Chest Videos Pt 1 Flashcards
Decompensated RHF and PE (166 cards)
1
Q
2 ways by which PA pressure minimally rises during exercise (how does the pulmonary vascular bed accommodate such a rise in flow)
A
- recruits more arterioles/capillary beds
- dilation
so PAP rises minimally during exercise despite large in crease in blood flow volume
2
Q
What part of the cardiac cycle does the RV perfuse during?
A
Most RV coronary perfusion occurs during systole and diastole, appreciable RV perfusion throughout the entire cardiac cycle
(opposite of LV that primarily perfuses during diastole)
3
Q
Causes of right heart failure
(a) excessive preload
(b) excessive afterload
A
RHF etiologies
(a) Excessive preload- fluid overload, intracardiac L to R shunt, extracardiac AV shunt, TR, PR
(b) Excessive afterload- PE, LHF, positive pressure ventilation
4
Q
Causes of right heart failure
(a) insufficiency inotropy
(b) insufficient lusitropy
A
Causes of RHF organized by
(a) Insufficient inotropy (contractility)- ischemia, sepsis
(b) Insufficient lusitropy = impaired relaxation = cardiomyopathy,constriction
5
Q
Example of cause of RV failure that may best be treated with
(a) IV fluids
(b) Diuresis
A
RV failure causes that respond to
(a) IV fluids- may help for causes due to high afterload such as PE, MI
(b) Diuresis for excessive preload = intracradiac or extracardiac shunt, fluid overload, TR/PR
6
Q
Mechanism by which positive pressure ventilation exacerbates RV dysfunction
A
- Increased RV afterload
- Reduced RV preload
7
Q
4 mechanisms of RV spiral/impairment during intubation
A
- Induction meds => hypotension = reduced RV perfusion
- Increased RV preload in flat position
- Apnea/hypoventilation => hypoxia which increases PVR
- Positive pressure ventilation => increased RV afterload and reduced RV preload
8
Q
Contingency planning for intubation a patient in RV failure
A
-A-line for continuous hemodynamic monitoring
-Aggressive preoxygenation to avoid hypoxia/hypoventilation
-Consider upright b/c flat position increases RV preload
-Consider awake b/c induction agents can cause hypotension => RV hypoperfusion
-Have a backup plan (VA ECMO)
9
Q
Overall management/treatment plan for RV failure
A
- Optimize while fixing underlying cause
-preload: fluid optimization
-inotropy: consider dobutamine
-afterload: consider pulmonary vasolidations - Fix underlying causes (RV ischemia, ARDS, PE)
- Always consider backup plan- VA ECMO
10
Q
Differentiate Wells and PESI score
A
Wells used for Pre-test probability for PE to determine next best diagnostic test
Low (<2): D-dimer has helpful negative predictive value
>2: Int or high risk
vs.
PESI- in pts with diagnosed PE can help determine severity of disease (mortality and long-term morbidity)
-low PESI can consider outpatient treatment
11
Q
List TTE findings suggestive of RV strain
A
-RA/RV dilation
-RV dysfunction (low TAPSE or TDI)
-McConnells (RV free wall hypokinesis with normal RV apical movement)
12
Q
Explain McConnells sign
A
McConnell’s sign = sign associated with acute PE
-RV free wall hypokinesis
-with normal RV apical movement since tethered to the hyperkinetic (adrenergically active) LV
13
Q
Explain the 60/60 sign for acute PE
A
Acute PE
-ePASP (TR gradient + RA pressure) < 60 mmHg given over 60 suggests chronicity
RA pressure by observing IVC during spontaneous breathing
TR gradient by continuous wave doppler through TV
-Pulmonary ejection acceleration time < 60 msec
Pulse wave doppler through pulmonic valve (in high parasternal short), measure time from beginning of blood flow to peak, when healthy blood will be ejected out faster
14
Q
Predictors of mortality in PE
A
-RV dysfunction, shock
-RV thrombus
-BNP over 100
-Elevated troponin
15
Q
List TTE signs of RV pressure overload
A
2019 ESC Guidelines for PE
16
Q
Differentiate use of biomarkers in classification of PE severity
A
2019 ESC guidelines use troponin as the biomarker to help risk stratify PE at time of diagnosis.
Does not quote BNP in table but footnotes that can provide ‘additional prognostic information’ but not validated yet
17
Q
Differentiate intermediate-high vs. intermediate-low risk PE
A
Not HDUS (not on pressors, no cardiac arrest) but high clinical severity/PESI score (makes it not low-risk) then differs by presence of either one, both, or neither
Intermediate-high risk = presence of BOTH RV dysfunction and elevated trop
Intermediate-low risk = presence of RV dysfunction, elevated trop, OR elevated PESI
18
Q
Guidelines definition of massive PE
A
Hemodynamic instability as defined by
1. cardiac arrest
2. obstructive shock with SBP < 90 or SBP < 40 points below baseline with pressor requirement not due to sepsis, arrhythmia, or hypovolemia
19
Q
What ‘risk’ are we categorizing in high/int/low risk PE?
