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ACNP Certification > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Blood Flow through the Heart

A
  1. Superior Vena Cava
  2. Right Atrium
  3. Tricuspid Valve
  4. RV
  5. Pulmonic Vavle
  6. Pulmonary Artery
  7. Lungs
  8. Pulmonary Veins
  9. Left Atrium
  10. Mitral Valve
  11. LV
  12. Aortic Valve
  13. Aorta
  14. Body
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2
Q

Heart Sound and Anatomical Locations

A

S1 = Mitral/Tricuspid (AV) valve closure

S2 = Aortic/Pulmonic (Semilunar) Valve closure

Systole = Period between S1-S2

Diastole = Period between S2-S1

S3 Ken-Tuck-Y, increased fluid states (CHF, pregnancy)

*Leading abnormal heart sound in CHF

S4 Ten-Ne_SSee, stiff ventricular wall (MI, LVH, Chronic HTN)

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3
Q

Valvular Dz

A

Mitral Stenosis: Loud S1 murmur, mid-diastolic, apical crescendo

Mitral Regurg: S3 with systolic murmur at 5th ICS MCL (apex), may radiate to base or left axilla, musical, blowing or high pitched

Aortic Stenosis: Systolic, blowing, rough, harsh murmur at 2nd ICS, *usually radiates to neck*

Aortic Regurgitation: Diastolic, blowing murmur at 2nd left ICS

Mitral

Regurg

Pulmonic Mr. Pass

Aortic

Stenosis

Systolic Murmurs

When? Beginning is Systolic, end is diastolic

Where? Mid-chest, 5th ICS = Mitral

Upper Chest= Aortic

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4
Q

Murmur Grades

A

I: Barely audible

II: Audible but faint

III: Moderately loud, easily heard, No thrill

IV: Loud, associated with + thrill

V: Very loud, heard with one corner of stethescope off chest

VI: Loudest, from the doorway

*III=no thrill, IV=thrill

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5
Q

Heart Failure Types

A

Cardiac Output is insufficent to meet metabolic needs of body

Types:

Systolic: Inability to contract reuslts in decreased CO

-(inotrope, dig)

Diastolic: Inability to relax and fill results in decreased CO

-(Dilator to help relax)

Acute- (L) abrupt onset usually follows MI or valve rupture

Chronic (R) develops as result of inadequate compensatory mechanisms over time to improve cardiac output

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6
Q

Cardiac Definitions

A

Preload: Filling pressure of the heart at the end of diastole

Afterload: Pressure against which the heart must work to eject blood during systole

Contractility: Strength and vigor of heart’s contraction during systole

Cardiac Index: Volume of blood pumped by the heart based on BSA per minute (L/min)

  • Greater the preload, the greater will be the volume of blood in the heart at the end of diastole*
  • Lower the afterload, the more blood the heart will eject with each contraction*
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7
Q

NYHA Functional Classification of HF

A

I: No limitations

II Slight limitation with physical activity but comfortable at rest

III: Marked limitation of physical activity but comfortable at rest

IV: Severe, inability to carry out any physical activity without symptoms, symptoms noted at rest

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8
Q

Left Heart Failure (Acute)

A
  • Dyspnea at rest
  • Coarse rales all lung fields
  • Wheezing, frothy cough
  • Appears generally healthy except with acute exacerbation
  • S3 gallop
  • Mitral regurg murmur (systolic, loudest at apex)

*Left failure =Lung

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9
Q

Right Heart Failure (Chronic)

A
  1. JVD
  2. Hepatosplenomegaly
  3. Dependent peripheral edema, result of increased capillary hydrostatic pressure
  • PND
  • Chronically ill appearance
  • Diffuse chest wall heave
  • Displaced PMI
  • Abdominal fullness
  • Fatigue on exertion
  • S3 and/or S4
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10
Q

