Critical Care Flashcards
1
Q
Cardiac tamponade: How does it make that cardiac tracing look?
A
Exaggerated X descent (RA and RV are affected first) and attenuated Y descent.
2
Q
What type of anesthesia could you give for tamponade?
What should you avoid?
A
Ketamine. Keep ventilation spontaneous.
Cardiac depression, vasodilation, and slowing of the heart rate should be avoided. Acute loss of preload, contractility, and heart rate can cause catastrophic circulatory collapse in the setting of cardiac tamponade. Epinephrine, therefore, is a useful medication in the management of cardiac tamponade and an infusion should be considered prior to induction of anesthesia.
3
Q
How to think of management for tamponade:
A
Hemodynamic goals for cardiac tamponade are best described as keeping the patient fast (tachycardia), full (hypervolemia), and tight (increased SVR). DO NOT SLOW HEART RATE!
4
Q
Constrictive pericarditis on CVP waveform:
A
Constrictive pericarditis causes an exaggerated X-descent and Y-descent on the CVP waveform.
5
Q
The key features of botulism syndrome:
A
B/l cranial nerve deficits
6
Q
Treatment of botulism: Above 1 and under one
A
Two types of antitoxin therapies are available – equine serum in patients older than one year old and human-derived immune globulin for infants less than one year of age.
7
Q
Formula to figure out how to neutralize acids by using sodium bicarbonate
A
Sodium bicarbonate (mEq) = 0.2 * patient weight (kg) * base deficit
8
Q
In patients with respiratory depression, can you give Bicarbonate?
A
Sodium bicarbonate should not be administered to a patient with respiratory depression or respiratory failure unless the patient is mechanically-ventilated
9
Q
In true pressure support mode, there is no ____. This means ___
A
In true pressure support mode, there is no backup rate; thus hypoventilation can occur particularly with a low respiratory rate.
10
Q
What are the 5 causes of hypoxemia?
A
Hypoventilation Low Partial pressure of O2 VQ mismatch poor diffusion right to left shunt
11
Q
Of the 5 causes of hypoxemia, which ones do NOT result in increased A-a gradient?
A
Hypoventilation and low partial pressure of O2.
12
Q
Classical finding of impaired diffusion (A-a stuff)
A
The classic clinical finding suggestive of impaired diffusion is a normal PaO2 at rest but a decreased PaO2 with increased cardiac output.
13
Q
T/F: A right-to-left shunt is never associated with an increased A-a gradient.
A
FALSE! It is always associated with an increased A-a gradient.
14
Q
Organophosphate poisons-how do they hurt? How do the modes of paralysis switch?
A
Organophosphates and related poisons including sarin nerve gas are acetylcholinesterase inhibitors that permanently bind to and prevent the function of the enzyme. This initially leads to a buildup of ACh within the neuromuscular junction resulting in brief spasms or a spastic paralysis. However, pre and post-junctional structures are soon destroyed, possibly due to the accumulation of toxic levels of calcium from continued stimulation, and a longer-lasting flaccid paralysis will result.
15
Q
Why make patients prone in ARDS?
A
Better VQ matching
Improved FRC
better drainage of secretions
16
Q
4 types of shock:
A
Cardiogenic, obstructive, distributive, hypovolemic
17
Q
Explain obstructive shock: whats usually happening?
A
Obstructive shock generally occurs in four clinical scenarios: tension pneumothorax, anterior mediastinal mass, pericardial tamponade, and pulmonary embolism. Since venous return to the heart is obstructed, central venous pressure (CVP) is elevated. Cardiac output (CO) is decreased. Systemic vascular resistance (SVR) is increased to compensate for reduced cardiac output.
18
Q
Why is PA occlusion pressure elevated in some types of shock, but not in others?
A
Because with ptx, mediastinal mass, and tamponade pulmonary artery occlusion pressure should be elevated. In PE-might not be elevated due to the fact that it tends to only affect the right side of the heart
19
Q
Cardiogenic shock: CO: CVP: SVR: PAOP:
A
Cardiogenic: CO is decreased, CVP is elevated, SVR is increased, and PAOP is increased.
20
Q
Distributive shock: What is it? CO, CVP, SVR, and PaOP?
A
Distributive shock is a failure of the vasculature to generate adequate SVR. In distributive shock, CVP is low, PAOP is low, SVR is low, and CO is high. Common causes of distributive shock are septic shock, anaphylactic shock, and neurogenic shock.
21
Q
Hypovolemic shock and CO,CVP, SVR, and PAOP:
A
Hypovolemic shock results from intravascular volume depletion. The body has a decreased preload (CVP and PAOP) as the primary hemodynamic derangement. Hypovolemic shock results in decreased CO, increased SVR, decreased CVP, and decreased PAOP.
22
Q
When, in brain death is confirmatory testing needed?
A
Only if the patient is under the age of 1
23
Q
Criteria for brain death:
A
Criteria are: two physician evaluation, no other causes that mimic brain death, coma with absent brainstem reflexes, and lack of respiratory drive by apnea testing.
24
Q
Other than age, when would you need a confirmatory test for brain death?
A
Confirmatory testing for brain death may be required in situations where clinical evaluation is compromised (severe facial trauma, pre-existing neurologic derangements prior to the incident) or where apnea testing is contraindicated such as significant hemodynamic instability, metabolic acidosis, or high levels of ventilatory support
25
Sepsis: How much fluid? Abx? Target MAP in sepsis?
Patients demonstrating sepsis-induced hypoperfusion should be initially resuscitated with at least 30 mL/kg of intravenous crystalloid within the first three hours. ABx-should be started at least 1 hour within finding out. Target MAP in sepsis: 65
26
which blood products have the lowest risk of TRALI? Why?
PRBCs-because the plasma fraction is removed
27
Which two products have the highest incidence of TRALI?
Plasma products and platelets: FFP, Cryo, platelets. Rb question that asked which person would be more likely to get TRALI, you'd also have to know which products they would require.
28
How is magnesium cleared?
the kidney.
29
Non-iatrogenic causes of hypermagnesemia:
Non-iatrogenic causes of hypermagnesemia include adrenal insufficiency, diabetic ketoacidosis, hemolysis, and hyperparathyroidism.
