ABA keywords Flashcards
Cardiac implications of Duchenne’s muscular dystrophy (48% 2012)
Fatty infiltration of the myocardium results in fibrosis and dilated cardiomyopathy with reduced ventricular function.
The posterobasal and lateral left ventricular wall are usually affected.
There is no correlation between the severity of skeletal and cardiac disease.
Cardiac disease may initially present on ECG as sinus tachycardia, prominent Q and inverted T waves. Echocardiography is initially normal but shows LV wall motion abnormalities as fibrosis progresses. Later, this may lead to systolic dysfunction, LV failure and sudden death.
ACE inhibitors and beta-blockers may helpful in treating cardiomyopathy in these patients.
ECT- seizure duration and anesthetic agents, 46% 2008
An adequate seizure in ECT lasts greater than 30 seconds.
Methohexital – gold standard for ECT, no change of seizure duration but better tolerated than etomidate secondary to ability to blunt hemodynamic response and better than propofol and thiopental because it does not decrease seizure duration.
Etomidate – it is also associated with myoclonus, a longer time to wake than methohexital and also does not block the hypertension and tachycardia often associated with ECT. Increases seizure duration.
Propofol and thiopental decrease seizure duration but blunt hemodynamic response.
Opioids are useful in the fact that they allow a lower dose of the anesthestic agent to be used, thus allowing faster wakeup and if using propofol or thiopental it will decrease the amount so the dose related decrease will help lengthen the seizure (i.e. you don’t have to give as much propofol so it won’t shorten the seizure as much).
Hyperventilation (hypocarbia) will lengthen seizure duration and thus effectiveness of ECT.
Postop management of myasthenia, 27%, 68% in 2009
Ensure that the patient is reminded prior to induction of the possibility of a prolonged intubation
Extubation: performed on awake patients and hopefully close to his/her baseline status. Reinstitute anticholinesterase medication, either by IV infusion or by reimplementation of the patient’s oral regimen.
Leventhal criteria: Predictive scoring system for the need for postoperative ventilation
1) duration of disease for 6 years or longer
2) chronic comorbid pulmonary disease
3) pyridostigmine dose >750 mg/d
4) VC < 2.9L
5) Other indicators include preoperative use of steroids, and previous episode of respiratory failure.
These predictors have not been widely validated. (1)
Drugs to avoid: Calcium Channel blockers, Magnesium, Aminoglycoside antibiotics as all of these may contribute to muscle weakness
Post-Op Bed: Patients should be monitored in either a ICU or step-down unit but NOT to a conventional surgical ward.
Acute treatment of increased ICP, 38% 2010
Elevating head of bed to improve venous drainage. Oxygenation and ventilation to keep PaO2 >100, PaCO2 30-35, use lowest possible AW pressures to not impede venous drainage, and keep MAP at pre-intubation level. Mannitol decreases blood viscosity, CBF unchanged while CBV and ICP decrease. Mannitol also reduces ICP by reducing cerebral parenchymal cell water, total effect takes 20-30min. Eventually Mannitol enters CSF and increases ICP. 3% Saline has similar osmotic effect as Mannitol. Other benefits include enhancement of cardiac output, reduction of inflammation, restoration of normal cellular resting membrane potential and cell volume, and stimulation of the release of atrial natriuretic peptide. NMB reduces ICP by avoiding coughing. Lidocaine can also blunt airway response and avoid increasing ICP w/ intubation. Sedation decreases anxiety, fear, and response to pain, all of which increase ICP. Steroids can reduce edema, especially in traumatic brain injury - steroids are harmful in the setting of TBI but may be exceedingly helpful in patients with intracranial tumors
Pseudotumor cerebri, LP effect, 52% 2011
Pseudotumor cerebri (aka Idiopathic Intracranial Hypertension) commonly causes headache, papilledema, and visual symptoms (and enlarged blind spot) in the setting of isolated elevations in ICP. Several mechanisms have been considered as possible explanations for the pathophysiology of IIH. These include an increased rate of CSF formation, a sustained increase in intracranial venous pressure, or a decreased rate of CSF absorption by arachnoid villi apart from venous occlusive disease. Females have 8 to 10 times the likelihood of males (esp. if overweight and of childbearing age). Frequently, the women are moderately or markedly overweight. IIH has a complex relationship to adrenal hormones. Rarely, IIH is a complication of Addison disease or Cushing disease. Improvement occurs after restoration of a normal adrenal state. Intracranial hypertension also occurs secondarily to occlusion of the intracranial venous sinuses. Diagnosis is made by lumbar puncture (CSF pressure > 25 mmHg with normal CSF composition) but requires exclusion of a mass lesion. Spontaneous recovery is possible however most practitioners advise treatment in order to prevent visual loss. Daily lumbar puncture was used in the past to lower CSF pressure to normal levels by removing sufficient fluid; 15 mL to 30 mL of fluid may be removed, but the value of this procedure is dubious. A CSF-shunt procedure, such as a lumboperitoneal shunt, is useful in patients with intractable headache and progressive visual impairment. It may dramatically relieve symptoms. Optic nerve decompression has its advocates as the procedure of choice to preserve vision. Weight reduction may help, acetazolamide and furosemide reduce CSF production. Repeated lumbar puncture may be of use. Surgical options include optic nerve fenestration and ventricular-peritoneal shunting
Sweat glands, innervation, 30% 2012
The sweat glands are innervated by the sympathetic nervous system and are part of the fight or flight response system. Their innervation consists of two parts, a preganglionic and postganglionic neuron. The preganglionic neuron is short, originates from the thoracolumbar region of the spinal cord, uses acetylcholine as its neurotransmitter, and synapses with the postganglionic neuron via a nicotinic acetylcholine. The postganglionic neuron for sweat gland innervation differs from other sympathetic postganglionic neurons in that it releases acetylcholine to act on muscarinic receptors; all other sympathetic postganglionic neurons, with the exception of the adrenal medulla, use norepinephrine.
