MEDSURG 2 FINAL EXAM.

MEDSURG 2 FINAL EXAM. Medsurg 2 FINAL EXAM Cardiac Assessment Cardiac Conduction System Generates and transmits electrical impulses that stimulate contraction of the myocardium SA node  AV node  Bundle of his (branches into right and left)  purkinjie fibers SA node which is the primary pacemaker of the heart o A patient has a HR of 90. Means The SA node is working because normal HR is 60-100 o If the HR falls below the normal value, there is a problem! AV node which is the secondary pacemaker of the heart o If the SA node malfunctions. The AV node will take over which has a lower rate such as 40-60 bpm Cardiac Action Potential Is the electrical cells generate and transmit impulses across the heart which will stimulate cardiac myocytes to contract. Stimulation of these myocytes occurs due to the exchange of electrically charged particles (ions) across the channels located in the cell membrane In resting or polarized state  o Sodium is the primary extracellular ion o Potassium is the primary intracellular ion Terms of Cardiac Action Potential o Depolarization: electrical activation of cell caused by influx of sodium into cell while potassium exits cell. THIS CREATES A POSITIVELY CHARGED INTRACELLULAR SPACE AND NEGATIVELY CHARGED EXTRACEULAR SPACE o Repolarization: return of cell to resting state caused by re-entry of potassium into cell while sodium exits o Refractory periods – cardiac cells must completely repolarize before they can depolarize AGAIN o 2 phases of refractory period  o Effective refractory period: phase in which cells are incapable of depolarizing. It is completely unresponsive to ANY electrical stimulus o Relative refractory period: phase in which cells require stronger-than-normal stimulus to depolarize Cardiac Hemodynamics • HR x SV = Cardiac Output • Cardiac output refers to the total amount of blood ejected by one of the ventricles in liters per minute. • The cardiac output in a resting adult is 4 to 6 L/min but varies greatly depending on metabolic needs • Cardiac output responds to changes in the metabolic demands of the tissues associated with stress, physical exercise, and illness o HR is affected by central nervous system activity and baroreceptor activity. o HR is determined by rate and rhythm – if it is regular or irregular o If HR is affected so is CO o If the heart is not stretching enough – cardiac output is affected o If the heart is not pumping – cardiac output is affected • Stroke volume is determined by  preload, afterload, and contractility o Preload: refers to the degree of stretch of the ventricular cardiac muscle fibers at the end of diastole. The end of Diastole is the period when filling volume in the ventricles is the highest and the degree of stretch on the muscle fibers is the greatest (when it is filled with more and more blood = the greater the stretch = the greater the force of contraction) o Diastole is the relaxation/filling phase of the ventricles and once these have filled  this is the preload. We can also refer to preload as the EVD (it is at the end of the diastolic phase). Preload is the amount the ventricle stretched! ▪ Think of a balloon (such as the more air you blow in, the greater the stretch) o Afterload: resistance to ejection of blood from the ventricles. This is the pressure required to overcome aortic pressure. The higher the aortic pressure the harder the ventricles have to work – (the LV must overcome the aortic pressure). The pressure in the ventricles work against to open the SL valves to pump blood out of the heart o Contractility: refers to the force generated by the contracting myocardium (the more forceful the more blood that is ejected) • If there is an issue with cardiac output = perfusion issue because there is an issue with oxygenation and flow components • Low HR = CO is affected • Increase in SV and HR = increase in CO Age Related changes in cardiac -Atria, LV, Valves (stiffen and no longer close properly), Conduction system, SNS (decreased response), aorta (stiffen), arteries (stiffen), baroreceptor response (more sensitive) History and Physical Health History which refers to the patient’s ability to recognize cardiac symptoms to know what to do when they occur it is essential for effective self-care management • Want CLEAR information when talking to the patient  Chief complaint, Hx present illness & past medical history/social history, Home meds, Nutrition, Allergies Physical Assessment (Cardiac specific) • General appearance, Skin and extremities • Blood pressure  pulse, and postural BP  Below 30 is reduction in CO • Arterial pulses  rate, rhythm, amplitude • Jugular venous pulsations  fluid accumulation/overload • Heart inspection and auscultation • Any deviations from normal? Meaning changes in how the patient responds to how they are feeling. Such as a patient with HF or circulatory issues will change their shoes due to their feet being swollen o Heart as a pump o Atrial/ventricular filling volumes o Cardiac output o Compensatory mechanisms ▪ What position does the patient lay in when they sleep? ▪ Tripod position  patient is leaning forward. This is an indication of respiratory distress MOST common clinical manifestation • Ask why the pt would feel like this? • Chest pain • SOB, dyspnea  fluid overload/pulmonary issue can lead to dyspnea • Peripheral edema • Weight gain • Abd distention • Fatigue • Dizziness, Syncope, Changes LOC due to