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FNP CV - Primary Care

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