SHOCK

ANESTHETIC
IMPLICATIONS AND
MANAGEMENT: AN
OVERVIEW

MODERATOR : DR J S DALI
PRESENTER : PRASHANTH
56 yr old natha, a farmer by occupation is brought to
the emergency with altered consciousness.
He is occasionally responding to commands and has
feeble pulses with gross tachycardia.
Accompanying attendant gives a history of reduced
appetite and abdominal pain since 1 week. Natha gives
a history of non passage of flatus or faeces since 3
days
Heart rate- 130/min. BP 70 systolic, rapid shallow
breathing evident.
Physical examination shows a grossly distended
abdomen with diffuse tenderness, reduced air entry in
both lower lobes of lungs with normal heart sounds.
“A momentary pause in the act of death.”

-John Collins Warren, 1800s

 DEFINITION

Syndrome in which tissue perfusion is reduced such

that blood flow is inadequate to meet cellular
metabolic requirements.

Alterations in one or more components of the

circulatory system that regulate cardiovascular
performance- intravascular volume,cardiac
function,arteriolar resistance,capillary
circulation,venules, venous capacitance circuit and
mainstream patency
CIRCULATORY PARAMETERS
C

Inflammatory mediators

Mitochondrial abnormalities

Accumulation of tissue CO2

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 presenting
with 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 dry
to 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 cases
of acute myocardial infarction

• Without treatment,associated with a 70-80%

mortality rate, and is the leading cause
of death in patients hospitalized for an acute
myocardial infarction
Natha after 6 days of admission in the
hospital suddenly develops a spike of fever
associated with tachycardia and warm
extremities. Pulses are well palpable.he has
persistent hypotension despite adequate fluid
resuscitation. Body fluids for appropriate
biochemiacal investigations are being sent.

Septic shock
SEPTIC SHOCK- pathophysiology
John is wheeled into the emergency after a
road traffic accident. The paramedics give an
alleged history of multiple puncture wounds on
the chest and dipping vitals. On examination,
his vitals are not recordable and breath sounds
are 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 pleural
decompression
 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 collision
and is rushed to the emergency unconscious.
His vitals are not recordable and his breathing
is irregular. Neck veins seem distended.
Multiple rib injuries and fracture of the sternum
is suspected on examination. The paramedics
have already inserted chest tubes B/L prior to
shifting suspectiong hemothorax.
Cardiovascular Trauma

Any patient with significant blunt or

penetrating trauma to chest has
heart/great vessel injury until proven
otherwise
 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 causing
cardiac tamponade. A subcostal view in early diastole shows a large
circumferential pericardial effusion compressing the heart, with the
right ventricle completely collapsed. (From Roy CL, Minor MA,
Brookhart MA, et al: Does this patient with a pericardial effusion have
cardiac tamponade? JAMA 297:1810-1818, 2007.)
 Cardiac Tamponade
• Management
– Secure airway
– High concentration O2
– Rapid transport
– Definitive treatment is pericardiocentesis
followed by surgery
 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 produces
shearing force on aortic arch
 Traumatic Aortic Aneurysm

• 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
 Traumatic Aortic Aneurysm
• Management
– High concentration oxygen
– Assist ventilation
– Suspect spinal injury
– Rapid transport
 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 to
foreign 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 the
alternate 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 2.6

anesthetics)
Data from French survey by Perioperative Anaphylactoid Reactions Study Group; 1648 patients, July 1994 to December 1996.
 Treatment (2)

• Initial therapy
1. Stop administration of antigen
2. Maintain airway with 100% oxygen
3. Discontinue all anesthetic agents
4. 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 treatment
1. Antihistamines (0.5–1 mg/kg diphenhydramine)
2. Catecholamine infusions (starting doses: epinephrine,
5–10 μg/min; norepinephrine, 5–10 μg/min, as an
infusion, titrated as needed)
3. Bronchodilators (inhaled albuterol or terbutaline with
bronchospasm)
4. Corticosteroids (0.25–1 g hydrocortisone; alternating
1–2 g methylprednisolone)
5. Sodium bicarbonate rarely needed (0.5–1 mEq/kg with
persistent hypotension and acidosis refractory to
volume 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 AND

CARDIAC EVENTS.......

DO WE NEED TO EDUCATE OURSELVES???

 ENTRY OF CRITICALLY ILL PATIENTS.

1. The Emergency Department

Victims ofmajor trauma requiring immediate operative
intervention fall into two categories:
* Major hemorrhage of any source that cannot be
controlled by simple resuscitative measures
* Patients with traumatic intracranial hemorrhage
* Patients presenting with acute general surgical
pathology 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

* leading cause of death under the age of 40 and the

third 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 – massive
Hemorrhage or crush injuries, massive CNS trauma
or (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 by

the American College of Surgeons since 1979
* Assessment, diagnosis and initial treatment carried out
simultaneously.
* 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 and

protected from further damage , hard cervical collar
mandatory.
* Unless immediate intubation is required, the cervical
spine 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
* 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 hypoventilation
and severe shock.

Circulation
* External hemorrhage to be controlled.
* Large bore catheters inserted and volume infused.
* Blood should be sent for blood gases and
crossmatching.
 Patient transfer to and from the OR

* The patient’s airway must be adequately secured.

