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Principles II > Perioperative Complications and Management, pt 1 > Flashcards

Perioperative Complications and Management, pt 1 Flashcards

1
Q

what is the most common dysrhythmia?

A

sinus tachycardia

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2
Q

define sinus tachycardia

A

HR > 100 bpm

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3
Q

what are the causes of sinus tachycardia?

A
  • 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
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4
Q

describe nonpharmacological treatments for sinus tachycardia

A
  • 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
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5
Q

describe pharmacologic management of sinus tachycardia

A
  • opioids narcotics (fentanyl blunts sympathetic response)
  • beta adrenergic blockers
  • preoperative anxiolytics
  • calcium channel blockers
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6
Q

define bradycardia

A

HR less than 60 bpm

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7
Q

what are causes of vagal responses that lead to sinus bradycardia?

A
  • 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
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8
Q

describe the oculocardiac reflex

A
  • 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
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9
Q

what are other causes of sinus bradycardia?

A
  • 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
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10
Q

what commonly used drugs used during anesthesia lead to sinus bradycardia?

A
  • narcotics (fentanyl, alfentanyl)
  • alpha 1 agonists (phenylephrine)
  • depolarizing muscle relaxants (Succs)
  • reversal agents (neostigmine)
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11
Q

what are treatment options for sinus bradycardia?

A
  • 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)
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12
Q

what is the second most common intraoperative complication?

A

hypotension

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13
Q

what should be checked first to be a cause of hypotension?

A

BP measurement error

  • transducer height or calibration error
  • overdamped invasive system
  • limb cuff oversize, loose, or improperly fitted
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14
Q

what may cause hypotension immediately after induction?

A

lack of decreased magnitude of surgical stimulation (decreased SNS before incision is made)

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15
Q

what are causes of decreased contractility that lead to hypotension?

A
  • volatile anesthetic agents
  • opioids
  • cardiac meds (beta blockers)
  • cardiac dysfunction: ischemia, electrolyte imbalance, acidosis/alkalosis, hypothermia
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16
Q

what are causes of decreased SVR that lead to hypotension?

A
  • 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
17
Q

what are causes of decreased venous return that lead to hypotension?

A
  • 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
18
Q

what are other causes of hypotension?

A
  • vasovagal response to surgical stimulation: decreased SVR and HR
  • dysrhythmias: tachyarrhythmias, Afib/aflutter (no atrial kick loses 30% of SV, reducing ventricular filling), bradyarrhythmias
19
Q

what is the first step to treat hypotension?

A

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
20
Q

after verifying BP reading is adequate, how should hypotension be treated?

A
  • 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
21
Q

how would ketamine help hypotension?

A
  • ketamine increases SNS outflow

- causes increased HR and vasoconstriction: SBP increases 20-40 mmHg in

22
Q

what are the risk factors for developing peri-op HTN?

A
  • increased age
  • smoking
  • renal disease
  • inadequate ventilation
  • preoperative h/o HTN
  • preoperative h/o angina
23
Q

how can HTN complicate surgery?

A
  • hemorrhage
  • ruptured suture lines
  • CVA
  • myocardial ischemia
  • dysrhythmias
24
Q

what are causes of perioperative hypertension?

A
  • 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)
25
Q

what causes an increase in endogenous catecholamine release?

A
  • 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
26
Q

describe management of HTN

A
  • 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
27
Q

describe perioperative hypoxia

A
  • reduced oxygen tension at the tissue level

- four categories: hypoxemia, anemic hypoxia, circulatory hypoxia, histiocystic hypoxia

28
Q

describe oxyhgb curve shifts

A
  • shifts right: easier unloading of O2 by hgb to tissues

- shifts left: more difficult unloading of O2 to tissues for any given PO2

29
Q

describe hypoxemia

A
  • decreased blood oxygen tension
  • low inspired oxygen (FiO2)
  • hypoventilation
  • V/Q mismatch
  • shunt
  • diffusion limitations
30
Q

describe circulatory hypoxia

A
  • 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
31
Q

describe anemic hypoxia

A
  • 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
32
Q

describe histiocystic hypoxia

A
  • 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
33
Q

how is perioperative hypoxia recognized?

A
  • 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.
34
Q

how is perioperative hypoxia managed?

A
  • 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
35
Q

describe effects of hypercarbia

A
  • CO2 > 90 can cause narcosis and additive MAC

- acidosis and hyperkalemia can result

36
Q

what are causes of hypercarbia?

A
  • 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)
37
Q

how can hypercarbia be recognized?

A
  • no return to zero baseline on capnograph
  • increased SNS outflow, hypoventilation, HTN, tachycardia
  • restlessness
38
Q

describe management of hypercarbia

A
  • 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

Principles II (18 decks)

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