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CM Critical Care Boards > Chest Videos Pt 1 > Flashcards

Chest Videos Pt 1 Flashcards

Decompensated RHF and PE

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
  1. recruits more arterioles/capillary beds
  2. dilation

so PAP rises minimally during exercise despite large in crease in blood flow volume

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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)

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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

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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

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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

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6
Q

Mechanism by which positive pressure ventilation exacerbates RV dysfunction

A
  1. Increased RV afterload
  2. Reduced RV preload
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7
Q

4 mechanisms of RV spiral/impairment during intubation

A
  1. Induction meds => hypotension = reduced RV perfusion
  2. Increased RV preload in flat position
  3. Apnea/hypoventilation => hypoxia which increases PVR
  4. Positive pressure ventilation => increased RV afterload and reduced RV preload
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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)

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9
Q

Overall management/treatment plan for RV failure

A
  1. Optimize while fixing underlying cause
    -preload: fluid optimization
    -inotropy: consider dobutamine
    -afterload: consider pulmonary vasolidations
  2. Fix underlying causes (RV ischemia, ARDS, PE)
  3. Always consider backup plan- VA ECMO
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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

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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)

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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

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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

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14
Q

Predictors of mortality in PE

A

-RV dysfunction, shock
-RV thrombus
-BNP over 100
-Elevated troponin

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15
Q

List TTE signs of RV pressure overload

A

2019 ESC Guidelines for PE

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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

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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

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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

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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)

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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)

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21
Q

3 main prongs of treatment for RV failure in acute PE

A
  1. optimize volume stats
  2. support blood pressure
  3. backup mechanical circulatory support
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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…)

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23
Q

List the absolute contraindications for fibrinolysis

A

Absolute contraindications to tPA

  1. CNS Bleeding risk
    -any history of hemorrhagic stroke
    -ischemic stroke in the past 6 months
    -CNS neoplasm
  2. 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
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24
Q

What level of hypertension is considered a relative contraindication to fibrinolysis?

A

Refractory hypertension (SBP > 180)

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25
Q

Long-term f/u for acute PE- when to assess for CTEPH

A

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

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26
Q

Proven benefits of thrombolysis (tPA)

A

-Improves outcomes in massive PE but unclear if difference in long-term mortality

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27
Q

IVC filter guidelines

A

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

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28
Q

Most common cause of acute liver failure in

(a) US
(b) Outside US

A

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

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29
Q

3 classes of drugs implicated in drug-induced liver injury (DILI) and classic examples

A

Drug induced liver injury

  1. Antimicrobials
    -bactrim
    -nitrofurantoin
    -INH
    -azoles
  2. Antiepileptics
    -phenytoin classically
  3. Herbal supplements
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30
Q

Tx for certain causes of acute liver failure

(a) HELLP
(b) Acute hep B
(c) Autoimmune hepatitis

A

Treating acute liver failure

(a) HELLP- deliver
(b) Acute hep B- entecavir (anti-viral)
(c) Autoimmune hepatitis- steroids

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31
Q

Buzzwords for etiology of acute liver failure in the following

(a) Pt with cancer (hypercoagulable)
(b) Mushroom hunter
(c) Keiser-Fleisher rings

A

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)

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32
Q

4 things that can causes transaminasis > 10,000

A

Transaminasis > 10,000 from just a few things

  1. APAP
  2. Hypoperfusion (cardiac arrest)
  3. Viral infection
  4. Poisonous mushrooms

most notably NOT EtOH

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33
Q

Mechanism of NAC

A

N-acetyl cysteine donates cysteine needed to conjugate NAPQI (toxic metabolite of APAP) into harmless metabolite glutathione