HF Diagnostics

A
  • BMP
  • BNP
  • U/A
  • CXR: Pulm edema, Kerley’s lines (squiggly lines suggest pulm edema), effusions
  • Echo: Contraction/relaxation, valvular function, EF
  • ECG: may show underlying problem, acute MI, dysrthymia
  • PFT’s for wheezing during exercise
  • ABG: may show hypoxemia or hypocapnia
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11
Q

HF Management Out-Patient

A

Non-Pharm

  • Sodium restriction (leading reason for decompensation is failure to comply with this!)
  • Rest/activity balance
  • Weight reduction
  • others

Pharm:

  • ACE inhibitor: pril
  • Diuretics: Thiazide, loop
  • Anticoagulation for AF
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12
Q

In-Patient Management of Acute Pulmonary Edema

A
  1. O2 while awating ABG’s
  2. Sitting or semi-Fowler position
  3. Morphine 2-4mg IVP, MR 20-30 min PRN, stop if hypercapnea occurs
  4. Furosemide 40mg IVP, MR in 10 min if no response
  5. If severe bronchospasm occurs, inhaled simpathomimetics (albuterol, terbutaline)
  6. If severe, afterload and preload reduction with nitroprusside, dyfralazine or others
  7. If CI remains low, dobutamine 2.5-20 mcg/kg/min (helps pump with increased CO, BP, HR, improves blood flow, decreases peripheral vascular resistance)
  • If SBP <100, Dopamine 5-20mcg/kg/min
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13
Q

HTN

A

Sustained elevation of SBP >140 or DBP > 90 at least 3 times on two different occasions

2 Types:

  • Primary/Essential: 95% of all cases, onset <55 years of age
  • Secondary: 5% of all cases, secondary to other known causes such as estrogen use, renal dz, pregnancy, endocrine disorders, * renal artery stenosis* (leading cause of secondary)

Exacerbating factors:

  • Smoking, obesity, excessive alcohol intake, use of NSAIDS, others
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14
Q

HTN Signs/Symptoms

A
  • Often silent killer
  • Elevated BP
  • Severe HTN*sub-occipital pulsating HA, early in morning and resolving throught the day*
  • *Epistaxis* in adult of no known reason
  • Dizziness/Lightheadedness
  • *S4 r/t hypertrophy
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15
Q

HTN Diagnostics

A
  • In uncomplicated HTN, labs usually WNL

Diagnostics to r/o:

  • Renal Vascular Dz
  • CXR if cardiomegaly suspected
  • Plasma aldosterone level to r/o aldosteronism
  • AM/PM cortisol level to r/o Cushings

U/A, CBC, BMP, Ca+, phos, uric acid, cholesterol, trigylcerides

ECG

PA and Lat CXR

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16
Q

JNC 7 Classifications

A

Normal <120 AND <80

Pre-HTN 120-139 OR 80-89

Stage I 140-159 OR 90-99

Stage II >160 OR >100

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17
Q

JNC 7 HTN Management- Non-Pharm

A

Life style changes:

Wight reduction

low sodium diet

avoid/reduce alcohol intake

relaxation/stress management

Exercise 30 min/day, most days week

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18
Q

JNC 7 HTN Management- Pharm

A

Stage I (SBP 140-159 or DBP 90-99)

  • Without compelling indications: thiazide diuretic, consider ACE/ARB, BB, CCB

Stage II (SBP >160 or DBP > 100)

  • 2 drug combination: thaizide type AND ACE or ARB, or CCB, or BB

With compelling indications:

  • HF: thiazide, BB, ACE, ARB, Aldosterone antagonist (spironolactone, elpirinone)
  • Post MI: BB, ACE, Aldosterone antagonist
  • High CVD risk: Thiazide, BB, ACE, CCB
  • CKD: ACE, ARB
  • Recurrent stroke prevention: Thiazide, ACE

*Goal=SBP<130/80 for pt’s with DM or CKD

*

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19
Q

Other HTN Pharm Considerations

A

Beta Bockers: effective for migraines and angina, in combination iwth diuretics, monitor for wheezing