Traumatic Brain Injury: CPP (33% in the year 2010
Mechanisms of morbidity: vascular injury leading to extradural hematoma (rapid expansion high mortality 20%), cortical bridging veins leading to subdural hematoma (slow expansion). Either mechanism leads to elevated ICP and decreased arterial inflow resulting in reduced cerebral perfusion pressure -> tissue hypoxia and cell death. TBI can result in loss of autoregulation. SAH is seen in 60% of TBI pts. ECG may show long QT, canyon-T waves, ST depressions and U-waves. Main treatment goal of TBI is to maintain CPP, although ICP vs. CPP management is controversial (see below). Brain Trauma foundation says PaCO2 less than 35 results in worse outcomes. Osmotic or loop diuretics work to reduce ICP.
AICD malfunction causes, 49% 2012
Similar to pacemakers, sensing problems, lead migration, and battery failure all occur in AICDs (usually within 3 months of implantation). A potential malfunction unique to the AICD is the inappropriate or lack of defibrillation of the device. Any of the above causes can lead to inappropriate therapy. The AICD may discharge inappropriately in response to rapid supraventricular rhythms such as atrial fibrillation, supraventricular tachycardia, or even sinus tachycardia. It also may fail to deliver appropriate shocks for v-tach or v-fib if the arrhythmia rate falls below the detection rate: as may be the case in patients on pharmacological rate therapy.
Pharmacologic management of atrial flutter, 37% 2010
Initial treatment of atrial flutter targets the rate control (which is frequently ~150 BPM). Drugs of choice include beta blockers such as esmolol (0.5 mg/kg IV bolus followed by 50-300 ucg/kg/min) and propranolol, or calcium channel blockers such as verapamil (5-10 mg IV) or diltiazem. Beta blockers and CCB are effective in prophylactic prevention of atrial flutter after postoperative thoracic or cardiac surgery. If a patient is hemodynamically unstable and/or has an excessively rapid ventricular rate you may consider an antiarrhthmic drug or synchronized DC cardioversion. If synchronized DC cardioversion is utilized in a non-emergent setting, the provider must be certain that the atrial flutter is new-onset, that a patient does not have thrombosis in the heart via echo, or that the patient has been adequately anticoagulated in order to prevent a thromboembolic event. Ibutilide, a class III antiarrhythmic (Corvert, 1 mg in 10 mL saline infused slowly over 10 minutes) is effective in converting new-onset atrial flutter patients to normal sinus rhythm 90% of the time. It may be repeated once, but the provider should be aware it has a potential risk of inducing torsades de pointes, so the patient needs to be monitored carefully for 4-8 hours after drug administration. Amiodarone (150 mg IV loading dose infused over 10 minutes, followed by 1 mg/min infusion for 6 hours, a 0.5-mg/min infusion for 18 hours, and then a reduced IV dose or oral dose) is also effective in converting atrial flutter to normal sinus ryhthm. Procainamide is another lesser used choice after rate is controlled.
CPB management, 33% 2009
Charge on imidazole ring of histidine. pH 7.40 (pCO2 = 40) at 37C, thus during hypothermia pCO2 is actually lower and pH is higher. Multiple independent, prospective randomized trials have shown that α-stat during moderate hypothermia produces better neurologic outcomes than using pH-stat [Stephan H. Br J Anaesth 69: 51, 1992; Murkin JM. J Thorac Cardiovasc Surg 110: 340, 1995; Patel RL. J Thorac Cardiovasc Surg 111: 1267, 1996]. ACC/AHA Class I Level A Recommendation for adults undergoing moderate hypothermic CPB
pH stat
pH 7.40 at actual core body temperature, CO2 often added, vasodilation. Impairs autoregulatory responses to changes in BP. May increase the risk of cerebral embolization, according to one study of 52 patients based on jugular venous oximetry [Kiziltan HT et al. Anesth Analg 96: 644, 2003]. Data in pediatrics are conflicting but probably favor pH stat management
latex allergy and foods, 50% 2010
There are particular foods and fruits that are known to produce a type of substance that is similar to the rubber latex. This is known as the latex-fruit syndrome. Fruits (and seeds) involved in this syndrome include banana, pineapple, avocado, chestnut, kiwi fruit, mango, passionfruit, strawberry, and soy, as well as potato and bell pepper [Wagner S, Breiteneder H. Biochem Soc Trans 30: 935, 2002]
