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Flashcards in CV/Pulm Deck (108):

Two different types of CCBs and their major ADRs

What Rx can you use to minimize the effect of the ADR?

  1. DHP (amlodipine, nefidepine)
    • peripheral edema (2/2 potent arteriolar dilator, HA, flushing, dizziness
    • add ACEi/ARB to decr. peripheral edema (2/2 post-capillary venodilation)
  2. Non DHP (diltiazem, verapamil)


Major ADR of Trastuzumab

Is it reversible or irreversible?

What increases the risk of this ADR?

cardiotoxicity, decreases LVEF

REVERSIBLE - can hold x4 weeks if LVEF decreases by >16% from baseline

Anthracycline (e.g. doxorubicin) and cyclophosphamide will increase risk of cardiotoxicity


What is a major ADR of doxorubicin?

 Is it reversible or irreversible?

cardiotoxicity (2/2 myocyte necrosis, destruction, fibrous tissue replacement)

NOT reversible 


MI involving inferolateral wall typically have what kind of symptoms/physical findings?

What would you treat this?

EKG leads affected in MI involving inferolateral wall

sinus bradycardia + AV block (2/2 incr in vagal tone)

give atropine (though if patient does not respond, undergo transvenous cardaic pacing)

II, III, aVF, V5, V6


What EKG findings would indicate thrombolytic therapy?

What EKG findings would inciate prior MI?

STE >1mm in two contigious leads

T inversions, Q waves


What kind of symptoms would manifest if patient had an anterior wall MI?

How would you treat this?

bradyarrhythmias (usually 2/2 damage to conduction system below AV node)

transvenous cardiac pacing


What defines Pulseless Electrical Activity (PEA)?

How does this differ from asystole?

What should you do if you see PEA?

PEA: presence of organized electrical activity (i.e ekg shows afib/sinus tach/etc) in the heart but w/o sufficient CO to produce a palpable pulse or measurable BP

  • initiate CPR (remember CAB guidelines) and give epi q2-3min until responsive

Asystole: no electrical activity, no pulse

  • shock


What is the mechanism of nitroprusside?

What is it commonly used for? 

What is the benefit of nitroprusside over other medications in its class?

What is the major ADR? In what patients is this risk greatly increased? How do you treat this?

potent vasodilator of arterial+venous circulation

used often in hypertensive emergency

has rapid onset/offset, allows you to titrate

cyanide toxicity - flushing, AMS, arrhythmias, tachypnea, metabolic acidosis. Risk esp in patients with ESRD/AKI. Tx: sodium thiosulfate


What is the treatment goal in patients with hypertensive urgency?

rapidly decrease diastolic BP to 100-105s over 2-6 hours. If not treated, it can ause increased cerebral perfusion pressure, resulting in cerebral edema/hypertensive encephalopathy (HA, N/V, confusion, agitation, seizure, coma)


Hypertrophic cardiomyopathy (HCM) vs Hypertrophic obstructive cardiomyopathy (HOCM)

When and how do you manage these patients?

Patients who show signs/symptoms of heart failure should be treated with 

  • ß blockers
  • verapamil/disopyramide can be added in patients with persistent symptoms
  • acohol septal ablation if they're refractory to medical management
  • Implantable cardioconverter defibrillator (ICD) if they have a history of cardiac arrest or vtach (to prevent sudden cardiac death)


4 defining features of Tetraology of Fallot

  1. RVOT obstruction (incr obs. = decr. pulm flow = cyanosis)
  2. overriding aorta
  3. RVH
  4. VSD (harsh holosystolic murmur, L 3rd/4th/ intercostal space, thrill)


Bicuspid Aortic Valve is diagnosed in your patient, what should you recommend to the patient?

What are the major complications of patients with bicuspid aortic valve?

screening ECHO in 1st degree relatives since this is AD w/ incomplete penetrance.


