Surgical Intensive Care Flashcards
A patient needs renal replacement therapy.
Who gets CRRT, who gets HD?
CRRT: Patients who have poor cardiovascular stability and cannot tolerate large fluid shifts over a short period of time.
HD: Patients who are cardiovascularly stable or who arrive with toxic ingestion.
Basically, CRRT is easier on hemodynamics, but less effective at reducing electrolyte concentrations and reversing uremia.
Tracheobronchomalacia diagnosis and ventilator management
>90% obstruction with exhalation during provocation maneuver
Definitive management is with tracheobronchoplasty, however ventilation with PEEP can also keep the tracheal cartilage open in order to ventilate.
Etiology of critical illness neuromyopathy
Two components:
- Use-dependence. If you aren’t using your muscles or nerves, they will become less efficient/weaker.
- Perfusion – poorly perfused muscle/nerve will not function as well.
Looking for edema in ICU patients
You want to look in the dependent positions, so posterior hip and pre-sacral regions are optimal in ICU patients lying supine.
If a patient has an S3 on exam, their PCWP is at least. . .
. . . 18 mmHg
Measuring SVR with a Swan-Ganz catheter
Calculated using MAP, CVP, and cardiac output (flow)
F = dP / R
R = dP / F
SVR = [MAP - CVP] / CO
Pulmonary, cardiovascular, and neuro assessment of readiness to extubate
Pulmonary: RSBI < 105, Inspiratory pressure < 25 cm H2O
Cardiovascular: PEEP < 5 cm H2O
Neuro: Mental status adequate
How to test pulmonary compliance with a ventilator
Set mode to volume control. For the volume, use lung-protective ventilation (6 mL/kg idela body weight)
Compliance = TV / (Ppleateau - PEEP)
Compliance > 60 is normal.
Special nutrition formulations for:
Hypoxic repsiratory failure
Renal failure
Cirrhosis
Hypoxic respiratory: Low RQ diet (less carb, more fat)
Renal failure: Low K, low Phos diet
Cirrhosis: High calorie, branched chain amino acid diet
Assessing a patient’s nutritional requirements (3 elements)
- Pre-morbid state (is the patient malnourished?)
- Stress level (very sick, or relatively stable?)
- Risks of the intervention (infection)
How many calories does the patient need?
Calories = BMR x Stress Factor x Ideal body weight
If they have sepsis, SF = 1.7. If they have large burns, SF= 2.0.
Usually for an inpatient, 17 x 1.5 x IBW = 25 x IBW, so:
25 kCal/kgIBW/day
Respiratory quotient
RQ = CO2 production / O2 consumption
For most people, this is 0.8
Why does muscle wasting occur, metabolically, in patients without exogenous glucose?
Gluconeogenesis requires pyruvate, which can only come from fermented glucose or amino acid skeletons – not from fats.
Ergo, when glucose stores run out, amino acids start to be pulled for pyruvate to participate in gluconeogenesis.
Nutritional composition of a typical tube feed
- Macronutrients:
- 30% carbohydrates (for protein-sparing effect)
- 40% protein (2g/kg/day if sick, 4 if really sick)
- 30% fat (cell membrane synthesis)
- Micronutrients and other:
- Fluid (minimal)
- Electrolytes
- Vitamins
- Minerals
- Additives (insulin, famotidine)
RQ of carbohydrates
1.0
RQ of fatty acids
0.6
What is the biggest risk of small bowel feeding over gastric feeding?
The small bowel can’t control the rate of digestion.
The pylorus is the filter for metabolic demand on the small bowel. Once stuff is in the bowel, the bowel must increase its metabolic demand to digest and absorb the nutrients.
In a patient with enteric hypoperfusion, this is effectively exercising an ischemic gut, and may result in enteric infarction.
Patient in the ICU has a high anion gap metabolic acidosis that is not fully explained by their lactate level.
What is the next best step?
Check the beta-hydroxybuyrate
They may be in DKA – especially nowadays with so many diabetics on SGLT2 inhibitors or other antihyperglycemics that keep glucose normal even when absolute insulin levels are low.
When is a Swan Ganz helpful?
- Acute aortic insufficiency, to assess hemodynamics and to use the pacing port for acute heart pacing.
- Mixed shock, to assess relative contributions from different etiologies and optimize cardiac output
Spontaneous breath vs Ventilator breath
Spontaneous breath: Intrathoracic pressure decreases, increasing venous return to the R heart.
Ventilator breath: Intrathoracic pressure increases, decreasing venous return to the R heart but increasing pulmonary venous return to the L heart.
Delta down
After a period of apnea, deliver a large-volume breath (8-15mL/kg) and measure the change in systolic blood pressures.
ΔDown = Ppeak, apnea - Ppeak, post-breath
Higher delta down predicts better fluid responsiveness.
Types of amiodarone-induced thyroid abnormalities
Amiodarone-induced thyrotoxicosis type I: Thyrotoxicosis in individuals with preexisting thyroid disease. Treated with methimazole or PTU.
Amiodarone-induced thyrotoxicosis type II: Thyrotoxiosis resulting from amiodarone-induced thyroiditis and destruction of glandular tissue. Best treated with glucocorticoids. May be followed by a hypothyroid period.
Amiodarone-induced hypothyroidism: Due to Wolff-Chaikoff effect from high iodine levels in amiodarone. Women and those with Hx of Hashimoto’s are at increased risk.
