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ACNP Exam > Cardio/Pulm > Flashcards

Cardio/Pulm Flashcards

1
Q

Four primary things to look for on PFT and what they mean

A

FVC - the total amount of air that can be put out
FEV1 - How much air comes out in the first second
FEV1/FVC - amt of air expelled in the first second compared to total volume expelled
PEFR - peak flow (max airflow rate achieved)

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2
Q

What is required for the diagnosis of asthma? What is used for monitoring asthma?

A

Spirometry (PFT) used for diagnosis
Peak flow is used for monitoring

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3
Q

Asthma treatment

A
  • SABA - emergency relief, albuterol
  • ICS - controlling persistent asthma
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4
Q

Exercise-induced asthma management

A
  • SABA 15-30min prior to exercise
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5
Q

Asthma controller medications

A
  • ICS (fluticasone, mometasone, budesonide, beclomethasone, ciclesonide) – preferred controller treatment for persistent asthma. use daily for optimal effect
  • ICS/LABA - (budesonide + formoterol, fluticasone + salmeterol, mometasone + formoterol) – should only be used in pts who are not controlled by ICS alone
  • Leukotriene receptor antagonists or leukotriene modifiers (montelukast) — allergic rhinitis, often used with ICS
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6
Q

Stepwise process for asthma management

A

Step 1 - SABA
Step 2 (mild asthma) - low dose ICS
Step 3 (moderate asthma) - low dose ICS + LABA
Step 4 (severe asthma) - medium dose ICS + LABA

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7
Q

Severe asthma exacerbation management

A

ED treatment
SABA + systemic corticosteroids

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8
Q

Warning signs of impending respiratory arrest

A

drowsiness or confusion
paradoxical throacoabdominal movement
absence of wheezing
bradycardia
absence of pulsus paradoxes
initial PEF or FEV1 < 25% of personal best/predicted value

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9
Q

What should you get for every asthma exacerbation

A

peak flow

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10
Q

Clinical findings for emphysema

A

increased AP diameter, hyper resonance (air trapping)

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11
Q

Clinical findings chronic bronchitis

A

normal AP diameter, normal percussion (resonance), increased Hct, copious blood tinged mucus

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12
Q

What is the electrolyte triad found in emphysema and chronic bronchitis

A

hypokalemia, hypochloremia, increased NaHCO3

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13
Q

COPD management

A

SABA (albuterol), LAMA (tiotropium), or LABA (salmeterol)

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14
Q

COPD exacerbation treatment

A

O2, bronchodilators (SABA), prednisone
Antibiotics (if increased dyspnea, incr sputum, incr sputum purulence)
NIV (BiPAP)

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15
Q

TB diagnosis and treatment

A

Latent TB - no symptoms
TB disease - significant cough > 3 weeks, chest pain, hemoptysis or sputum production, weakness/fatigue, weight loss, lack of appetite, chills, fever, night sweats
CXR - cavitary lesion
Treatment - isoniazid (INH), rifampin, ethambutol, pyrazinamide (RIPE)

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16
Q

Diseases caused by S. pneumoniae

A

COMPS
conjunctivitis
otitis media
meningits
pneumonia
sinusitis

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17
Q

Diseases caused by H. influenzae

A

COMPS
conjunctivitis
otitis media
meningitis
pneumonia
sinusitis

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18
Q

CAP treatment in persons with no significant comorbidities

A

doxycycline
azithromycin
amoxicillin

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19
Q

Broad spectrum treatment for HAP

A

Vancomycin or linezolid
+
Pipercillin tazobactam (Zosyn)
Cefepime
Levofloxacin
Imipenem
Amikacin

** Vancomycin + Pipercillin-tazobactam

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20
Q

VAP initial empiric treatment

A

3 antibiotics
Vancomycin or linezolid +
Pipericllin-tazobactam (Zosyn)
Cefepime
ceftazadime
imipenem
meropenem
aztreonam +
Levofloxacin
ciprofloxacin
Amikacin
Gentamicin
Polymyxin

** Vancomycin + Pipercillin-tazobactam + Levofloxacin

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21
Q

Etiology/Pathology of pneumothorax

A
  • Traumatic injury
  • Spontaneous - COPD, asthma, tall, thin males, marijuana smoking
  • air trapping and increased pressure can cause a medistinal shift –> compress the great vessels and heart (tension pneumothorax)
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22
Q

