Postanesthesia Recovery Flashcards
Which are the most common complications in the PACU?
Nausea and vomiting
Need for upper airway support
Hypotension
Most frequent cause of airway obstruction in the PACU
Loss of pharyngeal muscle tone in a sedated or obtunded patient
Most reliable clinical evaluation of residual NMB and indicator of pharyngeal muscle tone in the PACU
The ability to strongly oppose the incisor teeth against a tongue depressor
Correlates with an average TOF of 0,85
Causes of prolonged nondepolarizing neuromuscular blockade
1) drugs
- Inhaled Anesthetics
- Local anesthetics
- Cardiac Antiarrhythmics (procrainamide)
- Antibiotics (polymixins, aminoglycosides, lincosamides, metronidazole, tetecyclines)
- Corticosteroids
- Calcium Chanel blockers
- Danteolene
- Furosemide
2) Metabolic and physiologic states
- Hypermagnesemia
- Hypocalcemia
- Hypothermia
- Respiratory Acidosis
- Hepatic/renal failure
- Myasthenia syndromes
Causes of prolonged depolarizing NMB
1) Excessive dose of succinylcholine
2) Reduced plasma cholinesterase activity
- Decreased levels
- Extremes of age (newborn, old age)
- Disease states (hepatic, uremia, malnutrition, plasmapheresis
- Hormonal changes
- Pregnancy
- Contraceptives
- Glucocorticoids
3) Inhibited activity
- Irreversible (echothiophate)
- Reversible (edrophonium, neostigmine, pyridostigmine)
4) Genetic variant (atypical plasma cholinesterase)
Treatment of laryngospasm
1- Suctioning
2- Jaw thrust + CPAP up to 40 cm/h2o
If this fails
3- Succinylcholine (0,1 - 1 mg/kg IV or 4 mg/kg IM)
If this fails
4- Intubation with full dose of induction agent and NMBA
If airway edema is deemed significant enough to preclude extubation, which measures can facilitate resolution of edema?
1- sitting the patient upright to ensure venous drainage
2- diuretic administration
3- IV dexamethasone
Factors contributing to postoperative arterial hipoxemia by mechanism of hypoxemia
1) Right to left intrapulmonary shunt or ventilation perfusion mismatch
- Atelectasis
- Pulmonary Edema
- Aspiration of gastric content
- Pneumothorax
- Pulmonary embolus
2) Alveolar hypoventilation
- Residual effects of anesthetics and/or neuromuscular blocking drugs
3) Venous admixture
- Reduced cardiac output
- Congestive heart failure
4) Diffusion hypoxia
- From NO2 administration
5) Increase O2 consumption
- Shivering
6) Decrease O2 delivery
- Unrecognized disconnection of O2 source
- Empty O2 tank
Most common causes of transient postoperative arterial hypoxemia
Atelectasis
Alveolar hypoventilation
Cause, manifestations and treatment of Negative Pressure Postoperative Edema
Is a rare consequence of laryngospasm (or, less commonly, other upper airway obstruction). The etiology is multi factorial, but is clearly correlated with the generation of exaggerated negative intrathoracic pressure during inspiration against a closed glottis. The resulting negative pressure augments venous return, which in turn increases pulmonary hydrostatic pressures, promoting the movement of fluid into the intertitial and alveolar spaces.
The resulting arterial hypoxemia develops quickly (usually within 90 min) and is accompanied by dyspnea, pink frothy sputum, and bilateral fluffy infiltrates in the chest X ray.
Treatment is generally supportive and includes O2 supplementation, diuresis, and, in severe cases, positive pressure ventilation.
When treated, NPPE typically resolves in 12 to 48 hours
Brief description of TRALI
Transfusion-Related Acute Lung Injury usually manifests within 2 to 4 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets. TRALI occurs when recipient neutrophils become activated by donor plasma and then release inflammatory mediators which cause increased pulmonary vascular permeability resulting in pulmonary edema. Clinical manifestations include fever, pulmonary infiltrates on chest radiograph, cyanosis, and systemic hypotension. The sudden onset of hypoxemic respiratory failure can occur up to 6 hours after the conclusion of the transfusion, and TRALI may first present when the patient is in the PACU.
Treatment is supportive and includes supplemental oxygen and diuresis. Approximately 80% of patients will recover within 48 to 96 hours. Mechanical ventilation may be needed to support hypoxemia and respiratory failure, and vasopressors may be required to treat refractory hypotension.
Factors associated with postoperative hypertension
1) Cardiovascular
Preoperative hypertension
Hypervolemia
2) Respiratory
Arterial hypoxemia
Hypercapnia
3) Neurologic
Pain
Emergence agitation
Shivering
Nausea/vomiting
Increased intracranial pressure
Increased sympathetic nervous system activity
4) Drug-related
Withdrawal from β-blocker, clonidine
Withdrawal from opioids, benzodiazepines
Alcohol withdrawal
Substance use (e.g., cocaine, methamphetamine, phencyclidine)
5) Gastrointestinal/genitourinary
Bowel distention
Urinary retention
Diferencial diagnosis of hypotension in the PACU
1) Hypovolemic
Intravascular volume depletion
Persistent fluid losses
Ongoing third-space translocation of fluid
Bowel preparation
Gastrointestinal losses
Surgical bleeding
Increased capillary permeability
2) Distributive
Sepsis
Burns
Decreased vascular tone
Allergic reactions (anaphylactic)
Spinal shock (cord injury, iatrogenic high spinal)
Adrenal insufficiency
3) Cardiogenic
Myocardial ischemia or infarction
Cardiomyopathy
Valvular disease
Cardiac arrhythmias
Drug induced (β-blockers, calcium channel blockers, local anesthetic systemic toxicity)
4) Extracardiac/Obstructive
Pulmonary embolus
Pericardial disease
Cardiac tamponade
Tension pneumothorax
Pharmacologic treatments of hypotension caused by sympathetic nervous system blockade
Vasopressors, including ephedrine and phenylephrine
In one study of patients over 45 years of age undergoing noncardiac surgery 85% of patients with postoperative myocardial infarction complained of typical chest pain
(Characteristics and short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study. P J Devereaux et Al)
T or F
F
In one study of patients over 45 years of age undergoing noncardiac surgery only 35% of patients with postoperative myocardial infarction complained of typical chest pain