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Cardiovascular
FNP CV - Primary Care
| Question | Answer |
|---|---|
| When assessing HPI of pt c/o chest pain | focus on personal risk factors for CV disease |
| Ask all pts c/o chest pain | about their exercise tolerance |
| When assessing pt's with known angina | see if there has been a change in sx pattern |
| Change in angina sx pattern = | alteration in vessel patency such as accelerated atherosclerosis or vessel spasm |
| Atrial ectopic beats are__ | usually benign and can occur with excess caffeine, alcohol, or tobacco use |
| Ventricular ectopic beats are___ | usually indicate cardiac pathology and pt is at increased risk of sudden cardiac death |
| Dyspnea | shortness of breath |
| orthopnea | SOB when laying supine |
| Goal BP of pts over 60 | less than 150/90 |
| HTN meds for typical pts | thiazide diuretic, ACEI, ARB, CCB |
| HTN meds for African americans | thiazide diuretic, CCB |
| HTN meds for CKD pts | ACEI, ARB |
| When to recheck BP after starting initial HTN med | 1 month |
| If initial HTN med has not provided BP at goal | can up dose of 1st med or add additional meds from different classes for a total of up to 3 meds |
| What meds should not be used together for HTN | ARB and ACEI |
| Cause of essential HTN | no single cause, genetic & environmental factors = 95% of pts |
| cause of secondary HTN | possibly reversible; cardiac, renal and endocrinological problems or vasoconstricting meds = 5% of pts |
| Person to likely get HTN | AA female |
| Effects of HTN on arteries | high BP causes shearing force on arterial walls which injure endothelium = reaction of vasoconstriction, inflammation, platelet aggregation, lipid deposition = arteriosclerotic plaque formation |
| Target organs affected by HTN | brain, eyes, heart, kidneys, and peripheral arteries |
| Increased insulin levels affect on BP | increases sympathetic activity (which controls vasoconstriction) and causes hypertensive states |
| Sleep apnea affect on BP | can cause HTN b/c it activates sympathetic activity (vasoconstriction) and renin-angiotensin systems |
| Malignant HTN/HTN emergency/HTN crisis is___ | BP over 180/110 WITH end organ damage; treat with immediate IV meds |
| HTN urgency is___ | BP elevated WITHOUT end organ damage; treat with PO meds for 24-48 hrs |
| Pt presenting w/ severely elevated BP should have ___ included in their P/E | fundoscopy, ECG, UA, C XRY |
| Fundoscopy presentation of HTN end organ damage | papilledema, hemorrhages, exudates |
| Neuro presentation of HTN end organ damage | AMS, neuro deficits, dementia |
| ECG presentation of HTN end organ damage | myocardial ischemia or infarction, left ventricular hypertrophy (LVH) |
| Chest X-ray presentation of HTN end organ damage | heart failure or aortic dissection, |
| Renal presentation of HTN end organ damage | hematuria, proteinuria, elevated serum creatinine |
| To confirm diagnosis of BP | have pt do home ABMP or sequential home BP readings |
| Meds that cause HTN or worsen it | NSAIDS, COX 2 Inhibitors, decongestants, diet pills, Oral contraceptive, erythropoietin, tacrolimus, cyclosporine, steroids |
| Management of initial dx of HTN | try lifestyle changes for 1 month, if no progress begin meds |
| When to order ACEI (-pril) | when pt has HF or hx of MI, renal insufficiency or DM; S/E is a cough |
| When to order ARBs (-artan) | pt's with HF or DM; are more expensive them ACEI so should only order if pt gets a cough with ACEI |
| When to order beta blocker (-lol) | no longer used for primary management but can be used for pt's with angina, post-MI, atrial tachycardia, migraine HA, |
| When to use CCB | black pts, stable angina, |
| When to use alpha adrenergic antagonists (alpha blockers) for HTN | pts's with BPH |
| ASCVD recommends statins for what percentage of risk? | 7.5% |
| What do lipoproteins do? | Carry cholesterol in the bloodstream |
| How do LDL proteins work? | They go to inflamed areas in the blood vessel wall where they form fatty streaks and atherosclerotic plaques |
| Goal LDL and HDL | LDL = less than 40 HDL = more than 60 |
| What do HDL proteins do? | removes excess cholesterol from blood vessels to the liver where it is excreted in intestine as bile. |
| What is metabolic sydrome | various CVD and DM risk factors where the underlying path is related to insulin resistance |
| What conditions make up metabolic syndrome | any 3 of the following: increased BMI, elevated SBP, hypertriglyceridemia, hyperglycemia, lows HDL protein |
| What do coronary arteries do | coronary arteries provide arterial blood (O2 & nutrients) to heart and dilate as needed to increase oxygen delivery with changing metabolic demands of heart |