30
which 3 drugs are so broad spectrum that they can even treat gram negatives?
eftaroline, tigecycline, and TMP-SMX have the broadest spectrum of activity effecting both Gram positives and some Gram negatives
31
Early onset adult VAP is typically due to:
antibiotic-sensitive flora (Methicillin-sensitive Staphylococcus aureus (MSSA), H. influenzae, S. pneumoniae, and Proteus, Klebsiella, and Enterobacter species) and does not typically affect morbidity and mortality
32
Resuscitation of the drowning victim begins with: ____. Do NOT do what?
Rescue breaths FIRST, then chest compressions. DO NOT attempt to expel water from the lungs
33
classic clinical findings in cardiogenic shock: (6)
classic clinical findings in cardiogenic shock include (1) low cardiac output with jugular venous distension, (2) hypotension with peripheral and pulmonary venous congestion, (3) peripheral vasoconstriction, (4) cool extremities, (5) poor urine output, and (6) altered mental status.
34
Is the microcirculatory system preserved in cardiogenic shock?
No. Think about the fact that the oncotic pressures and all that stuff are changing.
35
Charcot Marie Tooth and Vincristine?
Avoid the two because ppl with CMT already have peripheral nerve issues
36
Cyclophosphamide can cause what?
hemorrhagic cystitis
37
Mercapotpurine and gout
Mercaptopurine is metabolized by xanthine oxidase. Xanthine oxidase is inhibited by Allopurinol, so if you have a patient with gout then be careful because the mercaptopurine can build up
38
Side effects of Transtuzumab and 6MP and methotrexate;
Trastuzumab: cardiotoxicity
| 5-FU, 6-MP, methotrexate: myelosuppression
39
4 Sites are recommended for IO:
he sternum, proximal tibia, distal tibia, and proximal humerus
40
Is there a difference in flow between humeral IO and tibial IO? complications of IO?
Humeral IO lines support almost twice the flow rates of tibial IO lines. Complications are rare, and they are easier to place than central.
41
What does an ABG and VBG show in cyanide toxicity as far as O2 and metabolic state?
An arterial blood gas analysis in a patient with cyanide toxicity may show normal oxygenation with metabolic acidosis; although depending on the time from exposure, the metabolic acidosis could be masked by respiratory compensation. A venous blood gas may reveal a high oxygen content, which may mirror that of the arterial blood gas, because oxygen is not being utilized for cellular respiration.
42
Role of sodium thiosulfate in cyanide toxicity?
Sodium thiosulfate was administered secondarily to remove the cyanide from the methemoglobin.
43
Why is sodium thiosulfate not really used anymore with cyanide toxicity?
Though previously a common treatment of cyanide toxicity, this approach had several problems: nitrites can precipitate hypotension and methemoglobinemia, with the latter being toxic.
44
So, what do we use now to tx cn toxicity?
Hydroxocobalamin works by combining with cyanide to form cyanocobalamin (vitamin B-12). Cyanocobalamin is renally cleared. The use of hydroxocobalamin became first line due to its low adverse risk profile, rapid onset of action, and ease of use in the prehospital setting;
45
If you cant find hydroxocobalamin, what can you give for CN toxicity? What if you have no IV?
amyl nitrite if no iv, and sodium nitrite -but both of these have fallen out of favor due to hypotension
46
How can cefepime directly cause worsening hypotension in a patient with pan-sensitive E. coli bacteremia?
LPS. efepime (and any antibiotic used to treat Gram-negative bacteria) may directly cause lysis of the outer bacterial membrane composed mainly of lipopolysaccharide (LPS)-it can release nitric oxide
47
What can vanco release that causes hypotension?
Histamine
48
Hydrocortisone is not indicated in the treatment of septic shock unless: ____. If you do give them, then how much do you give? Can you give steroids in anticipation of septic shock?
No steroids in septic shock unless patient not responsive to fluids or vasodilators. If given, give Hydrocortisone 200 mg IV per day should be administered; it can then be tapered once vasopressors are no longer required. Steroids are NOT recommended for patients with septic shock responsive to fluids or vasopressors nor are they indicated for sepsis in the absence of septic shock.
49
Hydrocortisone inhbiits what?
Nitric oxide synthesis.
50
T/F Blood should NOT be administered through the same line as TPN using Y-site or piggyback connections. Why or why not?
TRUE. It should not be administered through the same line as TPN. Because because dextrose causes hemolysis of red blood cells.
51
When taking patients on TPN back to the OR, what is critical to check? should you continue it? How can TPN affect CHF patients?
Electrolyte levels, liver enzymes (TPN can cause liver dysfunction). you should continue TPN if possible d/t hypoglycemia with rapid d/c of TPN. TPN can affect CHF patients by causing volume overload.
52
What is the alkaline drift seen in CPB?
here is a natural “alkaline drift” with hypothermia owing to the increase in gas solubility and reduction of the PaCO2.
53
pH stat mgmt: wht does it do as far as the alkaline drift?
A pH-stat management technique corrects the alkaline drift by maintaining a neutral pH during hypothermia.During pH-stat management, CO2 is added to the oxygenator or the CPB “sweep” may be reduced (the sweep mechanism removes CO2 from the CPB circuit). The addition of CO2 to the circuit increases total body CO2 in order to maintain pH neutrality despite the continuous reduction in core temperature.
54
What about alpha stat: What does it do as far as the alkaline drift?
Alpha-stat management allows the natural alkaline drift to occur without correction.
ALPHA IS DOWN FOR ALKALINE! IT'S NOT TRYING TO CHANGE IT!
55
Advantages of pH stat: Disadvantages?
increased speed of homogenous cerebral cooling through cerebral vasodilatation, reduced cerebral metabolic rate of oxygen demand (CMRO2) while providing increased cerebral blood flow (CBF), and improved oxygen delivery to tissue by counteracting the leftward shift of the oxyhemoglobin curve typical of alkalosis. Disadvantages of pH-stat management include an increased delivery of embolic load to the brain as a result of the cerebral vasodilatation as well as loss of cerebral autoregulation. Outcome data support the use of pH-stat management during congenital heart surgery as a result of the homogeneous brain cooling.
56
What is qSofa? why would anyone use qSofa?
qSOFA criteria are scored from 0-3 with one point for each of the following: altered mental status (GCS < 15), respiratory rate ≥ 22, and systolic blood pressure ≤ 100 mm Hg. can be used to identify adult ICU patients with a suspected infection that are likely to have a prolonged ICU stay or poor outcome. It may also be used in adult out-of-hospital, emergency room, and general ward patients with suspected infection to identify those that are more likely to have poor outcomes typical of sepsis.
