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CCRN > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q
  • Lub
    *AV (mitral / tricuspid) closure
  • Loudest at APEX (midclavicular, 5th intercostal
  • End of diastole, beginning of systole
A

S1

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2
Q
  • Dub
  • Closure of semilunar valves (aortic/pulmonic) valves
  • Loudest @ base (RIGHT sternal border, 2nd intercostal space)
  • Marks end systole, beginning of diastole
  • Splits on inspiration: wide, fixed splitting of this caused by R bundle branch block (RBBB)
  • Louder with pulmonary embolism
A

S2

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3
Q
  • Rapid rush of blood into a dilated ventricle
  • Occurs early in diastole, right after S2
  • Best @ APEX with the BELL of the stethoscope
    * ASSOCIATED W/ HEART FAILURE, MAY OCCUR BEFORE CRACKLES
  • Ventricular gallop “KENTUCKY”
  • Caused by: pulmonary hypertension and cor pulmonale | mitral, aortic, or tricuspid insufficiency
A

S3

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3
Q

Due to pericarditis, pain on deep inspiration, positional

A

Pericardial Friction Rub

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4
Q
  • Caused by atrial contraction of blood into a noncompliant ventricle
  • Occurs right before S1
  • Best heard at the APEX with the BELL of the stethoscope
  • Associated w/ myocardial ischemia, infarction, hypertension, ventricular hyperthrophy, AORTIC STENOSIS
  • Atrial gallop (TENNESSEE)
A

S4

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5
Q

Valvular disease / Septal defects (atrial or ventricular)

A

Murmur

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6
Q
  • Systolic - Diastolic = ?
  • 40-60 mmHg
A

Pulse Pressure

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7
Q

Indirect measurement of the cardiac output and stroke volume

A

Systolic blood pressure

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8
Q

A decrease in systolic pressure with little change or increase in diastolic pressure is ??? of pulse pressure; seen most often with ??? or ??? in cardiac output

A

Narrowing | severe hypovolemia | DROP

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8
Q

Indirect measurement of the systemic vascular resistance (SVR). A ??? in this that widens pulse pressure may indicate ???, ???, often seen in ???, ???.

A

Diastolic blood pressure | decrease | vasodilation | drop in SVR | sepsis | shock

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9
Q

??? perfused during diastole

A

Coronary arteries

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10
Q

Which is longer diastole or systole?

A

Diastole 1/3 LONGER than systole

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11
Q

Why do the CO and blood pressure drop during tachyarythymias?

A

No time for filling during diastole, therefore less output

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12
Q
  • Murmurs of ??? (regurgitation) occur when the valve is CLOSED
  • Chronic or acute?
A

INSUFFICIENCY | BOTH

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13
Q
  • Murmurs of ??? occur when the valve is OPEN
  • Chronic or acute?
A

STENOSIS | Chronic - develops over time, NOT ACUTE

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14
Q
  • Semilunar valves are (OPEN or CLOSE) during systole
  • Aortic / pulmonary stenosis
A

OPEN
Lub … Shhh … Dub
Sytolic murmur

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15
Q
  • AV valves are (OPEN OR CLOSE) during systole
  • Mitral / tricuspid insufficiency
  • Causes large, giant V-waves on the pulmonary artery occlusion pressure tracing if the patien has a pulmonary artery catheter
A

CLOSED
Lub … Shhh … Dub
Systolic murmur

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16
Q

??? Most common with acute MI, may result in a systolic murmur, head at the LEFT sternal border, 5th intercostal space

A

Ventricular Septal Defect
Associated with systolic murmur

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17
Q
  • Semilunar valves are (OPEN or CLOSED) during diastole
  • Aortic / pulmonary insufficiency
A

CLOSED | Diastolic murmur | Lub … Dub … SHHHH

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18
Q
  • AV valves are (OPEN OR CLOSE) during diastole
  • ??? is associated with atrial fibrillation due to atrial enalrgemetn that occurs over time
  • Triscuspid ???
A

OPEN | Mitral Stenosis | Stenosis

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19
Q

Myocardial ischemia or infarction can affect ??? valve function and lead to acute ??? valve regurgitation?