perfusion and oxygenation issues (brain likes oxygen) • We know diuretic is working if the pt is peeing a lot and they feel less fatigue/dyspnea Chest Pain • Identify Quantity, location, quality, radiation, duration of pain , Associated S/S • Assess  for other cardiac conditions and for other significant conditions • Angina Pectoris: uncomfortable pressure, squeezing, or fullness in substernal chest area. It can radiate across chest to the medial aspect of one of both arms and hands, jaw, shoulders, upper back, or epigastrium. (BOOK) • ACS: is the same as angina pectoris. Pain and discomfort ranges from mild to severe associated with SOB, diaphoresis, palpitations, unusual fatigue, and n/v (BOOK) • Pericarditis: sharp, severe substernal or epigastric pain which can radiate to necks, arms, and back. • Pneumonia, pulmonary embolism  sharp, severe substernal or epigastric pain arising from interior portion of pleura • Hiatal hernia, GERD  substernal pain described as sharp, burning, or heavy. Often mimics angina and can radiate to neck, arm, or shoulders. • Costochondritis  musculoskeletal disorders. This is a sharp or stabbing pain localized in anterior chest. Most often is unilateral and can radiate across chest to epigastrium or back • Vascular Diagnostic (laboratory values) Hematologic Studies • CBC  identifies the total number of white and red blood cells and platelets and measures the Hgb and Hct. The CBC is carefully monitored in a patient with cardiovascular disease • Hct: 45% • Hgb: 15% • Platelets: 150,000-450,000 • WBC: 4,500-10,500 • RBC: 5 Cardiac Biomarker – • serum biomarkers (can be used for a diagnosis of an MI) • CK: 22-198 U/L. A high amount = damage • CK-MB: 0-3.  Elevated CK-MB is indicator of acute MI; the level begins to increase within a few hours. • Myoglobin: 0-85 ng/mL.  This is a protein which can tell if tissues are damaged • Troponin: 0-0.4.  This is a protein that is a marker for the heart. Elevated means the patient is having a problem with their heart such as a heart attack • Myocardial cells that become necrotic from prolonged ischemia or trauma release specific enzymes (mentioned above). These substances leak into the interstitial spaces of the myocardium and are carried by the lymphatic system into general circulation • This bundle becomes important, timing is important. Look at when do you see these levels start to rise (usually within 4- 6hrs), when do they peak (15-20hrs), and when should you start to see a resolution (2-3 days) • If levels are not coming down, can mean that injury is extending…. Blood Chemistry • BUN: 10-20 mg/dL  An elevated BUN can mean dehydration • Creatinine: 0.7-1.4 mg/dL  This is a good indicator for renal function • Sodium: 135-145 mEq/L  Low or high do not directly affect cardiac function • Potassium: 3.5-5 mEq/L  Plays a major role in cardiac electrophysiologic function o Hypo: dysrhythmia, life-threatening ventricular tachycardia or ventricular fibrillation and predispose patients taking digitalis preparations to digitalis toxicity o Hyper: heart block, asystole, life threatening ventricular dysrhythmia • Magnesium (this is sometimes ADDED, it is not always on the blood chemistry): 1.8-3.0 mg/dL  This is necessary for the absorption of calcium, maintenance of potassium stores, metabolism of adenosine triphosphate. It plays a major role in protein and carb synthesis o Hypo: atrial and ventricular tachycardias o Hyper: depress contractility and excitability of the myocardium, causing heart block and if severe, asystole • Calcium: 8.5-10.5 mg/dL  This is necessary for blood coagulation, neuromuscular activity, and automaticity of the nodal cells o Hypo: slow nodal function and impair myocardial contractility which can put the patient at risk for a heart attack o Hyper: ventricular fibrillation Coagulation studies • Injury to a vessel wall or tissue can initiate the formation of a thrombus. This injury activates the coagulation cascade o PTT: 60-70 seconds Measures the activity of intrinsic pathway and is used to assess the effects of heparin o aPTT: 20-39 seconds o PT: 9.5-12 seconds.  This is used to monitor the level of anticoagulation with warfarin o INR: 2-3.5 This can be used to measure warfarin (professor said this is clinical). It is a laboratory value used to see how long blood takes to form a clot ▪ A 1  there is NOT enough anticoagulation medication ▪ A 2  there is ENOUGH medication on board BNP • Is a neurohormone that helps regulate BP and fluid volume. It is secreted from the ventricles in response to increased preload with resulting ventricular pressure • This is very specific for HF (over 100) • A BNP greater than 100 is suggestive of HF Cholesterol: • Normal  200 mg/dL • LDL: 130 mg/dL. This is the primary transporter of cholesterol and triglycerides into the cell. A high level of this can be bad because it can lead to heart disease, diabetes, and CAD • HDL: 40 mg/dL C-reactive protein • Protein produced by the liver in response to systemic inflammation • People with high hs-CRP levels (3 mg/L or greater) may be at greatest risk for CVD compared to people with moderate (1 to 3 mg/L) or low (less than 1 mg/L) Homocysteine • Linked to atherosclerosis because it can damage the endothelial lining of the arteries and promote thrombus formation • A 12-hour fast is necessary before drawing a blood sample for an accurate serum • Elevated homocysteine is indicative of a