57
What is a NM blocking drug whose metabolite is nearly as potent as its parent drug? whats the metabolite and who is at risk for it building up?
Vecuronium. 3-desacetyl metabolite is the most important since it has nearly 80% of the activity of vecuronium. It can accumulate in the setting of vecuronium infusions, particularly in patients with renal disease since this metabolite is renally cleared
58
Cisatricurium and atracuium metabolites
Cisatracurium (and atracurium) is primarily metabolized (80%) to laudanosine. This renally-cleared excitatory amine can precipitate seizures, but does not have neuromuscular blocking activity. The clinical significance of laudanosine was more important with atracurium
59
Best C diff test :
C. difficile bacterial antigen EIA can rapidly detect the presence of the bacteria, although asymptomatic carriers will also be positive.
60
First line of treatment forreating hyperkalemia with mental status and EKG changes is: _____. Why not CRRT?
to stabilize the myocardium with calcium to prevent a malignant arrhythmia and cardiac arrest.nsulin is administered in conjunction to temporize the potassium levels by causing intracellular influx. Dextrose is supplemented to prevent hypoglycemia with insulin administration.Continuous renal replacement therapy is the correct definitive treatment. In the setting of mental status and ECG changes, however, myocardial protection is the most urgent and best next first step.
61
Cardiogenic shock due to MI parameters:
SBP
PCWP
CI
The hemodynamic parameters seen are sustained hypotension for longer than 30 minutes with a systolic pressure less than 90 mmHg (or a decrease from baseline of 30 mmHg), a pulmonary capillary wedge pressure greater than 18 mmHg, and a cardiac index of less than 2.2 L/min/m^2.
62
What is the primary method of increasing oxygen delivery to the body at high altitude? Why does this happen? Initially what? then after a few days? What does this do to the body's pH and PaCO2?
increased minute ventilation as a result of hypoxic stimulation of peripheral chemoreceptors. Initially, this causes a respiratory alkalosis, however, after a few days the body compensates by increasing the bicarbonate loss in the kidneys. This helps normalize the body's pH, but the PaCO2 remains low.
63
T/F Minute ventilation starts to normalize after a while at high altitude? How does minute ventilation increase?
False. It stays high the entire time someone is at high altitude. RR rate increases, but VC and FRC stay the same.
64
Why is altitude weird-like, what makes things more difficult? Is the concentration of oxygen the same? What about the vapor pressure?
because the drop in barometric pressure at higher elevations results in a lower partial pressure of oxygen. Although the concentration of oxygen and vapor pressure remain the same, according to the alveolar gas equation, when the barometric pressure falls there is a decrease in alveolar oxygen
65
Does the partial pressure of water vapor change with high altitude?
No.
66
CO and high altitude?
It increases in order to improve oxygen delivery to the tissue the cardiac output increases as well.
67
Protein metabolism during the stress response.
First there is anabolism and THEN, there is catabolism. Lipid catabolism is part of the stress response, and so is catabolism from visceral muscles.
68
What part of the body does the ACA supply?
| and 4 parts of brain
medial surface of the parietal lobe, which includes part of the primary motor cortex. The part of the cortex which is located medially, is that which gives motor function to the lower limb
- 4 parts
- Prefrontal cortex: functions in motivation, planning, and organizing of complex behavior
- Supplemental motor area (dominant cortex): functions with Broca’s area for speech
- Motor cortex (lower limb)
- Sensory cortex (lower limb)
69
ACA stroke would lead to:
Anterior cerebral artery strokes tend to lead to behavioral abnormalities, aphasia (if dominant cortex is involved), and contralateral lower limb weakness and sensory deficits.
70
What is the purpose of phrenic nerve stimulators? Who gets them? What are the complications?
Phrenic nerve stimulators improve lung function and reduce atelectasis in patients with cranial or cervical spinal cord injuries but have multiple known complications.
Infections, injury of cervical electrodes during neck motion, paradoxical inward movement of chest in peds, infection
71
Go over chart of what is broken down/activated in lungs
Okay. Epi is not, histamine is NOT, angiotensin 2, oxytocin, and vasopressin are NOT, dopamine is not and pg1 and pg2 are not
72
Why do people with myotonic dystrophy have so many issues with possible aspiration?
Patients with myotonic dystrophy have an increased risk of pulmonary aspiration due to gastric atony and delayed emptying, intestinal hypomotility, and pharyngeal muscle weakness.
73
Any form of carotid sinus manipulation, such as carotid stent deployment, may result in stimulation of carotid baroreceptors located within the carotid sinus. This results in
sympathetic inhibition.
| The AFFERENT NERVE involved is #9-glossopharyngeal
74
The body receives chemo
this means that the chemoreceptors are in the carotid body, and the carotid sinus has the baroreceptors (sinus bradycardia)
75
What is mixed venous oxygen saturation in sepsis-increased or decreased? Why? What about microvascular shunting?
Increased-due to increased cardiac output. Microvascular shunting will also lead to increased MV O2
76
Uterine blood flow pre pregnancy vs at term
normal flow pre-pregnancy is approximately 50 to 100 mL/min with an increase up to 900 mL/min at term.
77
Does CSF bicarbonate decrease with altitude sickness?
Yes. It goes into bloodstream (2-3 days later) and then is excreted through urine.
78
can you get cerebral edema from high altitude?
High altitude cerebral edema (HACE) may be caused by a significant increase in cerebral blood flow leading to hyperemia in the setting of hypoxia.
79
Can you get pulmonary edema from high altitude? who is at the highest risk? Why? prophylaxis and treatment?
High altitude pulmonary edema (HAPE) is thought to be caused by increased pressure in the pulmonary vasculature. The increased pulmonary capillary permeability in patients with preexisting pulmonary hypertension may worsen their predisposition to developing HAPE. This is due to the further increase in pulmonary vascular resistance from hypoxic pulmonary vasoconstriction (HPV). Nifedipine and inhaled β2-agonists are used as prophylaxis and treatment to reduce HPV (most vasodilators impair HPV). Treatment strategy includes supplemental oxygen with gradual descent to lower altitudes
80
NitrIC oxide can result in what as far as platelets, disorders, and shifts, and what does it do to the P50?