  • endocarditis
  • AS/AR
  • aortic root dilation or ascending aortic dilation 
  • dissection


Effects of uncontrolled diabetes during pregnancy on the fetal heart

How is this managed?

excess glycogen deposition in the myocardium results in hypertrophy of cardiac musculature -> ventricular outflow obstruction -> cardiomyopathy/CHF

will spontaneously correct


How do EKG differ between sinus tachycardia, ventricular tachycardia, and paroxysmal supraventricular tachycardia (SVT) in terms of

wave form



sinus tachycardia - normal P waves, narrow QRS

ventricular tachycardia - WIDE QRS complexes (>0.12 sec). 

  • vagal manuevers
  • adenosine

paroxysmal supraventricular tachycardia (SVT) - narrow QRS w/ unidentifiable P waves, SUDDEN onset

  • adenosine
  • vagal maneuvers 
  • cardioversion (if unstable)


Long QT Syndrome can preciptate into this:

What are the inciting factors?

How would you treat it?

Torsade de pointes

inciting factors:

  • bradyarrhythmia
  • electrolyte imbalances
  • SSRI
  • hypothermia
  • HIV infection
  • adrenergic surge
  • hypERglycemia
  • hypOthyroidism
  • starvation


  • IV Mg (even if serum levels are WNL)
  • If patients do not respond: temporary transvenous pacing


A-fib Treatments (3)

  1. rate control w/ AV nodal blocking Rx for paroxysmal/first episodes
  • ß blocker, CCB, digoxin
  1. rhythm control for patients unable to achieve adequate rate control, recurrent episodes, symptomatic LV dysfunction
  • no structural heart dz: flecainide
  • LVH: amiodarone vs dronedarone
  • CAD w/o HF: sotalol vs dronedarone
  • CAD w/ HF: amiodarone, dofetilide
  • recurrent sx refractory to medical management: radiofrequency ablation


Wolf Parkinson White Syndrome

What is it? What can it cause?

In what patients is this syndrome most dangerous in and why? How should these patients be managed?

accessory pathway that bypasses AV node to cause ventricular contraction; mostly asymptomatic, but can cause paroxysmal SVTs

patients w/ a-fib who also have this syndrome can experience tachyarrhythmias, which can spiral into v-fib and subsequently syncope/death. Manage w/ cathether ablation


How do you differentiate between Wolf Parkinson White Syndrome and vasovagal?

vasovagal - neurocardiogenic response caused by decreased sympathtic drive (resulting in vasodilation) w/ increased parasympathetic response (causing bradycardia). Often presents w/ prodromal symptoms nausea, lightheadedness, pallor, diaphoresis. Diagnose w/ tilt table test

Wolf Parkinson White Syndrome - accessory pathway that bypasses AV node to cause ventricular contraction; mostly asymptomatic, but can cause paroxysmal SVTs (sudden onset of palpitations)


All patients w/ new-onset a-fib should undergo this assessment to estimate thromboembolic risk


Age >75

Vascular Dx (MI, PAD)
Age 65-75
Sex (female)


= 0 = no anticoagulation treatment

= 1 = initiate ASA, coumadin, or NOAc (dabigatran, rivaroxaban, apixiban)

= 2 = coumadin or NOAc


Patient on coumadin starts a medication that potentiate warfarin's effect. What should you recommend?

reduce coumadin dose by 25-50% and recheck PT/INR for several weeks until it stabilizes


How can CHF cause hyponatremia?

How is this managed?

decr CO -> decr perfusion pressure ->

  • incr ADH -> diluational hypernatremia
  • incr renin + NE -> incr H2O intake 

Tx: fluid restriction, tolvapatan (vasopressin receptor antagonist)


What is CHF?

How is it diagnosed?

What are some things you should order?

systolic dysfunction (impaired/inadequate ventricular emptying) + diastolic dysfunction (impaired vent relaxation) 

i.e. can't pump/can't fill

Diagnose via 2 major OR 1 major + 2 minor symptoms

Get EKG, CXR, pulse ox


What is the goal of treating patients w/ CHF?

decrease preload w/ diuretics, IV vasodilators (NTG, nitroprusside, nesiritide)


Four distinguishing features of cardiac tamponade

EKG findings?