A

MITRAL

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20
Q

Papillary muscle DYSFUNCTION (Grade I / II), loudest at ???

A

APEX

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21
Q

Papillary muscle RUPTURE (grade V or VI) loudest at ???, what type of emergency?

A

APEX | Surgical

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22
Q

Where can you hear ventricular septal defect?

A

Sternal Border, 5 ICS

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23
Q

What are nonmodifiable risk factors?

A

Age, sex, family history, genetics

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24
Q

What are modifiable risk factors?

A

Smoking, atherogenic diet, alcohol intake, physical activity, dyslipidemias, hypertension, obesity, diabetes, metabolic syndrome

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25
Q
  • Troponin (+)
  • ST depression
  • T-wave inversion on the ECG
  • Unrelenting chest pain
A

NSTEMI

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26
Q

What are the three types of acute coronary syndome?

A
  1. Unstable Angina
  2. Non ST elevation myocardial infarcation (NSTEMI)
  3. ST Elevation myocardial infarction (STEMI)
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27
Q
  • Chest pain at rest
  • Unpredictable
  • Relieved w/ NTG
  • Troponin (-)
  • ST DEPRESSION
  • or T-wave inversion on the ECG
A

Unstable Angina

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28
Q
  • Troponin (+)
  • ST elevation in 2 or more contiguous leads
  • Unrelenting CP
A

STEMI

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29
Q
  • A type of unstable angina associated with transient ST segement elevation
  • Due to coronarya artery spasm with or without atherosclerotic lesions
  • Occurs at rest, amy be cyclic (same time each day)
  • May be precipated by nicotine, ETOH, cocaine ingestion
  • Troponin (-)
  • NTG administration results in relief of CP, STs return to normal
A

Variant or Prinzmetal’s Angina

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30
Q

Management of Acute Chest Pain

A
  • ECG within 10 minutes to categorize
  • Aspirin ASAP
  • Anticoagulant - heparin or enoxaprine
  • Antiplatelet agents: clopidogrel (Plavix), Abciximab (Reopro), Eptifibatide (Integrilin), Tirofiban (Aggrastat) \
  • Beta Blocker - unless ACS due to COCAINE, cardioselective prefered (metoprolol vs noncardioselective (propanolol)
  • Contraindications - hypotension, bradycardia, use of phosphodiesterase inhibitor drugs such as sildenafil (viagra)
  • Treat pain - NTG / Morphine
  • History, risk factor assessment: lab assesment, cardiac biomarkers, lipid profile, CBC, electrolytes, BUN, creatinine, magnesium, PT, PTT
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31
Q

Changes in II, II, aVF

A

RIGHT coronary artery (RCA), inferior LV

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32
Q

Changes in V1, V2, V3, V4

A

LEFT anterior descending (LAD), anterior LV

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33
Q

Changes in V5, V6, I, aVL

A

CIRCUMFLEX, lateral LV

34
Q

Changes in V5, V6

A

Low lateral LV

35
Q

Changes in I, aVL

A

high lateral LV

36
Q

Changes in V1 & V2

A

RCA, posterior LV

37
Q

Changes in V3R, V4R

A

RCA, RIGHT ventricular infarct

38
Q
  • Associated with RCA occlusion
  • ST elevation II, III, aVF
  • Reciprocal changes in lateral wall (I, aVL)
  • Use beta blockers / NTG with caution
  • AV conduction disturbances - 2nd degree Type I AV block, 3rd deegree AV boock, sick sinus syndrome, sinus bradycardia
  • Systolic murmur - mitral valve regurgitation secondary to papillary muscle rupture (posterior papillary mucle has only one source of blood supply (RCA).
  • Tachycardia - higher mortality
  • R ventricular infarct and posterior MI
A

Inferior MI

39
Q
  • JVD at 45, high CVP, hypotension, BUT clear lungs, bradyarrhythmias
  • ST eelvation in V3R, V4R
  • Size of infarct will determine symptoms
  • Tx: Fluids / Positive inotorpes
  • Avoid: Preload reducers, nitrates/diuretics. Caution: BB -often cannot give due initial hypotension
A