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34
Q

Indications for NAC

A
  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

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35
Q

Key ammonia cutoff to consider RRT in pt with acute liver failure

A

Consider renal replacement if ammonia is > 200

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36
Q

Grade 0-4 of hepatic encephalopathy

(a) When start to get sleepy

A

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

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37
Q

Proposed mechanism of hepatic encephalopathy

A

Increased ICP

-presumably due to elevated NH4 crossing BBB and dragging in water

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38
Q

Acute or chronic causes of liver failure carry higher risk of hepatic encephalopathy

A

Acute&raquo_space; chronic for risk of hepatic encephalopathy, even highest in subacute

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39
Q

Why lactulose typically avoided in mgmt of acute liver failure

A

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

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40
Q

General approach to managing elevated ICP in hepatic encephalopathy

A

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

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41
Q

Key concepts in acute liver failure to trigger transplant referral

A
  1. Progressive lab abnormalities
    -coagulopathy
    -acidemia
    -hypoglycemia
  2. Development of complications
    -hepatic encephalopathy
    -AKI
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42
Q

2 prognostic models in acute liver failure

A

-MELD for synthetic dysfunction
-Kings college criteria

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43
Q

When to use the following in acute liver failure

(a) Levophed
(b) Glucocorticoids
(c) ICP monitoring

A

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

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44
Q

Mannitol vs. hypertonic saline in mgmt of hepatic encephalopathy in acute liver failure

A

Hypertonic saline- can use prophylactically for target Na 145-155

While mannitol (contraindicated in hyperosmolality and renal dysfunction) for acute, last ditch, temporary effect

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45
Q

What etiologies of acute liver failure typically recover, while which are more likely to require transplant

A

Acute tylenol toxicity typically recovers

Wilson’s disease, subacute drug toxicity, autoimmune hepatitis- less likely to survive w/o transplant (lower transplant-free survival)

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46
Q

Timeline cutoff for hyperacute, acute, subacute, chronic liver failure

A

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

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47
Q

Explain mechanism and proper use of hyperventilation in acute liver failure

A

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…

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48
Q

Typical clinical scenario of alcoholic hepatitis

A

Increased EtOH consumption over days/weeks- subacute jaundice (over 8 weeks), abdominal pain, fatigue

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49
Q

Scores that guide steroid initiation and duration in alcoholic hepatitis

A

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

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50
Q

Definition of spontaneous bacterial peritonitis

(a) Tx

A

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)

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51
Q

First line for SBP tx in PCN-allergic patient

A
  1. albumin! (1 g/kg)
  2. abx if can’t use third gen cephalopsporin (CTX or cefotaxime) = fluoroquinolone (cipro)
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52
Q

When to treat hyponatremia in cirrhotic

A

Really don’t treat, it’ll just make the retain more fluid

Treat if Na < 120 or any neurologic consequence (seizures)

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53
Q

Definition of hepatorenal syndrome

A

HRS: dx of exclusion
Cr > 1.5 unchanged after albumin challenge, stopping diuretic, and addressing alternative causes

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54
Q

Approach to HRS treatment

A

HRS treatment

  1. albumin to augment blood volume
  2. pressor (or midodrine) to augment MAP
  3. octreotide to combat splanchnic vasodilation
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55
Q

Typical LFT findings in alcoholic hepatitis

A

AST/ALT > 1.5, both < 400 with Tbili > 3.0 (so more cholestatic than hepatocellular pattern)

Transaminasis > 10,000 not consistent with alcoholic hepatitis

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56
Q

2 indications where albumin improves survival in liver failure

A

Albumin improved survival

  1. After large volume paracentesis > 5L
  2. Bacterial infections (peritonitis)
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57
Q

Mechanism of kidney injury in TLS

A

Tons of cells lyse and release nucleic acid, purine metabolism produces tons of uric acid which precipitates in renal tubules

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58
Q

Low-intermediate risk for TLS- what to pre-medicate with

A

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)

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59
Q

Methemoglobinemia

(a) Pathophys
(b) Explain why SpO2 = 85%

A

(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

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60
Q

Buzzword blood color

(a) Cherry red
(b) Chocolate brown

A

(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)