ECHO findings?

What should you do if you suspect this in patient?

  • Becks Triad: JVD, Hypotension, Diminished heart sounds
  • pulsus paradoxus (inspiratory decrease in SBP by >10mmHg)
  • EKG: low voltage QRS, electrical alternans
  • ECHO: RA/RV collapse during diastole, IVC dilation

--> pericardiocentesis


acute pulmonary edema - management and measures to achieve symptomatic relief?

  • O2 
  • IV diuretics (decr intravascular volume -> improved oxygenation -> symptomatic relief)
  • IV vasodilators (NTG, nitroprusside; improves preload and afterload, decr intracardiac filling pressures -> symptomatic relief)


What are the top 3 indications for lipid lowering therapy?

  1. clinically significant atherosclerotic disease (ACS, MI, angina, stroke, TIA, PAD)
  2. LDL >190
  3. Age 40-75 w/ DM


What areas do these blood vessels supply?




LCX - lateral wall of LV (V1-V4)

RCA - RV+inferoposterior wall of LV (II, III, aVF)

LAD - anterior wall of LV


Management of STEMI

What should you avoid?

cardiac cath within 90 minutes of initial medical contact

Avoid CCB - has been shown to increase mortality due to decreased BP w/ subsequent increased sympathetic activity


Patients w/ inferior wall MI can develop this complication:

What should you do in these situations? What should you avoid?

sinus bradycardia 2/2 increased vagal tone and SA node ischemia. Can ultimately lead to cardiogenic shock (hypotension, JVD, clear lung fields)


  • IV atropine
  • optimize preload via IVF

usually resolves within 24 hours, but if persistent, cardiac pacing

Avoid ß blockers/CCB, nitrates, diuretics, opioids since they can impair CO (resulting in profound hypotension)


What is pathognomonic of ACS? 

How do you differentiate btwn NSTEMI and unstable angina?

What should you do in either case?

prolonged episode of substernal CP + dyspnea relieved by NTG

NSTEMI - troponins increase

unstable angina - troponins do not change

Admit for serial tropinins to r/o MI/STEMI


patient presents w/ s/sx c/w unstable angina, what should you do?

coronary angiography ASAP to diagnose the degree/location of blockage in the coronary circulation. May ultimately need PCI/CABG


patient p/w s/sx c/w NSTEMI, what should you do?

What should you avoid?


  • O2
  • NTG
  • morphine
  • ß blocker
  • statin
  • ACEi/ARB
  • platelet P2Y12 receptor blocker (clopidogrel, ticagrelor)
  • ASA, anticoagulation


  • CCB due to hypotension, increase syncopal activity, and worse outcomes


patient has stable angina + decreased LVEF/wall hypokinesis. next step?

patient has stable angina + risk factors (DM, HTN, FHx). next step

coronary angiography


patient p/w elevated CK after running a marathon. He is on a statin. What should you do?

statins can potentiate muscle injury w/ prolonged vigorous exercise.

If patient is asymptomatic, d/c statin if CK >10x upper limit of normal. Restart statin once CK levels normalize

If patient has rhabdomyolysis, d/c statin (do not resume)


Compartment syndrome features (4)

What is the pathophysiology behind these features?

What is the ultimate sequelae if not treated appropriately?

How to diagnose?

How to treat?

  • pain out of propotion to injury (esp w/ repeated doses of pain meds)
  • pain on passive stretch
  • rapidly increasing/tense swelling
  • parasthesias (early, crawling/burning sensation)

pathophys: increased edema in an enclosed space, resulting in compression of neurovascular bundles and anoxic muscle necrosis (rhabdo), can result in ARF (esp in volume depleted states)

diagnose: worsening serial tissue pressures (if >30mmHg or difference btwn DBP and compartment pressure is <20-30mmHg), then urgent fasciotomy is indicated


transmural MI can result in pericarditis. What is a common physical finding? What would EKG show?