high risk for CAD, stroke, and peripheral vascular disease • Test results are interpreted as optimal (less than 12 mcmol/L), borderline (12 to 15 mcmol/L) and high risk (greater than 15 mcmol/L) ECG • Electrical currents of the heart • 12-lead ECG is used to diagnosed dysrhythmia, conduction, abnormalities, chamber enlargement, as well as myocardial ischemia injury, or infarction Continuous ECG • Used when patient is at risk for dysrhythmia • Detects abnormalities in the heart rate and rhythm Assessment • Meds, nutrition, elimination, activity, exercise, sleep, rest, self-perception/concept, roles, relationships, sexuality, reproduction, coping, stress tolerance, prevention strategies, General appearance • Bp  pulse pressure, postural BP changes • Arterial pulses pulse rate, rhythm, amplitude(force)- regular/irregular • JVD  indicative of fluid overload • Heart inspection/palpation/auscultation o S1, S2 (S3, S4) o S3 normally found in HF (or fluid overload) o S4 specific to CAD • Assessment of lungs respiratory overlap if pt has fluid overload • Assessment of abdomen ascites (how it impacts breathing and overload of heart) Diagnostic Evaluation Imaging: Chest X-ray  • size, position, contour of heart • reveals cardiac/pericardial calcifications • assists in diagnosis other conditions Fluoroscopy ECG  • Electrical activity of heart (12 lead- 12 different views of heart) • Diagnoses  Dysrhythmias, conduction abnormalities, chamber enlargement, myocardial ischemia, infarction, injury, electrolyte imbalances • Continuous ECG Standard care for pt w/ continuous monitoring o Monitors more than 1 lead at a time, monitors ST segments, provides visuals/audible alarms Cardiac Stress Testing Noninvasive procedure to evaluate response to stress. We are increasing the demand/workload of the heart on purpose since abnormalities are more than likely to be detected during times of stress/demand. The test is terminated when target HR is achieved or when the patient c/o myocardial ischemia Exercise: o Walks on a treadmill, bike, arm crank o Exercise intensity increases o Patient monitoring (EKG, VS) o Terminate test when  Target HR achieved or when ischemia occurs Pharmacologic: o Physical disability/deconditioned o Persantine and Adenocard IV o Mimic effects of stress o Dobutamine if no tolerance to exercise *GOAL of both tests  put stress on heart to determine if any of these 6 are present  Used to determine the following: • Presence of CAD • Cause of chest pain ischemia?? • Functional capacity of the heart after an MI or surgery • Effectiveness of antianginal or antiarrhythmic medications • Occurrence of dysrhythmias • Specific goals for physical fitness program Contraindications: • Severe aortic stenosis, Acute myocarditis or pericarditis, Severe HTN, Suspected left main disease, Heart failure • Unstable angina  this is a precursor for MI • MI within 48 hours Complications: AMI, cardiac arrest, heart failure, and unstable angina. o If the patient is having chest pain, the test must be stopped immediately Nursing Interventions: • NPO x 4 hours, Avoid stimulants such as caffeine and tobacco, Meds with sips of water • May instruct to hold beta blocking agents, theophylline, aminophylline before test (these drugs lower HR) • Appropriate attire, Sensations with medications Cardiac Evaluations Transesophageal echocardiography- • ultrasound of heart (EXTERNAL visualization) • Threading a small transducer through the mouth and into the esophagus • Topical agent is applied, and moderate sedation is used • Evaluating patient with many CVD such as HF, valvular heart disease, dysrhythmia, and many other conditions • Nursing Intervention: the patient is not to eat or drink anything for 6 hours. During the test the nurse will provide emotional support and monitor LOC, BP, ECG, and respiration, and SPO2. Food and fluid is withhold until patient is fully alert and the effects of the topical anesthetic agent are reversed, usually 2 hours after; if the gag reflex is intact the nurse can start feeding with sips of water Transthoracic echocardiography- • Noninvasive INTERNAL visualization • Ejection fraction – (amount of volume left after pump- looking at left side of heart) o if you can determine EF you can determine  Cardiac output. • Size, shape and motion of cardiac structures • Pericardial effusions, Determines chamber size, Etiology of heart murmurs, Function of heart valves, Ventricular wall motion Myocardial perfusion imaging- • performed after an acute MI to determine if arterial perfusion to the heart is compromised during activity and to evaluate extent or myocardial damage Computerized tomography (CT)- cardiac evaluation MRI- different glsnds to see different structures PET scan (a dye that you can swallow – machine lights up where there is a dysfunction) • Determines muscle injury- when there is muscle injury, the tissue isn’t going to be able to suck up the dye the same way Cardiac Catheterization A test that helps clinicians determine if you have CAD Invasive procedure with radiopaque arterial and venous catheters advanced into right and left heart which is guided by fluoroscopy. To look at vascularization The patient has an arterial line which will inject dye & they will be able to see where the blockage is • A catheter is inserted in either the femoral or radial artery, and once is it in the correct anatomical location, they are going to do a version of an x ray (fluoroscopy), we give dye through catheter, dye goes through the vessels, we look through fluoroscopy to see if there is a blockage- once they see the blockage, that's what we talk about what we are going to DO- PTCA that's the ACTION plan. Are we going to open a balloon? Place a stent? Depending on the vessel, how many vessels, that's what we determine what we are going to do. Gold standard for diagnosis of: • CAD, Coronary artery patency, Atherosclerosis extent, If revascularization is necessary, Pulmonary artery HTN, Valvular heart disease Complications: • Anaphylaxis from iodine o Iodine must be flushed out (check creatinine/BUN before & after) o Increase fluids after pt leaves catheter lab (IV fluids) o Monitor catheterization site for hematoma, damaged artery • Contrast induced nephropathy (CIN) increase baseline creatinine by 25% w/in 2 days of procedure • Bleeding (importance of applying pressure through: manual pressure, Femostop, quickseal/angioseal, sutures) Interventions: • Sedation so pt isn’t uncomfortable • Labs beforehand • Fast 8-12 hours prior • Transportation home • Explanation of procedure • Observe sit for bleeding/hematoma • Neurovascular assessment of extremity (pulses distally from insertion site, use doppler if pulses are not found) • Screening for dysrhythmia • Bedrest for 2-6 hours, positioning (pt must lie flat for a few hours) • Monitor CV status, chest pain, and VS • Monitor for CIN • Vascular status • BUN/creatinine • Dysrhythmia • After  the catheter must come out and pressure should be applied in the following ways: femoSTop, quickseal/angioseal, sutures Hemodynamic Monitoring Central Venous Pressure (CVP) that is inserted into the subclavian. Volume status is measured through volume status (able to receive a wave form; how much volume status the patient has centrally) • Measures filling pressure in RIGHT atrium/ventricle at end of diastole (PRELOAD) ▪ Hypervolemia or right sided HF greater than 6mm hg  indicates an elevated right ventricular preload ▪ Hypovolemia less than 2mm hg indicates reduced right ventricular preload o CVP 2-6 mm Hg o CVP reading of 10  too much fluid (hypervolemia) you would give a patient a diuretic for fluid overload. Give the patient Lasix and the CVP reading goes to 5, this is good. Pulmonary Artery Pressure Monitoring Central monitor that gives different readings of the heart • Assess LEFT ventricular function, Diagnose ethology of shock, Evaluate response to therapy, Administer medications, Place pacemaker, Measures cardiac chamber pressures Intra-arterial Blood Pressure Monitoring • Obtains direct and continuous BP measurement in critically ill patients with severe hypertension or hypotension • Obtain arterial blood gas specimen  ABG values • Radial artery Heart Failure Is a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood. It is the ventricles that are sick in the heart • Frequent flyers – around the holidays – educate pt to prevent it • 75 yrs of age (most common hospitalization- they have changes in heart) Risk Factors: CAD, cardiomyopathy, valvular disorders, renal dysfunction with volume overload, and systemic or pulmonary HTN Pathophysiology: Significant myocardial dysfunction occurs refers to stiffening of the heart & muscles wearing out Responsible for s/s of edema and SOB o Diastolic RIGHT HF: RV cannot eject sufficient amounts of blood and blood backs up in the venous system. This results in peripheral edema, hepatomegaly, ascites, anorexia, nausea, weakness, and weight gain. ▪ Characterized by stiff and noncompliant heart muscle ▪ The EJ is normal (55-65%) due to the position of the heart in the body ▪ Can occur by itself o Systolic LEFT HF: LV cannot pump effectively into systemic circulation. Pulmonary venous pressure increase and will result in pulmonary congestion with dyspnea, cough, crackles, and impaired oxygen exchange ▪ Characterized by a weakened heart muscle. ▪ Reduced EJ ▪ There is an alteration in ventricular function ▪ This can also result in right sided HF- bc whats backing up into the lungs can eventually start backing up into the right side o Chronic heart failure is frequently biventricular Diagnostic Studies: • Echocardiogram to confirm diagnosis of HF • Chest x-ray • 12-lead EKG serum electrolytes (CMP), liver function tests, CBC o We want to look at NA, water, and potassium on the patient • BNP (HR specific)  number over 100 (THIS WOULD BE ELEVATED) o 100-200 is fine o 300 is mild o 800-1000 BNP = SEVERE  FULL BLOWN CHF • C reactive protein looking for inflammation Clinical manifestations: characterized by s/s of fluid overload or inadequate tissue perfusion o Congestion  dyspnea, orthopnea, PND, cough, pulmonary crackles, weight gain, dependent edema, ascites, JVD, and fatigue o Low cardiac output  muscle wasting/weakness, lightheadedness/dizzy, resting tachycardia, pallor/cyanosis, and the kidney will start to shut down and not produce urine o **know what low C.O looks like in a pt* Systolic LEFT HF: everything will start to back up to the lungs Diastolic RIGHT HF: blood will stay and back up and go backwards into the circulatory system Diastolic RIGHT HF Systolic LEFT HF - LEFT FOR LUNGS *SWELLING GOING ON* • Edema can occur in the legs/feet/ankles as well. Everything will back up! • -If swelling in feet they are cold • When blood backs up edema occurs in abd, liver, legs (renal obstruction) • JVD due to fluid backing up and pressuring • Ascites • Hepatomegaly due to the liver getting bigger • Anorexia – loss of appetite, nausea, or abdominal pain may result from the venous engorgement and venous stasis with the abdominal organs • The feet start to swell – feet will feel cool/cold when there is edema • Nausea • Weight gain due to retention of fluid and sodium. So, we want to perform daily weights on the **Hallmark sign: patient will have a pink frothy sputum because the mucosal is irritated (blood tinged sputum) • SOB and O2 stats would be low • Fatigue • Coughing which will irritate the mucosal of the lungs – this is a dry nonproductive cough • Paroxysmal nocturnal dyspnea- sensation of SOB that awakens the pt • Crackles in the base of the lungs • Orthopnea which is difficulty breathing when lying flat (need to sleep in a recumbent position) • PND, pleural effusion, and pulmonary edema will occur because the fluid is backed up in the pulmonary system. • Patient will have a decrease in renal function – oliguria will occur • Patient will have a cerebral anoxia  confusion, irritability, dizziness, and lightheadedness (patient start becoming restless; a sign the patient is getting oxygen deprived). patient • Patient will start getting tired and fatigue – muscle weakness; patient can’t even stand up. • Heart sounds S3 and a gallop occurring • Require sitting in chair to sleep • Daily weight to know if edema is present (pt starts to gain weight bc of sodium/water retention) Complications: • hypotension, cardiogenic shock (inadequate blood flow), dysrhythmia, thromboembolism, pericardial effusion, and cardiac tamponade (fluid in pericardium builds up, resulting in compression of the heart) GOAL in management • Relieve symptoms, improve functional status, extend survival • Improve cardiac by reducing preload, afterload (through meds/diet) • Delay progression of HF Pharm therapy • **Diuretics (most important) o Admin Lasix to pt- diuresis the pt – GETS RID OF FLUID o Concern potassium  prevent hypokalemia  give pt potassium if labs are under 3.5 • ACE inhibitors decrease BP/afterload • ARBS decrease BP/afterload • Hydralazine vasodilator • Nitrates vasodilator • Beta blockers decrease afterload (lower everything) • Digitalis increase contractility • IV infusion increase C.O (milrinone, dobutamine) • Antiarrhythmic Nursing Mx CHF patient NEEDS HOPE – main treatment/nursing interventions for the patient • H  Head of the bed elevated 45 degrees (semi fowler/high fowler position) • O  give the patient Oxygen because they are deprived of oxygen • P  Push furosemide/Lasix/morphine which can be used to reduce to workload of the heart (afterload drug) • E  end sodium. NO SODIUM/EXTRA FLUID IN THE PATIENT’S DIET. Sodium is responsible for swelling up the cells • Promote activity intolerance o Bed rest for acute exacerbations o Encourage regular physical activity; 30–45 minutes daily o Exercise training o Pacing of activities o Wait 2 hours after eating for physical activity o Avoid activities in extreme hot, cold, or humid weather ▪ Due to the workload of the heart during these temperatures. We want to conserve the workload of the heart o Modify activities to conserve energy o Positioning; elevation of the HOB to facilitate breathing and rest, support of arms • Manage fluid volume o Perform daily weight o Auscultating the lungs o I&O o Fluid/sodium restriction. Sodium should be no more than 2g/day o Diuretic therapy; timing of meds • Control anxiety  o Talk to the patient to ease anxiety o Breathing exercises o Have a conversation with the patient • Monitor for complications  o Acute decompensated HF o Pulmonary edema o Kidney injury o Life-threatening dysrhythmia • Patient education Patient Teaching MAWDS: M  medication. Patient should avoid NSAIDs and be compliment with regimen A  activity. Patient should wait 2 hours after a meal for physical activity and avoid hot weather W  weight. 2-3 lb. in ONE DAY and 5 lb. in ONE WEEK. Patient should report to HCP D  diet. 2-3grams per day (book says 2) and fluid restriction (2L) or whatever HCP prescribes S  note worsening s/s • Medications • Diet: low-sodium diet and fluid restriction o Low sodium diet (no more than 2g/day) diet and avoiding excessive fluid intake. o This will decrease the amount of circulating blood volume, which will decrease myocardial work o Avoid canned or processed foods, eating fresh or frozen foods o Avoid salt use o Avoid excess in eating and drinking • Monitor for s/s excess fluid, hypotension, and symptoms of disease exacerbation, including daily weight • Know how and when to contact HCP o Gain in weight 2-3 lb in one day or 5 lb in one week o Increased swelling of ankles, feet, or abdomen o Persistent cough o Loss of appetite o Development of restless sleep; increase in number of pillows needed to sleep o Profound fatigue • Exercise and activity program • Stress management • Prevent infection • Include family and teaching o Especially the one who is cooking for the patient, must educate about diet restriction Other management strategies: • Oxygen therapy, PCI/CABG, biventricular pacemaker, ultra-filtration volume overload, nutritional therapy Hypertension This is the amount of resistance of blood pumping through the arteries. It is CO x PR. Cardiac output and peripheral resistance both increases with HTN • Silent killer • Hispanics, African Americans Classifications of BP according to JNC: o Normal 120 and 80 o