| What is Coronary artery disease (CAD)/ coronary heart disease (CHD) | arteriosclerotic plaque hinders optimal blood flor wan dilation of coronary arteries by sticking to coronary artery walls which causes obstruction and prevents vasodilation which impedes perfusion of myocaridum |
| angina pectoris cascade | arteriosclerosis prevents coronary vessels from dilation = insufficient O2 being delivered to myocardium=ischemia of heart muscle = anaerobic metabolism which produces lactic acid = tissue acidosis and irritation = chest pain = angina |
| What is atherosclerosis/arteriosclerosis | systemic disease affecting all arteries of body |
| If the pt presents with exertion angina__ | suspect CAD |
| Diagnostic tests for CAD | ECG, stress test, nuclear scanning and angiography can help determine extent of CAD and identify which vessels are affected |
| What is Nuclear Scanning | studies motion of left ventricle and measures ability to eject blood (normal ejection fraction is 55-75%). |
| Nuclear scanning rundown | When ischemia because of a narrowed artery is present, the part of the myocardium that artery serves shows a diminished wall contractility evidenced by pooled blood in that specific chamber. |
| Acute coronary syndrome consists of which dx | myocardial ischemia dx: stable and unstable angina, variant angina, and myocardial infarction |
| Stable angina is | predictable, and controlled with meds |
| Unstable angina is | newly diagnosed angina or unpredictable in pattern, frequency or severity; may lead up to acute MI |
| Population most likely to have an MI | AA men older than 65 |
| Stable angina | coronary occlusion that causes brief ischemia but is treatable and reversible |
| 2 types of MI | STEMI and NSTEMI (non STEMI) |
| STEMI | stands for ST elevation myocardial infarction; caused by OCCLUSIVE thrombus that leads to infarction of FULL THICKNESS of myocardial wall |
| NSTEMI | stands for non ST elevation myocardial infarction; caused by infarction from NONOCCLUSIVE thrombus that infarcts only PART of myocardial wall |
| Diagnostic test for MI | Troponin I and T |
| Cardiac Troponin levels | are proteins released from dead heart muscle and are NOT found in people with healthy hearts. Rise in 2-4 hours after MI and remain high for 7-10 days |
| ECG finding showing acute coronary artery occlusion | ST-segment elevation more than 1mm ; usually occurs due to thrombus |
| ECG finding showing myocardial ischemia | enlarged and inverted t-wave |
| ECG finding showing myocardial infarction | abnormal q-wave |
| Determine the location of myocardial damage and which coronary artery is damaged by | seeing which ECG lead has the abnormality |
| Manage stable angina | Nitro and rest, attacks normally 3-5 minutes and go away with treatment; if they don't go to ER |
| Heart failure is | cardiac output cannot meet body's demands |
| Systolic dysfunction of heart failure | ventricles can't eject an adequate amount of blood; left ventricle EF is less than 50% |
| Diastolic dysfunction of heart failure | ventricles can't fill up with sufficient amount of blood; let ventricle EF is 70% or more |
| Systolic dysfunction cascade/ forward failure | weak ventricles eject small amount of blood = hypoperfusion = stimulates sympathetic nervous system to constrict arteries and provoke renin angiotensin cascade = increased BP and blood volume = more work on ventricles |
| Diastolic dysfunction cascade/backward failure | elevated filling pressure builds up in ventricle. In let ventricle, blood builds up and goes into left atrium then pulmonary system = pulmonary edema; |
| Pulmonary edema signs | pink frothy sputum, dyspnea, cough, crackles |
| Left Ventricular Failure/left sided heart failure | most common type; HTN increases the resistance against the left ventricle resulting in increased workload which leads to left ventricular hypertrophy. |
| Normal ejection fraction | 55-70% |
| Right sided heart failure/ right ventricle failure | leads to venous system congestions; congestion of superior vena cava=jugular vein dissension; congestion of inferior vena cava= hepatomegaly, splenomegaly, and peritoneal edema (ascites) |
| Cor pulmonale | right sided heart failure from increased pulmonary HTN d/t chronic hypoxemia. the HTN causes right ventricle hypertrophy but the ventricle eventually fails and this failure is called cor pulmonate |
| Atrial natriuretic peptide (ANP) is secreted when___ | atrial stretch d/t increased hydrostatic pressure occurs; happens in heart failure |
| B-type natriuretic peptide (BNP) | rises in presence of heart failure, above 500 pg/ml= HF, |
| Best test to confirm heart failure | ECG, done after a BNP |