RIGHT VENTRICULAR INFARCT

RCA supplies the inferior wall of the LEFT ventricle, also supplies the R ventricle, therefore, about 30% of inferior wall MI patients also have a RV infarct

40
Q
  • Associated with LEFT anterior descending (LAD) occlusion
  • ST elevation V1-V4; precordial leads, V leads
  • Reciprocal changes (ST depression) in ferior wall (II, III, aVF)
  • May develop 2nd-degree Type II AV block or RBBB (the LAD supplies the common bundle of His) - ominous sign
  • Development of systolic murmur: possible ventricular septal defect
  • Higher mortality than inferior MI: Heart Failure
A

Aneterior MI

41
Q
  • ST elevation in V5, V6 (low lateral)
  • ST elevation in I, aVL (high lateral)
  • Generally involves LEFT circumflex artery
A

Lateral MI

42
Q

Treatment of STEMI

A
  • Determine bonset of infarct, if sypmtoms < 12 hours –> Reperfusion
  • PCI - door to balloon within 90 minutes
  • Fibronyltic drug therpy - standard is door to drug within 30 minutes

Eligibility Criteria
* ST elevation in 2 or more contuous leads or new onse]t LEFT bundle branch block (LBBB)
* Onset of CP <12 hours
* Chesst pain of 30 minutes in duration
* Chest pain unresponsive to sublingual (SL) nitroglycerin (NTG)

43
Q

Absolute Contraindications for Fibrinolytic Therapy (30 minutes door to dug administration)

A
  • Any prior intracranial hemorrhage
  • Known structural cerebral vascular lesion (arteriovenous malformation)
  • Known malignant intracranial neoplasm (primary or metastatic)
  • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours
  • Suspected aortic disseciton
  • Active bleeding or bleedin diathesis (excluding menses)
  • Significant closed-head or facial trauma iwthin 3 months
44
Q

Evidence of Reperfusion

A
  • Chest pain relief
  • Resolution of ST segement deviations due to return of blood flow
  • Marked elevation of troponin/CK-MB due to myocardial “stunning” when vessel opens
  • Reperfusion arrhytmia (VT, VT; accerlated idioventricular rhythm (AIVR); due to myocardial stunning vessel opens
45
Q

Treatment of NSTEM

A
  • No emergent reperfusion
  • Same meds as STEMI
  • If high risk score or continued chest pain, signs of instability, start GP IIb/IIIa inhibitors (Integrilin, Reopro) and prepare for diagnostic cardiac catherterization within 24 hours
46
Q

What is the difference between hypertensive emergency or CRISIS vs URGENCY?

A
  • Emergency: evidence of end organ damage (brain, heart, kidney, retina) that can be realted to acute hypertension –> needs critical care addmision
  • Urgency: w/o evidence of acute end organ damage –> usually no need for critical carea dmission
  • GREATEST RISK: STROKE
47
Q

Nitroprusside (Nipride)

A
  • Preload AND afterload reducer
  • Assess for cyanide toxicity secondary to drug metabolite (thiocyanate): mental status change (restless, lethargy), tachycardia, seizure, a need for increase in dose, unexplained metabilic acidosis, especially in those with renal impairment or when a drug is used >24 hours
  • Treatment for hypertensive crisis/urgency
48
Q

Labetalol (Normodyne, Trandate)

A
  • Intermittent IV doses preferred to a continuous infusion due to possibility of continuing the drug beyond the maximum dose of 300 mg
  • Duration of effects persist 4-6 hours after IV dose is discontinued
49
Q

Signs and Symptoms of PAD

A
  1. Pain (activity & rest)
  2. Pallor
  3. Pulse absent or diminished
  4. Paresthsia
  5. Paralysis
  6. Poikilothermia: loss of hair on toes or lower legs; glossy, thin, cool, dry skin (chronic sign of PAD)
  7. Cool to touch, minimal edema
50
Q