Prehypertension 120-139 and 80-89 o Stage 1 140-159 and 90-99 o Stage 2 160 and 100 ** ON TWO OR MORE MEASUREMENTS* JNC management objective  prevent complications/death  maintain 140/90 or lower  130/80 for ppl with DM or CKD Types: • Primary HTN (essential) blood pressure from an unidentified cause (most common 95%) • Secondary HTN  occurs when cause can be identified (least common 5%) o Renal disease, Hyperaldosteronism, Medications (prednisone), Pregnancy Pathophysiology: BP is the product of cardiac output multiplied by peripheral resistance. • CO is the product of the heart rate multiplied by stroke volume (CO= HR x SV) • Peripheral resistance: amount of pressure being put against blood vessel walls • Each time the heart contracts, pressure is transferred from the contraction of the heart muscle to the blood and then pressure is exerted by the blood as it flows through the blood pressure. o HTN results in  increased CO and increased peripheral resistance (constriction of blood vessels) o HTN result from  o increase of CO or peripheral resistance or both o Increased SNS activity related to dysfunction of ANS o Increased renal reabsorption of sodium, chloride, and water o Increased activity of RAA system: expansion of extracellular fluid volume and increased SVR o Decreased vasodilation of the arterioles related to dysfunction of the endothelium o Resistance to insulin action o Activation of immune system contributing to renal inflammation Risk Factors: MAJOR smoking, dyslipidemia, atherosclerosis, diabetes, impaired renal function, obesity, metabolic syndrome, obstructive sleep apnea, physical inactivity, age, and family history of CV disease o R  race o I  increased sodium and alcohol consumption o S  smoking/stress o K  decreased potassium (due to increased sodium- not getting enough vitamin D) o F  family history o A  advanced age o C  cholesterol (high) o T  too much caffeine – constricts vessels o o obesity o R  restricted activity o S  sleep apnea Diagnostic Studies: • Health hx/ Family hx— Is the patient a smoker? Does the pt snore? • Px examination o Assess the patient’s BP (take BP 5 minutes apart in both arms; can do a postural BP) o Calculate the patient’s BMI • Retinal examination • Laboratory  UA, blood chemistry, lipid profile, 12-lead EKG, and echocardiography Clinical Manifestations: • May reveal no other abnormalities other than elevated BP • elevated BP, retinal changes/hemorrhages, papilledema (swelling of optic disc) • Specific s/s may indicate vascular damage o CAD, angina, AMI, LVH, heart failure, increased creatinine and BUN, nocturia, CVA/TIA Complications: LVH, AMI, heart failure, CVA/TIA, CKD, PAD, and retinopathy. -Major contributor to death related to cardiac, cerebrovascular, renal and peripheral vascular disease • Micro organ damage: eyes and the kidney • Macro organ damage: heart, brain, and lungs CAKE o C  cardiovascular disease o A  br(a)in causing a stroke o K  kidney o E  eyes Nursing Interventions: Assessment • Measure BP Nursing dx • Knowledge deficit regarding relation of tx regimen and control of disease process • Noncompliance w/ therapeutic regimen related to S.E of prescribed therapy Interventions • Increasing knowledge, Promoting adherence to therapy, Promoting home and community-based care GOAL Prevent complications and death by achieving and maintaining a blood pressure lower than 140/90 mm Hg – 130/ 80 with DM, CKD pt Management prior to pharm  • First s/s of HTN: headaches, blurry vision, palpitations, chest pains, nsoe bleeds, dizzy • What needs to be done o Assess BP (both arms) o Family/ patient health hx o Calculate BMI o Look at meds o Educate pt on lifestyle modifications Pharmacological/Medical Management • Uncomplicated HTN  give diuretic, beta blocker, or both • Uncontrolled HTN  can be on many medications *TRY to prescribe simplest treatment, ideally on pill/day Types of drugs: o Diuretic (thiazide) ▪ Patient is first put on a diuretic such as thiazide diuretic this can remove sodium and water and also deplete potassium (therefore we must increase potassium in diet) o Beta blocker (olol) we do not give these to asthmatic patients o Central 2 alpha 2 agonist o Vasodilators o ACE inhibitors (pril) prevents vasoconstriction of blood flow (watch for dry cough and angioedema) o ARBS- Angiotensin II receptor blockers (sartan) o CCBS- Calcium channel blockers (pine) Patient Teaching/ Lifestyle modifications • Weight reduction • DASH diet o Grains: 7-8 servings per day o Vegetables 4-5 servings per day o Fruits 4-5 servings per day o Low fat/Fat free dairy 2-3 servings per day o Meat 2 or fewer servings per day o Nuts/seeds 4-5 servings per week • Dietary sodium restriction (2400 sodium DAILY) • Moderate consumption of alcohol (2drinks) • Regular physical activity (brisk walking 30min) Hypertensive Emergency Clinical dysfunction of a target organ. • These are acute, life-threatening BP elevated that require prompt treatment in an intensive care setting because of serious organ damage that may occur. • Extremely elevated BP can occur with HTN, pregnancy, AMI, dissecting aortic aneurysm which is fatal and blood pressure is beating against a vessel meaning this will then and break, or intracranial hemorrhage Nursing Mx o Close monitoring of patient’s BP and cardiovascular status o GOAL Reduce BP by 20-25% within the FIRST HOUR (25% of systolic and diastolic) o IV vasodilators that work very