UBP Book 4 Flashcards
What is the definition of major burns for adults?
Second-degree (partial-thickness) >25% BSA
Third-degree (full-thickenss) >10% BSA
If major burn present, risk respiratory compromise –> plan to intubate
Signs and symptoms of burn/inhalational airway injury
Singed facial hair
Burned mucosa
Cough
Stridor
Hoarseness
Difficulty breathing or swallowing
Pharyngeal edema
Upper airway inhalational injury can lead to glottic and periglottic edema, copious thick secretions, and airway obstruction.
Complications of sodium bicarbonate to treat acidosis
- Generates additional CO2 which then diffuse into cells –> worsens intracellular acidosis
- Leftward shift oxyhemoglobin dissociation curve (impaired delivery of O2 to tissues)
- hyperosmolar state 2/2 Na
But can consider NaHCO3 if pH <7.1
Cardiovascular changes expected following burn injury
First 24-48 hrs: decreased cardiac output (due to circulating myocardial depressant factors, increased SVR, contracted plasma volume, diminished response to catecholamines, decreased coronary blood flow)
After 24-48 hrs: hyperdynamic state with CO 2x normal, reduced SVR (circulating inflammatory mediators), interstitial fluid re-absorption, increased circulating catecholamines
Bone-cement implantation syndrome
Hypoxia, hypotension, dysrhythmias, pulm HTN, and decreased cardiac output associated with bone cement. Unclear etiology/poorly understood, but may be due to:
- increased intra-medullary pressure from expansion of bone cement can cause embolization of bone marrow debris
- Circulating methyl methacrylate monomers can cause reduced SVR
- Cytokine release during reaming can lead to pulm HTN
- embolized cement can lead to pro-inflammatory factor release
Tx: supportive w/ 100% O2, fluids, vasopressors
Note: bone cement is plexiglass!
Hyperthermia after burn injury
Major burn injury often leads to hypothalamus-mediated increase in core/skin temperature (may be part of hypermetabolic response to thermal injury)
Umbilical artery catheter position
Insert through iliohypogastric artery to level of T7-T9 (to avoid catheter tip migration into iliac arteries and malperfusion)
Complications of umbilical venous cannulation
- bleeding
- infection
- portal or mesenteric vein thrombosis
- portal cirrhosis
- liver abscess
- subcapsular hematoma
- cardiac tamponade
- endocarditis
What is the pathophysiology of retinopathy of prematurity?
Occurs prior to 44 weeks gestational age (vascularization of retina complete after this)
High oxygen concentration leads to vasoconstriction and obliteration of retinal vessels with subsequent relative hypoxia and abnormal neovascularization.
Relative contraindications to Mg therapy in pre-E
- cardiomyopathy
- recent MI
- Myasthenia Gravis
- impaired renal function
- CCB therapy (potentiates cardiotoxic effects)
Estimated blood volume
Premature 90-100
Term 80-90
3-12 months 70-80
> 1 year 70-75
Man 75
Woman 65
100-90-80-70
75-65
Postoperative apnea in neonates
Greatest risk up to 50-60 weeks post-conceptual age (approximately 1 year post conception)
Monitor 12-24 hours post op
Risk factors: chronic lung disease, hx apnea and bradycardia, narcotics, congenital anomalies, anemia, neurologic abnormalities
Metabolic derangements associated with pyloric stenosis? Fluid for resuscitation?
Hypokalemia hypochloremic hyponatremic metabolic alkalosis
Compensatory respiratory acidosis
Rehydrate with sodium chloride and potassium (important to replace sodium because renal conservation of sodium in a dehydrated infant leads to bicarbonate reabsorption and worsening metabolic alkalosis)
Dangers of metabolic alkalosis in the neonate
Leftward shift in hemoglobin oxygen dissociation curve
Reduced ionized Ca
Lowers seizure threshold
Osteogenesis imperfecta considerations
Abnormal Type I collagen synthesis. May present with:
- blue sclera
- fractures from minimal trauma (avoid NIBP, cricoid pressure, IO needles, succinylcholine)
- kyphoscoliosis
- femur/tibia bowing
- coagulopathy (platelet dysfunction, keep in mind for neuraxial)
- hearing loss
- hyperthyroidism
- craniocervical instability
- cardiac disease (MR, AR, aortic dissection)
- macroglossia
- quadriparesis
- megalocephaly
- shorter neck
Potentially difficult airway and avoid cricoid pressure. Low threshold for art line. Neuraxial ok but be careful and check for coagulopathy.