A
PE severity classification correlating with risk of early death (in-hospital or 30 day)
20
Q
Caveats of volume resuscitation in acute PE
A
-consider if low CVP/collapsible IVC if c/f concomittant hypovolemia
-be careful of volume overloading the RV and worsening ventricular interdependence (reduce cardiac output)
21
Q
3 main prongs of treatment for RV failure in acute PE
A
- optimize volume stats
- support blood pressure
- backup mechanical circulatory support
22
Q
Distinguish recommendation for use of lytics in high-risk vs. intermediate-risk PE
A
High-risk (refractory hypotension) with low bleeding risk- consider lytics
for intermediate risk it’s wishy washy! (likely not testable…)
23
Q
List the absolute contraindications for fibrinolysis
A
Absolute contraindications to tPA
- CNS Bleeding risk
-any history of hemorrhagic stroke
-ischemic stroke in the past 6 months
-CNS neoplasm - Internal Bleeding Risk
-Major trauma, surgery (surgery within 10 days at noncompressible site), or head injury in the past 3 weeks
-Bleeding diathesis (increased susceptibility to bleed- thrombocytopenia, some hemophilia)
-Active bleeding
24
Q
What level of hypertension is considered a relative contraindication to fibrinolysis?
A
Refractory hypertension (SBP > 180)
25
Long-term f/u for acute PE- when to assess for CTEPH
After 3-6 months of anticoagulation assess symptoms (dyspnea or functional limitation)
Per guidelines only get TTE if symptoms present, but clinically we often recheck if anything above a low-risk
26
Proven benefits of thrombolysis (tPA)
-Improves outcomes in massive PE but unclear if difference in long-term mortality
27
IVC filter guidelines
2021 ACCP guidelines on IVC filters
NO if anticoagulating the patient
YES if contraindication to AC and presence of proximal DVT
-JAMA 2015: IVC filters did not reduce recurrence rate in intermediate PE
28
Most common cause of acute liver failure in
(a) US
(b) Outside US
Cause of acute liver failure
(a) MC in US = Drug-induced liver injury, most commonly APAP
(b) Outside US- viral, acute hep B and concomitant hep E
29
3 classes of drugs implicated in drug-induced liver injury (DILI) and classic examples
Drug induced liver injury
1. Antimicrobials
-bactrim
-nitrofurantoin
-INH
-azoles
2. Antiepileptics
-phenytoin classically
3. Herbal supplements
30
Tx for certain causes of acute liver failure
(a) HELLP
(b) Acute hep B
(c) Autoimmune hepatitis
Treating acute liver failure
(a) HELLP- deliver
(b) Acute hep B- entecavir (anti-viral)
(c) Autoimmune hepatitis- steroids
31
Buzzwords for etiology of acute liver failure in the following
(a) Pt with cancer (hypercoagulable)
(b) Mushroom hunter
(c) Keiser-Fleisher rings
Acute liver failure
(a) Hypercoagulable- think Budd Chiari
(b) Mushroom hunter- amanita poisoning (think farmer who eats mushrooms in the forrest)
(c) Wilson's (copper overload)
32
4 things that can causes transaminasis > 10,000
Transaminasis > 10,000 from just a few things
1. APAP
2. Hypoperfusion (cardiac arrest)
3. Viral infection
4. Poisonous mushrooms
most notably NOT EtOH
33
Mechanism of NAC
N-acetyl cysteine donates cysteine needed to conjugate NAPQI (toxic metabolite of APAP) into harmless metabolite glutathione
34
Indications for NAC
1. APAP for sure but also indicated in
2. non-APAP drug induced liver injury
-best effect if started early (as in before hepatic encephalopathy)
So basically is routine for any acute liver failure that could be drug-related, generally start in all ALF then can stop if find viral or clot
35
Key ammonia cutoff to consider RRT in pt with acute liver failure
Consider renal replacement if ammonia is > 200
36
Grade 0-4 of hepatic encephalopathy
(a) When start to get sleepy
Hepatic encephalopathy
0 = normal
1 = mild confusion, short attention span (might not be noticeable to someone who doesn't know the patient)
2 = disoriented, personality change, inappropriate behavior (noticeable even if don't know patient)
3 = somnolent (a)
4 = obtunded, coma
37
Proposed mechanism of hepatic encephalopathy
Increased ICP
-presumably due to elevated NH4 crossing BBB and dragging in water
38
Acute or chronic causes of liver failure carry higher risk of hepatic encephalopathy