How do you treat this?

pericardial friction rub

EKG: sinus tach, diffuse STE, PR segment depression

Tx: ASA (avoid NSAID due to concerns of myocardial rupture)


Patient p/w asymptomatic low LVEF. Management and rationale?

Start ACEi/ARB - delays onset of symptomatic heart failure and potentially prolongs survival


patient w/ peripartum cardiomyopathy is contemplating another pregnancy? What do you recommend?

get TTE and if LVEF is low, avoid pregnancy


CP 2/2 cocaine - what two things should remain high on your radar and why? 

EKG demonstrates STE, what medications should you administer?

What should you aovid? 

If the initial management does not alleviate the CP, what is the next logical step?

  1. coronary artery thrombosis (due to vasoconstrition/vasospasm and prothrombotic state 2/2 platelet activation)
  2. MI/aortic dissection (esp in the first four hours of use)

Give benzo (to decrease anxity/agitation, HTN, tachycardia -> reduce myocardial ischemia), nitrates or CCB, ASA

Avoid ß blockers (can cause further vasospasm)

If not responsive

  • Get coronary angiography to r/o coronary thrombus
  • phentolamine (a-antagonist) to reduce coronary vasospasm, NTG, nitroprusside


Pt w/ history of PAD/TIA has normal cholesterol levels. What should you do?

start statin regardless of baseline cholesterol levels. 

can also start ASA or clopidogrel if presenting w/ symptomatic PAD to reduce risk of ischemic stroke, MI or CV death


PAD management

if initial management fails to alleviate symptoms, what medication should you start next?


  • ASA/clopidogrel
  • statin
  • exercise program to reduce symptoms, increase walking distance

If symptoms persist:

  • start cilostazol (vasodilator via phosphodiesterase inhibitor)


lightening injuries treatment

CPR, vasopressors, defibrillator if patient is in v-fib


what are the indication for antibiotic ppx to avoid bacterial endocarditis?

what common produres is antibiotic ppx not indicated?

at risk procedures:

  • dental manipulations
  • respiratory tract procedures
  • patients w/ ongoing GI/GU/skin/MSK infections
  • cardaic surgeries

not indicated/low-risk procedures

  • prostatectomy, foley placement
  • C-sections/vaginal deliveries


most likely cause of death in young patients who experienced exertional CP, presyncope, syncope, and SCD?

anomalous coronary artery


Criteria for Long QT Syndrome in men? women?

men: >450 msec 

women: >470 msec


TCA overdose symptoms


if not responsive to initial therapies?

CNS changes (AMS, seizures, respiratory depression) secondary to inhibition of central GABA receptors

anticholinergic effects - dry mouth, blurry vision, dilated pupils, flushing, hyperthermia, urinary retention

tx: Benzo (GABA agonists), NaHCO3 (increases pH such that TCA becomes non-ionized/less available for binding

if not responsive: lidocaine, Mg


Acute MR



exam findings


  1. ruptured mitral chordae tendinae (flail leaflets) from MVP, infective endocarditis, trauma, rheumatic disease
  2. papillary muscle rupture 2/2 MI/ischemia (usulaly 2-7 days after infarct)


  • rapid onset of pulmonary edema
  • hypotension progressing to cardiogenic shock
  • RHF 2/2 pulmonary HTN

exam findings:

  • decreshendo systolic murmur at LLSB
  • incr JVP
  • diaphoresis
  • pallor/cool extremities 2/2 poor tissue perfusion


Ehler Danlos vs Marfan

major features

cardiac findings

Ehler Danlos

  • major features: hernia, thracolumbar sciolosis, pes planus
  • cardiac findings: MVP

Ehler Danlos

  • major features: lens dislocation, retinal detachment, spontaneous PTX
  • cardiac findings: MVP + aortic root dilation --> dissection vs AR


when is vavular surgery indicated in patients w/ MR?

when LVEF <60 and patient has symptoms of exertional dyspnea, fatigue, overt heart failure


patient p/w dyspnea/CP w/ exertion, CXR showing prominent pulmonary arteries, loud SD and EKG showing R axis deviation.

