NSG 3313 Exam 3 Study Guide PDF

NSG 3313 Exam 3 Study Guide Chapter 21 Preload, Afterload, Cardiac Output, CVP, SV o Preload: refers to the degree of stretch of the ventricular cardia muscle fibers at the end of diastole ▪ Volume of blood in ventricles at...

NSG 3313 Exam 3 Study Guide Chapter 21 Preload, Afterload, Cardiac Output, CVP, SV o Preload: refers to the degree of stretch of the ventricular cardia muscle fibers at the end of diastole ▪ Volume of blood in ventricles at the end of diastole (end of diastole pressure) ▪ Increased in: Hypervolemia, Regurgitation of cardiac valves, heart failure o Afterload: resistant to ejection of blood from the ventricle, the second determinant of stroke volume. ▪ Resistance left ventricle must overcome to circulate blood ▪ Resistance going out pressure exerting to push blood flow out of ventricles ▪ Increased in: Hypertension, Vasoconstriction ▪ Increased Afterload= increased Cardiac workload o Cardiac Output: a product of the stoke volume (the amount of blood ejected from the left ventricle during systole) and heart rate. ▪ CO- the total amount of blood ejected by one ventricle in one minute ▪ Stroke volume + heart rate = cardiac output o CVP: ▪ Central Venous Pressure (GOOGLE ANSWER) ▪ The blood pressure in the vena cava, near the heart’s right atrium ▪ It’s a measure of how much blood is returning to the heart and how well the heart can pump blood back into the arterial system o SV: ▪ SV= the amount of blood ejected from one ventricle per heartbeat Stress Test: o Purpose: ▪ Determines what heart condition you have by putting stress on the heart ▪ Why they are having shortness of breath, chest pain and other symptoms ▪ Changes in ECG o Assessment: ▪ Make sure patient is stable ▪ Monitor vital signs ▪ Looking for ECG changes ▪ Example: pt on treadmill, starts having shortness of breath Nurse intervention: have patient stop and rest Chapter 22  Conduction of heart (need to know normal pathway o SA node, AV node, the bundle of HIS, left and right bundle branches, Purkinje fibers o 60-100 bpm o SA Node is Pacemaker EKGs- what each wave indicates Analyzing the ECG strip o Used to determine cardiac rate and rhythm o A 1-minute strip contains 300 large boxes and 1500 small boxes o Count large boxes from QRS to QRS and divide into 300 Example – if you count 2 large boxes between QRS – 300/2 = 150bpm o P wave: atrial depolarization o QRS: ventricle depolarization/ repolarization o Normal Sinus Rhythm ▪ Rate: 60-100 bpm ▪ Rhythm: regular ▪ P wave normal ▪ PR-i: consistent 0.12-0.20 sec ▪ P: QRS is 1:1 ▪ Indicative of good cardiovascular health. However, an increase of 10 bpm or more in the resting heart rate increases the risk for sudden cardiac death, atrial fibrillation, heart failure, CAD, stroke, and cardio disease  Sinus Bradycardia o Less than 60 beats per minute o P wave normal and consistent in front of QRS o PR-i: consistent interval between 0.12 and 0.20 sec o P: QRS- 1:1 o Management ▪ Depends of s/s ▪ If symptomatic- may need atropine ▪ Transcutaneous pacing ▪ Use of catecholamines o Nurse Action ▪ Assess patient (make sure led are on) ▪ Ask patient fatigue, light-headed (symptoms of bradycardia) ▪ Treatment is determined by if they are symptomatic ▪ Atropine, pacer (may be needed if symptoms) ▪ No symptoms- monitor ECG and vital signs Sinus Tachycardia o Rate is greater than 100 bmp o Rhythm is regular o P wave is normal and consistent but may be buried in T wave o PR-i: consistent but may be buried o 1:1 ratio o Management ▪ Depends on s/s ▪ If symptomatic may need to be synchronized cardioversion  ▪ Adenosine ▪ AV blocking meds o Nurse Actions ▪ Assess patient ▪ Treating underlying cause ▪ Make sure its an accurate reading ▪ Does patient have fever, in pain, dehydrated o If you find a patient is unresponsive ▪ Assess patient first ▪ Check for pulse ▪ Airways (make sure they are breathing ▪ Call for help and start CPR if no pulse or breathing Ventricular Dysrhythmias premature ventricular complex (PVC) o An impulse that starts in the ventricle and is conducted before the next NSR complex o Ventricular rate- depends on underlying rhythm o Irregular rhythm due to early QRS o QRS is 0.12 sec or longer and shape is abnormal o P wave- visibility depends on timing