Acute >> chronic for risk of hepatic encephalopathy, even highest in subacute
39
Why lactulose typically avoided in mgmt of acute liver failure
Lactulose doesn't improve survival in acute liver failure, and can often just cause gut distention that can be a big issue if need to go to the OR for transplant
Not used in acute liver failure even if ammonia is sky high
40
General approach to managing elevated ICP in hepatic encephalopathy
Elevated ICP management
-HOB 30 degrees
-minimize stimulation
-protect airway if needed
-treat fever and seizures
-avoid hyponatremia (goal Na 145-155)
-levo for goal MAP > 75 to maintain CPP
-can consider mannitol acutely if kidneys are ok
41
Key concepts in acute liver failure to trigger transplant referral
1. Progressive lab abnormalities
-coagulopathy
-acidemia
-hypoglycemia
2. Development of complications
-hepatic encephalopathy
-AKI
42
2 prognostic models in acute liver failure
-MELD for synthetic dysfunction
-Kings college criteria
43
When to use the following in acute liver failure
(a) Levophed
(b) Glucocorticoids
(c) ICP monitoring
Acute liver failure
(a) Any signs of hepatic encephalopathy- consider pressors for goal MAP > 75 to maintain CPP
(b) Glucocorticoids- not routine (ex: not for viral, drug-induced). Yes for severe EtOH or autoimmune hepatitis
(c) ICP monitoring not routinely recommended, follow clinically
44
Mannitol vs. hypertonic saline in mgmt of hepatic encephalopathy in acute liver failure
Hypertonic saline- can use prophylactically for target Na 145-155
While mannitol (contraindicated in hyperosmolality and renal dysfunction) for acute, last ditch, temporary effect
45
What etiologies of acute liver failure typically recover, while which are more likely to require transplant
Acute tylenol toxicity typically recovers
Wilson's disease, subacute drug toxicity, autoimmune hepatitis- less likely to survive w/o transplant (lower transplant-free survival)
46
Timeline cutoff for hyperacute, acute, subacute, chronic liver failure
Hyperacute- 0-1 days (ex: huge tylenol ingestion, hep A)
Acute- 1-4 days (ex: hep B)
U
Subacute- < 26 weeks (ex: gradual APAP or non-APAP drug, pt taking supplement for months)
Chronic: > 26 weeks
47
Explain mechanism and proper use of hyperventilation in acute liver failure
Blowing off CO2 (hyperventilation) => intracranial vasoconstriction = less blood flow into brain = lower ICP
Super temporary and then there's rebound hyperemia so only really use if pt herniating and getting rolled to OR for transplant...
48
Typical clinical scenario of alcoholic hepatitis
Increased EtOH consumption over days/weeks- subacute jaundice (over 8 weeks), abdominal pain, fatigue
49
Scores that guide steroid initiation and duration in alcoholic hepatitis
Alcoholic hepatitis
-if discriminatory factor > 32: initiate prednisolone
-on day 7 use Lille score to determine if should continue steroids, b/c if not improving will D/c given increased risk for infection and GI bleed
50
Definition of spontaneous bacterial peritonitis
(a) Tx
SBP: peritoneal fluid PMN > 250 with negative gram stain (if positive gram stain then it's overt peritonitis)
(a) Tx- albumin 1 g/kg + antibiotic (CTX)
51
First line for SBP tx in PCN-allergic patient
1. albumin! (1 g/kg)
2. abx if can't use third gen cephalopsporin (CTX or cefotaxime) = fluoroquinolone (cipro)
52
When to treat hyponatremia in cirrhotic
Really don't treat, it'll just make the retain more fluid
Treat if Na < 120 or any neurologic consequence (seizures)
53
Definition of hepatorenal syndrome
HRS: dx of exclusion
Cr > 1.5 unchanged after albumin challenge, stopping diuretic, and addressing alternative causes
54
Approach to HRS treatment
HRS treatment
1. albumin to augment blood volume
2. pressor (or midodrine) to augment MAP
3. octreotide to combat splanchnic vasodilation
55
Typical LFT findings in alcoholic hepatitis
AST/ALT > 1.5, both < 400 with Tbili > 3.0 (so more cholestatic than hepatocellular pattern)
Transaminasis > 10,000 not consistent with alcoholic hepatitis
56
2 indications where albumin improves survival in liver failure
Albumin improved survival
1. After large volume paracentesis > 5L
2. Bacterial infections (peritonitis)
57
Mechanism of kidney injury in TLS
