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● Atrial Fibrillation ○ Impact of Atrial Fibrillation ■ It increases a person’s risk of stroke by 4 to 5 times. ■ AFib causes about 25% of ischemic strokes by causing blockage of blood flow to the brain. ■ AFib doubles the risk of heart-related deaths. ■ The absence of contraction of the atria can result in a loss of cardiac output anywhere from 15 - 30% due to the absence of an "atrial kick," contributing to heart failure. ○ Risk Factors ■ Advancing age* ■ High blood pressure* ■ Coronary artery disease* ■ Cardiomyopathy ■ Obesity ■ European ancestry ■ Athletes ■ Diabetes ■ Heart failure ■ Hyperthyroidism ■ Chronic kidney disease ■ Heavy alcohol use ■ Rheumatic heart disease ■ Valvular heart disease ■ Enlargement of the chambers on the left side of the heart ■ Pericarditis/myocarditis ■ Sleep Apnea ○ Valvular vs Non-Valvular AFib ■ Valvular: AF in the presence of moderate-to-severe mitral stenosis (potentially requiring surgical intervention) or in the presence of an artificial (mechanical) heart valve ■ Non-valvular: AF in the absence of moderate-to-severe mitral stenosis or a mechanical heart valve ○ Clinical Presentation ■ Many people do not experience any symptoms and are unaware of their diagnosis – Sometimes it is an incidental finding upon examination ■ Symptomatic presentation: ● General fatigue ● Rapid and irregular heartbeat ● Fluttering or “thumping” in the chest ● Dizziness ● Shortness of breath and anxiety ● Weakness ● Faintness or confusion
● Fatigue when exercising ● Sweating ● Chest pain or pressure- (Call 911) ○ Physical Exam ■ On PE : Irregular heart rhythm – this is the hallmark finding of AFib, tachycardia (typically 110s-140s), hypotension ■ Possible findings in someone with AF include: ● JVD, rales or effusions from HF ● Murmurs suggest stenosis or regurgitation. ● LE edema (HF or DVT), ● Exophthalmia (bulging eyes) ● Signs of stroke, including facial droop, arm weakness, and slurred speech ■ Possible PE findings correspond with diseases coexisting with AF or being high risk for AF rather than the disease presentation itself ○ EKG ■ There are no visible P waves (no measurable PR interval) & an irregularly irregular QRS complex. The ventricular rate is frequently fast. ■ *GOLD standard ■ ■ ○ Classifying AFib ■ Paroxysmal AF ● AF that terminates spontaneously or with intervention within 7 days of onset ● Episodes may recur with variable frequency ■ Persistent AF
○ for patients who don’t tolerate loss of atrial kick (hemodynamic instability): ■ Synchronized cardioversion ■ Pharmacologic cardioversion: dofetilide, flecainide, propafenone, ibutilide, or amiodarone (consider long half-life, pulmonary toxicity, thyroid dysfunction) ■ Chadsvasc - To determine stroke risk ● ● ■ Anticoagulation ● Vit K antagonist ○ Warfarin (serum monitoring: goal INR 2-3) ● Direct Thrombin Inhibitor ○ Dabigatran (Pradaxa) - 150 mg PO BID (no serum monitoring) ● Factor Xa Inhibitors ○ Rivaroxaban, Edoxaban, & Apixaban (no serum monitoring) ○ Xarelto (Rivaroxaban) - 20 mg PO QD ■ (if switching from warfarin to Xarelto, d/c warfarin & start Xarelto when INR < 3) ○ Eliquis (Apixaban) - 5 mg PO BID