It can decrease platelet aggregation, Inhaled nitric oxide (NO) can result in methemoglobinemia resulting in a left shift in the oxyhemoglobin curve and a decrease in the P50
81
What does nitrIC oxide do? What does it selectively dilate? What does it improve, while reducing what?
Nitric oxide causes vasodilation through the production of cGMP and is useful in the treatment of pulmonary hypertension. Because it is delivered in an inhaled form and is rapidly taken up by hemoglobin, nitric oxide selectively dilates pulmonary vasculature in areas of greater ventilation and improves V/Q matching with a reduction in dead space ventilation.
82
Nitric causes methemoglobinemia-explain-what is the ultimate result?
Methemoglobin is formed by the nitrosylation of Fe2+ to Fe3+ by NO and results in hemoglobin that is unable to release oxygen and causes a left shift in the oxyhemoglobin dissociation curve. These effects result in tissue hypoxia.
83
NitrIC oxide-what does it do to platelets?
Nitric oxide also has inhibitory effects on platelets and is produced by the vascular endothelium as an endogenous mediator to prevent inappropriate clot formation.
84
Why does NitrIC oxide NOT lower systemic blood pressure?
NO does not significantly affect systemic blood pressure because it is scavenged quickly by circulating hemoglobin in the lungs.
85
What does nitrIC oxide do to PaO2? How?
nhaled NO tends to improve arterial PaO2 by improving V/Q matching and decreasing dead space ventilation.
86
Explain primary, secondary, and tertiary adrenal insufficiency
This can be termed primary adrenal insufficiency when the adrenal gland is unable to produce hormones when stimulus from the pituitary gland is adequate. Approximately 70% of primary insufficiency occurs secondary to autoimmune destruction of the gland and the remaining 30% occurs secondary to other causes (cancer, amyloidosis, acquired immunodeficiency syndrome, infections). Secondary adrenal insufficiency occurs when the anterior pituitary does not secrete adrenocorticotropic hormone (ACTH, also referred to as corticotropin) or the hypothalamus does not secrete corticotropin-releasing hormone (CRH). There are numerous causes of secondary adrenal insufficiency. Tertiary adrenal insufficiency most commonly occurs secondary to exogenous administration of glucocorticoidsTertiary adrenal insufficiency occurs following abrupt cessation of high-dose glucocorticoid therapy.
87
What is functional adrenal insufficiency and why does it matter?
Subnormal production of corticosteroids in the absences of structural defects in the hypothalamic-pituitary-adrenal axis is termed functional adrenal insufficiency and it is the most common cause found in patients with critical illness in the intensive care unit
88
Who might need to be stress dosed?
It should be anticipated in patients who have received 30mg of hydrocortisone per day for more than three weeks. In patients on chronic exogenous steroids for more than 1 to 2 weeks, it is important to taper the medication to allow adrenal gland recovery. It can take up to 6 to 12 months for the adrenals to completely recover.
89
Normal pulmonary artery pressure:
8-20
90
What is phosphate necessary for, and what are some common conditions that can cause hypophosphatemia?
Phosphate is necessary for a variety of functions that include bone structure, cell membrane structure, energy metabolism, and acid-base buffering. In patients who are critically ill, there are some commons reasons for hypophosphatemia: It can also cause skeletal muscle weakness.
- Trauma
- Sepsis
- Refeeding
- Metabolic acidosis
- Respiratory alkalosis
- Medications (insulin, diuretics)
- Renal replacement therapy
91
hypophosphatemia and the oxygen dissociation curve:
Hypophosphatemia decreases 2,3-diphosphoglycerate (2,3-DPG) causing a left shift in the oxyhemoglobin curve. These patients will have poor oxygen release at the level of the peripheral tissues as a result.
92
Replacement of phosphate can lead to lowering of which other electrolyte?
It can lead to hypocalcemia
93
What level of phosphate can cause prolonged QT?
HYPERphophatemia
94
```
Refeeding syndrome causes which electrolyte derrangements?
phoshpate
sodium
calcium
magnesium
potassium
glucose?
```
Refeeding syndrome causes hypophosphatemia, hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia, and hyperglycemia.
95
Is Tissue Factor increased in sepsis?
Yes
96
When is TPN considered? What are indications for TPN?
TPN is considered when a patient will not be able to take enteral nutrition for greater than 5-7 days. Indications for TPN include bowel obstruction, short bowel syndrome, and active GI bleeding. Other relative indications exist such as fistula, pancreatitis, and severe burns.
97
Two most common risks (in order) of TPN, and why?
Infection is the most common risk of TPN and thrombophlebitis is the next most common risk, particularly with peripherally delivered TPN.
eripheral veins cannot tolerate an osmolarity of more than 750 mOsm/L (the equivalent of 12.5% dextrose) so that the fluid volume that can be tolerated limits the caloric intake. Therefore, this route is used mainly for supplementation or short-term feeding.
98
Cholecystitis and TPN:
Cholecystitis can occur with the use of TPN. The GI tract is not used during TPN administration. Therefore, the gallbladder is not stimulated to contract and thus CCK release does not occur. This promotes cholestasis and increases the likelihood of cholecystitis. Cholecystitis can be a severe complication of TPN.
99
When considering lines, which one has the highest rate of infection? The lowest?
When considering a central line the femoral region has the highest rate of infection and the subclavian has the lowest.
100
Why are intubated patients at a higher risk for VAP? Which med is best to use in this scenario?
PPIs and VAP?
Sucralfate compared to H2 and PPI for prevention of gastric bleeding?
Reductions in gastric acidity and volumes increase bacterial overgrowth and the incidence of ventilator-associated pneumonia.
Sucralfate may be considered to have the advantage over H2-blockers and PPIs in this regard because sucralfate does not change the pH of gastric fluid. A majority of meta-analyses found that sucralfate therapy decreased the incidence of ventilator-associated pneumonia compared to H2-antagonists.he rate of ventilator-associated pneumonia was found to be greater in the groups receiving a PPI than groups receiving sucralfate.
Sucralfate is less effective in regards to prophylaxis against gastrointestinal bleeding than either a PPI or H2-blocker. For that reason, it is not commonly used for stress ulcer prophylaxis.
101
Methhemoglobinemia treatment in normal patients vs those with G6PD? Why?
Methylene blue in regular patients, ascorbic acid in those with G6PD.
