Perioperative Complications and Management, pt 1 Flashcards
what is the most common dysrhythmia?
sinus tachycardia
define sinus tachycardia
HR > 100 bpm
what are the causes of sinus tachycardia?
- increased endogenous catecholamine release
- pre op anxiety
- surgical stimulation from incision
- direct laryngoscopy and tracheal intubation
- noxious/painful stimuli
- inadequate anesthetic depth
- hypoxia
- hypercarbia
- excessive tourniquet inflation time
- emergence
- reflex response to hypotension and hypovolemia
- fever or malignant hyperthermia
- pulmonary embolus
- pheochromocytoma (tumor adrenal medulla causing epi and NE release)
- meds
- vagolytics (antimuscarinics used w/ NMB reversal & antisialagogue)
- sympathomimetics
- muscle relaxants (pancuronium)
- volatile anesthetics (Des initial rapid uptake)
- thyrotoxicosis
describe nonpharmacological treatments for sinus tachycardia
- verify tachycardia isn’t artifact or ESU interference (look @ pulse oximeter)
- determine and treat underlying cause
- ensure adequate oxygenation and ventilation
- adequate anesthetic depth
- correct hypovolemia or hypotension
describe pharmacologic management of sinus tachycardia
- opioids narcotics (fentanyl blunts sympathetic response)
- beta adrenergic blockers
- preoperative anxiolytics
- calcium channel blockers
define bradycardia
HR less than 60 bpm
what are causes of vagal responses that lead to sinus bradycardia?
- vagal response to surgical manipulation
- bowel manipulation
- abdominal insufflation
- peritoneum stimulation (cervix)
- lumbar spine traction (prone)
- neck surgery or retractor use or stimulation
- tracheal intubation or extubation
- direct laryngoscopy
- ophthalmic surgery optic pressure or traction of extraocular muscles
describe the oculocardiac reflex
- involves the trigeminovagal reflex arc (afferent trigeminal, efferent vagus)
- produces bradycardia in 90% of patients
- increased OC reflex in hypercarbia
- antimuscarinics such as atropine do not prevent reflex
what are other causes of sinus bradycardia?
- high level sympathetic block (neuraxial anesthesia)
- blocked efferent cardio-accelerator fibers (T1-T5)
- increased predominance of parasympathetic response mediated by vagus
- Trigeminal nerve stimulation
- electroconvulsive therapy (parasympathetic outflow from shock; pretreat with glycopyrrolate)
- Volatile anesthetics (halothane, sevoflurane)
- Hypoxia- esp. in neonates and children
what commonly used drugs used during anesthesia lead to sinus bradycardia?
- narcotics (fentanyl, alfentanyl)
- alpha 1 agonists (phenylephrine)
- depolarizing muscle relaxants (Succs)
- reversal agents (neostigmine)
what are treatment options for sinus bradycardia?
- may not require Rx if hemodynamically stable
- maintain oxygenation and ventilation
- may require decreasing depth of anesthesia
- remove/extinguish vagal stimulus
- antimuscarinics (atropine or robinul)
- chronotropic agents (isoproterenol)
- cardiac pacing (rare)
what is the second most common intraoperative complication?
hypotension
what should be checked first to be a cause of hypotension?
BP measurement error
- transducer height or calibration error
- overdamped invasive system
- limb cuff oversize, loose, or improperly fitted
what may cause hypotension immediately after induction?
lack of decreased magnitude of surgical stimulation (decreased SNS before incision is made)
what are causes of decreased contractility that lead to hypotension?
- volatile anesthetic agents
- opioids
- cardiac meds (beta blockers)
- cardiac dysfunction: ischemia, electrolyte imbalance, acidosis/alkalosis, hypothermia
what are causes of decreased SVR that lead to hypotension?
- volatile agents
- opioids
- benzodiazapines
- various other drugs administered during anesthesia
- sympathetic outflow blockade (neuraxial)
- increased parasympathetic tone
- sepsis
- vasoactive metabolites (tourniquet release, anaerobic respiration)
- allergic reactions (increase histamine release)
- hypoxemia
what are causes of decreased venous return that lead to hypotension?
- hypovolemia: fasting, bowel prep, vomiting/diarrhea, acute hemorrhage, diuretic/diuresis
- vena cava compression or retractor use
- increased venous capacitance, pooling of blood
- increased intrathoracic pressure: PEEP, excess Vt
- pneumothorax and cardiac tamponade
- dramatic position changes
what are other causes of hypotension?
- vasovagal response to surgical stimulation: decreased SVR and HR
- dysrhythmias: tachyarrhythmias, Afib/aflutter (no atrial kick loses 30% of SV, reducing ventricular filling), bradyarrhythmias
what is the first step to treat hypotension?
re check the BP and ensure it is not erroneous
- check transducer calibration and assess damping
- confirm appropriate cuff size and fitting
- palpate and assess peripheral pulses
- assess any acute pulse oximetry waveform changes
- assess any acute capnography waveform changes (decrease EtCO2)
- confirm adequate oxygenation and ventilation
after verifying BP reading is adequate, how should hypotension be treated?