■ (2.5 mg PO BID if 2 of the following apply: older than 80 years, weight < 60 kg, or Cr >1.5) ● Nonvitamin K antagonist oral anticoagulants (NOACs) are contraindicated in patients with clinically significant mitral stenosis or mechanical valves. ■ Bleeding Risk Assessment ● ● ○ Other Treatments ■ Watchman Device: left atrial appendage (LAA) closure device that is permanently implanted. Closes off the left atrial appendage so that clots that form within the LAA can’t enter circulation ● It is indicated for patients with non-valvular Afib at risk for stroke ● Alternatives for patients who can’t be on anticoagulation (h/o bleeding, high-risk for bleeding, drug interactions, etc) ● Risks: LAA rupture during device implant; infection; pt will probably still need to take ASA ■ Pacemaker for slow heart rate ● Deep Vein Thrombosis (DVT) ○ Virchow’s Triad ■ 3 broad categories of factors that are thought to contribute to thrombosis ● Endothelial Damage ○ Endothelial Dysfunction ■ Smoking ■ Hypertension ○ Endothelial Damage ■ Surgery ■ Catheter (PICC lines) ■ Trauma ● Hypercoagulability ○ Hereditary
○ Well’s Score ■ If the score is greater than 2, then a diagnostic study must be ordered ■ ○ Diagnostic Tests ■ Duplex venous ultrasound of the leg/s: ● 97% sensitivity for proximal DVTs ● Cannot detect distal DVT (whole leg ultrasound order) ■ D-dimer level - small fibrin fragments are produced & released into the blood when fibrin blood clots are broken down by plasmin. Not specific to DVT ● It will not help with post-surgical patients because of the natural inflammatory process after surgery ● False positives in infection, inflammation, pregnancy, trauma, surgery, & hemorrhage ● Less sensitive with distal DVT’s ■ Venography/MRI ● Iliac vein thrombosis ○ Management ■ May be treated as an outpatient unless in cases of limb ischemia, symptoms of PE, significant comorbidities (ESRD), functional limitations, high bleeding risk, or non-adherence → Send to ER ■ Outpatient : calf DVT, clinically stable, and low-risk bleeding ● Coumadin and Pradaxa/Savaysa require at least 5 days of parenteral injections ● Low Molecular Weight Heparin (LMWH) ○ Enoxaparin (1 mg/kg BID or 1.5 mg/kg OD) BID for at least 5 days ○ Fragmin 100 units/kg BID or 200 units OD ● LMWH + Vitamin K Antagonist ○ Coumadin 5-10 mg OD for 2 days, then adjusted to 2- INR for 24 hours ● LMWH +
○ Abigatran (Pradaxa) 150 BID or Edoxaban (Savaysa) Patient weight >60 kg: 60 mg once daily, ≤60 kg: 30 mg once daily ● Factor Xa Inhibitor: do not require parenteral anticoagulation ○ Eliquis 10 mg BID for 7 days, followed by 5mg BID ○ Xarelto 15 mg BID for 21 days, followed by 20 mg OD ○ Inpatient Management ■ Unfractionated heparin is preferred in patients who are at high risk: massive DVT (iliofemoral), severe renal insufficiency, symptoms of PE, high bleeding risk, hemodynamic instability, comorbid conditions or morbid obesity ● Herparin IV in hospital setting: 80 units per kg IV bolus, then maintenance infusion of 18 units/kg/hr of IV continuous infusion; further adjustment per nomogram ● Transition to Coumadin: INR must be between 2-3 for 24 hours ● Initiate Eliquis, Pradaxa, or Xarelto within 2 hours after discontinuing heparin infusion. ○ Bleeding Risk ■ ○ Management Distal DVT ■ Thrombophlebitis ● Patients with distal DVT are at lower risk for embolization, approximately half that of those with proximal DVT, & resolve spontaneously without therapy ○ If symptomatic, then must be treated; low risk for bleeding. ■ 1/3 will develop into proximal veins ○ “Surveillance with serial ultrasound” may be indicated. ■ low-risk patients: minor thrombus, no history, - D-Dimer, non-diagnostic US or at high risk for bleeding ■ Survey patients every week for 2 weeks to assess for extension to the proximal veins