  • (metoprolol, propranolol, atenolol, nadolol (corgard), acebutolol (sectral)

CCB: Effective for Caucasians, not 1st line, monotherapy if BB contraindicated, effective for AF, ATach, migraine or DM

  • Dilt, verapamil (calan), amlodipine (Norvasc), nicardipine (Cardene), felodipine(plendil)

Diuretics: Effective for AA, elderly with isolated HTN, CHF (Lasix)

ACE “Pril”: Caucasians <65, **durg of choice in DM**, watch for cough and bronchospasm (in HF switch to ARB)

  • Captopril (Capoten), enalapril (Vasotec), benazepril (Lotensin), ramipril (Altace)
    1. Adrenergic Inhibitors (Central/eripheral, alpha blocker)
  • No standard of care for these, use as adjunct therapy
  • Clonidine (catapress), methyldopa (aldomet), guanethidine (Ismelin), guanadrel (hylorel), prazosin (mini-press), doxazosin (cardura), labetalol (Normodyne/Trandate), carvedilol (coreg)

ARB: well tolerated

  • Used for HTN, HFm preventing kidney damage in pts with DM or HTN
  • Most serious SE’s are: kidney failure, liver failure, allergic reactions, angioedema, decreased WBC
  • Common SE’s cough, hyperkalemia, low BP, dizziness, HA, drowsiness, diarrhea, abnormal taste, rash
  • Candesartan (Atacand), eprosarta (Teveten), irbesartan (Avapro), telmisartan (Micardis), valsartan (Diovan), losartan (Cozaar)

*Use as few meds as needed at lowest dose to get to desired goal*

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20
Q

JNC 8 Tx Threshholds

A

No classifications

Tx Threshholds

  • Do not tx adult <60 until reach 140 OR 90, then tx to <140AND 90
  • Tx adults >60 once >150 AND/OR 90, tx to <150 and 90
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21
Q

JNC 8 Important Recs

A
  • CKD in Non-AA, thiazide type diuretic, CCB, ACE or ARB
  • In AA= thiazide diuretic CCB, Grade B
  • Tx goal: return in one month F/U, then increase drug or add drug
  • Do NOT use ACE and ARB together
  • Refer to specialist if 3 or more drugs are needed

Lifestyle changes:

  • Restrict sodium, DASH diet, weight loss
  • Increase to 40 min exercise most days
  • Stress management planning
  • Reduce or eliminate alcohol <2 drinks for men, < 1 for women daily
  • Smoking cessation
  • Watch lytes: K, Mag, Ca+
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22
Q

JNC 8 Common Pharm

A

Thiazide type diuretic-*1st line*

ACE “pril” cause vasodilation, block sodium water retention, watch for cough

ARB “sartan” - reserved for those with ACE intolerance

BB

CCB

Aldosterone antagonists/Central blockers/Alpha antagonists

Special considerations

*neither age nor gender affects agent responsiveness

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23
Q

HTN Urgency

A

SBP>180 or DBP >110 without target organ damage

Require BP reduction within hours to days

MAy be associated with HA, epistaxis, anxiety

  • Upper level stage 2 HTN
  • HTN with disc edema
  • Progressive target organ complications
  • Severe peri-operative HTN

Management

  • Oral therapy such as clonidine, captopril, nifedipine, loop diuretics
  • Rarely needs parenteral tx (don’t overtx pt)
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24
Q

HTN Emergency

A

Rare situations that require immediate (w/in 1 hr) BP reduction to prevent or limit end organ damage

Generally SBP> 180/ DBP >120 with target organ dysfunction

*Initial tx goal to reduce MAP by no more than 25% w/in 2 hrs*

  • **Malignant HTN: fundoscopic changes include flame shaped retinal hemorrhage, soft exudates and **papilledema (swelling of optic disc with blurred margins)
  • HTN encephalopathy
  • Intracranial hemorrhage
  • Unstable angine
  • Acute MI
  • Acute LV failure with pulmonary edema
  • Dissecting aortic aneurysm
  • Ecclampsia

Management:

  • If requiring IV agents, critical care bed, invasive arterial pressure monitoring
  • Sodium nitroprusside (Nipride) is a potent vasodilator, *drug of choice*, IV at .25 to 10 mcg/kg/min

**AVOID rapid, severe drops in BP as cerebral infarction may occur**

Pressure should be lowered acutely to SBP 160-180 range then gradually with oral therapy over a period of days!