quickly ▪ Nitroglycerin IV ▪ Nipride IV ▪ This is not the time to leave the patient. we will look at the pump and see how the patient is reacting to the medication and based on this we will increase/decreased the dose Hypertensive Urgency Describes a situation in which BP is very elevated but there is no evidence of impending or progressive target organ damage. • These are classified as URGENCIES (pressures above 180 mm Hg systolic and/or above 120 mm Hg diastolic) Clinical Manifestations: Elevated BP, HA, nosebleed and anxiety Nursing Mx • oral agents can be given which will normalize BP in 24-48 hours • Close monitoring of patient’s BP and cardiovascular status Dysrhythmia – ECG Disorders of the formation/conduction or both of the electrical impulses of the heart. These disorders can cause disturbances of the: • Rate, Rhythm- Both rate and rhythm Normal electrical conduction originates in the SA node. It is 60-100BPM • Stimulation of SNS will increase HR • Stimulate of PNS will reduce HR ECG: An ECG is used to monitor the electrical activity of the heart and it can reflect: o Ischemia, Infarction, Electrolyte disturbances, Drug toxicity, Enlarged cardiac chambers On an ECG we will see: o Impulse conduction time intervals, HR, Rhythm/regularity WE WILL NOT SEE PUMPING ACTION, BLOOD PRESSURE, AND CARDIAC OUTPUT An ECG will contain intervals such as o P wave: atrial depolarization which is 0.04-0.12 seconds o QRS complex: ventricular depolarization which is 0.12 seconds o T wave: ventricular repolarization (relaxation) o PR interval: time needed for sinus node stimulation, atrial depolarization, and conduction through the AV node which is 0.12-0.20 seconds o ST segment: isoelectric line which represents early ventricular repolarization Each box is equal to 5 The small box inside is 0.04 seconds Each box is .20 seconds because 0.04 x 5 is equal to 0.20 seconds PQRST wave P wave  represents atrial depolarization (the atria contracting) • The P wave is normally upright and is 0.04-0.12 seconds • 2.5 mm in height (or less) o So, there should be 1-3 small little boxes! ▪ Why? Because 1 little box is equal to 0.04 and 0.04 x 3 little boxes is 0.12 • There should be one P wave for every QRS complex – the P wave should be rounded and upright QRS complex  represents ventricular depolarization (the ventricles are contracting) • A normal QRS complex is less than 0.12 seconds o So, there should be 3 little boxes! ▪ Why? Because 3 little boxes x 0.04 would equal 0.12 • Disturbances in the conduction such as the bundles branches in the ventricles can disrupt the normal QRS complex T wave  represents repolarization of the ventricles • A normal T wave is upright and lasts 0.16 seconds (according to picmonic) • The resting phase • A tall, peaked, or inverted T wave may be caused by electrolyte imbalances, ischemia, or myocardial infarction PR interval  measured from the beginning of the P wave to the beginning of the QRS complex and represents the time needed for sinus node stimulation, atrial depolarization, and conduction through the AV node • A normal PR interval is 0.12-20 seconds o So, this would be 3 small boxes or 1 big box ▪ Why? Because 3 little boxes x 0.04 is equal to .12 and one big box is equal to 0.20 seconds ST segment  represents early ventricular repolarization • Normally isoelectric  meaning it will stay on the line ECG Interpretation: STEP 1: Heart rate: We determine rate with the RR interval • Rate can be regular/irregular depending on how even the RR interval is o Bradycardia is 60 BPM o Tachycardia is 100 BPM • Use the evaluation 1-minute strip for regular rhythm o Count the number of boxes within an RR interval and divide 1500 by that number (example in notes) o ONLY USED FOR REGULAR RHYTHM • Use the six-second method for irregular rhythm o Look at the little ticks at the top – 30 big boxes is equal to 6 seconds and count the R intervals between those 3 ticks o Count the number of RR intervals in 6 seconds and multiply by 10 o OR COUNT 30 BOXES (ACCORDING TO VIDEO) and count the RR intervals and x STEP 2: Heart rhythm • Measure the intervals between R-to-R (ventricular rhythm) • Measure the intervals between P-to-P waves (atrial rhythm) o If the intervals are the same or if the difference between the intervals is less than 0.8 seconds throughout the strip, then it is regular o If the intervals ae different then it is irregular STEP 3: P waves • Should be 0.04-0.12 seconds (1-3little boxes) • Are the P waves present, occurring regularly, is there one for each QRS complex, are they SMOOTH, ROUNDED, AND UPRIGHT IN APPEARANCE? STEP 4: PR Interval • Should be 0.12-0.20 seconds (3 little boxes or 5) • Are the PR intervals greater than 0.20 seconds? • Are they constant across the EKG strip? STEP 5: QRS Complex • Should be 0.12 seconds (3 little boxes) • Is the QRS complex greater or less than 0.12 seconds? Overall Appearance • Evaluate the ST segment for elevation or depression o ST segment elevation is indicative of injury to the heart o ST segment depression can equal ischemia and can be indicative of digoxin toxicity • Evaluate the T waves: upright, negative, or peaked Normal Sinus Rhythm Have the following characteristics: o Ventricular/atrial rate: 60 to 100 bpm in the adult o Ventricular and atrial rhythm: Regular o QRS shape and duration: Usually normal, but may be regularly abnormal QRS 0.04 to 0.20 seconds (should all look the same) o P