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61
Q

Most common cause of acquired methemoglobinemia

A

Drug-induced
-antimalarials: dapsone
-topical anesthetics: benzocaine, lidocaine <– can be added to street drugs

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62
Q

Clinical features of methemoglobinemia

A

Neurologic symptoms of tissue hypoxia typically
Then metabolic acidosis (from lactate)

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63
Q

Differentiate hyperleukocytosis and hyperviscosity syndrome

(a) Cause
(b) Mgmt

A

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

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64
Q

Differentiation syndrome

(a) Cause
(b) First line treatment

A

Differentiation syndrome from (a) use of ATRA to help differentiate promyelocytes in APLM to neutrophils

(b) Steroids

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65
Q

First line treatment for HLH

A

HLH- hypermacrophage huge cytokine storm sitch

First line treatment- etoposide and steroids

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66
Q

Uncommon but possible cause of tissue hypoxia side effect of high dose iNO

A

iNO doses > 80ppm carries risk of methemoglobinemia

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67
Q

Typical clinical scenarios for

(a) Methemoglobinemia
(b) Carbon monoxide poisoning

A

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
Q

Differentiate clinical features of methemoglobinemia and carbon monoxide poisoning

A

Both present with tissue dysoxia- CNS manifestations

69
Q

Differentiate treatment of methemoglobinemia and carbon monoxide poisoning

A

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
Q

Indication for methylene blue in methemoglobinemia

A

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
Q

TEG interpretation- order of abnormalities guiding resuscitation

A

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
Q

What part of TEG expect to be abnormal on heparin

A

Heparin inhibits clotting factors => expect start of clot formation (R-time) to be prolonged

73
Q

RBC abnormality on smear expected in

(a) Autoimmune hemolytic anemia
(b) TTP

A

Spherocytes (small, dense RBCs) in AIHA or drug-induced hemolysis

vs.

Schistocytes in MAHA (DIC, TTP), fragmented from shearing forces

74
Q

What’s more common- TACO or TRALI

A

TACO way more common

TACO 1:100
TRALI 1:10,000

75
Q

FFP

(a) Amount of volume per unit
(b) Empiric dosing to correct coagulopathy

A

FFP

(a) 250cc per unit
(b) Generally want 15 ml/ kg so in 70 lb patient ~1L FFP

76
Q

Differentiate apheresed vs. pooled platelets

A

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
Q

Platelet cutoff for

(a) CVL insertion
(b) Thora

A

Plt > 20,000 for both CVL insertion and thora

78
Q

Expected fibrinogen rise from 1 pooled unit of cryo

A

Cryo (fibrinogen, vWF, factor VIII and XIII, fibronectin)- expect rise in fibrinogen of about 70 per unit of cryo

79
Q

Mechanism of tXA

A

Inhibits fibrinolysis (clot breakdown) by blocking plasminogen binding to fibrin => fibrin not broken down so clot lasts longer

80
Q

Top indications for tXA

A

Best results when used within 3 hours of major trauma or postpartum bleeding

Not useful in massive GI bleed

81
Q

Describe the abnormality in TEG seen with

(a) Heparin use
(b) Uremic platelets
(c) Hyperfibrinolysis

A

(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
Q

PLASMIC score utility

A

PLASMIC score = pre-test probability for TTP

If high enough- start plasma exchange prior to ADAMST13 activity coming back low

83
Q

Describe mechanism of TTP

A

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
Q

Explain 3 key features of lab diagnosis of DIC

A

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
Q

Differentiate apixaban and dabigatran mechanism

A

Apixaban, edoxaban, rivaroxaban all factor Xa inhibitors (on up the pathway from thrombin)

While dabigatran is a direct thrombin (factor IIa) inhibitor

85
Q

Mechanism of argatroban

A

Argatroban and bival are direct thrombin inhibitors, like dabigatran

86
Q

Indication for idarucizumab vs. andexanet alpha

A

Idarucizumab reverses dabigatran (direct thrombin/factor IIa inhibitor)

