Random Flashcards
Calculation of BP in different sites (example the arm cuff, and asking what’s the brain pressure?)
The difference in blood pressure at 2 different sites equals the height difference in cm (between cuff pressure and desired pressure sure) multiplied times the conversion factor 0.74.
TrueLearn Insight : A mnemonic to help remember which comes first (pressure or height) is “pH” or “pH 15 20”, where a pressure of 15 mmHg correlates to a height of 20 cm.
Pulse ox reading differences between CO vs methemoglobinmia?
The both would increase PaO2 with supplemental oxygen. However, in contrast, a patient with CO poisoning would most likely have a pulse-ox that is falsely elevated to 100% even while breathing room air since carboxyhemoglobin resembles oxyhemoglobin to a standard pulse oximeter. With methemoglobinmia the pulse ox would read 85-88%
What exacerbates acute intermittent porphyria?
P450 inducers Barbiturates BZDs Nifedipine Glucocorticoids Acute alcohol
These patient should be kept normothermic and well hydrated.
What electrolyte dearrangement must be corrected in anesthesia transplanted liver who is reviving massive blood transfusion?
Hypocalcimia
Citrate toxicity causes ionized hypocalcemia, manifested as hypotension and decreased pulse pressure, QT prolongation, and potential for arrhythmias.
Citrate toxicity causing severe hypocalcemia during liver transplantation is well documented and is manifested as hypotension, narrow pulse pressure, increased intraventricular end-diastolic pressure, and increased central venous pressure
What anti-depressant medication would be relative C/I to use methylene blue and why?
SSRI/SNRI or MaO inhibitors
Methylene blue is a MAO-A inhibitor and may cause serotonin syndrome in patients taking antidepressants. Suggestive symptoms include postoperative delirium and postoperative fever. Treatment is mostly supportive although cyproheptadine, a serotonin receptor antagonist, can be attempted.
what medications used to prevent epistaxis in nasal intubation? Local anesthetic is a choice?
vasoconstrictors such as oxymetazoline and phenylephrine
Lidocaine ointment is helpful in treating the pain of a nasotracheal intubation as well as functioning as a lubricant, particularly in awake intubations. however, does not prevent epistaxis. The only local anesthetic that would be useful for reducing epistaxis in this setting would be cocaine but it carries the risk of inducing arrhythmias.
Airway edema classified to subglottic vs supraglotic, what are the causes of either?
Supraglottic edema most often occurs following surgical instrumentation, secondary to impaired venous drainage (head down or prone position), the formation of a hematoma, excessive fluid administration, or due to coexisting conditions (preeclampsia/eclampsia, angioedema).
Subglottic edema most often occurs following traumatic intubation attempts or due to damage from the endotracheal tube (prolonged intubation, excessive cuff pressure, tight-fitting tube, patient bucking on the ETT).
Subglottic edema is much more common in children due to the smaller diameter of their airway.
Time expected to see post-extubation laryngeal edema ?
usually presents within 30-60 minutes of extubation as stridor although it can present up to 6 hours post-extubation.
Mgmt of post-extubation laryngeal edema?
1) 100% oxygen + head elevation to help improve venous drainage
2) asses for emergent re-intubation
3) nebulized racemic epinephrine
4) Heliox.
Steroids remain controversial and need several hours for effect.
Hoe nebolizer epi and heliox benefits in laryngeal edema?
- nebulized racemic epinephrine: alpha-adrenergic receptor stimulation in the airway resulting in mucosal vasoconstriction, causing a decrease in the amount of fluid present in the airway. It will also cause beta-adrenergic stimulation in the bronchial tissue resulting in bronchodilation, which will not alleviate the edema but can help any component of bronchoconstriction present)
- Heliox: ( it develops less resistance “because of its light density” when passing through the stenosis/edema resulting in less patient effort needed to get the same volume of gas.