■ 50% of the population has elevated cholesterol, & 73.5 million adults (31.7%) have high LDL. ■ Fewer than 1 out of every 3 adults (29.5%) with high LDL cholesterol has the condition under control. ■ Less than half (48.1%) of adults with high LDL cholesterol receive treatment to lower their levels. ■ Male > female ■ Increased with age ○ Risk Factors ■ Family hx ■ Obesity/metabolic syndrome ■ CHD and equivalent ■ High saturated fat diet ■ Physical inactivity ■ Smoking ■ DM ■ Age ○ Definition ■ Primary hyperlipidemias: are probably genetically based ■ Secondary hyperlipidemia: ● Diabetes ● thyroid disease ● renal disorders ● liver disorders ● Cushing's syndrome ● Obesity ● alcohol consumption ● drug-associated – steroids, estrogen ○ Question ■ Using the ACC/AHA lipid management guideline, what specific diagnostic tool would you use to help determine the treatment plan for the patient’s cholesterol? What is the patient’s estimated risk score? ● http://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/ ■ ASCVD Risk Calculator ● ASCVD 10-year risk: 4.0% ■ Using the most current lipid guidelines, what is the treatment plan for this patient? Please provide a rationale. ● ASCVD risk score = 4% ○ No medication. ○ Emphasize lifestyle management. ■ If the patient was male, would your treatment plan change? Be specific and explain how and why. ● ASCVD risk score: 10.1%
● *Shared decision-making – include patient’s 10-year atherosclerotic disease risk ○ Answer ■ Moderate intensity statin ○ ATP 4 Lipid Guidelines ■ 4 statin benefit groups: ● HIGH-INTENSITY STATIN ○ 1 - Age > 21 with a history of ACVD (heart disease/stroke/PAD) = high-intensity statin ○ 2 - Age 20-75 with LDL >190 = high-intensity statin ● MODERATE INTENSITY STATIN ○ 3 - Age 40 – 75 with DM, LDL 70 – 189 = moderate-intensity statin ■ unless > 7.5%, consider high-intensity statin or multiple risk factors ○ 4 - Age 40 – 75 – no CVD or DM with calculated 10-year CV risk of ■ 5% - 7.4% = discussion ■ > 7.5% = moderate intensity ■ *consider coronary artery calcium scoring, ● if <100, can avoid statin or moderate intensity, especially > ● if >100, moderate statin ■ >20% - high intensity ○ High-Intensity Statin: lowers LDL–C ~ ≥50% ■ Indicated for: ● Clinical ASCVD age < 75 ● LDL-C ≥190 mg/dL ● Diabetics age 40–75 with LDL-C 70–189 mg/dL & 10 yr ASCVD risk ≥7.5% ● Age 40–75 – ASCVD >20% ■ The following are considered high-intensity statins: ● Atorvastatin 40–80 mg ● Rosuvastatin 20–40 mg ○ Moderate Intensity Statin: lowers LDL-C by ~ 30% to 49% ■ Indicated for: ● Clinical ASCVD age ≥ ● LDL-C ≥190 mg/dL (if unable to tolerate high-intensity statin) ● Diabetics age 40–75 with LDL-C 70–189 mg/dL & 10 yr ASCVD risk ≤7.5% ● Nondiabetics ages 40–75 with LDL-C 70–189 mg/dL & 10 yr ASCVD risk ≥7.5% ■ The following are considered moderate-intensity statins: ● Atorvastatin 10–20 mg
● Rhabdomyolysis ● Muscle aches – obtain CPK ● Heart Failure ○ Definition ■ a pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues ■ structural or functional impairment of ventricular filling or ejection of blood. ■ Since not all patients present with fluid overload, the term “heart failure” is preferred over “congestive heart failure.” ○ Epidemiology ■ 6.2 million people in the US ■ At least 650,00 newly diagnosed cases yearly ■ Approximately 50% die within 5 years of diagnosis ■ As age increases, HF is the primary diagnosis in >1 million hospitalizations annually ■ 13.4% of death certificates list HF on them. ■ Costs more than $30.7 billion annually, including health services, medication, and lost productivity. ○ ○ Etiology ■ HTN & CAD are the 2 most common risk factors ■ Other risk factors: CKD, DM, Afib, CVA, & valvular disease