Ankle Brachial Index (ABI)

A
  • Test to assess for PAD
  • Assess the adequacy of lower extremity perfusion (normal >.90)
  • Divid the ankle pressure by the brachial pressure on the same side
  • Only need to know what a normal ABI is
51
Q

PAD - additional diagnostic testing / patient care / medications

A

Testing: doppler ultrasound / arteriography
Patient Care: embolectomy, bypass graft, angioplasty
* Bed in REVERSE Trendenlenburg
* DO NOT elevated the affected extremity - will decrease perfusion
* Medications: thrombolytics, anticoagulants (heparin), antiplatelet agents (ASA, clopidogrel), vasodilators

52
Q

Acute Symptomatic Caroid Artery Disease
S/s| Diagnostic Testing

A

S/s
* Transient ischemic attack (TIA)
* Moncular visual disturbances
* Aphasia
* Stroke

Diagnostic Testing
* Angiography (GOLD STANDARD): risk of stroke during exam
* Carotid duplex ultrasound
* Computed tomopgraphy angiograhy (CTA)
* Magnetic resonance angiography (MRA)

53
Q

Acute Symptomatic Caroid Artery Disease
Treatment / Post Procedure Monitoring

A

Treatment
* Carotid endarterectomy (CEA)
* Carotid stenting
* Aspirin
* Statin Therapy

Post Procedure Monitoring
* Frequent neuro / motor check
* Close BP / HR monitoring - labile BP and bradyarrhythmia with hypertension, hypotension, or bradycardia
* Bleeding
* May develop HYPERperfusion syndrome with the s/s of a headache ispsilateral to the revascularized carotid artery, focal motor seizures, and/or an intracerebral hemmorrhage

54
Q

Wolff-Parkinson-White (WPW)

A

Genetic conduction abnormality in which an abnormal conduction pathway exists that allows a reentrant tachycardia pathway to bypass the normal AV node conduction pathway, resulting in supraventricular tachycardia. Primarily seen in those younger than 30 years old
* When in NSR - ECG shows a short PR interval and the presence of a DELTA wave (seen as a slow rise of the initial upstroke of hte QRS)
* WPW results in supraventricular tachycardia (SVT) when the abnormal pathway takes over, but may present as PRE-EXCITED ATRIAL FIBRILLATION (irregular rhythm, rates of 150 beats/minute or greater, and a wide QRS)

55
Q

SVT S/s

A
  • Palpiations, dizziness, chest pain, SOB, and syncope
56
Q

Wolff-Parkinson-White Treatment

A
  • Radiofrequency ablation to eliminate reentrant pathway
  • If UNSTABLE SVT is present, perform syncrhonzied cardioversion or adminster adenosine
  • If pre-excited A-fib is present, administer beta blockers, amiodarone, or procainamine IV

** Do NOT give adenosine, digoxin, or calcium channel blockers for pre-excited AF; these agents may enhance antegrade conduction through the abnormal pathway by increasing the refractory period in the AV node, resulting in ventricular fibrillation **

57
Q

Prolongation of QT interval
(causes / treatment)

A

QT prolongation may lead to TORSADES DE POINTES

Causes
* Amiodarone, quinidine, haloperidol, procainamide
* HYPOkalemia, HYPOcalcemia, HYPO magnesemia

Treatment for torsades VT
* Magnesium

58
Q

Pacemaker Codes

A

First Initial - Chamber paced
Second initial - chamber sensed
Third initial - response to sending
* I - inhibits (pacer detects intrinsic cardiac activity and witholds its pacing stimuli) … demand
* D - Inhibits and triggers (pacer detects intrinsic cardiac acitvity and fires a pcing stimulus in response
* O - none

59
Q

3 Basic Pacer Malfunctions

A
  1. Failure to pace (no spike at all when expected)
  2. Failure to capture (spikes without a QRS for ventricular pacing)
  3. Failure to sense (pacing in native beats)
60
Q