* Ventilation must be adequate, either spontaneous or
mechanical. Manual ventilation unpredictable and
unreliable.
* Lifting of patients on and off stretchers is a cause of
inadvertant extubation.
* Blood pressure must be maintained with a combination
of fluids and inotropic agents.
* Patient monitoring must be appropriate to ensure safe
transfer.
* Consideration should be given to pharmacological
sedation and muscle relaxation.
* Communication between transferring and receiving
staff .
* Planning to minimize delays and waiting in OR
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 equivalent
battery-powered syringe pumps if required.
* There is no excuse for battery-powered equipment
becoming exhausted, oxygen cylinders emptying or
drug syringes running out.
 Patient positioning
* Lines, tubes and bags- Every piece of equipment inserted
into the patient is there for a reason.
* Patients may not have had a full primary
and secondary survey.. the cervical spine should stay fixed
* Patient should not be moved without a formal log-rolling
technique being used.
* Edematous , weakened skin prone to tearing, bruising and
vulnerable 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

* Circle system ventilation with carbon dioxide absorber

and 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

* 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 volume
and 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 vs
elective ventillation
 ANAESTHETIC AGENTS

INDUCTION AGENTS:
Thiopentone
Etomidate
Propofol
Ketamine

OPIOIDS:
Morphine
Fentanyl
Remifentanyl

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 (N O) – due to low blood gas solubility
2

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.
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 to
induction.
* Communication and timing with theater staff,
surgeons, porters, etc., to eliminate delays in
potentially difficult circumstances and environments.
 Intraoperative monitoring

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 the
right ventricle,
* guide to fluid requirements, and
* infusion of irritant drugs, e.g. inotropes, vasopressors
and IV nutrition.
 End points of fluid therapy

Reduction in tachycardia and improvement in blood

pressure 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 matter
how much fluid is given (in the patient undergoing IPPV)
The role of the anesthetist in outcomes

* Obvious clinical errors.

* Choice of anesthetic agents.
* Hemodynamic control
* Ischemia. Volatile agents (and probably opiates) in
Preconditioning.
Adapting ACLS to the Perioperative
Period

Anesthesiology Centric ACLS by Andrea

Gabrielli, 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 in
the perioperative setting:
Anesthetic
o Intravenous anesthetic overdose
o Inhalation anesthetic overdose
o Neuraxial block with high level sympathectomy
o Local anesthetic systemic toxicity
o Malignant hyperthermia
o Drug administration errors

Respiratory
o Hypoxemia
o Auto PEEP
o Acute Bronchospasm
Cardiovascular

o Vasovagal reflex
o Hypovolemic and/or hemorrhagic shock
o Tension Pneumothorax
o Anaphylactic Reaction
o Transfusion Reaction
o Acute Electrolyte Imbalance (high K)
o Severe Pulmonary Hypertension
o Increased intraabdominal pressure
o Pacemaker failure
o Prolonged Q-T syndrome
o Acute Coronary Syndrome
o Pulmonary Embolism
o Gas embolism
o Oculocardiac reflexes
o Electroconvulsive therapy
Recognizing cardiac arrest in the
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 to
remember . . .
CPR for patients under general anesthesia need not be
preceded by “Annie! Annie! Are you okay?”
Instruct appropriate personnel to start effective CPR.
Discontinue the anesthetic and surgery
Call for help, defibrillator
Bag mask ventilation if ETT not in place followed by immediate
endotracheal intubation if feasible FiO2 = 1.0
Don't stop CPR unnecessarily! Capnography is a more reliable
indicator of ROSC than carotid or femoral arterial pulse
palpation.
Capnograph to confirm advance airway positioning and
effective CPR
Hand 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, fiberoptic
bronchoscopy, consider exchanging the airway. Continue CPR.
Open all IVs to wide open
Cardiac arrest in association with
neuraxial 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 a
variety of clinical procedures.

Clinically, the only unifying feature of this

syndrome is the degree of surprise among the
caregivers of these patients.
Prevalence of cardiac arrest at 1.8 per 10,000
patients (neuraxial), with more arrests occurring in
patients with spinal anesthesia versus epidural (2.9
vs. 0.9 per 10,000 ;P = 0.041)
(Anesth Analg 2005;100:855-865).

In 46% (12/46) of the cases cardiac arrest was

associated with recurrent specific surgical events
(cementing of joint components, spermatic cord
manipulation, manipulation of a broken femur, and
rupture of amniotic membranes).

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

Subarachnoid block contributed directly to the
arrest.
Shock: “rude unhinging of the machinery of
life.”

Samuel D. Gross, 1872

Further reading:

1. Surviving sepsis campaign 2008

http://www.survivingsepsis.org

2 2009 Focused Updates: ACC/AHA Guidelines

for the Management of Patients
With ST-Elevation Myocardial Infarction
J. Am. Coll. Cardiol. 2009;54;2205-224

3. Anesthesia for The High Risk Patient

Ian McConachie, second edition, cambridge publications
2009

4. Textbook of critical care 5th edition, fink, elsevier

saunders 2005