○ Left-Sided Heart Failure ■ HFrEF (Systolic Failure) ● LV loses the ability to contract due to ischemic changes ● The heart cannot pump out adequate blood ● Known as heart failure with reduced ejection fraction (HFrEF) ● Defined as EF below 40% (normal is 55-60%) ● There is also heart failure with mildly reduced EF (HFmrEF) ■ HFpEF (Diastolic Failure) ● LV loses its contractility due to stiffness ● The heart can’t fill properly during diastole ● Known as heart failure with preserved ejection fraction (HFpEF) ● EF is normal - usually at least 50% in these patients. ○ Types of Heart Failure ■ Acute vs Chronic ● Acute : rapid onset, worsening of HF (previously termed decompensated HF) ● Chronic : there is longstanding S/S of HF, and the patient is being treated ■ Right-Sided Heart Failure ● The most common cause is left-sided failure ● Also caused by lung diseases like pulmonary HTN, COPD, pneumonia, etc. ● Increased fluid pressure is transferred back through the lungs, damaging the right side. ● Blood backs up in the body’s veins. ○ Clinical findings: jugular venous distention (JVD), hepatomegaly, hepatojugular reflux, peripheral edema, anasarca, ascites, etc. ○ Cardinal Manifestations of Heart Failure ■ dyspnea and fatigue, which can make activity difficult ( SOB is the most common symptom)
● Stage D. treatment-resistant heart failure requiring specialized intervention ○ Physical Exam Findings ■ Dyspnea, Fatigue, Edema ■ Neuro – lethargy, confusion ■ Lung – rales/crackles ■ CV - S3 (early sign of HF) ● +JVD, hepatojugular reflux ● Peripheral edema ● Increase in abdominal girth ■ ○ Management of Heart Failure ■ Pharmacologic ● ACE inhibitors (combat RAAS activation)/ ARBS ○ Improves clinical symptoms and functional status. ○ Improves mortality and decreases hospitalizations. ○ Monitor renal function and K+ ○ ● Beta Blockers (combat SNS activation) ○ Improves clinical symptoms and functional status.
○ Improves mortality and decreases hospitalizations. ○ Decreases risk for arrhythmia. ○ Patients with systolic BP < 85 mmHg, HR < 60 beats per minute, & decompensated heart failure usually excluded. ○ Caution in asthma ○ Do not stop abruptly, taper over 1-2 weeks to D/C ○ ● Vaptans (vasopressin antagonists) ● Diuretics ○ Loop: furosemide (Lasix); torsemide (Demadex) ○ Aldosterone antagonist – spironolactone (Aldactone) - Potassium sparing = for HFrEF NYHA Class III-IV ○ goal of diuresis use is to eliminate congestion. ○ Monitor renal function, K+, especially if used in conjunction with ACE inhibitors or ARBs ○ ● SGLT2 inhibitors ○ With or without diabetes ○ Dapagliflozin (Farxiga) 10 mg daily ○ Empagliflozin (Jardiance) 10 mg daily
■ Non-Pharmacologic Interventions ● Daily Weights ○ Early A.M. (same time daily) ○ Before a meal/drink ○ After urination ○ The same amount of clothing ○ Same scale ○ Call when there is a 2lb weight gain in 24 hours or 5 lbs in 1 week ● Dietary Restrictions ○ 2 grams Na intake ○ 2 L fluid intake for those with more severe heart failure and reduced renal function (ie: dialysis pt) ● Education and Follow-up ○ HF patient/family education ○ Follow up within 1 week post-discharge ● Treatment of Co-morbidities ○ Treatment of hypertension. ○ Treatment of hypercholesterolemia. ○ Treatment of diabetes mellitus. ○ Management of metabolic syndrome.