Implantable Cardioverter-Defibrillator (ICD) Tierd Therapy

A
  • Shock - defibrillate or synchronized cardioversion
  • Burst pace - sense tachyarrhythmia, provide a series of beats fater than the tachyarrhythmia, and the nsudden stop with the hope of the recovery of the SA node)
  • Pacing for bradyarrhythmias
61
Q

Difference systolic / diastolic dysfunction in heart failure

A

Systolic Dysfunction
EF 40% or less, problem with ejection

Diastolic Dysfunction
EF is >50%, problem with filling, ejection is OK

62
Q

BNP

A

B-type natriuretic peptide (BNP) - released when ventricle is under wall stress in attempts to dialte and decrease ventricular pressure

Elevates when the LEFT ventricular is under stress (left ventricular failure) or, to a lesser degree, BNP eleveates when the R ventricule is under stress (pulmonary hypertension, pulmonary embolism)

63
Q

Pathophysiology of Acute Decompensated Systolic Dysfunction
&
Summary of systolic v diastolic HF

A

See page 38

64
Q

American heart Association (AHA) Stages of Heart Failure

A
  • Stage A: High Risk: no evidence of dysfunction
  • Stage B: Heart disorder or structural defect; no symptoms
  • Stage C: Heart disorder or structural defect, with symptoms (past or present)
  • Stage D: End-stage cardiac disease; with symptoms despite maximal therapy (inotropic or mechanical support)
65
Q

NYHA Heart Failure Classes

A
  • Class I - Ordinary activity does not cause symptoms, EXTRAORDINARY activity results in heart failure symptoms
  • Class II -Comfortable at rest, but ORDINARY activity results in heart failure symptoms
  • Class III - Comfrtable at rest, but MINIMAL activity cause HF symptoms
  • Class IV - Symptoms of heart failure occur at REST; there is severe limitation of physical activity
66
Q

Q What are the 3 indicators of successful reperfusion?

A
  • Pain cessation
  • Short runs of V-tach
  • Reversal of ST segment elevation with return to baseline
  • Increase in CK or troponin - reperfusion injury of muscle elevates cardiac biomarkers
67
Q

Q. What medication is not recommended for a patient experiencing Anterior MI (V2, V3,V4)?

A

A. Propanolol - noncardioselective medicaiton - works on cardiac muscles and lung muscles which may cause bronchoconstriction.

A beta blocker is beneficial for an acute MI, as they decrease the work of the heart and increase the threshold for v-tach. Anti-platelets and anti-coagulants are also indicated for acute MI

68
Q

Q An anterior MI can cause which type of heart block?

A

A. Second-degree, Type II

Acute anterior MI is generally due to LAD occlusion. LAD supplies the bundle of His, so an LAD occlusion could result in a second-degree Type II heart block. If symptomatic bradycardia were to occur, the patient may require transcutaneous pacing. Other 3 types of heart blocks are due to SA node or AV node ischemia, which is generally occur with an RCA occlusion (inferior wall MI)

69
Q

Approriate drug therapy for dialted cardiomyopathy is aimed toward:

A

Increasing contractility and DECREASING both preload and afterload

70
Q

Post acute MI, pt c/o of chest pain and fever, pain increasing with deep inspiration and is relieved when he leans forward. There are non-specific ST changes int eh precordial leads of the ECG. The nurse anticipates that this patient will most likely need treatment for?

A

Dressler’s Syndrome - is the pericarditis that may result after an acute MI

71
Q

A patient admitted with an NSTEMI develops acute shortness of breath, a recurrence of chest pain, and a loud systolic murmur at the apex of the heart. What most likely occurred?

A

Developed acute mitral valve regurgitation.

The location of the murmur, at the APEX of the heart (midclavicular, 5th ICS) is one clue to the naswer. Regurgitation occurs when the valve should be closed, and mitral valve should be closed during systole. Mitral valve stenosis, occurs when mitral valve is open, also mitral valve stenosis cannot be acute, it develops gradually / chronically.

72
Q

C/o sudden dyspnea 5 days s/p an acute MI (ST elevation in II, III, aVF, with ST depression I and aVL). Anxious, diaphoretic, and hypotensive. Development of loud holosystolic murmur at the apex (Midclavicular, 5th ICS) that radiated to the axilla. Crackles but no S3 sound at the apex. Cause of deterioration?