of PVC o PRi is less than 0.12 sec o Ratio is 0:1 or 1:1 VTACH VFIB  PEA ASYSTOLE Any pulseless rhythms must initiate CPR Abnormal rhythms/Unresponsive patients- Assessment and treatment o S3- third heart sound – can relate to heart failure ▪ Heard early in diastole during period of rapid ventricular filling as blood flows from the atrium into a noncompliant ventricle ▪ Lub-dub-dub ▪ Best heard over the apical area with the patient in the left lateral position ▪ Heard after S2 o S4-Fourth Heart sound- Can relate to hypertensive heart disease  ▪ Occurs late in diastole ▪ Heard just before S1 is generated during atrial contraction as blood forcefully enters a noncompliant ventricle ▪ LUB lub dub ▪ Best heard over the tricuspid area with the patient in supine position o Opening Snaps and Systolic clicks ▪ Open snaps: are abnormal diastolic sounds heard during opening on an AV valve Sound is caused by high pressure in the left atrium that abruptly displaces, or snaps open a rigid valve leaflet It occurs long after S2 to be mistaken for a split S2, and too early in diastole to be mistaken for an S3 ▪ Systolic click: stenosis of one of the semilunar valves creates short, high- pitched sound in early diastole, immediately after S1 Results of the opening of a rigid and calcified aortic or pulmonic valve during ventricular contraction o Murmurs ▪ Are created by turbulent flow of blood in the heart ▪ Causes of turbulence may be a critically narrowed valve, a malfunctioning valve that allows regurgitant blood flow, a congenital defect of the ventricular wall ▪ Characteristics include timing in the cardiac cycle, location on the chest wall, intensity, pitch, quality, and pattern of radiation o Friction Rub ▪ A harsh, grating sound that can be heard in both systole and diastole ▪ It is caused by abrasions of the inflamed pericardial surfaces for pericarditis ▪ Can be confused for a murmur CPR o Know how to assess patient, rate of compressions and rate of rescue breathes ▪ Compressions in a minute ▪ Resue breathes ▪ Ratio to compressions to breathes 30 COMPRESSION-2 BREATHS o Cardiopulmonary resuscitation provides blood flow to vital organs until effective circulation can be reestablished. Following the recognition of unresponsiveness, a protocol for basic life support is initiated. o The resuscitation process begins with the immediate assessment of patient breathing and consciousness, then call for assistance, as CPR is performed most effectively with the addition health care providers and equipment Chapter 23 Myocardial Infarction: Heart attack -Acute Coronary Syndrome: Acute onset of Ischemia that leads to myocardial death STEMI vs NSTEMI- STEMI- Patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. NSTEMI- Patient has elevated cardiac biomarkers but no definite ECG changes (less damage to the myocardium) EKG changes: 12 lead EKG, Cardiac Biomarkers, cardiac catheterization Labs: Elevated Troponin (there is damage to the heart) *High cardiac troponin Clinical manifestations: Angina, Substernal chest pain, elephant on chest Treatment: Oxygen 1st Intervention, Nitroglycerin, Morphine, Aspirin Nitro contraindication: Viagra and low blood pressure Nursing interventions: hook them up to monitor, 12 lead, oxygen, start an IV Patient education: lifestyle modifications, discharge teaching/monitoring for cardiac symptoms, appropriate exercise, stopping smoking, low salt and fat diet, knowing medications, and taking them correctly. Cardiac cath: -Post-care assessments/priorities. Check for puncture site and make sure there is no hematoma or bleeding, look distally. CAD- Risk factors- Modifiable: (My notes) Hyperlipidemia, Tobacco use, Hypertension, Diabetes, Metabolic syndrome, Obesity, Physical inactivity, Chronic inflammatory conditions (Lupus, Rheumatoid arthritis, HIV/AIDS, and Chronic Kidney Disease. Nonmodifiable: (My notes) Family history of CAD, increasing age, Gender, Race (higher in African Americans), History of premature menopause and pregnancy associated disorders such a preeclampsia, and primary hypercholesterolemia Patient education: focus on modifiable Stop smoking, diet and exercise CABG: post-op priority care: making sure the heart is still pumping appropriately or fluid retention.  