While andexanet alpha reverses anti-Xa DOACs (apixaban)

87
Q

Mechanism of atropine

(a) Why ineffective in complete heart block

A

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
Q

Mechanism of glucagon in bradycardia due to BB or CCB toxicity

A

Glucoagon activates L-type calcium channel independent of beta-receptor (adrenergic tone) so makes the muscle work despite beta blockade

Temporary effect

89
Q

Describe what VVI pacemaker mode is

A

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
Q

Role of placing magnet over a

(a) Pacemaker
(b) Defibrillator

A

(a) magnet over pacemaker inhibits sensing

(b) magnet over defibrillator inhibits shock therapy

91
Q

Explain why atropine might fix sinus bradycardia from an inferior MI within first 6 hours after MI

A

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
Q

What to expect on baseline EKG for patient with WPW

A

Short PR, delta wave

93
Q

Duration of post-op AFib that prompts consideration of anticoagulation

A

AFib very common post-op, if persists for > 48 hours consider AC

94
Q

Why is amiodarone typically better at rate control for AFib than digoxin in the acute ICU setting?

A

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
Q

What to consider if facing a regular narrow-complex tachycardia not responsive to cardioversion

A

Ectopic or multifocal atrial tachycardia won’t respond to cardioversion
(while AFib/flutter typically will)

96
Q

Why want to avoid adenosine in patient with known WPW

A

Block the AV node- leave only accessory pathway available => Vfib/flutter

97
Q

Why might consider using adenosine in stable wide complex tachycardia

A

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
Q

EF cutoff for HFrEF vs. HFpEF

A

HFrEF for EF < 40%

HFpEF > 50%

99
Q

Differentiate NYHA class II vs. III

A

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
Q

Differentiate NYHA class III vs. IV

A

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
Q

Distinguish main mechanism/effect of nitroglycerin vs. nitroprusside

A

Nitroglycerin = peripheral venodilator = lower preload

Nitroprusside = peripheral arterial dilator = lowers afterload (SVR)

102
Q

Explain how dobutamine is an inodilator

A

Dobutamine-
Beta 1 = inotrope
Beta 2 = peripheral vasodilator

103
Q

Limits of IABP

(a) Amount of augmented cardiac output
(b) Arrhythmia

A

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
Q

Maximal flow rate of

(a) IABP
(b) Impella
(c) VA ECMO

A

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
Q

At what part of the cardiac cycle does IABP

(a) Inflate
(b) Deflate

A

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
Q

Explain how IABP changes the aortic pressure during systole and diastole

(a) Compare assisted to unassisted diastole
(b) Compare assisted to unassisted systole

A

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
Q

At what part of the cardiac cycle does IABP inflate?

A

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
Q

IABP vs. Impella

(a) Flow rate
(b) Anticoagulation requirement

A

(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
Q

Cutoffs used to signify increased need for LV mechanical support

(a) CI
(b) CPO

A

(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
Q

PAPi cutoff to trigger escalation of R-sided mechanical support

A

PAPi < 0.6 or evidence of severe RV dysfunction on TTE- escalation of RV mechanical support

PAPi = (sPAP-dPAP) / RA

111
Q

Describe how the cerebral autoregulation curve is shifted in ppl with chronic hypertension

(a) Clinical consequence

A

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
Q

Differentiate hypertensive urgency from emergency

A

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
Q

Which antihypertensive drip comes with risk of cyanide toxicity?