Tons of cells lyse and release nucleic acid, purine metabolism produces tons of uric acid which precipitates in renal tubules
58
Low-intermediate risk for TLS- what to pre-medicate with
Low-intermediate risk TLS pre-medicate with fluids to flush out kidneys and allopurinol to reduce production of uric acid (what precipitates in renal tubules) from purines (nucleic acid released from dead cells)
59
Methemoglobinemia
(a) Pathophys
(b) Explain why SpO2 = 85%
(a) Methemoglobinemia- increase in the oxidized form of iron (Fe3+) that oxygen cannot bind to causing a functional anemia
(b) SpO2 stuck at 85% b/c the different color blood (not oxidized) absorbs light of a different color not readable by pulse ox
60
Buzzword blood color
(a) Cherry red
(b) Chocolate brown
(a) Cherry red blood seen in carbon monoxide poisoning
-house fires, smoke
(b) Chocolate brown blood seen in methemoglobinemia (oxidized Fe3+ cannot bind to O2) typically acquired from drug-exposure that donates oxidizing agent and induces methemoglobin formation (ex: dapsone, topical anesthetics like benzocaine)
61
Most common cause of acquired methemoglobinemia
Drug-induced
-antimalarials: dapsone
-topical anesthetics: benzocaine, lidocaine <-- can be added to street drugs
62
Clinical features of methemoglobinemia
Neurologic symptoms of tissue hypoxia typically
Then metabolic acidosis (from lactate)
63
Differentiate hyperleukocytosis and hyperviscosity syndrome
(a) Cause
(b) Mgmt
Hyperleukocytosis (WBC > 50-100,000)
(a) Tons of blasts/WBCs in AML typically b/c blasts are large and less deformable
(b) Cytoreduction
Hyperviscosity due to increased circulating immunoglobulins, typically in (a) multiple myeloma or Waldenstrom's macroglobulinemia
(b) Mgmt = plasmaphoresis and chemo
64
Differentiation syndrome
(a) Cause
(b) First line treatment
Differentiation syndrome from (a) use of ATRA to help differentiate promyelocytes in APLM to neutrophils
(b) Steroids
65
First line treatment for HLH
HLH- hypermacrophage huge cytokine storm sitch
First line treatment- etoposide and steroids
66
Uncommon but possible cause of tissue hypoxia side effect of high dose iNO
iNO doses > 80ppm carries risk of methemoglobinemia
67
Typical clinical scenarios for
(a) Methemoglobinemia
(b) Carbon monoxide poisoning
Clinical scenario
(a) Methemoglobinemia (chocolate-red blood, SpO2 85%) from drugs that donate oxidizing agent. Antimalarials (dapsone), topical anesthetics (benzocaine)
ex: traveler receiving anti-malarial ppx
ex: undergoing bronchoscopy gets too much topical lidocaine
(b) CO poisoning- house fire, smoking
68
Differentiate clinical features of methemoglobinemia and carbon monoxide poisoning
Both present with tissue dysoxia- CNS manifestations
69
Differentiate treatment of methemoglobinemia and carbon monoxide poisoning
Treatment
-Methemoglobinemia (oxidized Fe3+ that can't carry O2) = methylene blue, to reduce back to Fe2+ that can hold O2
-CO: HFNC or hyperbaric
70
Indication for methylene blue in methemoglobinemia
Methylene blue reduces Fe3+ (can't hold O2) to Fe2+ (normal)
-indicated if methemoglobin > 30%
OR
if methemoglobin 20-30% with symptoms (lactic acid, CNS)
71
TEG interpretation- order of abnormalities guiding resuscitation
Initial formation of clot (R-time) for lotting factors
Strength of clot fibrinogen (k-time and alpha angle)
Max amplitude (clot strength) platelets
Lysis- if excess use TXA
72
What part of TEG expect to be abnormal on heparin
Heparin inhibits clotting factors => expect start of clot formation (R-time) to be prolonged
73
RBC abnormality on smear expected in
(a) Autoimmune hemolytic anemia
(b) TTP
Spherocytes (small, dense RBCs) in AIHA or drug-induced hemolysis
vs.
Schistocytes in MAHA (DIC, TTP), fragmented from shearing forces
74
What's more common- TACO or TRALI
TACO way more common
TACO 1:100
TRALI 1:10,000
75
FFP
(a) Amount of volume per unit
(b) Empiric dosing to correct coagulopathy
FFP
(a) 250cc per unit
(b) Generally want 15 ml/ kg so in 70 lb patient ~1L FFP
76
Differentiate apheresed vs. pooled platelets
Apheresed platelets- donor comes in, donates whole blood, platelets removed from single donor and rest of blood returned
-less antigenic
vs.