Look at urine and blood pressure to see if still getting blood flow. (End organ perfusion) Angina- Know the different types Stable: can be relieved by rest, usually triggered by walk Unstable: can’t be relieved with rest, can come on anytime, not triggered by activity or event. Variant : can vary Know medications for MI/CAD and MOA and patient education: It can vary depending on the patient BUT are they on Plavix or Aspirin (prevents platelets from forming clots) Heparin drip- Lab to monitor: aPPT Range: over 100 STOP the infusion 60: GOOD 30: LOW Chapter 25 Heart failure: Key Diagnostic Test- B-type natriuretic peptide Clinical manifestations (Right vs Left), Right: edema , distended kneck veins, ascites Left: Lungs, dyspnea, orthopnea Risk Factors: MI, increased aging, valve abnormalities Patient education: Low sodium diet, Daily weights (same scale everyday at the same time, same clothing) Heart failure- decrease in cardiac output Compensatory mechanisms: RAAS and Sympathetic nervous system Vital Sign changes: increase in Blood pressure RAAS activation System: Mechanism: Reduced renal blood flow triggers the release of renin, which converts angiotensinogen to angiotensin I, then to angiotensin II, a potent vasoconstrictor. Angiotensin II stimulates aldosterone release, leading to sodium and water retention. Effect: Vasoconstriction increases blood pressure, and fluid retention increases blood volume, both aimed at improving perfusion. However, these lead to increased afterload, worsening the heart's workload and contributing to fluid overload (edema). Pulmonary edema Clinical manifestations: pink frothy sputum, crackles Nursing interventions: sit them up, elevate the head of the bed, and use diuretics to pull fluid off LVAD: (Left Ventricular Assist device) Utilized for patients with heart failure, buys them time until heart transplant (portable) Chapter 26 Atherosclerosis- plaque build-up Risk factors: Modifiable/Nonmodifiable (page 828) (smoking, diabetes, hypertension, high fat diet, stress, sedentary lifestyle /// non mod age, genetics Patient Education: modifiable risk factors, exercise, diet ect. PVD/PAD/Venous Insufficiency- Clinical manifestations, patient educations, complications, and treatments Peripheral artery disease (PAD) is a common circulatory problem in which narrowed arteries reduce blood flow to the limbs, usually the legs. Clinical Manifestations: More common in the lower extremities - Hallmark manifestation is intermittent claudication: 5 P’s (Pain, Pale, Paresthesia, Pulseless, Paralysis), Ulcerations, gangrene, nail changes, and muscle atrophy, Pulse changes - Manifestations in the upper extremities include: arm fatigue and pain Patient Education: Daily foot hygiene- wash between toes with mild soap and lukewarm water, rinse, pat dry. Cut toe nails straight across after showering, wear soft loose cotton socks (allows air to circulate), wear extra socks when cold, avoid heating pads, hot tubs, inspect feet daily for redness, cuts, blisters, dryness (if occurs call provider), avoid sandals, wear leather shoes with extra depth toe box, use cream and lotions with emollient, avoid compression socks, do not cross legs, stop using nicotine products, participate in regular exercising such as walking to stimulate circulation, no medication used on feet unless prescribed, avoid using alcohol, iodine, adhesive products, etc -Shiny color, no hair on legs, *FEET DOWN* PAD- A as in feet down Complications: Urine output, venous pressure, mental status, pulse rate and volume- indicates fluid imbalances; Bleeding can result from the heparin given during surgery or form an anastomotic leak; A hematoma may form; Thrombosis (from leg crossing); Severe leg crossing; Severe edema, pain, decreased sensation of toes and fingers indicate compartment syndrome Treatments: Pharmacologic- Trental or Pletal, Antiplatelets and Statins, Cilostazol- phosphodiesterase III inhibitor (a direct vasodilator that inhibits platelet aggregation) Endovascular- Stents, balloon angioplasty, and atherectomy Surgical- Endarterectomy, Bypass Grafting Chronic Venous Insufficiency/ PVD: Results from obstruction of the valves in the veins or a reflux of blood through the valves. PVD- V as in feet up, elevate legs / inspect daily Pathophysiology: Venous