A

Acute Mitral regurgitation due to paillary muscle rupture or dysfunction

Inferior wall MI which is due to RCA occlusion. This may cause papillary muscle dysfunction or rupture of the mitral valve because it supplies the area of the left ventricle where this valve is attached.

Although RV infarct could result in RCA occlusion, RV infarct does not result in holosytolic murmur at the APEX of the heart or lung.

73
Q

A patient with a diagnosis of cardiogenic shock now requries high dose dopaine (greater than 10 mcg/kg/min) to maintain her blood pressure, and the cardiologist is planning to start IABP therapy. This therapy will benefit the patient because it will:

A

Decrease afterload with balloon deflation and increase diastolic augmentation with balloon inlfation.

Cardiogenic shock results in decrease cardiac output and tehrefore a drop in coronary artery perfusion and compensatory vasoconstriction. Deflation decreases afterload and work of the left ventricle. Inflation of the balloon is beneficial because it boluses blood into the coronary arteries, increasing perfusion.

74
Q

Which drug would most likely be given to a patient with hypertrophic cardiomyopathy?
A. Metoprolol
B. Digoxin
C. Dopamine
D. Dobutamine

A

A. Metoprolol

Hypertrophic cardiomyopathy results in problems with filling. A decrease in heart rate provided by a beta blocker such as metoprolol would increase the filling time.

Diastolic dysfunction does NOT cause a problem with ejection, and the EF is normal. The other three choices may be indicated for systolic dysfunction.

75
Q

A patient is admitted with ST elevation V2, V3, V4. Four days after admission, the patient suddenly developed a holosystolic murmur at the lower left sternal border, chest pain, and hypotension. What complication should the nurse expect?

A

Ventricular septal defect - LEFT STERNAL BORDER murmur

This scenario describes an acute anterior STEMI, caused by occlusion of LAD. This type of MI is most likely to result in VSD. The location of the murmur is important, mitral valve disease-related problems do not cause murmurs to be loudest at the LEFT sternal border, whereas VSD would result in a murmur at this locaiton.

76
Q

Postoperative patient suddenly develops chest pain, extreme weakness, dyspnea with ST elevation in II, III, and aVF, 92/62, HR 58, RR 28, clear lungs and heart sound assessment reveals an S4 with no murmurs. In addition to preparing for a PCI, which intervention would the nurse anticipate?
A. Nitroglycerin drip and aspirin
B. Lasix and atropine
C. Trancutaneous pacing / morphine
D. Aggressive fluid adminsitration and R sided ECG

A

Acute inferior STEMI associated with RCA which may result in an RV infarct which this patient has signs of (hypotension with clear lungs). Definitive treatment is PCI. Fluid administration will help increase coronary artery perfusion by correcting hypotension and ensure adequate RV preload. R sided ECG may help confrim the RV infarct.

Nitroglycerin, diuretics, and morphine may decrease preload, which would worsen the hypotension.

77
Q

An 80-year-old female presents with chief complaint of acute shortness of breath. BP 180/102, HR 105, RR 32, lung crackles bilaterally, SpO2 88%, S4 heart sounds upon auscultation. ECG - ST w/ LEFT ventricular hypertrophy pattern, CXR - normal heart size / pulmonary vascular cong\estion, EF 55%. Which drug should be avoided?
A. CCB
B. Digoxin
C. Low dose diuretics
D. Oxygen

A

Digoxin

This patient presents with heart failure due to diastolic dysfunction (hypertension, left ventricular hypertrophy, EF >45%). Patient has a problem with FILLING, not ejection. Digoxin - a positive inotrope, may incraese wall stress and worsen filling of the LEFT ventricle

78
Q

Pt w/ LEFT internal carotid artery stent placed, lastest assesment reveals AOx4, weakend RIGHT hand grasp and RIGHT facial droop, stable VS, dry procedure site. Pt most likely experiencing?
A. R cerebral hemorrhage
B. Hyperperfusion syndrome
C. Acute cerebrovascular insufficiency
D. Hypovolemia

A

Acute cerebrovascular insufficiency

Contralateral motor weakness and aphasia may be signs of cerebrovascular insufficiency due to LEFT stent patency issues.

