POST INTUBATION

HYPOTENSION
• Introduction
• Definition
• Pathophysiology
• Prediction of the crash
• Approach to post intubation hypotension

OUTLINE
• Endotracheal intubation and the transition from negative
pressure breathing to PPV is a dangerous time
• >20% of patients experience post intubation hypotension
• Studies have shown that the presence of hypotension is an
independent predictor of in-hospital mortality and
increased length of stay in the ICU

INTRODUCTION
• Drop in BP:
• Systolic BP < 90mmHg
• 20% drop from initial systolic BP
• MAP drops < 65mmHg
• Initiation of vasopressor
• Within 30 minutes post intubation (or 60 minutes)
• Stable before intubation
• Some include timing: 30, 60 minutes pre intubation

DEFINITION
• Decreased venous return is an expected phenomena following
intubation
• Intubation causes catecholamine surge from the airway stimulation
• Pre medications given prior to intubation blunt this catecholamine
surge resulting in hypotension
• PPV leads to increase intrathoracic pressure that is transmitted to the
right atrium, hence causing reduced venous return
• Decreased PO intake and dehydration are common in the critically
ill patients

• How?
• Change in breathing dynamics
• Medications prior to intubation; reversal of sympathetic state
• Mechanical ventilation related/complications
• Clinical deterioration

PATHOPHYSIOLOGY
PREDICTION OF THE CRASH
• Shock index
• CKD
• Intubation
indication: acute
respiratory failure
• Age
• Various studies are poorly powered to show specific
factors
• 2 most commonly cited:
• Shock index
• Weight
• Clinical gestalt and knowledge of the underlying
pathophysiology are more reliable

PREDICTION OF THE CRASH

• Shock index is an inverse surrogate of cardiac work such
that elevated SI is associated with deteriorating cardiac
performance

Shock index = HR/SBP

Normal SI: 0.5 – 0.7

• Elevated SI is an early sign of shock despite otherwise

normal vital signs
APPROACH TO POST
INTUBATION HYPOTENSION
 ACIDOSIS
• Patients with profound metabolic acidosis typically have a high minute
ventilation, as a mean of compensation
• If minute ventilation not set to match the patients’ metabolic needs, PaCO2
HOW raises, severe acidaemia occurs, and may lead severe cardiovascular collapse

• ABG
POST-
INTUBATION

• Post intubation ventilator settings need to provide minute ventilation that

approximates pre-intubation level
MANAGEMENT • Aim for pre intubation ETCO2/PaCO2
 MV in men = 4 x BSA
MV in women = 3.5 x BSA

Normal minute ventilation at rest = 100ml/kg IBW

Increased by 20% in metabolic acidosis

MV = TV x HR

Expected PaCO2 = (1.5 x HCO3) + 8

 ANAPHYLAXIS
• Any patient may develop allergy reaction to any medications
• Allergen/antigen  B cells  IgE  mast cells  release of
HOW histamine  increase vascular permeability and vasodilation

• Detection: look for body rashes; other signs of anaphylaxis

POST- can be subtle and difficult to elicit in intubated patients
INTUBATION

• Prevention: ask allergy history

MANAGEMENT
• 1st line: Adrenaline
 HEART: TAMPONADE
• Obstructive shock
• Patient with penetrating chest trauma is an obvious trigger for
HOW bedside cardiac ultrasound

• Elderly patients on anticoagulants with minor falls, and end stage

renal disease patients may have occult / borderline tamponade that
POST only declares itself after a change to positive pressure ventilation
INTUBATION

• Increase the threshold for intubation (in trauma)

• Avoid high ventilatory pressures
Mx • Pericardiocentesis/ Thoracotomy
HEART: PULMONARY HPT
• Hypervolemia, hypoxia, and hypercarbia are known to worsen
their right heart function
• Fluid boluses are unlikely to help an overloaded, distended right
HOW ventricle, and may worsen LV impingement

• Avoid intubation if possible

• Vasopressors and inotropes, rather than fluid boluses, are often
required in shock to augment cardiac output and reduce the
Mx risk of exacerbating right ventricular ischemia
• Pulmonary vasodilators
 STACKED BREATHS
• Patients with obstructive lung pathology who are not able to completely
exhale prior to the next breath being initiated  air trapping  increased
intrathoracic pressure  decrease venous return overtime, and cause
HOW hypotension, and eventual arrest