Pooled platelets- plts removed from whole blood of 4-6 donors then pooled to make a unit
77
Platelet cutoff for
(a) CVL insertion
(b) Thora
Plt > 20,000 for both CVL insertion and thora
78
Expected fibrinogen rise from 1 pooled unit of cryo
Cryo (fibrinogen, vWF, factor VIII and XIII, fibronectin)- expect rise in fibrinogen of about 70 per unit of cryo
79
Mechanism of tXA
Inhibits fibrinolysis (clot breakdown) by blocking plasminogen binding to fibrin => fibrin not broken down so clot lasts longer
80
Top indications for tXA
Best results when used within 3 hours of major trauma or postpartum bleeding
Not useful in massive GI bleed
81
Describe the abnormality in TEG seen with
(a) Heparin use
(b) Uremic platelets
(c) Hyperfibrinolysis
(a) R-time = initial clot formation, requires clotting factors so prolonged in heparin
-correlates with INR, PT, PTT
(b) Platelets reduced in number or function- lower max amplitude
(c) Increased clot breakdown (low stability) = high LY30 (lots of clot broken down within 30 mins)
82
PLASMIC score utility
PLASMIC score = pre-test probability for TTP
If high enough- start plasma exchange prior to ADAMST13 activity coming back low
83
Describe mechanism of TTP
ADAMST13 activity low, so vWF remains uncleaved on endothelium walls so platelets stick to the walls and eat up platelets and cause intravascular hemolysis
84
Explain 3 key features of lab diagnosis of DIC
DIC- lab evidence that all 3 parts of the coagulation system are hit
1. Thrombocytopenia- primary hemostasis impaired, can't make platelet plug
2. Consumption of coagulation factors (high INR, high PTT, low fibrinogen) b/c all used up to activate fibrin. Fibrin + platelet plug = blood clot (secondary hemostasis)
3. Fibrinolysis = overactive clot breakdown = elevated D-dimer
85
Differentiate apixaban and dabigatran mechanism
Apixaban, edoxaban, rivaroxaban all factor Xa inhibitors (on up the pathway from thrombin)
While dabigatran is a direct thrombin (factor IIa) inhibitor
85
Mechanism of argatroban
Argatroban and bival are direct thrombin inhibitors, like dabigatran
86
Indication for idarucizumab vs. andexanet alpha
Idarucizumab reverses dabigatran (direct thrombin/factor IIa inhibitor)
While andexanet alpha reverses anti-Xa DOACs (apixaban)
87
Mechanism of atropine
(a) Why ineffective in complete heart block
Atropine- blocks sympathetic tone to AV node => improves/increases conduction through AV node
(a) Ineffective in 2nd degree type 2 and complete heart block where the conduction abnormality is below the AV node
88
Mechanism of glucagon in bradycardia due to BB or CCB toxicity
Glucoagon activates L-type calcium channel independent of beta-receptor (adrenergic tone) so makes the muscle work despite beta blockade
Temporary effect
89
Describe what VVI pacemaker mode is
PSA- pace, sense, action
V- pacing the ventricle
v- sensing the ventricle
i- inhibit, when the pacemaker sees a regular ventricular rhythm it inhibits further pacing activity
90
Role of placing magnet over a
(a) Pacemaker
(b) Defibrillator
(a) magnet over pacemaker inhibits sensing
(b) magnet over defibrillator inhibits shock therapy
91
Explain why atropine might fix sinus bradycardia from an inferior MI within first 6 hours after MI
If sinus brady is due to increased vagal tone in the first 6 hours following an anterior wall MI, and not just disrupted perfusion to the SA node
Atropine will inhibit parasympathetic tone to the AV note => increase HR
92
What to expect on baseline EKG for patient with WPW
Short PR, delta wave
93
Duration of post-op AFib that prompts consideration of anticoagulation
AFib very common post-op, if persists for > 48 hours consider AC
94
Why is amiodarone typically better at rate control for AFib than digoxin in the acute ICU setting?
Digoxin works to directly inhibit AV node to inhibit SVTs- dependent on cathecholamine state typically low in the ICU
While amio has multiple targets/mechanisms of action to work on
95
What to consider if facing a regular narrow-complex tachycardia not responsive to cardioversion
Ectopic or multifocal atrial tachycardia won't respond to cardioversion
(while AFib/flutter typically will)
96
Why want to avoid adenosine in patient with known WPW
