Post operative hypotension

This si a common complication that can cause hypoperfusion and inadequate delivery of O2 and
substrates to organ systems. The risks of complications depends on the preoperative blood pressure

Ghe cause of post operative hypotension is due to

1. Decreased preload
a. Hypovolaemia
b. Vasodilation
c. Restriction of venous return
i. Surgical
d. Elecated intrathoracic pressures
e. Position of the patient
f. Pericardial tamponade
g. PE
2. Decreased contractility
a. Due to the effects of inotropic depressant drugs
b. Arrhythmias
c. Cardiomyopathies
d. CHF
e. Ischaemia
f. Infarction
g. Hypoxaemia
h. Valve disease
i. Increase in afterload (abrupt)
3. Decreased afterload
a. Vasodilation
b. Sepsis
c. Anaphylaxis
d. Endocrine issues
i. Addisonian crisis
ii. Hypothyroidism
iii. Hypoglycaemia
1. Check venilation is adequate or not
 2.
DDx

 Rule out false measurements

 Large cuffs lead to low values
 Decreased preload secondary to hypovolaemia is one of the most common causes in the PACU
 Failure to replace preoperative fluid deficit
 3rd space losses can continue 24-48hrs post operation
 Blood loss can be occult
 Decreased preload secondary to increase venous capacitance from a regional block
 Spinal or epidural anaesthesia increases venous capacitance by interfering with SNS
regulation of venous tone
 Decreased preload secondary to positive intra-thoracic pressure from mechanical ventilation or
tension pneumothorax compressing the veins and impeding venous return
 Acute pericardial tamponade aso impedes ventricular filling
 Decreased cardiac output secondary to decreased stroke volume
 Cardiac ischaemia, infarction, pulmonary emboli, air emboli can cause ventricular
dysfunction leading to deceased SV
 Cardiac arrhythmia leading to decreased CO
 Decreased afterload
 Systemic sepsis nterfering with arteriolar constriction, generating low resistance and high
output
 Transfusion reaction

Tx
 Indications for intervention includes
 20-30%reduction in systemic arterial systolic pressure from chronic pre-op levels
 Sx of vital organ hypoperfusion
 Administer O2
 IV infusion rate should be increased to max due to hypovolaemia (most common cause)
 Trendelenburg positioning might be helpful
 Vitals taken
 HR
 RR
 Check medication hx. Any drugs/ infusions that can cause vasodilation should be stopped
 ECG
 ABG
 CXR
 Definitive therapy dependent on the cayse
 Infusion of crystalloid solutions  hypovolaemia
 Sympathomimetics pressures e.g. phenylephnne or ephedrine that increases SVR and
venous return can be used to maintain pressure until volume is infused
 Tension pneumothorax must be immediately evaculated
 If fluid administration 300-500mL does not improve hypotension, consider other causes
 If myocardial dysfuction not related to ischaemia, drugs that augment contractility e.g.
dopamine, dobutamine with systemic vasodilators are used to restore CO and BP
 Is due to iscahemia, resolution of the ischaemia restores baseline cardiac function
 upport of aortic diastolic pressure with an alpha receptor agonist such as phenylephrine and
reduction of LVEDP with nitroglycerin can be useful to maximize the coronary artery
pressure gradient
 Control of heart rate with analgesics for pain, sedatives for anxiety. or beta receptor blockers is
essential

If hypotension occurs coincident with severe metabolic acidemia, bicarbonate should be given i.v.
while the cause is remedied. Severe hypoxemia or respiratory acidemia mandates tracheal intubation
and mechanical ventilation with supplemental oxygen. Sinus bradycardia unrelated to hypoxemia
usually responds to iv administration of atropine. Refractory bradycardia caused by sinus node
disease or complete heart block must be managed with artificial cardiac pacing. Digitalization or
calcium channel blockade reduces the ventricular rate from acute onset atrial fibrillation, whereas
paroxysmal atrial tachycardia often disappears with maneuvers or drugs that change cardiac
conduction rates. If hypotension from a tachydysrhythmia is severe, immediate low-energy direct
current cardioversion (50 joules) is indicated.

Hypotension caused by a low SVR in the setting of a high cardiac output (i.e. sepsis, or end stage
liver disease) is treated with an alpha-adrenergic agent (i.e. phenylephrine infusion). Hypotension
caused by sympathectomy from regional anesthesia, usually responds to low levels of alpha
stimulation. If decreased SVR is caused by acidemia, correction of pH is necessary before pressor
therapy will be effective.

 x
shock and hypotension
 shock is the state of cellular and tissue hypoxia due to reduced O2 delivery and or increased
consumption
 it most commonly occurs when there is circulatory failure and manifests as hypotension
 there are 4 main types
 distributive
 septic
 SIRS
 Neurogenic
 Anaphylactic
 Toxic shock
 End stage liver disease
 Endocrine
 Cardiogenic
 MI
 Arrhythmias
 Valve or ventricle septal rupture
 Hypovolameic
 Haemorrhagic
 Non-haemorrhagic fluid loss
 Obstructive
 PE
 Pulmonary HTN
 Pneumothorax
 Constrictive pericarditis
 Restrictive cardiomyopathy

Features that are highly suspicious of shock include:

●Hypotension – note that in the early stages of shock, the patient can be hypertensive
●Tachycardia – early compensatory mechanism in Pts with shock. Younger pts develop
severe and persistent tachycardia before bcoming hypotensive. Be aware of medication
use as BBlockers and others can change this
●Oliguria – shunting of blood flow to other organs, direct injury to the kidneys or due to
volume depletion
●Abnormal mental status – altered sensorium in shock is due to poor perfusion or
metabolic encephalopathy. It is a continuum that begins with agitation, then confusion
or delirium and ends in obtundation or coma
●Tachypnea – early compensatory mechanism in patients with shock and metabolic
acidosis
●Cool, clammy, cyanotic skin – this is due to compensatory peripheral vasoconstriction
that redirects blood centrally to maintain organ perfusion. A cyanotic, mottled
appearance is late feature of shock. NOTE that cool clammy skin s also due to
ischaemia from underlying peripheral arterial vascular disease. Warm hyperemic skin
does not exclude shock as it can appear in the ealy phases of distributive shock, prior
 to the onset of vasoconstriction or in terminal shock (due to the failure of compensatory
vasoconstriction)
●Metabolic acidosis – the presence of high anion gap metabolic acidosis should always
raise the suspecision of shock, AKI or toxin ingestation
●Hyperlactatemia – either in conjunction with metabolic acidosis or not, the presence is
associated with adverse outcomes including the development of shock

Initial Mx
 ABCs
 Airway  unless suspect tension pneumothorax in which drainage will reverse the shock
 IV access 14-18G + IV fuids  should not be delayed for a detailed clinical assessment
 Patients should be assessed for the need for an immediate or early intervention so that
lifesaving therapies can be administered promptly


 x