic Reactiono Transfusion Reactiono Acute Electrolyte Imbalance (high K)o Severe Pulmonary Hypertension

o Increased intraabdominal pressureo Pacemaker failureo Prolonged Q-T syndromeo Acute Coronary Syndromeo Pulmonary Embolism

o Gas embolismo Oculocardiac reflexeso Electroconvulsive therapy

Recognizing cardiac arrest in theOR:



OR:

- EKG with pulseless rhythm (V-tach, V-fib)

- Loss of pulse X 10 seconds

- Loss of end-tidal CO2

- Loss of plethysmograph

BLS/ACLS in the OR –Some key points toremember . . .

CPR for patients under general anesthesia need not bed d b “A i ! A i ! A k ?”



preceded by “Annie! Annie! Are you okay?”Instruct appropriate personnel to start effective CPR.Discontinue the anesthetic and surgeryCall for help, defibrillatorBag mask ventilation if ETT not in place followed by immediate

endotracheal intubation if feasible FiO2 = 1.0Don't stop CPR unnecessarily! Capnography is a more reliable

indicator of ROSC than carotid or femoral arterial pulsepalpation.Capnograph to confirm advance airway positioning and

effective CPRHand ventilate rate 8 -10, VT to chest rise, TI one second with

100% oxygen – assess for obstruction, if none, institute

mechanical ventilation. If obstruction, suction, fiberopticbronchoscopy, consider exchanging the airway. Continue CPR.Open all IVs to wide open



Cardiac arrest in association withneuraxial anesthesia :



remains the most mysterious cause of morbidity

and mortality

Its existence would be controversial

has been well documented as an occurrence in

younger otherwise healthy patients undergoing avariety of clinical procedures.

Clinically, the only unifying feature of thissyndrome is the degree of surprise among thecaregivers of these patients.

Prevalence of cardiac arrest at 1.8 per 10,000



Prevalence of cardiac arrest at 1.8 per 10,000patients (neuraxial), with more arrests occurring in

patients with spinal anesthesia versus epidural (2.9vs. 0.9 per 10,000 ;P = 0.041)(Anesth Analg 2005;100:855-865).

In 46% (12/46) of the cases cardiac arrest wasassociated with recurrent specific surgical events(cementing of joint components, spermatic cordmanipulation, manipulation of a broken femur, andrupture of amniotic membranes).

In 54% (14/26), the anesthetic technique, i.e.

Subarachnoid block contributed directly to thearrest.









Shock: “rude unhinging of the machinery of

life.”

Samuel D. Gross, 1872

Further reading:



1. Surviving sepsis campaign 2008http://www.survivingsepsis.org

2 2009 Focused Updates: ACC/AHA Guidelinesfor the Management of PatientsWith ST-Elevation Myocardial Infarction

J. Am. Coll. Cardiol. 2009;54;2205-224

3. Anesthesia for The High Risk PatientIan McConachie, second edition, cambridge publications2009

4. Textbook of critical care 5th

edition, fink, elseviersaunders 2005

http://www.survivingsepsis.org/

http://www.survivingsepsis.org/

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Shock Uncut Version