Note: Due to the long halflife of amiodarine (50-100 days), these effects may persist long after discontinuation of the medicaiton.
Adrenal insufficiency in sepsis
While this is a well-documented phenomenon, and steroids have been shown to help some patients, conventional AI testing (Cosyntropin stimulation, etc) has not been shown to be helpful in determining who will benefit from corticosteroids.
So, we just give corticosteroids to anyone who has hypotension resistant to fluids and pressors, as well as those with baseline corticosteroid therapy (stress dosing). In other words, those with clinical adrenal insufficiency.
CYP inhibitors and inducers on corticosteroids
Paradoxically, both can decrease the level of circulating corticosteroids:
CYP inducers can increase cortisol catabolism
CYP inhibitors can reduce cortisol synthesis
Lots of patients in the ICU have hypotension and require sedation.
So, why don’t we use etomidate?
Because these patients are also at risk for adrenal insufficiency, which could be devastating if they are already hypotensive.
Etomidate’s one major complication is that it can cause adrenal insufficiency via dose-depedent inhibition of enzymes involved in cortisol synthesis. Even single-dose etomidate may produce clinically significant adrenal insufficiency in septic patients, and etomidate has been shown to increase all-cause mortality in the ICU.
For these reasons, ketamine is the preferred rapid-sequence induction agent in critically ill ICU patients.
Sleep-wake cycle problems in critically ill patients
- Many either have or are receiving high levels of cortisol. Cortisol is known to inhibit sleep.
- Septic patients have continuous, non-fluctuating secretion of melatonin.
Both of these serve to derange the sleep-wake cycle and increase the risk and severity of delirium.
In whom is the Hgb goal > 10g/dL instead of >7 g/dL?
- Patients with active hemorrhage
- Patients with significant lactic acidosis
- Patients with coronary ischemia
Management of euthyroid sick syndrome
Really nothing.
Characterized by a decrease in T3 followed by a decrease in T4 within 24-48 hours, due to inhibition of T4 to T3 conversion and increased rT3. TSH remains normal to low.
While it may be an adaptive mechanism, it is associated with increased mortality despite an absence of hyper- or hypo-thyroid symptoms.
No treatments have been shown to be effective. So, we do nothing but prognosticate.
Vasopressin and sepsis
In sepsis, the V1 receptor may be downregulated.
This results in relative vasopressin deficiency, and these patients may benefit from low-dose exogenous vasopressin.
Clinically, this just makes vasopressin our 2nd-line vasopressor in patients with septic shock (after norepinephrine).
pO2 / FiO2
P/F < 300 indicates acute lung injury (ALI)
P/F < 200 suggests ARDS, particularly when there is new bilateral alveolar infiltrate on CXR
Multiorgan dysfunction syndrome
All in the name. Basically, organ dysfunction begets organ dysfunction. Macrophage cytokine release in the setting of organ dysfunction is thought to be the instigating factor of the syndrome.
Biggest risk factor is circulatory failure within the first 24 hours of admission.
MODS takes days to weeks to develop following the initial insult.
Anesthetics that preserve respiratory drive
Ketamine: Also increases sympathetic outflow (and ICP). NDMAR antagoist.
Dexmetomadine: Also decreases sympathetic outflow. Centrally acting alpha-2 agonist.
It is generally advisable to withhold enteral feeding from patients in the ICU until. . .
. . . these patients are fully resuscitated and have adequate blood pressures
In a previously healthy patient with no evidence of malnutrition, how long can you go before it is no longer justifiable to withhold parenteral nutrition?
7-10 days
Traditional markers of malnutrition (albumin, prealbumin, transferrin, retinol-binding protein) . . .
. . . change with acute phase response and cannot be used in the ICU
Enteral nutrition should be initiated for a new ICU patient. . .
. . . within 24-48 hours of admission OR as soon as fluid resuscitation is complete and the patient is hemodynamically stable
Why do we tend to prefer small bowel feeding in the ICU?
To reduce the risk of aspiration, particularly in patients with severe brain injury (the lack of vagal input results in gastroparesis).
“Trickle” feeds
Prevent mucosal atrophy in ICU patients, but do not improve immunologic function and infectious outcomes
What is an acceptable gastric residual volume (in the absence of other signs of intolerance)?
< 500 mL
Fluid of less than this amount is not associated with increased risk of aspiration or pneumonia
Enteral lipids should generally consist of. . .
. . . an anti-inflammatory, anti-oxidant lipid profile
This includes omega-3 oils and borage oil, which have been shown to reduce the ICU length of stay, duration of MV, and overall mortality.
Don’t miss complications of aortic dissection
Acute cardiac tamponade
Acute aortic regurgitation (especially bad i/s/o aortic dissection therapy)
Acute RCA coronary syndrome (contraindication to intravascular inervention)
Acute limb ischemia, anterior circulation stroke, mesenteric and renal involvement/embolism
Impulse control in aortic dissection
Reduce the amount of time that the vessel is experiencing high pressure
- HR control – reduce the frequency of systolic pressure exposure
- Pressure control – reduce the magnitude of systolic pressure
Start with a beta blocker (to avoid reflex tachycardia – often esmolol), then afterload reducer (dihydropyridine CCB, hydralazine, nitroprusside, etc).
Initial IV nutrition regimen
30 kcal/day, 1g protein/kg body weight