Why? Methylene blue provides an electron receptor for the reduction of methemoglobin using NADPH produced from the hexose phosphate pathway. In a patient with G6PD deficiency the hexose phosphate pathway is dysfunctional and free radicals develop, which causes red blood cell lysis. Ascorbic acid does not have the hemolytic effect that methylene blue does in a G6PD deficient patient.
102
Methhemoglobinemia occurs when?
Methemoglobinemia occurs when hemoglobin becomes oxidized from Fe2+ to Fe3+. Methemoglobin is unable to bind oxygen and causes a functional anemia, in addition to left shifting the oxygen dissociation curve. Methemoglobin has an absorbance of 630 nm, which correlates to an oxygen saturation of 84-86% on pulse oximetry. Co-oximetry should be used to aid in the diagnosis and treatment of methemoglobinemia. If unavailable, blood can be sent for a methemoglobin level.
103
When would you use amyl nitrite, and what does it do?
Amyl nitrite is used to treat cyanide toxicity. Amyl nitrate oxidizes Fe2+ to Fe3+. Cyanide binds to methemoglobin more actively than it binds to normal hemoglobin. Thus, by inducing a low-level of methemoglobinemia the methemoglobin in turn can sequester cyanide as cyanmethemoglobin.
104
Methylene blue and MAOI's
Additionally, methylene blue is a potent reversible monoamine oxidase inhibitor (MAOI) and may interact with serotonergic psychiatric medications leading to life-threatening serotonin syndrome.
105
Appropriate Tidal volumes in ARDS are derived from:
The appropriate tidal volume is derived from the predicted body weight (PBW), which can be approximated by the following:
Males: 50 + 2.3 * (height in inches - 60)
Females: 45.5 + 2.3 * (height in inches - 60)
106
What are plateau pressures, and what should they be in ARDS?
reduction in mortality when patients with ARDS were mechanically ventilated at tidal volumes using 6 mL/kg of PBW and plateau pressures ≤ 30 cm H2O.
107
What is the strong ion difference?
SID (Strong Ion Difference) = [strong cations] - [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] - [Cl- + lactate-]
108
What are strong ions? Why are they considered strong?
Strong ions are cations and anions that exist as charged particles dissociated from their partner ions at physiologic pH. Thus, these ions are "strong" because their ionization state is independent of pH.
109
SID and alkalosis vs acidosis:
Disturbances that increase the SID increase the blood pH (alkalosis) while disorders that decrease the SID lower the plasma pH (acidosis). So, low pH or SID is associated with acidosis and high pH or SID is associated with alkalosis.
110
Why does aggressive administration of saline NOT increase the SID?
Aggressive administration of normal saline can cause a hyperchloremic metabolic acidosis due to decreased SID. Cl- administration decreases the SID and produces an increase in water dissociation and hence H+ concentration. The reason why this occurs with saline administration is that, although saline contains equal amounts of both Na+ and Cl-, the plasma does not. When large amounts of salt are added, the Cl- concentration increases much more than the sodium concentration.
111
Why does severe diarrhea cause an INCREASE in the SID?
Severe diarrhea will result in a decrease in the strong ion difference (SID). The body normally reabsorbs much of the water and electrolytes but when severe diarrhea exists large amounts of strong cations (K+ and Na+) will be lost. If this loss is persistent, the SID will decrease and metabolic acidosis will occur
112
How does the tetanus toxin travel?
The tetanus toxin from Clostridium tetani travels via neuronal retrograde transport up the motor neuron and enters the presynaptic terminal of inhibitory interneurons within the spinal cord.
113
Clostridium botulinum prevents the vesicular release of acetylcholine at the
NMJ
114
In a patient with known sepsis, how is septic shock defined?
In a patient with known sepsis, septic shock can be clinically diagnosed by the combination of a vasopressor requirement necessary to maintain a mean arterial pressure > 65 mmHg and a lactate > 2 mmol/L despite adequate volume resuscitation.
115
What is the Q sofa, (in vs out of ICU) and is it used to diagnose septic shock?
In the ICU, Q sofa can tell you the extent of end organ dysfunction. For infected patients in non-ICU settings, the quickSOFA (qSOFA) score can be used to identify patients at high risk for poor sepsis-related outcomes. The qSOFA score consists of:
- Respiratory rate > 22/min (1 point)
- Altered mental status (1 point)
- Systolic blood pressure < 100 mm Hg (1 point)
Scores of two or greater are associated with poor outcomes, however, the qSOFA score is not used to formally diagnose sepsis or septic shock.
116
Copper and Zinc in TPN:
Copper and zinc levels are also decreased which may contribute to anemia and impaired wound healing respectively.
117
Liver and TPN: what's albumin doing and what does that mean? what about PT/INR? AST/ALT, and alk phos in TPN?
Liver dysfunction is a potential complication of chronic TPN therapy, evidenced by increased AST, ALT, and alkaline phosphatase. The albumin level should increase over time with TPN. An increase in serum albumin with parenteral nutrition has been identified as one of the most powerful predictors of improved postoperative outcome
118
Do patients on TPN require supplementation with K+
Yes
119
Absolute indications for TPN:
Absolute indications for parenteral therapy include short gut syndrome, small bowel obstruction, active gastrointestinal bleeding, pseudo-obstruction with complete intolerance to food, and high output enterocutaneous fistulas (unless a feeding tube can be passed distal to the fistula). A high-output fistula is defined as > 500mL/day.
120
T/F: Patients will have metabolic alkalosis with TPN
FALSE: they can have metabolic acidosis
121
Should TPN be discontinued in the OR.
NO. TPN should not be abruptly discontinued as it may result in hypoglycemia. For patients coming to the operating room on TPN, the infusion should typically be continued. If the infusion is stopped, glucose levels should be checked at least every hour.
122
How do you get propofol infusion syndrome?
Propofol infusion syndrome is a rare complication of high-dose (> 4-5 mg/kg/hr or > 65-80 mcg/kg/min), long-term (> 24 hours) propofol administration. It has been described more commonly in children, though adult patients are also at risk.
123
Pathophysiology of propofol infusion syndrome? Which organ systems can it affect?
The pathophysiology of PRIS relates to propofol’s ability to impair cellular free fatty acid utilization and mitochondrial activity leading to inadequate aerobic metabolism and increased reliance on anaerobic metabolism. Cardiac and skeletal muscle are particularly susceptible leading to muscle damage or necrosis that can cause cardiac failure and rhabdomyolysis. Additional downstream effects include lactic acidosis, hyperkalemia, and renal failure.