Block the AV node- leave only accessory pathway available => Vfib/flutter
97
Why might consider using adenosine in stable wide complex tachycardia
Stable wide complex regular tachycardia- SVT w/ aberrancy (or underlying BBB) vs. monomorphic VT
If SVT with aberrancy (less likely than VT but possible) may break with adenosine, and if stable then have time before shocking
(can also try vagal maneuvers)
98
EF cutoff for HFrEF vs. HFpEF
HFrEF for EF < 40%
HFpEF > 50%
99
Differentiate NYHA class II vs. III
NYHA Class I- no functional limitation
NYHA Class II- able to perform ordinary physical activity, slight limitation with exertion
NYHA Class III- dyspnea with ordinary activity, no symptoms at rest
NYHA Class IV- dyspnea at rest or unable to perform any activity without symptoms
100
Differentiate NYHA class III vs. IV
NYHA Class I- no functional limitation
NYHA Class II- able to perform ordinary physical activity, slight limitation with exertion
NYHA Class III- dyspnea with ordinary activity, no symptoms at rest
NYHA Class IV- dyspnea at rest or unable to perform any activity without symptoms
101
Distinguish main mechanism/effect of nitroglycerin vs. nitroprusside
Nitroglycerin = peripheral venodilator = lower preload
Nitroprusside = peripheral arterial dilator = lowers afterload (SVR)
102
Explain how dobutamine is an inodilator
Dobutamine-
Beta 1 = inotrope
Beta 2 = peripheral vasodilator
103
Limits of IABP
(a) Amount of augmented cardiac output
(b) Arrhythmia
IABP
(a) 0.5 L/min of augmented cardiac output
(b) Can have difficulty synching with systole/diastole (tries to inflate at dicrotic notch at beginning of diastole) if AFib
104
Maximal flow rate of
(a) IABP
(b) Impella
(c) VA ECMO
Max flow rate
(a) IABP- 0.5 L/min
(b) Many types of impellas but generally 3-5 L/min
(c) VA ECMO up to 7 L/min
105
At what part of the cardiac cycle does IABP
(a) Inflate
(b) Deflate
IABP
(a) Inflates in diastole to augment coronary perfusion
(b) Deflates in systole to reduce LV afterload
Overall improve cardiac output by about 0.5 L/min
106
Explain how IABP changes the aortic pressure during systole and diastole
(a) Compare assisted to unassisted diastole
(b) Compare assisted to unassisted systole
IABP
Aortic pressure:
(a) Augmented diastole > unassisted diastole because balloon is inflated in diastole (inflates at the dicrotic notch when aortic valve closes)- increases coronary artery perfusion
(b) Augmented systole < unassisted systole because balloon deflates to reduce LV afterload
107
At what part of the cardiac cycle does IABP inflate?
Technically inflates at the dicrotic notch (start of diastole, closure of aortic valve)
IABP inflates during diastole- augmenting coronary perfusion
IABP deflates during systole, reducing LV afterload
108
IABP vs. Impella
(a) Flow rate
(b) Anticoagulation requirement
(a) IABP augments cardiac output by 0.5 L/min, while impella can augment 3-5 L/min depending on the type
(b) IABP does not require AC while impella does
109
Cutoffs used to signify increased need for LV mechanical support
(a) CI
(b) CPO
(a) Cardiac Index < 2.2
CI = CO / BSA
(b) Cardiac power output (watts) < 0.6 should trigger escalation of L-sided MCS (mechanical support)
CPO = (MAP x CO) / 451
110
PAPi cutoff to trigger escalation of R-sided mechanical support
PAPi < 0.6 or evidence of severe RV dysfunction on TTE- escalation of RV mechanical support
PAPi = (sPAP-dPAP) / RA
111
Describe how the cerebral autoregulation curve is shifted in ppl with chronic hypertension
(a) Clinical consequence
Cerebral autoregulation = concept that intracranial vessels dilated and constrict in response to MAP to provide a consistent cerebral perfusion pressure over a decently broad range of systemic pressures
In chronic hypertensives curve remains the same shape (middle plateau) but shifts to the right- so brain maintains CPP at a higher MAP
(a) Can get cerebral ischemia at otherwise normal BPs if drop a chronic antihypertensive too low
112
Differentiate hypertensive urgency from emergency
Both: SBP over 180, SBP over 110
Emergency when some sign of end organ damage:
headache, AMS, lethargy/confusion
cardiac ischemia
pulmonary edema
reduced UOP/elevated Cr
113
Which antihypertensive drip comes with risk of cyanide toxicity?