What is your diagnosis?

How do you make the diagnosis?


Diagnosis: Pulmonary HTN

Tests: ECHO

Tx: Bosentan endothelialn receptor antagonist), prostanoid, or PDE5 inhibitor


Multifocal Atrial Tachycardia

EKG findings


EKG findings

  • P waves have ≥ 3 different morphologies 
  • variable PR and RR segments
  • narrow QRS complexes
  • up to 200bpm


  • AV nodal blocking agents (ß blockers, non-DHP CCB (verapamil, diltiazem)


EKG findings of patients w/ a-fib w/ RVR


absent p waves

irregularly irregular

varying R-R intervals

narrow QRS complex tachycardia

treatment: ß blockers, non-DHP CCB (verapamil, diltiazem)


First thing to do in patient w/ blunt chest trauma

get EKG

if normal - NTD

if abnormal  (i.e. new BBB, sinus tach, STD/STE, etc) - get FAST exam and ECHO for tamponade, thrombi, hemopericardium, vavular abnormalities


acute aortic dissection treatment (2)

1) morphine

2) IV ß blocker (target BP 100-120); preferred esmolol, propranolol, labetalol

  • esomolol has a short half life, allows for rapid titration of BP/HR
  • nitroprusside if ß blockers do not work


define the parameters for hypovolemic shock in terms of 


cardiac index (pump function)

SVR (afterload)


preload: decr

cardiac index (pump function): decr

SVR (afterload): incr 

MVO2: decr 


define the parameters for cardiogenic shock in terms of 


cardiac index (pump function)

SVR (afterload)


preload: incr

cardiac index (pump function): decr

SVR (afterload): incr 

MVO2: decr


define the parameters for septic shock in terms of 


cardiac index (pump function)

SVR (afterload)


preload: normal or decr

cardiac index (pump function): incr (compensatory)

SVR (afterload): decr

MVO2: incr


complication of PCI

cardiogenic shock 2/2 abrupt coronary occlusion -> impaired contractility of myocardium


common causes of secondary HTN in young folks? older folks?

young folks - renal parenchymal disease, coarctation of aorta (brachial-to-femoral pulse delay)

older folks - hyperaldosteronism, renal artery stenosis 2/2 atherosclerosis, FSGS (esp in AA males), OSA, pheochromocytoma, cushing, thyroid dysfunction


initial studies indicated in syncope (3)





mitral stenosis murmur

low-pitched diastolic rumble heard best at cardiac apex (5th intercostal space), L mid clavicular line


Coumadin management if INR was:

>3 but <5

5 - 9


>3 but <5: hold 1-2 days or decrease dose

5 - 9: hold/resume when INR therapeutic; add 1-2.5mg Vit K PO if there is increased risk of bleeding

>9: hold and give 2.5-5mg Vit K PO, FFP, factor VIIa, prothrombin complex concentrate


mechanical heart valves require long-term treatment with what and why?

How does mitral valve differ from those of aortic valves?

80 mg ASA + coumadin (INR 2-3 for aortic valve, INR 2.5-3.5 for mitral valve) because there is a 2x risk of thromboembolism (if patients can't tolerate coumadin, give 75-325mg ASA)


Acute limb ischemia is managed depending on the severity of ischemia:




viable - cath vs surgical revascularization

threatened (severe pain at rest, sensory/motor loss, delayed cap refill, inaudible doppler, incr risk of myonecrosis) - surgical revascularization 

non-viable - amputation

*ALL should get anticoagulation immediately*


Mitral stenosis

exam findings

CXR findings

EKG findings

TTE findings

exam: loud S1, loud P2 if pulm HTN is involved. Hoarseness (2/2 compression of recurrent laryngeal nerve by enlarged LA)

CXR: LAE, flattened L heart border, dilated pulm vessels

EKG: P mitrale (broad-notched P waves), atrial tachyarrhythmia, RVH (tall R waves in V1+V2)

TTE: MV thickening/decreased mobility, coexisting MR


sick sinus syndrome

what is it? what causes it?


how to diagnose it?