124
Impaired free fatty acid utilization in propofol infusion syndrome can cause what?
Hypertriglyceridemia, hepatomegaly, and hyperlipidemic pancreatitis
125
Why do PRIS people have green urine?
PHenol
126
Why is use of broad spectrum antibiotics for several days NOT recommended in ARDS? Can you use them-ever?
The use of broad spectrum antibiotics for several days is NOT recommended in the treatment of acute respiratory distress syndrome (ARDS), as it may promote antibiotic-resistant organisms and select for resistant strains of pathogens already present in the ICU. Broad spectrum antibiotics may be used initially, but sputum cultures and antibiotic sensitivities should be obtained so that the antibiotic regimen can be tailored accordingly.
127
When are plateau pressures measured?
Plateau pressures are measured after the inspiratory pause during volume-cycled ventilation.
128
Supportive modalities for ARDS:
Supportive modalities include tracheal intubation and mechanical ventilation with low tidal volumes, low plateau pressure, high FiO2, and PEEP. Conservative fluid management is also employed. A long-term course of broad spectrum antibiotics is NOT recommended.
129
Complications of enteral nutrition:
Enteral nutrition is not without complications as there is an increase in risk of aspiration, especially if the head of the bed is not elevated above 30 degrees and with the use of larger feeding tubes which compromise the competence of the lower esophageal sphincter. There is also a risk of sinusitis with the use of nasogastric tubes, especially when left in for prolonged periods of time. Diarrhea is common, especially if the product contains sorbitol. Hypophosphatemia is actually more common with enteral versus parenteral nutrition and can lead to muscle weakness and difficulty in ventilator weaning because there is a lack of phosphate to generate ATP.
130
Why should one have enteral nutrition?
Other than maintaining gut integrity, Reasons given include decreased cost, easier formulation, decreased risk of infections, no need for intravenous access, and ability to deliver a wider array of nutrients. Because of these benefits and the associated morbidity and mortality of malnutrition, early initiation of enteral feeding is recommended.
131
Tetanus travels by: ____ And once inside,
by retrograde axonal transport and trans-synaptic spread. Once inside central inhibitory interneurons, the light chain is released and cleaves specific SNARE proteins (soluble N-ethylmaleimide-sensitive attachment protein receptors).
132
Are central nerves involved in tetanus? What about in botulism?
Tetanus toxin travels via retrograde axonal transport from peripheral to central neurons. Botulinum toxin from Clostridium botulinum only affects peripheral motor neurons and prevents release of acetylcholine into the neuromuscular junction, leading to a flaccid paralysis.
133
Is there autonomic dysfunction in tetanus?
Tetanus toxin also enters brainstem and sympathetic nervous system neurons leading to autonomic dysfunction.
134
What initially helps compensate for an acute respiratory acidosis? Explain-what happens at the level of the RBC?
Plasma protein buffers like hemoglobin and other plasma proteins. Primarily intracellular buffering via proteins (hemoglobin in the red blood cells) and phosphates help with the initial buffering capability. In the red blood cell, carbon dioxide reacts with water to form bicarbonate and hydrogen ions. The bicarbonate exchanges for chloride across the red blood cell membrane, resulting in higher plasma bicarbonate levels
135
Later Compensation for respiratory acidosis occurs through
occurs through an increase in the plasma bicarbonate levels.
136
Is excretion of hydrogen ions an ACUTE compensation mechanism for respiratory acidosis?
NO
137
renal response to resp acidosis:
Renal retention of bicarbonate is important as a compensatory mechanism, however this does not occur immediately. The renal compensation for a respiratory acid-base disorder takes time to develop (usually hours to days depending on the clinical situation).
138
What is respiratory quotient? What is the number generally used? what has the lowest quotient and can help with ventilator weaning?
A lower RQ would decrease CO2 production and may improve the chances of successful ventilator weaning. Respiratory quotient refers to the amount of CO2 produced per unit of O2 consumed to a specific energy substrate. Generally the number 0.8 is used for the Q due to a relatively high mix of carbohydrates and proteins in the diet. Lipids have the lowest Q at 0.7 and thus will result in a decrease in CO2 production compared with carbohydrates (Q of 1) and proteins (Q of 0.8).
139
ABG directly measures which parameters? Which ones does it derive from these directly measured ones?
Arterial blood gas analysis directly measures pH, PaCO2, and PaO2. Other parameters such as base excess (or deficit), bicarbonate, and SaO2 are calculated or derived from the directly-measured parameters.
140
Cyclosporine is what, and what type of toxicity are people on it at risk for?
Cyclosporine is a calcineurin inhibitor that is used to prevent organ transplant rejection and carries a risk of nephrotoxicity, not pulmonary toxicity.
141
Tacrolimus carries a risk of :
Nephrotoxicity
142
Does sirolimus carry a risk of nephrotoxicity?
No
143
Can you get refeeding syndrome with enteral nutrition?
Yes
144
Pt on enteral feeds has leukocytosis and fever but no change in labs or abdominal pain-what are you thinking?
Sinusitis
145
Four indications for a trach:
1) Emergency airway access
2) Airway access for continuing mechanical ventilation
3) Functional or mechanical upper airway obstruction
4) Decreased/incompetent clearance of tracheobronchial secretions
146
Trachs do what to airway resistance and work of breathing?
They increase airway resistance, but decrease work of breathing?
147
Compared to an open surgical approach, percutaneous tracheostomy has some advantages
Avoids deep neck dissection
- Can be performed by non-surgeons
- Can be performed at bedside (lowers costs/delays)
- Lower incidence of stoma infection
- Lower incidence of significant bleeding
148
Absolute contraindications for perc. trach:
- Active infection at the site of tracheostomy
- Uncontrolled bleeding disorder
- Unstable cardiopulmonary status (shock, extremely poor ventilatory status)
- Patient unable to stay still
- Abnormal anatomy of the tracheolaryngeal structures
149
Trachs and peds? What are some surprising things under which trachs can still be done?
Obesity
- Neutropenia
- History of sternotomy
- Spinal cord injury
- Repeat tracheostomy
150
Possible complication of tracheostomy, and how would it present?