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25
Q

Angina

A

Decreased blood flow thru vessel=>ischemia

Types:

  1. Stable: (classic or chronic) Exertional-nost common
  2. Prinzmetal’s: Occurs at various times, including rest (coronary vasospams=>influx of Ca+, tx with CCB)
  3. Unstable (pre-infarction, rest or crescendo, coronary syndromes)
  4. Microvascular (Metabolic syndrome)
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26
Q

Angina Signs/symptoms

A
  • Chest discomfort lasting several minutes
  • Exertional precipitated by activity, subsides with rest
  • NTG shortens or prevents attacks

Exam findings:

  • Signs of peripheral areterial dz
  • Levine’s sign=Clenched fist (squeeze vs elephant sitting/MI)
  • Transient S4 not uncommon during angina
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27
Q

Angina Diagnostics

A
  1. ECG may be normal with down sloping of ST segment or T wave peak or inversion during attack
  2. Exercise ECG
  3. Serum lipids-biggest contributor to cardiac dz
  4. Coronary angio *definitive diagnostic procedure but not indicated solely for diagnosis
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28
Q

Total cholesterol target

A

<200

29
Q

Triglycerides Target

A

<150

30
Q

HDL Target

A

>40 Male

>50 Female

31
Q

LDL Target Healthy persons

A

<100 mg/dL

32
Q

LDL Target for Pt’s with Cardiac Dz OR DM

A

<70

33
Q

ASCVD risk

A

Pooled cohort equation for 10 yr risk

Age

sex

race

t chol

HDL chol

SBP

DM

Smkg

34
Q

Angina Management

A
  1. Reduction of risk factors
  2. Manage diet
  3. Lower LDL
  4. Low dose ASA
  5. Common pharmacotherapy: Nitrates, BB, CCB
  6. Common pharmacotherapy for hypercholesterolemia: Statins, Niacin, Fibrates (gemfibrozil/Lopid)
35
Q

MI

A

Contributes to leading cause of death in adults in US

“clot on plaque”

  • Only 1/3 pts give hx of typical anginal pain
  • Most MI’s occure at REST: pain is similar to angina but more severe
  • NTG has little effect
36
Q

MI Signs/Symptoms

A
  1. Cold sweats
  2. Syncope
  3. Impending doom
  4. Apprehension
  5. Light-headedness
  6. Dyspnea
  7. Cough
  8. N/V
37
Q

MI Exam Findings

A
  1. Dysrhythmias
  2. S4 very common
  3. Wheezing
  4. Pulmonary crackles
  5. Low grade fever 1st 48 hrs
  6. Tachycardia
38
Q

MI Diagnostics

A

ECG changes -almost 30% have no initial changes

  • Peaked T waves, ST elevation, Q wave development (may not have Q waves in 30-50% MI’s)
  • I,AVL, V5, V6- Left lateral wall
  • II,III, AVF- Inferior wall
  • V2-V4 Anterior wall
  • AVR, V1-Right

Cardiac enzyme elevation above normal w/in 4-6hrs (trop-t, trop-I, CKMB), remain high 3 days to 3 weeks