S/s of pneumothorax

A

acute onset of SOB
tachypnea
pleuritic chest pain

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23
Q

Pneumothorax physical exam findings

A
  • hyper resonance to percussion
  • absent breath sounds on injured side
  • hypotension
  • distended neck veins (late sign)
  • tracheal deviation
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24
Q

Pneumothorax diagnostic study of choice

A

CXR - air in pleural space with absent lung markings

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25
Q

Pneumothorax treatment

A
  • needle decompression - first line therapy
  • chest tube for patients with symptoms or >2cm
  • tension pneumothorax - emergent needle decompression with 14G or 16G IV in the 2nd ICS MCL followed by chest tube placement
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26
Q

ARDS etiology and pathophysiology

A

inflammatory lung condition c/b direct or indirect injury to the lungs

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27
Q

Diagnostic and inclusion criteria for ARDS

A
  • bilateral diffuse infiltrates c/b non-cardiogenic pulmonary edema/pulm capillary leak
  • PAWP/PCWP < 19 mmHg (no evidence of L arterial HTN)
  • PaO2/FiO2 < 200
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28
Q

Goals of ventilation for ARDS

A
  • treat the underlying cause, support oxygenation, CO, ventilation
  • optimize lung recovery to prevent lung injury
  • PEEP = 5, PaO2 55-80, plateau pressure <30
  • check plateau pressure q4h, if > 30 decr VT by 1mL/kg, if < 25 increase VT by 1mL/kg
  • pH goal 7.3-7.45 - if pH is low increase RR, if pH is high decrease RR
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29
Q

Hemothorax etiology & pathophysiology

A
  • blood accumulation in pleural space caused by some form of traumatic injury (usually) or injury to adjacent structures
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30
Q

S/s of hemothorax

A

dyspnea, tachypnea, pleuritic chest pain

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31
Q

physical exam findings for hemothorax

A

dullness to percussion (fluid accumulation)
decreased breath sounds on injured side
signs of hypovolemic shock

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32
Q

hemothorax diagnostic study of choice

A

CXR - blood in pleural space (white out)

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33
Q

Treatment for hemothorax

A

chest tube placement, autotransfusion, open thoracotomy in the presence of uncontrolled bleeding

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34
Q

Pulmonary embolism etiology/pathophysiology

A

thrombus in the arterial system of the lung preventing effective perfusion (not a ventilation problem)
most commonly d/t DVT, also seen in oncologic patients

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35
Q

signs/symptoms of pulmonary embolism

A

dyspnea, pleuritic chest pain, cough, hemoptysis

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36
Q

physical exam findings for pulmonary embolism

A

tachycardia + tachypnea
rales and S4 heart sound

37
Q

pulmonary embolism diagnostic study of choice

A

CTA ***
D-dimer has high sensitivity, poor specificity

38
Q

Treatment for pulmonary embolism

A

** anticoagulation - unfractionated LMWH, Warfarin (INR 2-3), rivaroxaban 15mg bid 3 weeks then 20mg daily
IVC filter (if anticoagulation is contraindicated), thrombectomy (large PE), or thrombolysis (TPA) (PE with shock or massive PE with a high risk of shock)

39
Q

Describe the characteristics of a transudative pleural effusion

A

Transudative (water)
often c/b CHF, constrictive pericarditis, cirrhosis
SG < 1, protein < 3, LDH < 200

40
Q

Describe the characteristics of an exudative pleural effusion

A

exudative (cellular material)
often c/b lung parenchymal infection, malignancy, pulmonary embolism
SG > 1, protein > 3, LDH > 200

41
Q

Treatment for pleural effusion

A

if known to be from fluid overload (CHF or cirrhosis) –> diuresis
Symptomatic effusions - thoracentesis
infections effusions -antibiotic therapy, if 1/2 the hemithorax or empyema is present then place a tube thoracostomy

42
Q

Equation for BP

A

BP = HR x SV x PVR
if you increase any part of this equation you increase BP and vice versa

43
Q

What is the primary concern with HTN and what types of things are we looking for

A

Target organ damage
Brain - stroke, vascular (multi-infarct) dementia
CV - atherosclerosis, MI, LVH, HF
Kidney - hypertensive nephropathy, renal failure
Eye - hypertensive retinopathy

44
Q

Lifestyle modifications for HTN and dislipidemia - what is most effective

A

weight reduction (most effective)
DASH diet, Na+ restriction, physical activity, alcohol moderation

45
Q

Three primary medications used for HTN

A

diuretics (thiazide)
ACE/ARBS
CCB

46
Q

Thiazide diuretics adverse effects

A

Na+, K+, Mg++ depleting
Less effective with GFR < 30 (loop diuretics are helpful with lower GFR, but not for BP)