EKG findings?


what it is: inability of SA node to generate an adequate HR, usuallydue to age-related degeneration of the conduction system/fibrosis of SA node, ischemia, infiltrative cardiac disease

symptoms: bradycardia +/- tachycardia (afib, palpitations)

diagnose: holter monitor

EKG findings: sinus bradycardia, sinuses pauses (delayed P waves), SA nodal exit block (dropped P waves)

Treatment: pacemaker +/- rate control medications if there is tachyarrhythmias present


Where are AAAs typically located?

Who do you normally screen

how are AAAs typically managed?


screen >65M who smoke


  • stop smoking!
  • ASA/statin
  • repair if >5.5cm, rapidly enlarging (>0.5cm in 6 mo), or if the AAA is associated w/ PAD or aneurysm


Patient underwent CABG two days ago and has developed edema, ascites, and evidence of hepatic congestion. What is the diagnosis?

What would you see on EKG? CXR?

constrictive pericarditis - due to continued pericardial inflammation resulting in a thickened, fibrous pericardium. 

EKG: non-specific vs low-voltage QRS complexes

CXR: calcified cardiac borders


XR findings of lung nodules favoring malignancy

>0.8 cm

interval changes/increase

irregular borders (spiculated or scalloped)

ground glass apperance

eccentric calcifications


CXR demonstrates a pulmonary nodule. What is the next step?

if previous XRs demonstrate SAME lesion - no further testing

if there is no prior imaging OR interval growth compared to prior XRs - get CT Chest

  • benign - serial CT
  • indeterminate - PET if >0.8 cm or serial CT if <0.8cm
  • suspicious - excision via video-assisted thoracoscopy


What is the annual screening protocol for lung cancer? 

screen patients annually with a low-dose CT Chest if they have a >30 PY + current smoker OR quit within last 15 years


Post-op hypoxemia has different diagnoses depending on the timing of when it occurs:



1-5 days

2-5 days

>5 days

  • Immediate - airway obstruction (often 2/2 endotracheal intubation or residual anesthesia)
  • Early - bronchospasm
  • 1-5 days - pneumonia
  • 2-5 days - atelectasis
  • >5 days - PE


COPD Hypoxemia

what causes it? 2

what happens when you supplement with O2?


  • VQ mismatch (areas of low VQ mismatch aka low airflow due to loss of elastic tissue, bronchiolar collapse, mucus plugging, bronchospasm)
  • poorly ventilated areas further undergo hypoxic vasoconstriction to improve gas exchange in areas that are well ventilated

effects of O2 supplementation

  • increaes ventilation -> increase perfusion (due to alleviation of the hypoxic vasocontriction) -> improved gas exchange


What is the utility of VQ scans in a patient w/ suspected PE?

VQ scan is not always diagnostic, it is LESS sensitive than helical CT or CTPA. Therefore a negative VQ scan does NOT rule out PE, esp in patients w/ high clinical suspicion of PE (OCP use, smoke)


Poor prognosticator in patients with PE

elevated troponins - presumably due to acute R heart overload 2/2 large PE


SIRS criteria (4)

When does it become sepsis?