Echo for wall motion, EF assessment

Leukocytosis 10-20 on 2nd day

39
Q

MI Management

A

**Door to fibrinolytics-30 min, Door to cath lab-90 min**

  1. ASA 325 mg chew and swallow (decrease plt aggregation)
  2. NTG CL
  3. O2 therapy
  4. IV KVO- 3 PIV’s total
  5. 12 lead ECG and tele monitor
  6. Morphine 2-4mg IVP
  7. Furosemide for pulm edema 40mg IVP
  8. if no contraindication: metoprolol 5 mg IV x 3 doses at 2 min intervals, then 50 mg orally Q6 hrs starting 15 min after last IV dose
  9. ACE most beneficial when pts have failure or large infarction, otherwise should only be considered after fibrinolytics, ASA, BB and nitrates
  10. Heparin vs LMH (lovenox 1mg/kg)
  11. Monitor therapeutic coag values
40
Q

Normal Coag Values

A

INR 0.8-1.2

ACT 70-120

aPTT 28-38 sec

PT 11-16 sec

pTT 60-90 sec

41
Q

Therapeutic Coags

A

INR in MI: 2.5-3.5 x normal

INR Coumadin 2-3

ACT 150-190 or >300 sec post PTCA/Stent

aPTT, PT, pTT all 1.5-2.5 x normal

42
Q

Indications for Pharm Revascularization

A
  1. Unrelieved chest pain >30 min and <6 hrs WITH:
  2. ST segment elevation >0.1 mV in 2 or more contiguous leads

Absolute contraindications: Active bleeding or risk thereof, including abnormal coag values (check plts as well- 150-400 normal)

43
Q

Venous Thrombosis

A

Partial of complete occlusion of a vein by thrombus with secondary inflammation to wall of vessel, may be superficial or deep

Causes:

  • Immobility
  • Female
  • Post-op
  • Prolonged BR
  • Oral contraceptives, esp smokers
  • Hypercoagulability
44
Q

Superficial Thrombosis

A

Sudden onset pain

Localized heat/erythema

Low grade temp

No labs needed

Management:

  • Elevation
  • Warm compress
  • NSAIDS
  • D/C oral contraceptives
45
Q

DVT

A

Suden onset pain

Painor tenderness while walking

May present as dull ache or tightness

Physical exam:

  • Edema distal to occlusion
  • low grade temp
  • Skin cool to touch

Management:

  • BR with elevated extremity until tenderness subsides 7-14 days
  • Walking gradually reintroduced
  • Lovenox 1mg/kg Q 12 h OR
  • Heparin infusion for 7-10 days
  • Coumadin x 12 weeks
  • Consultation when anti-coag therapy instituted
46
Q

PVD

A

Atherosclerotic narrowing of lumen of arteries resulting indecreased blood supply to the extremities

Causes:

  • Atherosclerosis
  • similar risk factors as CAD
  • Peak incidence 40-70 yrs
  • Hyperlipidemia
  • smkg
  • DM
47
Q

PVD Sign/Symptoms

A

Calf pain (claudication)

Cold/numbe extremities

Pain at rest

48
Q

PVD Exam Findings

A
  • Shiny/hairless skin
  • dependent rubor
  • Pallor when feet elevated
  • Cyanosis
  • Ulcerations
  • Reduced pulses
49
Q

PVD Diagnositics

A
  • Doppler US
  • ABI (ankle-brachial index)
  • XR may show calcification
  • Arteriography: most definitive test
50
Q

PVD Management

A
  1. Stop smkg and all tobacco use
  2. Exercise (1hr per day, stopping during pain and resuming when pain stops to devlop collateral circulation)
  3. Pentoxifylline (Trental)
  4. Cilostazol (Pletal)
  5. Weight reduction as needed
  6. Manage DM and hyperlipidemia
  7. Angioplasty
  8. Bypass
  9. Amputation
51
Q

Chronic Venous Insufficiency (CVI)

A

Impaired venous return d/t either destruction of valves, changes d/t deep thrombophlebitis, leg trauma, or sustained elevation of venous pressure

  • More common in women than mes
  • Genetic predisposition
  • Hx of leg trauma, ?assoc with varicose veins
52
Q

CVI Signs/ Symptoms

A
  1. Aching LE’s relieved by elevation
  2. Edema after prolonged standing
  3. Night cramps of LE’s
53
Q