| How to manage heart failure | ACEI (if not tolerated then ARB), diuretics for volume overload (thiazide for mild HF and loop for severe), beta blocker to slow HR and decrease work of heart |
| When to notify PCM with weight gain in heart failure | more than 3 pounds in a day or 5 pounds a week |
| A fib clinical presentation | hypotension, diaphoresis, dizziness, syncope, possible stroke |
| Evaluate pt's with A fib for risk of ___ | stroke d/t potential for blood clots, using CHADS2 scoring 1 point for - CHF, HTN, age more than 75, DM, and 2 points for stroke or TIA |
| premature atrial contractions (PAC) | usually insignificant and occur in young people who drink too much caffeine, nicotine, or alcohol, or other stimulant - no treatment |
| Digoxin affect on arrythmias | commonly causes AV blocks and b/c it has a narrow therapeutic window, toxicity occurs easily which can cause arrhythmia of any kind. |
| A fib ECG strip findings | irregularly irregular heart beat, 100-180 beats per min from ventricle rate, 350-600 beats per min for atrial rate, no discernible p waves, QRS usually normal |
| PAC ECG findings | rate of 60-100, regular rhythm until premature beat, |
| SVT ECG findings | regular rhythm w/ rate of 150-250 beats per minute |
| A flutter ECG findings | atrial rate of 250=350 beats per min, p waves march out, |
| PVS ECG findings | rate of 60-100 beats per min, QRS complex is wide and bizarre |
| anticoagulation in A-fib | started when pt's are afib longer than 48 hrs; warfarin will be started draw PT and INR; goal INR 2-3, check INR weekly until established then check monthly |
| Treat A fib | amiodarone to covert to NSR, synchronized cardioversion if pt in distress |
| SVT treatment | vagal maneuvers, adenosine rapid IV push in emergency, synchronized cardio version for symptomatic pts |
| Heart block treatment | First degree - observational second degree type 1 = observe only unless bradycardia then temporary pace maker type 2= permanent pace maker, third degree is emergency |
| A heart murmur is__ | sound of turbulent blood flow; normally blood flow is silent |
| Benign systolic ejection murmur | heard in 80% of thin adults and children; best heard at left sternal border; normal occurence |
| Hemic murmur | heard during anemia, exercising, or fever; resolves when underlying cause is gone, no heart problems |
| aortic sclerosis murmur | d/t fibrotic and calcific changes to aortic valve |
| aortic stenosis is___ | inability of aortic valve to open effectively |
| best clinical sign of aortic stenosis | narrowed pulse pressure on blood pressure |
| mitral regurgitation | inability of mitral valve to close - allow blood to flow from left ventricle to left atrium |
| Causes of valvular disorders | bacterial endocarditis, rheumatic fever, and aortic calcifications. |
| Definitive procedure to diagnose heart valve disorders | 2 dimensional echocardiography |
| Peripheral Artery Disease (PAD) most common manifestation | lower extremity claudication - cramping pain that starts with activity and is relieved by rest |
| Pathophysiology of PAD | usually caused by atherosclerosis, plaque builds up and obstructs blood flow to lower extremity muscles. When muscles start to move they need more oxygen via blood but cannot get it = pain d/t ischemia |
| Sign of severe PAD | pain at rest, weak pulse, pallor, paresthesia, coolness of extremity, muscle atrophy, diminished hair growth, hard discolored toenails |
| how to tell difference between chronic venous insufficiency and PAD | raise pt's legs for several minutes, when they are placed down again PAD= pale dusky red extremities venous insufficiency = improved color |
| PAD diagnostic tests | doppler flow study: ankle-brachial index (comparing arm and ankle BPs; normal ration is more than 0.9. |
| DVT Virchow's triad | hypercoaguability, endothelium wall injury, venous stasis; clots usually occur when 2 of the 3 are present |
| What is chronic venous insufficiency | valvular incompetence that results in lower extremity edema, skin discoloration, and ulceration d/t poor venous flow |
| Where do most DVTs originate | at or above popliteal vein |
| Common causes of a hypercoagulabilty state | estrogen use, pregnancy, neoplasms |
| PAD management | manage HTN and DM, keep legs dependent, no tight stockings or bandages, antiplatelet therapy (aspirin) |
| Chronic venous insufficiency management | light exercise, compression stockings, weight loss, elevate legs throughout the day |
| DVT management | low molecular weight heparin (lovenox for outpatient), along with warfarin |
Created by:
Aprilj90
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