• Detection: ventilator waveforms

• causes: (1) inadequate expiratory time (2) too high respiratory rate
POST (3) long inspiratory time (4) prolonged expiration from
INTUBATION bronchoconstriction

• Increase expiratory time; adjust IE ratio; increase inspiratory flow rate

• Reduce respiratory rate
Mx • Bronchodilators
Expiratory flow
doesn’t return to
baseline Pressure wave:
while performing
Start of next breath an expiratory hold,
the waveform rises
above baseline

60

40

20

0
200 400 600

-20

-40

-60
 HYPOVOLAEMIA
•Occult hypovolemia can be unmasked by the physiologic insult that occurs
when patients are switched from spontaneous ventilation to positive
pressure ventilation
HOW

• Clinical judgement
POST
INTUBATION

• Fluid resuscitation
• Reduce PEEP
Mx
 INDUCTION AGENT
• Any sedative agent that takes away an individual’s conscious
drive to survive could potentially result in post intubation collapse
HOW • Side effects of any other medications used for RSI

• Diagnosis of exclusion
POST
INTUBATION

• Fluid boluses
• Reduce sedation dose
Mx • Vasopressors
 TENSION PNEUMOTHORAX
• Obstructive shock
• Risk of those with obstructive lung disease with
HOW increasing pressure or those on high pressure settings

• Detection: clinical, bedside USG, *CXR**

POST
INTUBATION

• Needle thoracocentesis, chest tube

Mx
ELECTROLYTES
• Succinylcholine has a well known set of contraindications due to the risk
of succinylcholine associated hyperkalemia
• Several case reports exist of patients who have had profound
HOW hyperkalemia without obvious risk factors

• High index of suspicion should the rhythm change

• ABG/RFT
POST

• Lytic cocktail
Mx
• Heffner, A.C.; Swords, D.S.; Nussbaum, M.L.; Kline, J.A.; Jones, A.E.
Predictors of the complication of postintubation hypotension during
emergency airway management. J. Crit. Care 2012, 27, 587–593
• Green, Robert S. and Elham Sabri. “EM Advances Evaluation of the
incidence, risk factors, and impact on patient outcomes of postintubation
hemodynamic instability.” (2012)
• Smischney NJ, Demirci O, Diedrich DA, et al. Incidence of and Risk
Factors For Post-Intubation Hypotension in the Critically Ill. Medical
Science Monitor : International Medical Journal of Experimental and
Clinical Research. 2016;22:346-355
• Ron M Walls, Michael F Murphy. Manual of Emergency Airway
Management 3rd edition. 2008
• Rebelem website http://rebelem.com/post-intubation-hypotension-the-ah-
shite-mnemonic/ (accessed 5th August 2017)

REFERENCES
DKA: WHEN TO
INTUBATE?
WHY QUESTION?
• Sick DKA patients typically have extremely low bicarbonate
levels, for which they are compensating with a respiratory
alkalosis
• Acidosis will worsen in:
• Failed intubation
• Poor understanding of ventilator setting to match the patients’
metabolic needs
• With the exception of a patient who has truly developed
respiratory muscle fatigue (and lost the ability to generate a
compensatory respiratory alkalosis), intubation will typically
worsen the patient
How about risk of aspiration in
patients with altered mental status?

• It may be best to avoid intubation as long as the patient is

protecting their airway
• If mental status changes are due to DKA, improvement
often occurs rapidly
• Ultimately this is a clinical decision which must be made
at the bedside by an experienced physician
• If there is doubt, close observation and serial evaluation
may be helpful
• Most important is the understanding of its
pathophysiology and ventilation strategy

WHEN TO INTUBATE THEN?

REFERENCES
• Acid base physiology
http://www.anaesthesiamcq.com/AcidBaseBook/ab8_2b.php
(accessed 5th August 2017)
• PULMCrit(EMCrit) website https://emcrit.org/pulmcrit/four-
dka-pearls/ (accessed 5th August 2017)
• Duncan, Russell et al. Decreased Glasgow Coma Scale Score
Does Not Mandate Endotracheal Intubation in the
Emergency Department. Journal of Emergency Medicine ,
Volume 37 , Issue 4 , 451 - 455