(a) Clinical features of cyanide toxicity
Nitroprusside = peripheral arterial dilator to reduce LV afterload (reducing SVR), causing significant drop in BP
Metabolizes in cyanide
(a) Lactic acidosis and AMS
114
Treatment of cyanide toxicity from nitroprusside drip
IV thiosulfate
115
First-line antihypertensive during HTN emergency when end organ damage is:
(a) Cardiac
(b) Brain
HTN emergency
(a) ACS- nitroglycerin to reduce cardiac preload
(b) Brain- CCB (nicardipine)
116
Special circumstances for hydralazine for HTN
(a) First line
(b) Contraindicated
Hydralazine
(a) First line in pregnancy
(b) Contraindicated in aortic dissection b/c of risk of reflex tachycardia
117
Differentiate BP goal for ICH vs. ischemic stroke
BP goals
-ICH:
Initial BP 150-220: lower to SBP < 140
If initial BP > 220: rapidly lower to < 220 then gradually to < 140-160
-Ischemic stroke:
if no tPA: SBP < 220
before tPA must be < 185/105, 24h after tPA < 185/110
118
Explain pathophys of how HTN emergency causes CNS dysfunction
MAP too high- cerebral autoregulation can't keep CPP within normal range => CPP elevates causing endothelial damage, loss of vascular integrity
119
BP goals for ischemic stroke before and after TPA
ICS: SBP < 185/110 for tPA, < 180/105 after tPA
vs. SBP goal 150-220 for ICH
120
BP goal for hypertension in ACS
Goal SBP < 140mmHg within the first one hour, but importantly DBP > 60 to maintain coronary perfusion pressure
121
Differentiate surgical vs. nonsurgical aortic dissections
Aortic dissection- if involves ascending aorta (type I) requires surgery
If ascending aorta not involved- manage medically (or consider endovascular stent) with SBP goal < 120 and HR < 60 within the first hour
122
SBP and HR goal for medical management of aortic dissection
Aortic dissection-
SBP goal < 120 and HR < 60 within the first hour
123
Typical dual agent regimen for BP/HR management in aortic dissection
Typically start with beta blocker to avoid reflex tachycardia from vasodilator
1. beta blocker: IV esmolol
2. vasodilator: nitroprusside (but beware of cyanide toxicity)
124
Definition of severe preeclampsia
Severe preelampsia: SBP over 160 and/or DBP over 110 after 20 weeks of gestation with some evidence of end organ damage (at least one of the following):
-headache, visual disturbance
-pulmonary edema
-proteinuria
-PLt < 100,000
-Cr > 1.1
125
SBP goal in severe preeclampsia
SBP < 140 in severe (severe being SBP > 160 or SBP > 110)
126
3 drugs safe to treat HTN in pregnancy
Labetalol
Hydral
CCB (nicardipine)
127
Purpose of IV Mg in preeclampsia
IV Mg for seizure prophylaxis
128
Goal BP drop (both acutely and subacutely) for hypertensive encephalopathy
Initial target 15-25% drop in MAP over the first hour, then to < 160/100 at 6 hours
129
First line mgmt for HTN crisis from catecholamine surge from pheochromocytoma
Phentolamine = alpha blocker
130
STEMI door to balloon time for
(a) Patient presenting to PCI-capable hospital
(b) Patient presenting to non-PCI capable hospital
STEMI
(a) 90 minutes
(b) 120 minutes if a transfer
131
For STEMI patient presenting to non-PCI capable hospital- timeline for when to give lytics (when transfer/balloon time will be how delayed?)
For a STEMI that presents to non-PCI capable center, if can't get them transferred within 30 minutes with plan for time from presentation to balloon < 120 minutes- give lytics within first 30 minutes
132
Post-lytics for STEMI- keep patient at non-PCI capable hospital if chest pain resolves and EKG improves?
No! Even if they get lytics still transfer to PCI-capable center, they do better
NEJM 2009 Transfer-AMI: routine early PCI after STEMI s/p lytics did better with transfer
133
Outcome of NICE-SUGAR NEJM trial on ICU sugar control
NICE-SUGAR 2009 NEJM- increased mortality for tight (81-108) glucose control over liberal (under 180)
134
Nutrition in the ICU, guideline stance on
(a) enteral vs. parenteral
(b) early vs. late
(c) High vs. low protein
Nutrition in the ICU
(a) Enteral within 24-48 hours, parenteral no benefit within first 7 days (so wait)
(b) Better if within first 48 hours, maybe some signal for first 24 hours. but can start low (hypocaloric) and ramp up
(c) No difference (though signal that higher protein is worse in renal failure)
135
Nutrition in the ICU guideline stance on how to monitor tolerance of enteral feeding
By clinical parameters, no longer guideline to routinely check residual volumes
If checking, no need to hold unless over 500cc
136
Difference in feeding obese pts in the ICU
Higher protein needs
-still start early (within 24 hrs) despite concept of potentially higher reserve
-start with hypocaloric regimen to increase insulin sensitivity
137
How to improve survival in refeeding syndrome
Intentional underfeeding of at risk patients- survival better in patients with strict caloric management (not automatically starting at full feeds)
138
ICU feeding/nutrition guidelines on
(a) NG vs. NJ
(b) Glutamine supplementation
ICU feeding guidlines
(a) No diff btwn NG and NJ- so feel free to use the stomach. Can consider NJ in pts with particular high aspiration risk but no proven benefit
(b) No benefit to glutamine or any other antioxidant supplementation
139
ICU feeding/nutrition guidelines on
(a) When to start enteral feeds
(b) When to start parenteral feeds
140
What is actually measured by BP cuff
MAP- then SBP and DBP derived
-measured via oscillometry
141
CVP tracing, line up with EKG
(a) A-wave
(b) V-wave
(a) A-wave (atrial contraction) just after P-wave (starts in the PR interval)
(b) V-wave (atrial filling against closed tricuspid valve during ventricular diastole)- starts in T-P interval
142
By convention at what part of the acv curve do you measure CVP?