47
Q

ACE inhibitors (-pril suffix) adverse effects
ARBS (-sartan suffix)

A

risk of hyperkalemia, renal impairment when used with aldosterone antagonist, cough, angioedema

Priority medication for HTN control in individuals with DM

DO NOT USE DURING PREGNANCY

48
Q

CCB (-ipine suffix) adverse effects

A

ankle edema

AVOID USE IN HF, RENAL, OR HEPATIC IMPAIRMENT

49
Q

Aldosterone antagonist adverse effects

A

gynecomastia with prolonged use (in men) risk for hyperkalemia

50
Q

Hypertensive urgency characteristics

A

HTN with minimal or no acute target organ damage
SBP > 180 DBP > 120

51
Q

Hypertensive emergency characteristics

A

HTN with acute target organ ischemia and damage
Neuro - encephalopathy, stroke, papilledema
CV - ACS, HF, pulmonary edema, aortic dissection
Renal - proteinuria, hematuria, acute renal failure

52
Q

When treating hypertensive emergency what factors should you be monitoring

A

urine output (decreased), Cr (increased), or mental status (decrease) – this may be an indication that lower BP cannot be tolerated

53
Q

Therapy for hypertensive urgency

A

lower BP over a few hours with oral agents
goal is to return BP in outpatient setting over days/weeks/months

54
Q

Therapy for hypertensive emergency

A

decrease MAP by approx 25% within minutes-2hrs with IV agents.
consider a-line
Goal is DBP < 110 within 2-6hrs

55
Q

Common pharmacologic agents for hypertensive emergency

A

nitroprusside
labetalol
nicardipine
nitroglycerin
esmolol
hydralazine

56
Q

Patho/etiology for CAD

A

result of endothelial damage
elevated LDL, endothelial dysfunction, vascular inflammation

57
Q

Differentiate angina from MI

A
  • change from typical anginal pattern, associated symptoms
  • regional abnormality on ECG
  • troponin changes
58
Q

Stable angina s/s, diagnostic findings, treatment

A

symptoms occur with activity & relieved with rest or nitrate
diagnostic findings no cardiac enzyme elevation
treatment - prophylactic therapy – lower lipids, nitrates, ASA, lifestyle modification

59
Q

unstable angina s/s, diagnostics, and treatment

A

symptoms occur with activity and/or at rest and not easily relieved with rest or nitrates
no cardiac enzyme elevation may have signs of ischemia on ECG (ST depressions) during a symptomatic episode
treatment - nitrates, BB, ACE/ARB, morphine, ASA, ADP blocker (clopidogrel), heparin (if admitted)

60
Q

NSTEMI s/s, diagnostics, and treatment

A

symptoms occur with activity and at rest
cardiac enzymes are elevated, signs of ischemia on ECG (ST depressions)
treatment - nitrates, BB, ACE/ARB, morphine, ASA, ADP blocker (clopidogrel), heparin (if admitted)

61
Q

STEMI s/s, diagnostics, and treatment

A

symptoms usually occur at rest and not relieved with rest, may improve with high doses of nitrates
cardiac enzymes are elevated, ST elevation on ECG
treatment - ASA 325mg, SL nitrates, antiplatelet agents, heparin, cardiac cath/PCI, fibrinolysis if PCI is delayed

62
Q

absolute contraindications for fibrinolysis

A

hx of cerebrovascular event
non-hemorrhagic stroke or head trauma < 3mo ago
cranial or spinal trauma < 2mo
known bleeding diathesis
active internal bleeding

63
Q

guidelines of initiation of fibrinolysis

A

delayed PCI
goal (if presenting to PCI facility) door to balloon < 90min
goal (if presenting to non-PCI facility) door to balloon 120min
if fibrinolysis therapy is chosen, goal is < 30min of hospital presentation

64
Q

ACS post hospital care

A

ABCDE
A ASA, anticoagulants, ACE/ARBs, aldosterone antagonist
B beta blockers, BP control
C cholesterol control, cigarettes (smoking cessation)
D diet, DM control
E education, exercise

65
Q

Anterior & septal leads + coronary artery associated

A

V1, V2, V3, V4
LAD

66
Q

Lateral leads + coronary artery associated

A

I aVL V5 V6
left circumflex

67
Q

Inferior leads

A

II, III, aVF
RCA or Left circumflex

68
Q

Treatment for congestion c/b heart failure

A

LMNOP
L - lasix (furosemide), monitor urine output
M - morphine
N - nitrates (vasodilation)
O - oxygen (consider BiPAP)
P - position (upright with legs over bed)

