Cardiovascular Flashcards

Question

What are nonmodifiable risk factors?

Answer 1

Age, sex, family history, genetics

Answer 2

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

Answer 3

1. Unstable Angina 2. Non ST elevation myocardial infarcation (NSTEMI) 3. ST Elevation myocardial infarction (STEMI)

Answer 4

Unstable Angina

Answer 5

Variant or Prinzmetal's Angina

Answer 6

* 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

Answer 7

RIGHT coronary artery (RCA), inferior LV

Answer 8

LEFT anterior descending (LAD), anterior LV

Answer 9

CIRCUMFLEX, lateral LV

Answer 10

Low lateral LV

Answer 11

high lateral LV

Answer 12

RCA, posterior LV

Answer 13

RCA, RIGHT ventricular infarct

Answer 14

Inferior MI

Answer 15

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

Answer 16

Aneterior MI

Answer 17

Lateral MI

Answer 18

* 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)

Answer 19

* 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

Answer 20

* 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

Answer 21

* 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

Answer 22

* 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

Answer 23

* 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

Answer 24

* 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

Answer 25

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

Answer 26

* 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

Answer 27

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

Answer 28

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)

Answer 29

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

Answer 30

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)

Answer 31

* Palpiations, dizziness, chest pain, SOB, and syncope

Answer 32

* 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 ***

Answer 33

QT prolongation may lead to TORSADES DE POINTES Causes * Amiodarone, quinidine, haloperidol, procainamide * HYPOkalemia, HYPOcalcemia, HYPO magnesemia Treatment for torsades VT * Magnesium

Answer 34

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

Answer 35

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)

Answer 36

* 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

Answer 37

Systolic Dysfunction EF 40% or less, problem with ejection Diastolic Dysfunction EF is >50%, problem with filling, ejection is OK

Answer 38

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)

Answer 39

See page 38

Answer 40

* 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)

Answer 41

* 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

Answer 42

* 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

Answer 43

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

Answer 44

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)

Answer 45

Increasing contractility and DECREASING both preload and afterload

Answer 46

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

Answer 47

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.

Answer 48

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.

Answer 49

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.

Answer 50

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.

Answer 51

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.

Answer 52

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.

Answer 53

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

Answer 54

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

Answer 55

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).

Answer 56

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

Answer 57

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

Answer 58

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).

Answer 59

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

Answer 60

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

Answer 61

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.