Hypertension, Distended veins, Inability of valves to close Clinical Manifestations: resulting edema, altered pigmentation, pain, and stasis dermatitis. The patient may see s/s less in the morning and more at night. Complications: Severe post thrombotic syndrome, stasis ulcers, *Venous ulcers*, DVT’s, Stasis Ulcer; Warm, red, swollen / Lots of fluid Patient Education: Skin kept clean, dry, and soft. Signs of ulceration are immediately reported to physician, make sure to elevate the legs for 15-20 4xd, compress the legs, at night elevate the foot of the bed about 15 cm (6 inches). Avoid crossing legs, and legs dangling on the side of the bed. CVI Management/ Treatment: Elevate the legs, Avoid Constrictive clothing, Compression Stockings, Encourage Activity (Walking), Report signs of ulceration, Nursing education Raynaud’s disease- form of intermittent arteriolar vasoconstriction that results in coldness, pain, and pallor of the fingertips. clinical manifestations : Pallor-→ Cyanosis→Redness Treatment: CCB’s calcium channel blockers, such as amlodipine, avoid triggering stimuli (emotional factors/cold, avoid smoking, cold, and otc decongestions) **Educate and avoid triggers** Femoral, popliteal bypass: -Post-op care: Assess pulse of affected extremities every 15 minutes at first. pedal pulses are there and distal to graft site you know you have blood flow. Ulcers- Venous vs Arterial. ** Know the defining characteristics of the different ulcers Venous: shallow leg or ankle, irregular border, discoloration (ischemia and cell death) Arterial: Top of foot, toes or heels, ischemia → severe pain  **MAIN DIFFERENCE** venous superficial irregular border, arterial “whole punch appearance.” Abdominal Aortic Aneurysm- -Most common cause: atherosclerosis -if untreated will result in rupture and death - Clinical manifestations: masses, scars, mass pulsating, may have pain Signs of HF or listening for bruit more common in men, whites, and age of 65 and older, and smokers Nursing action/treatment: blood pressure control/ prevent the rupture **NORMAL ANERURYSM: A weak point in the wall of an artery. Chapter 27 Hypertension- 130/80 NEW 140/90Test Types/Categories: Pre, stage 1 and 2 (pg 166)  Primary vs Secondary Primary: no identifiable cause 90-95% of Americans have it Secondary: has an identifiable cause (thyroid, drug use, hyperparathyroidism) 5-10% of Americans have it Complications: prevent death and damage of arterials, like TIA/ stroke, Left ventricular hypertrophy, MI, HF, Chronic kidney disease, Retinal Hemorrhage Patient education: Pt needs to understand disease, lifestyle changes, medications, smoke cessation, exercise promotion, limit alcohol, and reduce salt intake Dietary modifications: low sodium/fat diet Risk Factors: aging, African American, CKD, diabetes, alcohol, family HX, men more likely than women until older, being obese, poor diet, poor exercise, tobacco use Clinical Manifestations: vision changes and headache otherwise **silent killer Medications – patient education page 872-873 Thiazide diuretics: first line diuretics hydro, cloprothiazole Side effect: dry mouth, thirst, weakness, drowsiness, lethargy, muscle aches, muscular fatigue, tachycardia, GI disturbances Therapeutic effects: Decrease in blood volume, renal blood flow, and cardiac output (decreased blood pressure); Depletion of extracellular fluid; Overall treatment to remove excess fluid/ over-load condition to lower blood pressure. Ace inhibitors: RAS system – Can cause hyperkalemia Side effect: dry cough CCB: amlodipine, nifedipine: vasodilation **foot/ankle swelling Patient Education: -written instructions on medication regimes - follow up appointments -avoid abrupt withdrawal Hypertensive Crisis- BP >180/100 – 180/120 Two types: Emergency and Urgency Emergency: (damage to target organs) (ELEVATED BUN AND CREATININE) Decrease mean arterial pressure (MAP) by 20- 25% for the first hour (IV MEDS) Treatment for Emergency: Vasodilators- Nitroglycerin and Sodium Nitroprusside: Slow push for IV medications Urgency: No evidence of emergency, YET over 24-48 hours Severe headache, nosebleeds (close monitoring) Oral agents are Okay Three causes: poorly controlled, undiagnosed, abruptly stop medication. Risk: smoking, obesity, poor diet high sodium