HR >90

RR>20 OR PaCO<32mmHg

WBC >12K (or <4k w/ >10% bands)

Sepsis if there is a source of infection


Septic patient becomes hypotensive. What should you do? 3

IVF until CVP is 8-12mmHg

vasopressors if persistently hypotensive despite aggressive fluid resuscitation (i.e. MAP<65 after CVP raised to 8-12mmHg)

exogenous steroids if SBP <90 for >1 hour despite IVF and vasopressors


primary cause of hypophosphatemia

what are the effects of this?

continuous glucose infusions

impaired ATP generation resulting in 

- muscle weakness (may be difficult to wean from vent)

- decr. cardiac contractility resulting in cardiomyopathy

- decr 2,3-DPG, resulting in L shift of oxygen-hemoglobin dissociation (results in decr. O2 delivery to tissue)


When is an IVC filter indicate for PE?

indicated for patients for which anticoagulation is contraindicated (i.e. head bleed) or low cardiopulmonary reserve


common effect of hypocalcemia

prolonged QT


how can you tell if someone has a zinc deficiency?

if they've had recent diarrhea, diuresis, malnutrition, burns, chronic renal failure

usually p/w skin rash, infections


What is ARDs commonly due to?

How would you manage vent settings to reduce mortality rate?

pulmonary contusions 2/2 chest wall trauma, usually takes several hours for clinical/radiological signs to develop

low-tidal volume mechanical ventilation

limit plateau pressure <30mmHg


What is croup caused by?





causes larynx/trachea inflammation -> stridor, hoarse cough, hoarse voice. Can occur w/ agitation or activity.

diagnosis: XR steeple sign

treatment: steroids +/- epi for moderate/severe croup


patients recently extubated experiences stridor and respiratory failure. What should you do?

reintubate and mechanical ventilation


What kind of vent setting is preferred for ARDS?

What is the PaO2 goal? O2 saturation goal? How are these two achieved?

LTVV - low tidal volume ventilation. Allows for permissive hypercapnia to maintain alveolar hypOventilation and prevents vent-associated lung injury

PaO2 goal: 55-80mmHg

O2 sat goal: 88-85%

achieve goals by adjusting FiO2 and PEEP


multiple/recurrent episodes of bacterial pneumonia in a particular lung lobe in a male smoker - why would this happen?

how would you confirm the diagnosis?

likely 2/2 partial obstruction of the bronchus or branch of the bronchus supplying a particular lobe aka endobronchial obstruction (bronchogenic carcinoma if elderly, carcinoid tumor in young non smoker)

results in inability to clear secretions, resulting in stasis and recurrent pneumonias

confirm diagnosis w/ flexible bronchoscopy


Single most important factor in determining prognosis in patients w/ COPD

FEV1 (and age)


Management of acute asthma exacerbations

How do you determine if someone needs hospitalization?

short acting bronchodilators (albuterol)

add PO steroids if symptoms persist

hospitalize if patient has hypoxemia, difficulty speaking, use of accessory muscles, reduced peak expiratory flow >50% from baseline


Patient has asthma-like symptoms at the beginning of her exercise sessions. Next step in management?


bronchoprovocation test - a fall in FEV1 >10% is positive, >15% is diagnostic.

short acting ß2 agonist (SABA before exercise)


Lung Ca CXR findings

Large cell carcinoma
Squamous cell carcinoma


nodular thickening of pleura
cavitary lesion in a bronchus
large peripheral mass
pulmonary fibrosis

Asbestosis - pulmonary fibrosis 
Mesothelioma - nodular thickening of pleura
Large cell carcinoma - large perihilar mass
Squamous cell carcinoma - cavitary lesion in a bronchus


Lung Ca hormonal effects

Small cell
Sqamous cell



Small cell - hyponatremia 2/2 SIADH
Sqamous cell - hypercalcemia 2/2 PTHrp production


how does peak expiratory flow differ in severe vs moderate asthma exacerbation?

what medication should you start patients on if they present w/ severe vs moderate asthma exacerbation?

What if the patient continues to deteriorate despite initial therapies?

(remember peak expiratory flow = FEV1)

severe <40% of baseline = start short acting ß agonist (SABA)

moderate 40-69% of baseline = start SABA + ipratroprium

if p/w s/sx of impending respiratory failure/status asthmaticus --> intubate immediately to secure airways


Asthmatics can develop hypersensitivity reaction to this particular mold

What kinds of findings would clue you into this?