RF of pulmonary artery rupture during PAC placement?
hypothermia (it increases catheter stiffness), anticoagulation, old age, and pulmonary hypertension
Compliacations of pulmonary artery placement (PAC)?
arrhythmia, valve damage, infection, PA rupture or infarction, thromboembolism, endocardial damage and misinterpretation of data
Interestingly the risk of endocarditis increase two-fold with use of non-heparin coated PACs.
stimulation of bronchoconstriction via 3 mechanisms?
- Main by parasympathetic nervous system (muscurinic receprots) via the vagus nerve. “ hypoxia & HTN can stimulate vagus nerve through carotid sinue/body to central nucleus ambiguous)
- Alpha receptor stimulation
- Excitation of NANC neurons by substence P & neurokinin A
Most common cause of perioperative retinal arterial occlusion is ?
Improper patient positioning resulting in external compression of the eye.
Postop visual loss due to ischemia of —– optic in cardiac vs spine surgeries?
Cardiac procedures, anterior ischemic optic neuropathy while spine surgery in the prone position, posterior ischemic optic neuropathy seems to be the predominant cause.
An easy way to remember ION would be the location of the surgery predicts the type – posterior spine surgeries = posterior ION and anterior cardiac procedures = anterior ION.
cardiac cases, related to emboli, thrombotic events, ischemic reasons, or even due to oncotic pressure changes.
In spine surgery the risk seems to be related to ischemia and/or patient position.
What pressure changes to PIP & Pplateau with Airway Resistance? DDX?
Increased PIP, Unchanged Pplateau
- Airway compression
- Bronchospasm
- Foreign body
- Kinked endotracheal tube
- Mucus plug
- Secretions
What pressure changes to PIP & Pplateau with Pulmonary Compliance (Elastic Resistance)? DDX?
Both increase( Increased PIP, Increased Pplateau)
- Abdominal insufflation
- Ascites
- Intrinsic lung disease
- Obesity
- Pulmonary edema
- Tension pneumothorax
- Trendelenburg position?
What is the initial compensation mechanism for acute respiratory acidosis ?
Increase plasma Bicab through plasma protein buffering (Hgb in RBC CO2 reacts with H2O to produce HCO3 and hydrogen, which this bicarbonate will exchange with CI to dump it in blood and raise blood HCO3)
Then urinary excretion of CI to reabsorb HCO3 happens later hours-days.
Will you have aspiration pox in asymptotic hiatal hernia repair?
Yes the asymptomatic and symptomatic at risk for aspiration even if no GERD sx because of esophagus dysfunction.
correcting high INR with Vit K?
No bleeding + INR <5 + elective then withholding warfarin for several days warfarin (1/2 t is 2-4 days).
No bleeding + INR >5 + surgery > 24 hrs then give Vit K
Bleeding, or INT> 10-> high dose Vit k (5-10 mg)
How do you correct high INR for urgent/emergent cases or active bleeding?
PCC (prothrombin complex concentrates) + Vit K
2 form of PCC; 4 factors (1972) and 3 factors (192) which factor 7 should be supplemented
S/E TRALI, and transfusion associated circulatory overload.
Ventilation goals in bronchipleural fistula?
End expiratory pressure
Short inspiration time
Low TV
Low RR
Spontaneous ventilation preferred over PPV.
Lung isolation decreases pressure and volume ( the theory of its benefit, ventilating both lungs may cause barotrauma and voluteuma to healthy lung since higher pressure needed to overcome through the fistula teak)
Mgmt of bronchopleural fistula?
Lung isolation with double lumen.
High frequency jet ventilation (delivers small TV under high pressure) but this causes hyperinflation and HD instability
If all falls then ECMO
Post op A-fib risks?
- cardiac/thoracic surgeries also large abdomen/vascular procedures
- present cardiac or Lung dis (HTN, valvular, copd/asthma …)
- intraop volume status (hypo triggers catecholamines from decreased i2 delivery, and increased catecholamines triggers AF) (hypervolemia also triggers AF through atreual mechanical stretch)
Whats the BP conversion number for change in cuff height ?