A right cerebral hemorrhage would result in LEFT sided weakness and is not usually associated with post carotid placement.

S/s of hyperperfusion syndrome do not include contralateral motor weakne]ss

79
Q

Mr. Jones has an exacerbation of her HF, s/s - jugular venous distention, peripheral edema, and abdominal discomfort. Clinical signs specific to?
A. Acute LEFT ventricular failure
B. Chronic RIGHT ventricular failure
C. Acute RIGHT ventricular failure
D. Chronic dehydration

A

B. Chronic R Ventricular Failure

Acute right ventricular failure may result in JVD, but not peripheral edema or abdominal discomfort (which is due to liver engorgement).

80
Q

What pulse change might a nurse expect in teh presence of cardiac tamponade?
A. Pulsus alternans
B. Pulsus paradoxus
C. Pulsus magnus
D. Pulsus bisferiens

A

Pulsus paraxodus is fluctuatipon of the systolic blood pressure with inspiration and expiration by more than 12 mmHg, best seen when an arterial line is in place. Inspiration increases thoracic pressure, when combined with fluid surrounding the heart in cardiac tamponade, inspiration further decreases venous return to the heart, leading to a drop in systolic pressure by >12 mmHg during the inspiratory phase of breathing.

Pulsus alterans - change in amplitude of systolic waveform from beat to beat, usually indicative of severe LEFT ventricular failure

Pulsus magnus is a bounding pulse

Pulsus bisferiens is a double pulse and is not covered on the CCRN

81
Q

A patient with mitral regurgiation develops atrial fibrillation with a heart rate of 88 beats/minute and a BP of 118/75. Which of the following may be indicated?
A. BB and vasopressors
B. Cardiac glycosides and CCB
C. BB & CCB
D. antiarrhythmics and angiotensin aconverting enzyme inhibitors

A

Scenario describes the development of atrial fibrillation with a controlled ventricular response & stable BP. Even with a normal BP, the development of atrial fibrillation drops the cardiac output by 20-25% due to loss in atrial kick provided by a NSR.

A cardiac glycoside (such as digoxin) may be beneficial since it is a weak positive inotrope that may compensate for the loss of atrial kick and calcium channel blockers will keep the heart rate controlled.

Pressors are not needed in this case

BB / CCB would decrease heart rate too much. Ace Inhibitors would offer no benefit

82
Q

Which are predominant signs of LEFT ventricular systolic dysfunction?

A

S3 heart sounds, new cough, bibasilar crackles, EF less than 40%

S3 heart sounds are indicative of high LEFT ventricular pressure. A new cough and lung cracklesare signs of pulmonary edema secondary to elevated LEFT ventricular end-diastolic pressure (PAOP).

83
Q

Complete heart blocks with ventricular rates of 30 beats / min are usually seen in what type of STEMI / occlusion?

A

Inferior MI w/ RCA occlusion. Transcutaneous pacing would be an appropriate treatment for an unstable patient with complete heart blocks.

84
Q

RV infarct is associated with which teype of MI?

A

Inferior MI (II, III, aVF) - associated with RCA occlusion - RCA supplies the blood to the R ventricular muscle wall thus associated with RV infarct.

85
Q

The following drugs are all considered positive inotropic drugs that primarily affect the beta-1 receptors in the heart EXCEPT:
A. Dopamine drip at 12 mcg/kg/min dose
B. Dopamine drip at 5 mcg/kg/min dose
C. Dobutamine drip at 7 mcg/kg/min dose
D. Milrinone at 7 mcg/kg/min dose

A

At high doses (>10 mcg/kg/min), dopamine stimulates alpha receptors in the arteries and causes vasocontriction. The other 3 drugs/doses affect mainly the beta-1 receptors in teh heart, producing a positive inotropic effect.

CCRN (2 decks)

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