Tracheoesophageal fistula-It would present with an air leak.
151
Why exactly does hypophosphatemia occur in TPN?
Hypophosphatemia is most commonly caused by an increase in intracellular movement of phosphate, which occurs with glucose loading during total parenteral nutrition (TPN) administration
152
Can hypophosphatemia result in hemolytic anemia?
yes
153
3 Causes of severe hypophosphatemia?
1) Refeeding syndrome
2) Diabetic ketoacidosis
3) Large decreases in PCO2 (e.g. hyperventilation during hypercarbic respiratory failure)
154
CAn you get refeeding syndrome with regular oral intake?
Yes
155
Diuretics and phosphate loss? At which part of the kidney?
Diuretics can cause increased phosphate loss and therefore phosphate deficiency. Diuretics are one of the most common drugs that cause hypophosphatemia. Phosphate is primarily resorbed in the proximal tubules of the kidney. Therefore, diuretics acting at the loop of Henle or collecting ducts have less of an effect of phosphate excretion. Diuretics like acetazolamide cause significant phosphate loss
156
Catecholamines and phosphate? Are catecholamines increased in critically ill patients?
Catecholamines are increased in critically ill patients. Catecholamines causes an increase in phosphorous uptake by cells, like insulin. Activation of beta receptors by catecholamines cause an increase in phosphorous uptake by cells. TPN causes a transcellular shift of phosphorous just like catecholamines. However, TPN-induced hypophosphatemia is caused by a transcellular shift as a result of glucose/insulin, not catecholamines.
157
The rate of transmission after a needle stick in a patient with HIV is
0.03%
158
Would anyone ever get single HIV drug prophylaxis?
NO
159
T/F:
No post exposure prophylaxis is necessary for exposure to a patient with unknown HIV status who is low risk for HIV.
160
Hep B/Hep C needlesticks:
Hep B-easier to get if stuck
| Hep C-harder to get, but more likely to progress to chronic
161
When would you do 2 drug HIV prophpylaxis?
Two drug prophylaxis is recommended when there is exposure to a known HIV patient and the exposure is superficial or exposure occurs with a solid needle. Additionally, two drug prophylaxis is considered when the patient is of unknown HIV status but high risk for infection. A typical two drug regimen of zidovudine and lamivudine for 4 weeks is recommended in this type of exposure.
162
When would you do 3 drug HIV prophylaxis?
Three drug prophylaxis is recommended in severe exposure when the patient is known to have HIV or AIDS. A severe exposure includes visible blood on the device, a large hollow bore needle, a deep puncture, or a needle that was in the patient’s artery or vein. Prophylaxis includes a 4 week course of a three drug regimen.
163
Abx for multi-drug resistant organisms assoc with VAP:
look at photo
| Basically-make sure linezolid and vanco are on board
164
Risk factors for patient being exposed to MDR organisms:
In a hospital more than 5 days at the time of diagnosis
- Have history of prior antibiotics use
- Have recent hospitalization within 90 days
- Are admitted from a nursing home, long-term care facility, or dialysis center
165
In a patient with septic shock, should you use low dose dopamine to support renal function?
No.Use of a low-dose (1-5 mcg/kg/min) dopamine infusion does not improve renal function or survival in patients with septic shock
166
How does dopamine work as it relates to infusions?
Dopamine raises mean arterial pressure by increasing cardiac output and, to a lesser extent, systemic vascular resistance. Dopamine effectively improves urine output by either improving overall hemodynamics, exerting a direct diuretic effect, or by decreasing the release of antidiuretic hormone via baroreceptor responses.
167
Steroids and sepsis? dosing?
Although high-dose corticosteroids for the treatment of septic shock are of no benefit, lower doses (e.g., hydrocortisone 200-300 mg/day) can reduce dependence on vasopressors and expedite the resolution of shock. Corticosteroids, regardless of dose, do not confer a mortality benefit. The 2012 recommendations advocate the use of a corticosteroid infusion in order to better control blood glucose levels, compared with steroid boluses.
168
Hgb target according to the Surviving Sepsis peeps
he most recent Surviving Sepsis guidelines recommend a hemoglobin target of 7-9 g/dL in the absence of tissue hypoperfusion, ischemic coronary artery disease, or acute hemorrhage.
169
Diagnostic criteria for ARDS;
Diagnostic criteria for ARDS include hypoxemia (PaO2/FiO2 ≤ 300), acute onset within 7 days of a known clinical insult, bilateral opacities on chest imaging, and pulmonary edema not explained by another cause (e.g. cardiac).
170
T/F: Orthodexia is NOT seen in Hepatopulmonary syndrome.
FALSE-it is
171
What is hepatopulmonary syndrome? What gradient is increased and in what setting? Why does position matter for them?
Hepatopulmonary syndrome is defined as intrapulmonary vascular dilatations and increased alveolar-arterial (A-a) oxygen gradient, in the setting of end-stage liver disease.Hypoxia is improved when the patient lies flat (platypnea) and is worsened when the patient stands (orthodeoxia). The intrapulmonary vascular dilations cause increased perfusion relative to ventilation. Standing further worsens this ventilation-perfusion mismatch since gravity causes increased perfusion and pooling in the less-ventilated lower lung segments.
172
Treatment of HPS:
Treatment of HPS is supportive until hepatic transplantation may be performed. Symptoms of HPS typically resolve within months to a year following transplantation.
173
Diagnosis of HPS: How is the presence of intrapulmonary vascular dilations (IVPDs) confirmed?
Diagnosis requires a room-air, sitting position arterial blood gas indicating an abnormal gas exchange (i.e. A-a gradient > 20 mm Hg, PaO2 < 60 mm Hg) and contrast-enhanced echocardiography (CEE) confirming the presence of IPVDs. The presence of IPVDs is confirmed if CEE shows agitated saline bubbles in the left atrium after at least 3-6 cardiac cycles have passed following IV administration. If saline bubbles appear in the left atrium after 1-2 cardiac cycles, the presence of intracardiac shunts (e.g. PFO) cannot be ruled out. If the CEE is positive but there are confounding factors such as cardiopulmonary disease, then a technetium-99m-labeled lung perfusion scan or pulmonary arteriography may help confirm the diagnosis.