The conversion is 0.75 mm Hg per 1 cm change in height relative the reference point (e.g. the level of the heart), adding when the cuff is below and subtracting when the cuff is above the level of the point of reference.
(pH = 15 20) 15 mmHg = 20 cm change
how preterm labor caused in pregnents with spinal cord injury?
Autonomic hyperreflexia results from the absence of central inhibition on the sympathetic neurons in the spinal cord below the injury. Uterine contractions can stimulate autonomic hyperreflexia. This can result in vasoconstriction, therefore fetal hypoxia and bradycardia.
Neurogenic shock vs Autonomic hyperreflexia?
Neurogenic shock following acute high spinal cord injuries (SCI) is associated with severe bradycardia and hypotension from unopposed vagal or parasympathetic activity and loss of cardiac accelerator fibers (if injury is above T1-T4). There is a loss of sympathetic function, which cannot oppose vagal response during stimulation. (so during DL; Nerve transmission unable to activate the thoracic sympathetic)
Autonomic hyperreflexia begins 2-3 weeks following acute injury. It may occur with stimulation below the level of spinal cord injury leading to uninhibited sympathetic stimulation. Approximately 85% of cases occur with SCI above the T5 level.
Lung volumes? the capacities (there is 3) - - FRC= residual volume + ….
- VC = All except ….
- TLC= Everything
- functional residual capacity is the RV + ERV (expiatory reverse volume).
- RV
DDx for delayed emergence or awakening?
Anesthesia related (residual anesthetic/ms relaxants, psudocholinesterase deficiency, excessive narcotics)
Metabolic (hypothermia, hypoxia, hypercarbia, hypo Na/Ca/glucose, renal/hepatic dysfunction)
Intracranial event (stroke/CVA, seizure, increased ICP)
Ondansetron is known to cause QTc prolongation in nearly 20% of patients but its very rarely clinically significant, why?
The prolongation is typically 20-30 msec or less, which is clinically insignificant (though statistically significant) except in patients with already prolonged QTc intervals or those with additional risk factors for prolonged QTc intervals (e.g. hypokalemia, hypocalcemia, hypothyroidism, history of myocardial infarction, long QT syndrome, and recent use of other medications that prolong the QTc interval).
Further prolongation of the QTc interval potentially places patients at risk for the development of arrhythmias, notably torsades de pointes. This lead to placement of a black box warning on the medication in the U.S. in 2011 by the Food and Drug Administration. However, it is worth noting this warning was focused on the 32 mg single IV dose. Current recommendations are that no single dose be larger than 16 mg IV.
Common side effects of Zofran?
- QTc prolongation (20%, very rarely clinically significant).
- headache (11%)
- transient AST/ALT increases (5%),
- constipation (4%), rash (1%), flushing/warmth (< 1%), and dizziness (< 1%).
5 types of PONV medications used?
when is the re-dosing of zofran can be considered?
is metoclopramide recommended for PONV?
1) 5-HT3 receptor antagonist (e.g., ondansetron): Do not re-dose unless more than 6 hours have elapsed since the last dose was administered, including in the immediate post-operative period. An adverse effect is QTc prolongation.
2) NK-1 receptor antagonist (e.g., aprepitant): more effective than ondansetron. Recommended to give prior to the start of surgery.
3) Corticosteroids (e.g., dexamethasone): recommended dosing is 4 mg at the beginning of the surgery due to long onset time.
4) Dopamine-2 receptor antagonist (e.g., droperidol, metoclopramide): droperidol is effective as an anti-emetic. Recommended dosing is 0.625 to 1.25 mg at the end of surgery. Metoclopramide is considered a weak anti-emetic. The effective dose for metoclopramide is 25 to 50 mg. Metoclopramide 10mg is not recommended for PONV. Also, metoclopramide is not recommended as an antiemetic for patients who have received prophylactic ondansetron intraoperatively.