69
Q

Treatment for poor perfusion c/b HF

A

IV vasodilators - nitroglycerin, nitroprusside, nesiritide
inotopic agents - dobutamine, milrinone
ultrafiltration
mechancial circulatory support (IABP, LVAD, RVAD)
cardiac transplant

70
Q

What are the type types of infectious cardiac disease

A

endocarditis and pericarditis

71
Q

Pericarditis

A

inflammation of the pericardium
usually d/t viral infection
c/b non-radiating pain, sharp, stabbing, knife-like chest pain over PMI
friction rub (maybe)
ECG - global concave ST elevations
pain relieved by position change
symptomatic treatment with NSAIDS

72
Q

Endocarditis

A

infection of the endocardium
c/b bacteria** and fungi
high risk in patients with valvular disease & increased risk of pathogen introduction (IV drug users)
changing cardiac murmur
PE - acutely septic patient
Oslers nodes, janeway lesions, splinter hemorrhages
treatment - vancomycin

73
Q

Three cardinal signs for cardiac tamponade

A

elevated jugular venous pressure, distant heart sounds, hypotension
(compression of cardiac chambers dye to increased pericardial pressure)

74
Q

What drug is used to reverse BB OD

A

glucagon

75
Q

Clinical presentation of ACS in the elderly (>75yo)

A

dyspnea
neuro symptoms - syncope, weakness, and acute confusion
chest pain or pressure < 50%

76
Q

point of maximum impulse - what is it, the normal location

A

a palpable sensation of the underlying left ventricle

5th ICS, MCL

size of the impulse is about a nickle, gentle tab by one finger, timing is about 1/3 of systole

77
Q

Displaced PMI - what does it mean

A
  • PMI is usually displaced laterally - indicates increased LV volume
    usually forceful – pressure overload or HTN
78
Q

Things to consider if you are unable to palpate the PMI

A

left lateral decubitus position enhancement, or consider other conditions – thick chest wall, obesity or COPD

79
Q

S1 - significance, heard best

A

marks the beginning of systole (pumping) c/b closure of the mitral and tricuspid valves

best heard at the apex wit the diaphragm

it is the “lub” of lub dub

heard simultaneously as the carotid upstroke

80
Q

S2 - significance, heard best

A

marks the END of systole - produced by closure of the aortic and pulmonic valves

heard best at the base with the diaphragm

it is the “dub” of lub dub

81
Q

physiologic split S2 - significance and heard best

A

fixed spit, no change with inspiration – often found in uncorrected septal defect

paradoxical split - narrows or closes with inspiration – found it conditions that delay aortic closure (LBBB)

best heard in the pulmonic region

82
Q

pathologic S3 - significance and heard best

A

marker of ventricular overload and/or systolic dysfunction

heard best in early diastole “hooked” on the back end of S2 - low pitched, heard best with bell

S3 can be correlated with HF but associate it with other findings such as dyspnea, tachycardia, crackles

Lub-Dub-dub

83
Q

S4 - significance, and heard best

A

Marker of poor diastolic function - often found in poorly controlled HTN or recurrent myocardial ischemia

heard in LATE diastole, “hooked” onto the front of S1

S4-S1-S2

84
Q

Different pathology between systolic and diastolic cardiac murmurs

A

Systolic - benign or pathologic
Diastolic - always pathologic

85
Q

pneumonic for systolic murmurs

A

MR PASS wins the MVP award
Mitral Regurgitation
Physiologic (innocent, functional)
Aortic Stenosis
systolic
Mitral Valve Prolapse

86
Q

pneumonic for diastolic murmurs

A

MS. ARD
Mitral Stenosis
Aortic Regurgitation
Diastolic

87
Q

systolic murmur is likely benign if

A

negative hx
lower grade (<III/VI)
no radiation
S1 and S2 are intact
no heave or thrills
PMI WNL
softens or disappears with supine to stand position change

88
Q

Systolic murmur is likely pathologic if, what is the next step

A

abnormal hx
higher grade (IV/VI)
radiates to neck, axilla, or other locations
S1 and S2 are obliterated
+ thrill or heave
PMI is displaced
increase in intensity with supine to standing

89
Q

difference between a radiating murmur and a carotid bruit

A

bruit - softer, unilateral, different sound than that in the chest

radiating murmur - louder, bilateral, same sound and timing as in the chest

ACNP Exam (6 decks)

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