CVI Exam Findings

A
  1. Trophic changes with brownish discoloration
  2. Stasis leg ulcers
  3. Edema of LE’s
  4. Dermatitis
  5. Cool to touch
54
Q

CVI Diagnostics

A

None specific to CVI dx

Testing to r/o edem r/t HF and other causes

55
Q

CVI Management

A
  1. Bed rEst with legs elevated to diminish chronic edema
  2. Support hose
  3. Weight reduction as needed
  4. Treat dermatitis or ulcers
  5. Adute weeping dermatitis:
  • WEt compress
  • 0.5% hydrocortisone cream after compress
  • systemic ATB only if active bacterial infection
56
Q

Pericarditis

A

Inflammation of pericardium. HX imprtant to accurate dx!

Causes:

  • Viruses *most common cause*
  • Post MI
  • Renal failure
  • Neoplasm, TB, Septemia
  • Endocarditis
  • Collagen dz
  • Drug/Trauma induced
  • Idiopathic (viral)
57
Q

Pericarditis Signs/ Symptoms

A
  • Localized restrosternal/precordial CP, pleuritic in nature
  • Pain increased by deep inspiration, swallowing, recumbent position
  • Pain releived by sitting forward
  • SOB secondary to pain with inspiration
58
Q

Pericarditis Exam Findings

A
  • Pericardial friction rub characteristically present
  • Pleural friction rub may also be present
  • Fever based on underlying cause
59
Q

Pericarditis Diagnostics

A
  • ST eleation in all leads
  • Return of ST to WNL in few days followed by temp T wave inversion
  • ESR elevation
  • BC if suspected bacterial cause
  • CBC to r/o infection or leukemia
  • Echo confirms presence of pericardial fluid
  • BMP
60
Q

Pericarditis Management

A
  • **NSAIDS are mainstay of Tx**
  • Ibuprofen, Indomethicin
  • Corticosteroids only when total failure of NSAIDS over several weeks with relapsing
  • Dexamethasone may releive pain in few hours. Prednisone 60mg daily then tapered
  • Codeine 15-60mg QID
  • Monitor for tamponade
61
Q

Endocarditis

A

Infection of the endothelial surface of the heart.

Usually affects the valves.

Infective endocarditits must be considered in all pts with heart murmur and FUO!

Causes:

Bacteria!!

Valvular heart dz, rheumatic, bicuspid aortic valve/mitral valve prolapse with significant regurg

Recent dental/mouth surgery

GU or Respiratory instrumentation

Congential heart dz

Prolonged IV or TPN

Burns

HD

62
Q

Endocarditis Signs/ Symptoms

A
  • Fever and malaise
  • Night sweats and weight loss
  • Sick feeling
63
Q

Endocarditis Exam Findings

A
  1. Murmur, maybe absent in 30% pts
  2. Med to high fever
  3. Osler’s nodes: painful, red nodules in distal phalanges
  4. Petechie, purpura, pallor
  5. Splinter hemorrhage
  6. splenomegaly in 50%
  7. Janeway lesions-small painful macules on palms and soles
  8. Roth spots: small retinal infarcts, white encircled by hemorrhage
64
Q

Endocarditis Diagnostics

A
  1. WBC normal or elevated, always left shift with bands
  2. Echo
  3. BC 3 at 3 sites
  4. ESR elevated
65
Q

Endocarditis Management

A

Patients who aren’t acutely ill looking and have no signs of HF or major embolic events, ATB are preferably withheld until BC available

In all other pts, empiric ATB started:

  • PCN G 2 million units IV q 4 H in combination with Gent
  • Nafcillin 2 gm IV q 4 H
  • Vanc MRSA
  • Others
66
Q

Heart failure causes physiologic changes in the body due to what process?

A

an increase in capillary hydrostatic pressure

67
Q

Which murmur is associated with syncope?

A

Aortic stenosis

68
Q
A

ACNP Certification (17 decks)

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