(a) Clinical features of cyanide toxicity

A

Nitroprusside = peripheral arterial dilator to reduce LV afterload (reducing SVR), causing significant drop in BP
Metabolizes in cyanide

(a) Lactic acidosis and AMS

114
Q

Treatment of cyanide toxicity from nitroprusside drip

A

IV thiosulfate

115
Q

First-line antihypertensive during HTN emergency when end organ damage is:

(a) Cardiac
(b) Brain

A

HTN emergency

(a) ACS- nitroglycerin to reduce cardiac preload
(b) Brain- CCB (nicardipine)

116
Q

Special circumstances for hydralazine for HTN

(a) First line
(b) Contraindicated

A

Hydralazine

(a) First line in pregnancy
(b) Contraindicated in aortic dissection b/c of risk of reflex tachycardia

117
Q

Differentiate BP goal for ICH vs. ischemic stroke

A

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
Q

Explain pathophys of how HTN emergency causes CNS dysfunction

A

MAP too high- cerebral autoregulation can’t keep CPP within normal range => CPP elevates causing endothelial damage, loss of vascular integrity

119
Q

BP goals for ischemic stroke before and after TPA

A

ICS: SBP < 185/110 for tPA, < 180/105 after tPA

vs. SBP goal 150-220 for ICH

120
Q

BP goal for hypertension in ACS

A

Goal SBP < 140mmHg within the first one hour, but importantly DBP > 60 to maintain coronary perfusion pressure

121
Q

Differentiate surgical vs. nonsurgical aortic dissections

A

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
Q

SBP and HR goal for medical management of aortic dissection

A

Aortic dissection-
SBP goal < 120 and HR < 60 within the first hour

123
Q

Typical dual agent regimen for BP/HR management in aortic dissection

A

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
Q

Definition of severe preeclampsia

A

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
Q

SBP goal in severe preeclampsia

A

SBP < 140 in severe (severe being SBP > 160 or SBP > 110)

126
Q

3 drugs safe to treat HTN in pregnancy

A

Labetalol
Hydral
CCB (nicardipine)

127
Q

Purpose of IV Mg in preeclampsia

A

IV Mg for seizure prophylaxis

128
Q

Goal BP drop (both acutely and subacutely) for hypertensive encephalopathy

A

Initial target 15-25% drop in MAP over the first hour, then to < 160/100 at 6 hours

129
Q

First line mgmt for HTN crisis from catecholamine surge from pheochromocytoma

A

Phentolamine = alpha blocker

130
Q

STEMI door to balloon time for

(a) Patient presenting to PCI-capable hospital
(b) Patient presenting to non-PCI capable hospital

A

STEMI

(a) 90 minutes
(b) 120 minutes if a transfer

131
Q

For STEMI patient presenting to non-PCI capable hospital- timeline for when to give lytics (when transfer/balloon time will be how delayed?)

A

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
Q

Post-lytics for STEMI- keep patient at non-PCI capable hospital if chest pain resolves and EKG improves?

A

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
Q

Outcome of NICE-SUGAR NEJM trial on ICU sugar control

A

NICE-SUGAR 2009 NEJM- increased mortality for tight (81-108) glucose control over liberal (under 180)

134
Q

Nutrition in the ICU, guideline stance on

(a) enteral vs. parenteral
(b) early vs. late
(c) High vs. low protein

A

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
Q

Nutrition in the ICU guideline stance on how to monitor tolerance of enteral feeding

A

By clinical parameters, no longer guideline to routinely check residual volumes

If checking, no need to hold unless over 500cc

136
Q

Difference in feeding obese pts in the ICU

A

Higher protein needs
-still start early (within 24 hrs) despite concept of potentially higher reserve
-start with hypocaloric regimen to increase insulin sensitivity

137
Q

How to improve survival in refeeding syndrome

A

Intentional underfeeding of at risk patients- survival better in patients with strict caloric management (not automatically starting at full feeds)

138
Q

ICU feeding/nutrition guidelines on

(a) NG vs. NJ
(b) Glutamine supplementation

A

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
Q

ICU feeding/nutrition guidelines on

(a) When to start enteral feeds
(b) When to start parenteral feeds

140
Q

What is actually measured by BP cuff

A

MAP- then SBP and DBP derived
-measured via oscillometry

141
Q

CVP tracing, line up with EKG

(a) A-wave
(b) V-wave

A

(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
Q

By convention at what part of the acv curve do you measure CVP?