How to medically optimize pyloric stenosis
History: frequency/volume emesis, number of wet diapers, weight change since birth, lethargy, last feeding
Physical: volume status, muscle tone, level of consciousness
Labs: CBC, BMP, ABG, UA, glucose
- empty stomach with OGT
- hydrate with NS until making urine, then add potassium. Add glucose if low blood sugar.
- target evidence of clinical hydration, normal pH, Na >130, K >3, Cl >85, HCO3 < 30, and UOP 1-2cc/kg/hr
CPB Centrifugal vs. roller pump
Roller pump:
- forward flow from partial compression of tubing
- not sensitive to preload or afterload
Pros: reliable amount of flow based on pump speed, can delivery pulsatile flow
Cons: increased RBC damage, risk over-pressurization (tubing separation or rupture), preload occlusion leading to negative-pressure cavitation and microbubbles
Centrifugal pump:
- forward flow from rotational force
- preload and afterload sensitive
Pros: will stop if significant amount of air entrained, less damaging to RBC, avoids over-pressurization, cavitation, delivering large amounts of air to patient
Cons: no pulsatile flow, can only partially compensate for decreased forward flow 2/2 increased distal pressure
Alpha-state vs. pH-stat
Alpha-stat: CO2 not added despite reduction in partial pressure that occurs with hypothermia. Primary mechanism of brain injury in adults thought to be 2/2 embolic events rather than ischemia–increasing CBF by adding CO2 may be harmful, avoid by using alpha-stat. 2019 EACTS/EACTA/EBCP recommendation is to use alpha-stat in adults undergoing mild to moderate hypothermic CPB due to improved neurologic outcomes in several trials from 1990
pH-stat: CO2 is added to compensate for reduction in partial pressure with hypothermia to enhance CBF (facilitate cooling). Used in pediatrics since mechanism of brain injury thought to be mostly 2/2 ischemia not embolic events.
Sequelae of acute mitral regurgitation
Acute MR = acute volume overload of the relatively noncompliant left atrium
Acute MR leads to LA and LV volume overload without compensatory LV dilation, resulting in increased LA and LVEDP. This causes decreased cardiac output, pulmonary congestion and edema, and RV failure. Additionally, elevated LVEDP can worsen myocardial ischemia (coronary perfusion pressure = Ao DBP - LVEDP)
Pulmonary capillary wedge tracing changes in acute MR
Prominent v wave, loss of x descent, rapid y descent
Normal pulmonary capillary wedge tracing waves
a = atrial contraction
c = elevation of MV during early systole
v = venous return against closed MV
x = downward displacement of atrium during systole
y = decrease in atrial pressure as MV opens during diastole
Potential causes of ventricular failure when weaning from byapss
- Inadequate coronary blood flow from hypotension, coronary emboli, coronary vasospasm, tachycardia
- Inadequate myocardial preservation
- Graft failure (if CABG)
- Increased afterload (if regurgitant valve was repaired/replaced–loss of pop-off)
- Valve failure
- Hypoxia
- Inadequate preload
- Reperfusion injury
- Acidosis
- Electrolyte abnormalities
Reason for difference between radial arterial pressure and central aortic pressure after CPB
Peripheral vasodilation occurs during rewarming, so radial arterial pressure may be up to 30mmHg lower than femoral/central aortic pressure. Usually resolves within 45 min of separation from bypass.
What is pulsus paradoxus?
A reduction in systolic pressure with inspiration
Negative intrathoracic pressure –> increased venous return –> increased RV volume –> septum bulges into LV because of tamponade –> decreased LV stroke volume
Definitions of OSA, obstructive sleep hypopnea syndrome, obesity-hypoventilarion syndrome, and Pickwickian syndrome
OSA: complete cessation of airflow for > 10 sec >5 times per hour of sleep with >4% decrease in SpO2
OSH: 50% reduction in airflow for >10 sec >15 times per hour of sleep with >4% decrease in SpO2
OHS: obesity, daytime hypercapnia (PaCO2 > 45), nocturnal hypoxia, and polycythemia in the absence of alternative causes of hypoventilation
Pickwickian syndrome: severe form of OHS with pulm HTN and RV failure (WHO Group 3 PH) - think P in Pickwickian goes with PH
How will you maintain anesthesia for obese patients with severe OSA?
For obese patients at increased risk for respiratory depression, my goal is to use short-carting agents without active metabolites that allow for rapid return of airway reflexes and do not have respiratory depressant effects.
Some options:
- desflurane
- remifentanil
- cisatracurium (if poor liver function)