How do you diagnose this?


Aspergillus (Allergic bronchopulmonary aspergillosis, ABPA)


history of asthma
peripheral blood eosinophilia >500/mm3
lung infiltrates in upper lobes
serum IgE >1000ng/mL
precipitating serum antibodies to Aspergillus fumigatus

diagnosis: skin prick test for molds/Aspergillus. If POS, get a serum total IgE and precipitating serum antibodies

treatment: PO steroids


endotracheal rapid-sequence intubation (RSI) involves a two part sequence of medications. What are they?

sedative: etomidate, propofol, midazolam

paralytic agent: succinylcholine, rocuronium


Massive PE

signs and symptoms

ECG findings

ECHO findings

s/sx: hypoxia w/ clear CXR, hypotension, tachycardia

ECG: RBBB (sign of RV strain), atrial arrhythmia, inferior Q wave, ST changes

ECHO: increased RV size, decreased RV contractility, presence of RV thrombus, functional tricuspid regurgitation (2/2 dilation of tricuspid annulus)


patient being treated for TB develops a new pleural effusion.

next step?

do thoracentesis, which is diagnostic and therapeutic

effusions are usually an enhanced immunologic response and are usually exudates w/ lymphocytic predominance


most reliable method for verifying proper endotracheal tube placement

capnography (qualitative waveform or colormetric analysis) - non-invasive technique used to measure CO2 in exhaled breath


How does asthma differ from COPD in terms of:

FEV1/FVC ratio


  • pattern - obstructive
  • FEV1 - reduced
  • FEV1/FVC - reduced
  • DLCO - normal


  • pattern - obstructive
  • FEV1 - reduced
  • FEV1/FVC - reduced
  • DLCO - reduced


When is an IVC filter indicated?

complications of anticoagulation (substantial GI bleed)

contraindications to anticoagulation (head bleed)

failure of anticoagulation in the setting of a known DVT/PE


How is OSA differentiated from benign snoring?

presence of:

  • upper airway structural abnormalities
  • daytime hypersomnolence
  • nocturnal choking
  • gasping
  • apnea w/ oxygen desaturation
  • HTN


what are the two ventilator adjustments for improving oxygenation (i.e. PaO2)

what are the two ventilator settings used to regulate PCO2?

improving oxygenation: PEEP and FiO2

improving PCO2 levels: respiratory rate and tidal volume


How can you use ABG to tell if a patient has ARDS?

PaO2/FiO2 ratio < 200mmHg w/ PEEP of 5

compares oxygen level in the blood vs oxygen concentration that is breathed to determine if there is any problems with how the lungs tranfer oxygen to the blood


Are oral antibiotics indicated for acute bronchitis?

in an otherwise healthy individual, no, since most are of viral etiology

in COPD patients, antibiotics are indicated when there are ≥2 of the following features:

increased sputum purulence, sputum volume, or dyspnea , those requiring mechanical ventilation


metoclopramide can cause symptoms including deviation of head/eyes and involuntary tongue movements. How do you treat this?

acute dystonic reaction/extrapyramidal symptoms

tx: diphenhydramine IV (initial) or benztropine IV (if not respnosive)


main cause of M&M in patients w/ Marfan syndrome?

aortic root disease manifesting as aneurysmal dilation, aortic regurgitation, or dissection

should be routinely screened w/ TTE or CT chest to check for progressive aortic disease 


FDA established pregnancy risk categories A, B, C, D, X to define the level of fetal risk from medications used during pregnancy. What are they?

A = safe in pregnancy

B = likely safe in pregnancy

C = used if the potential benefit clearly outweighs fetal risk 

D = high risk but may be acceptable in some circumstances

X = unacceptable 


What 4 medications can potentiate the effects of digoxin and result in digoxin toxicity?