174
Hepatopulmonary syndrome is the triad of
the triad of IPVDs, increased A-a gradient, and hepatic failure
175
IPVDs in hepatopulmonary syndrome and that pathophys:
his is due to excessive circulating levels of pulmonary vasodilators, namely nitric oxide (NO). Excess levels of NO are present in patients with hepatic failure and these levels further increase in the setting of HPS. The IPVDs include dilated precapillary vessels and arteriovenous (AV) connections along the pleura. The IPVDs result in hypoxia due to ventilation-perfusion mismatch, AV shunting, and reducing the transit time of the red blood cell within the alveoli.
176
What is portopulmonary HTN? Suggestive criteria?
Increased pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) are characteristic of portopulmonary hypertension (PPH). This condition arises in patients with liver cirrhosis and may be treated with pulmonary vasodilators (e.g. inhaled NO, IV epoprostenol). Criteria suggestive of PPH include mean PAP >25 mm Hg and PVR >120 dynes * sec/cm^5.
177
Which PAPs suggest high perioperative mortality? At what point is that pressure a contraindication to liver transplantation?
Mean PAP > 35 mm Hg in a liver failure patient is suggestive of high perioperative mortality risk. Mean PAP ≥ 50 mm Hg is an absolute contraindication to liver transplantation.
178
It would seem to make sense that if you abruptly stop TPN, and then start an insulin AND glucose infusion everything will be okay right?
Wrong. If TPN must be stopped, starting an insulin infusion, even with a simultaneous glucose infusion, increases the risk of hypoglycemia.
179
Which type of solutions of TPN will reduce the incidence of hypoglycemia after stopping TPN?
Using TPN solutions with lower glucose-to-lipid ratios (e.g., 70:30, 50:50) prior to discontinuation can reduce the incidence of hypoglycemia after abrupt cessation of TPN.
180
What are ways to decrease risk of hypoglycemia following cessation of TPN?
The risk of hypoglycemia after abrupt TPN discontinuation can be decreased by using TPN with a lower glucose-to-lipid ratio, stopping concomitant insulin infusions, and starting intravenous glucose with frequent blood glucose monitoring. Starting insulin upon TPN discontinuation increases the possibility of an acute hypoglycemic episode
181
Patients at higher risk of refeeding syndrome have lower levels of what?
pre-albumin
182
People on TPN can have higher insulin levels-explain, what does this put them at risk for?
Continuous high-carbohydrate TPN infusions can produce high blood insulin concentrations. This is the body’s attempt to compensate for significantly elevated blood glucose levels. Hypoglycemia can ensue upon abrupt discontinuation of TPN, which necessitates starting intravenous glucose and frequently monitoring blood glucose.
183
Drugs most commonly known to cause drug fever:
Medications that most commonly cause drug fever include amphotericin, cephalosporins, penicillins, phenytoin, procainamide, and quinidine. Treatment involves stopping an offending medication and is otherwise supportive.
184
In cirrhotic patients, portal hypertension is often associated with a hyperdynamic circulatory syndrome-what does this entail?
high cardiac output, reduced systemic vascular resistance, and reduced arterial pressure
185
SvO2 in a cirrhotic patient:
Mixed venous oxygen saturation increases with development of a hyperdynamic state. As liver disease progresses, more AV collateral circulation forms which further increases the hyperdynamic state of cirrhosis. AV fistulas bypass capillary beds, where oxygen extraction occurs, and this increases the mixed venous saturation. Conditions where mixed venous oxygen saturation is increased are: septic shock, AV fistulas, cirrhosis, hypothermia, and hyperoxia.
186
Pathophys of cirrhosis (hyperdynamic state and why), renin, SVR?
Cirrhosis causes a hyperdynamic cardiac state with increased cardiac output and decreased systemic vascular resistance secondary to vasodilating factors (e.g. nitric oxide). The fall in systemic vascular resistance promotes renin release and sodium retention by the kidneys. Additionally, mixed venous oxygen saturation rises with increased cardiac output and AV collaterals.
187
Patient gets radiation exposure; when you think about the thyroid, what should you administer?
Potassium iodide is effective at reducing I-131 uptake by the thyroid and reduces the incidence of radiation exposure related thyroid complications.
188
Does SID take into account HCO3-, phosphate, and albumin?
Yes
189
SIRS and Severe sepsis-do they exist anymore?
Not really
190
What is the pressor of choice when it comes to treating hypotension in patients with brain death?
Vasopressin
191
```
Ten major donor management goals in brain death with organ procurement (DMDs)
-MAP:
CVP:
Final Sodium
pressors?
Pao2/FiO2 ratio
pH on ABG
Glucose
UOP:
LVEF:
Hgb:
```
- MAP 60-120 mmHg
- CVP 4-12
- Final Na ≤ 155, or 135-160 mmol/L
- Pressors < 1 ideal, or low dose pressor
- PaO2/FiO2 ratio > 300 (PaO2 > 300 on 100% FiO2, 5 PEEP)
- pH on ABG 7.25-7.5
- Glucose < 150
- Urine Output 0.5-3 mL/kg/h
- LV EF (%) > 50
- Hgb > 10 mg/dL
192
What is the CAM-ICU and what are the questions? If the first two are positive, then what are the second two?
It is an assessment tool used to evaluate if patients are in delirium.
1. Is there an acute change in mental status or fluctuating course – yes/no
2. Is the patient inattentive or easily distracted – yes/no
If the answer to both 1 & 2 are yes continue to 3 and 4. If either 1 or 2 has an answer of no than the patient does not have delirium per CAM-ICU screen.
3. Is there an altered level of consciousness or RASS other than 0 – yes/no
4. Does the patient experience disorganized thinking – yes /no
193
RASS Score:
Look at photo
194
The optimal clinical PEEP level in ARDS should result in
Adequate perfusion and a PaO2 of 60 mm Hg or greater, with an adequate hemoglobin level at FiO2 of less than 50%.
195
Increasing positive end-expiratory pressure (PEEP) can improve oxygenation through:
Redistribution of extravascular water and increased functional residual capacity (FRC) through distention and recruitment of alveoli, and decreased shunt.
196
Negative side of high PEEP:
High PEEP has also significant cardiovascular effects such as diminished cardiac output due to decreased venous return to right heart, right ventricular dysfunction, and alterations in left ventricular distensibility.
197
What is the last test in brain death, and after that-is confirmatory testing needed?
Apnea testing is the last step in clinical assessment of brain death. Confirmatory testing is optional for death determination in adults.