(a) and what part of respiratory cycle

A

Measure CVP at base of c-wave, is C-wave no visible then take the mean of the a-waves

(a) end expiration

143
Q

End expiration higher or lower pressure during

(a) Spontaneous breathing
(b) PPV

A

(a) Spontaneous breathing
end expiration pressure is higher

(b) Mechanical ventilation- end expiration pressure is lower

144
Q

How to differentiate wedge from CVP tracing

A

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
Q

Typical cause of large v-waves in

(a) CVP tracing
(b) PAWP tracing

A

(a) CVP tracing = TR
(b) PAWP tracing- reduced LA compliance: MR, VSD, volume overload

146
Q

RHC findings classic for pericardial tamponade

A

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
Q

Describe phenomenon of overwedging of PA catheter

A

Erroneous pressure measurement when balloon traps catheter against vessel wall- pressure continues to rise

-inaccurate measurement and increased risk of PA rupture

148
Q

Describe mechanical ventilation’s effect on

(a) LV preload and afterload
(b) RV preload and afterload

A

Mechanical ventilation

(a) Reduces LV afterload, increases LV preload
(b) Reduces RV preload, increases RV afterload

149
Q

Pt on mechanical ventilation- what degree of pulse pressure variation is associated with fluid responsiveness

A

12-15% increase in pulse pressure during inspiration suggests on the steep portion of the Frank-Starling curve => fluid responsive

150
Q

Change in IVC diameter with inspiration during

(a) Spontaneous breathing
(b) Mechanical ventilation

A

(a) During spontaneous breathing, negative inspiratory pressure with inspiration with reduce IVC diameter

(b) During positive pressure ventilation, inspiration => increase in IVC diameter

151
Q

What percent of IVC diameter variability predicts fluid responsiveness

A

12% change

152
Q

Limitations of stroke volume/pulse pressure variation

A

-Best when breaths are the same size => limited in spontaneous breathing
-Best when stroke volume relatively similar => not great in arrhythmias

153
Q

Best method to assess fluid responsiveness in spontaneously breathing patient

A

Passive leg raise b/c not depending on same size breaths like other pulse pressure variation methods (PPV, VTI)

154
Q

Best method to assess fluid responsiveness in pt with AFib

A

Irregular HR/differing cardiac output- use VTI averaged multiple

Passive leg raise better than PPV

155
Q

Rare complication of stacked fentanyl doses that can worsen respiratory failure

(a) Tx

A

Stiff chest/wooden chest syndrome

(a) Tx = depolarizing paralytic- succinylcholine

156
Q

Pt on multiple sedatives (lorazepam, propofol) develops worsening metabolic acidosis

A

Check for propylene glycol toxicity (diluent of ativan gtt)- check osmolar gap

Check for PRIS- elevated TGs, renal failure (rhabdo), hyperkalemia

157
Q

Benzo antagonist

A

Flumazenil

158
Q

Ketamine

(a) Use in neurointubation
(b) Heart failure patients
(c) Effect on airways

A

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
Q

In what pts does tXA decrease moratlity

A

-post-partum hemorrhage and severely injured trauma patients

160
Q

Mechanism of tXA

A

tXA = antifibrinolytic, prevents breakdown of clot

161
Q

Mgmt of chest tube noted to be intraparenchymal

A

Place another large bore (that can handle blood) before you pull it

162
Q

Malignant hyperthermia

(a) When to consider
(b) Triggers
(c) Clinical features aside from fever…

A

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
Q

Indication(s) for dantrolene

A

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
Q

Dantrolene mechanism

A

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
Q

Data for or against

(a) Use of lung protective ventilation intra-op for abdominal surgeries
(b) Abdominal surgery intra-op BP goal

A

(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

CM Critical Care Boards (5 decks)

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