5) Anti-cholinergics (e.g. scopolamine patch): need to apply prior to going back to the operating room due to its 2 to 4 hour onset time. Can cause visual changes, dry mouth, and dizziness.
PONV Risk Factors in Children?
PONV Risk Factors in Adults Age < 50 years old Female gender History of PONV or motion sickness Non-smoker
PONV Risk Factors in Children Age > 3 years old History of nausea/vomiting (in the child or relative) Strabismus surgery Surgery > 30 minutes
perioperative factors associated with increasing and decreasing PONV
Increases Incidence of PONV
Duration of anesthesia
Opioid use (especially post-operatively)
Surgery (laparoscopic, cholecystectomy, gynecological)
Use of nitrous oxide/volatile agents
Decreases Incidence of PONV Adequate hydration??? Avoid nitrous oxide??/volatile agents Minimize opioid use Regional anesthesia (avoid general anesthesia) Use of propofol
Neostigmine dosage for reversal?
0.07 mg/kg neostigmine, up to 5 mg maximum
Risk factors for Postoperative cognitive dysfunction (POCD) ?
Advancing age, lower educational level, and a history of previous cerebral vascular accident with no residual impairment.
what is laryngospasm? who is at risk?
Reflex adduction of the true and false vocal cords and linits air move in.
results from light plane of anesthesia, extubation during stage II, oropharyngeal secretions, or in patients with recent respiratory tract infections.
It occurs more frequently in children, in those with reactive airway disease, and those who have second-hand smoke exposure.
Laryngospasm management?
100% oxygen with positive pressure < 20 cm H2O, Larson maneuver, ( 3-5 seconds of pressure to the retromandibular notch), optional IV anesthetic ( 3-5 seconds of pressure to the retromandibular notch), and last resort IV succinylcholine (0.5 mg/kg).
Goals to prevent PONV?
While we would like to prevent PONV in order to decrease PACU stays, avoid unexpected admissions, and improve patient satisfaction, vomiting and retching have been associated with severe side effects. This includes aspiration, suture dehiscence, esophageal rupture, subcutaneous emphysema, or pneumothorax.
Where dose seretonin released from? and how nausea & vomiting develops?
Toxic substances can lead to the release of serotonin from the enterochromaffin cells in the gut wall.
Serotonin is released near afferent vagal nerve endings of the gut wall that travels to the dorsal brainstem through the nucleus tractus solitarius.
Toxins and drugs are thought to cause nausea and vomiting through stimulation of the chemoreceptor trigger zone. The CRTZ is located in the area postrema at the bottom of the 4th ventricle. (The CRTZ is outside of the blood-brain barrier and leads to nausea and vomiting through the direct action of drugs and toxins on the CRTZ, and not through the release of serotonin.)
Salted emergence can be caused by neostigmine or glycopyrolate?
Glyco, the anticholenergic agent not the reversal anticholeaterase
Lower extremity sensation test after block:
L1 -> inguinal ligament L2 -> later side of thigh L3 -> medial thigh L4 -> medial side of first toe L5 -> lateral side of second toe
Flexion of hip -> L1 + 2
Extension of knee -> L3 + L4
Flexion of knee -> L5 - S2
NaHCO3 effect to consider when administering
- Transit increase in EtCO2 and PaCO2
- Increased ICP (the CO2 generates when bicarbonate binds to H+ produces CO2 which will increase cerebral BF and increase ICP)
- transit decrease in Ca & K
- hypotension due to hypoCa and ventricular depression effect as well as redistribution of blood to plum vascular)
Intraop Anaphylaxis mgmt ?
Remove all considered allergen. Remove all latex D/C meds Intubation? IVF bolus ~50 mL/kg Epi 0.01 mg/kg D/C anesthetic
Cause of acute hemolytic transfusion anemia
ABO incompatibility
Cause of febrile transfusion rxn?
Donor cytokines and Ab reacting to recipient leukocyte