- determine and treat underlying cause
- volume expansion, restore fluid status (fluid bolus)
- lighten anesthetic depth or reduce opioid use if able (apply awareness monitor, increase paralysis)
- reposition patient or place in trendelenburg
- consider ketamine in pts. prone to hypotension
- vasopressors (sympathomimetics and/or inotropes; no ephedrine if HR up; no phenylephrine if HR low)
- treat dysrhythmias with vagolytics and antidysrhythmics
- reduce tidal volume or PEEP (may require and increase in rate)
- chest tube placement or pericardiocentesis
how would ketamine help hypotension?
- ketamine increases SNS outflow
- causes increased HR and vasoconstriction: SBP increases 20-40 mmHg in
what are the risk factors for developing peri-op HTN?
- increased age
- smoking
- renal disease
- inadequate ventilation
- preoperative h/o HTN
- preoperative h/o angina
how can HTN complicate surgery?
- hemorrhage
- ruptured suture lines
- CVA
- myocardial ischemia
- dysrhythmias
what are causes of perioperative hypertension?
- increased endogenous catecholamine release
- hx of HTN
- increase intracranial pressure (rebound HTN)
- systemic vasoconstrictor absorption of epi or phenylephrine
- rebound HTN resulting from d/c of BP meds
- distended bladder
- aortic cross clamping
- indigo carmine dye
- exaggerated drug effects d/t MAOI use (HTN crisis)
what causes an increase in endogenous catecholamine release?
- pre-operative anxiety
- surgical stimulation from incision
- direct laryngoscopy and tracheal intubation
- noxious/painful stimuli
- inadequate anesthetic depth
- hypoxia
- hypercarbia
- excessive tourniquet inflation time
- emergence
describe management of HTN
- increase depth of anesthesia
- IV opioid narcotics
- preoperative anxiolytics
- evacuate urine from distended bladder
- beta blockers (labetalol, esmolol, metoprolol)
- vasodilators (Nipride, NTG, hydralazine)
- calcium channel blockers
- ACEI, angiotension receptor blocker, alpha 1 blocker, alpha 2 agonist
describe perioperative hypoxia
- reduced oxygen tension at the tissue level
- four categories: hypoxemia, anemic hypoxia, circulatory hypoxia, histiocystic hypoxia
describe oxyhgb curve shifts
- shifts right: easier unloading of O2 by hgb to tissues
- shifts left: more difficult unloading of O2 to tissues for any given PO2
describe hypoxemia
- decreased blood oxygen tension
- low inspired oxygen (FiO2)
- hypoventilation
- V/Q mismatch
- shunt
- diffusion limitations
describe circulatory hypoxia
- inadequate cardiac output
- adequate carriers (Hgb)
- all conditions that reduce HR and/or SV will reduce CO: symptomatic bradycardia, hypovolemia, reduced venous return (preload)
- inadequate volume over time: insufficient delivery (supply) to meet metabolic demand
describe anemic hypoxia
- low hemoglobin concentration
- hgb with a decreased affinity for oxygen (abnormal hgb)
- Tx: transfusion of PRBCs: rarely indicated if hgb > 10gm/dL; nearly always indicated if hgb less than 6 gm/dL
describe histiocystic hypoxia
- cell is unable to utilize delivered oxygen
- CO poisoning (shifts oxyhgb curve left): binds cytochrome c and disrupts oxidative metabolic processes in the mitochondria; correction requires O2 at three atmospheres
- nipride produces cyanide toxicity: cyanide (CN-) binds to mitochondrial cytochrome oxidase disrupting aerobic metabolism; inhibits oxidative phosphorylation; prevents ATP synthesis
how is perioperative hypoxia recognized?
- dark blood in the wound
- ABGs
- pulse oximetry
- cyanotic mucous membranes is unreliable and late sign (absence of cyanosis doesn’t mean pt. is oxygenated; oxyhgb sat usu.
how is perioperative hypoxia managed?
- determine the correct cause (4 categories): treatment based on cause
- supplemental O2: increase FiO2, correct hypoventilation, bronchodilators
- increase O2 delivery (CO): inotropes, chronotropes, fluid volume
- correct V/Q mismatch: PEEP, VCM, decrease volatiles (inhibit hypoxic pulmonary vasoconstriction)
- PRBC transfusion
describe effects of hypercarbia
- CO2 > 90 can cause narcosis and additive MAC
- acidosis and hyperkalemia can result
what are causes of hypercarbia?
- decreased CO2 elimination
- hypoventilation
- opioids, benzos, volatile agents, high neuraxial, residual NMB
- inadequate vent settings
- increased airway resistance
- increased EtCO2 rebreathing (low flow in closed circuit or exhausted CO2 absorption)
- increased CO2 production
- hypermetabolic state: hyperthyroid, pheochromocytoma, hyperthermia, shivering
- reperfusion, tourniquet release
- CO2 abdomen insufflation (CO2 injected)
how can hypercarbia be recognized?
- no return to zero baseline on capnograph
- increased SNS outflow, hypoventilation, HTN, tachycardia
- restlessness
describe management of hypercarbia
- increase minute ventilation
- decrease anesthetic level in spontaneous ventilating pts.
- use narcotic and benzo reversal agents
- increase fresh gas flow or create an open system (2x Vm)
- change CO2 absorber
- reduce dead space