(a) and what part of respiratory cycle
Measure CVP at base of c-wave, is C-wave no visible then take the mean of the a-waves
(a) end expiration
143
End expiration higher or lower pressure during
(a) Spontaneous breathing
(b) PPV
(a) Spontaneous breathing
end expiration pressure is higher
(b) Mechanical ventilation- end expiration pressure is lower
144
How to differentiate wedge from CVP tracing
Compare to EKG tracing, for CVP a-wave will be shortly after EKG's P-wave, while in wedge it'll be at the end of the QRS
V-wave in CVP at the end of the T-wave, while deeper in the T-P interval in wedge
So basically wedge R-shifted from CVP b/c takes mroe time for pressure be transduced backwards
145
Typical cause of large v-waves in
(a) CVP tracing
(b) PAWP tracing
(a) CVP tracing = TR
(b) PAWP tracing- reduced LA compliance: MR, VSD, volume overload
146
RHC findings classic for pericardial tamponade
Pericardial tamponade
-equalization of RA, PA diastolic, and wedge pressure
-prominent x-descent (exaggerated atrial relaxation)
-loss of y-descent (loss of rapid early diastolic filling)
147
Describe phenomenon of overwedging of PA catheter
Erroneous pressure measurement when balloon traps catheter against vessel wall- pressure continues to rise
-inaccurate measurement and increased risk of PA rupture
148
Describe mechanical ventilation's effect on
(a) LV preload and afterload
(b) RV preload and afterload
Mechanical ventilation
(a) Reduces LV afterload, increases LV preload
(b) Reduces RV preload, increases RV afterload
149
Pt on mechanical ventilation- what degree of pulse pressure variation is associated with fluid responsiveness
12-15% increase in pulse pressure during inspiration suggests on the steep portion of the Frank-Starling curve => fluid responsive
150
Change in IVC diameter with inspiration during
(a) Spontaneous breathing
(b) Mechanical ventilation
(a) During spontaneous breathing, negative inspiratory pressure with inspiration with reduce IVC diameter
(b) During positive pressure ventilation, inspiration => increase in IVC diameter
151
What percent of IVC diameter variability predicts fluid responsiveness
12% change
152
Limitations of stroke volume/pulse pressure variation
-Best when breaths are the same size => limited in spontaneous breathing
-Best when stroke volume relatively similar => not great in arrhythmias
153
Best method to assess fluid responsiveness in spontaneously breathing patient
Passive leg raise b/c not depending on same size breaths like other pulse pressure variation methods (PPV, VTI)
154
Best method to assess fluid responsiveness in pt with AFib
Irregular HR/differing cardiac output- use VTI averaged multiple
Passive leg raise better than PPV
155
Rare complication of stacked fentanyl doses that can worsen respiratory failure
(a) Tx
Stiff chest/wooden chest syndrome
(a) Tx = depolarizing paralytic- succinylcholine
156
Pt on multiple sedatives (lorazepam, propofol) develops worsening metabolic acidosis
Check for propylene glycol toxicity (diluent of ativan gtt)- check osmolar gap
Check for PRIS- elevated TGs, renal failure (rhabdo), hyperkalemia
157
Benzo antagonist
Flumazenil
158
Ketamine
(a) Use in neurointubation
(b) Heart failure patients
(c) Effect on airways
Ketamine
(a) Can cause increased ICP so generally contraindicated in neuro intubations
(b) Watch for immediate hypertension/tachycardia, then latera is a direct negative inotrope
(c) Can cause laryngospasm but bronchodilation
159
In what pts does tXA decrease moratlity
-post-partum hemorrhage and severely injured trauma patients
160
Mechanism of tXA
tXA = antifibrinolytic, prevents breakdown of clot
161
Mgmt of chest tube noted to be intraparenchymal
Place another large bore (that can handle blood) before you pull it
162
Malignant hyperthermia
(a) When to consider
(b) Triggers
(c) Clinical features aside from fever...
Malignant hyperthermia
(a) Minutes after anesthesia- typically inhaled anesthetic or succinylcholine
(b) ^ meds above
(c) Fever within minutes of RSI or up to 90 minutes post-induction, rapid rise in EtCO2 (due to jump in metabolic rate), muscle rigidity, CK elevation, tachycarrhtyhmia
163
Indication(s) for dantrolene
Inhibits intracellular calcium release in skeletal muscles (inhibits ryantidine receptor) => blocks skeletal muscle contraction
First line for malignant hyperthermia (after anesthesia), off-label can be used for NMS
164
Dantrolene mechanism
Inhibits intracellular calcium release in skeletal muscles (inhibits ryantidine receptor) => blocks skeletal muscle contraction
First line for malignant hyperthermia (after anesthesia), off-label can be used for NMS
165
Data for or against
(a) Use of lung protective ventilation intra-op for abdominal surgeries
(b) Abdominal surgery intra-op BP goal
(a) Yes, using lower TVs reduced PNA, sepsis, NIV requirement) for intra-abdominal surgeries
(b) Data supporting personalized/individualized BP goal (within 10% of baseline) vs. pressors for SBP > 80