wave: Normal p wave and consistent shape; always in front of the QRS (should be one for every QRS) o PR interval: Consistent interval between PR interval 0.12 and 0.20 seconds o P:QRS ratio: 1:1 ***EVERYTHING IS NORMAL*** Sinus Bradycardia • HR less than 60 BPM; the sinus node will create impulses at a slower rate than normal Have the following characteristics: o Ventricular and atrial rate: Less than 60 bpm in the adult o Ventricular and atrial rhythm: Regular o QRS shape and duration: Usually QRS normal, but may be regularly abnormal o P wave: Normal P wave and consistent shape; always in front of the QRS o PR interval: Consistent interval between PR interval 0.12 and 0.20 seconds o P:QRS ratio: 1:1 Etiology: vomiting, hypoxia, medications, well-conditioned athletes, coughing/straining, AMI, carotid sinus pressure, and IICP Clinical Manifestations: SOB, decreased LOC, angina, hypotension, EKG changes (ST segment changes PVC’s) Management: • treat symptoms increase HR  administer atropine IV 0.5mg • withhold medications (beta blockers), decrease vagal stimulation, and pacemaker *** EVERYTHING NORMAL EXCEPT HR WHICH IS BELOW 60*** Sinus Tachycardia • HR from 100-160 BPM; sinus node creates impulses at a faster than normal rate. It does not start or stop suddenly Have the following characteristics: o Sinus tachycardia has the following characteristics (see Fig. 26-7): o Ventricular and atrial rate: Greater than 100 bpm in the adult, but usually less than 120 bpm o Ventricular and atrial rhythm: Regular o QRS shape and duration: Usually QRS normal, but may be regularly abnormal o P wave: Normal P wave and consistent shape; always in front of the QRS, but may be buried in the preceding T wave (THEY ALL LOOK ALIKE) o PR interval: Consistent interval between PR wave 0.12 and 0.20 seconds o P:QRS ratio: 1:1 Etiology: exercise, fear/anxiety, MI, CHF, fever, stimulants, hypovolemia, medications, pain, and infection Clinical Manifestations: decreased filling time of the heart as the HR increases, which will cause reduced cardiac output which can result in syncope and hypotension • If this persists and the heart cannot compensate for the decreased ventricular filling time  patient will develop pulmonary edema Management: Abolish the cause • Beta-blockers • Vagal maneuvers such as carotid sinus massage, gagging, bearing down against closed glottis (having a bowel movement), forceful and sustained coughing, applying a cold stimulus to the face • Adenosine (may be considered to interrupt tachycardia) • Calcium-channel blockers • Increased fluid/sodium ***EVERYTHING NORMAL EXCEPT HR WHICH IS OVER 100*** Atrial Flutter (SAW TOOTH) • Occurs in the atrium; creates an atrial rate between 250-400 times/minute (ventricular rate 75-150) Have the following characteristics: o Ventricular and atrial rate: Atrial rate ranges between 250 and 400 bpm; ventricular rate usually ranges between 75 and 150 bpm. o Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but may be irregular because of a change in the AV conduction. o QRS shape and duration: Usually QRS normal but may be abnormal or may be absent. o P wave: P wave is Saw-toothed shape; these waves are referred to as F waves. o PR interval: Multiple F waves may make it difficult to determine the PR interval. o P:QRS ratio: 2:1, 3:1, or 4:1 Etiology: hypoxia, PE, pneumonia, MI, hyperthyroidism, cardiac surgery Clinical Manifestations: chest pain, dyspnea, hypotension, diaphoresis Management: AIMED AT CONTROLLING VENTRICULAR RATE o Unstable: cardioversion o Stable: beta blockers, CCB, digitalis, and adenosine (these slow HR) SAW TOOTH SHAPED P WAVES WHICH CAN BE REFERRED TO AS FLUTTER WAVES THEY ARE NOT CONSISTENT PR INTERVAL NOT MEASURED BECAUSE THE P WAVES ARE NOT NORMAL P: QRS RATIO WILL VARY Regular atrial activity with a saw tooth appearance HR 100 BPM is uncontrolled HR 150 BPM is a rapid ventricular rate Atrial Fibrillation • PT IS AT HIGH RISK FOR CLOTS • Rapid, disorganized and uncoordinated twitching of atrial muscle Has the following characteristics: o Ventricular and atrial rate: Atrial rate is 300 to 600 bpm; ventricular rate is usually 120 to 200 bpm in untreated atrial fibrillation. RATE OVER 100 o Ventricular and atrial rhythm: Rhythm Highly irregular o QRS shape and duration: Usually QRS normal (but not evenly spaced out), but may be abnormal o P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen and referred to as fibrillatory or f waves o PR interval: PR INTERVAL Cannot be measured (atria is not contracting) o P:QRS ratio: Many:1 Etiology: advanced age, valvular disease, CAD, HTN, s/p open heart surgery, DM, obesity, hypothyroidism, ETOH, OSA, excessive caffeine, hypoxia, stress, electrolyte imbalance, and PE Clinical Manifestations: palpitations, fatigue, malaise, SOB, exercise intolerance, chest pain, and pulmonary Complications: patient is at risk for HF, myocardial ischemia, and embolic event such as a stroke Management: Depends on the cause and duration, patient’s age, symptoms and co morbidities ABCDE A: anticoagulant B: beta blocker C: cardiac ablation D: digoxin E: electro cardioversion • Stable: Adenosine, Digoxin, Calcium channel blockers, Beta blockers, Amiodarone • Unstable o Cardioversion for AF 48 hours old (Acute onset) ▪ Be CAREFUL WE CARDIOVESION BECAUSE WE PUT THE PATIENT AT A HIGHER RISK FOR A CLOT. WE DO NOT WANT TO SHOCK THESE CLOTS INTO THE SYSTEM ▪ Avoid Cardioversion if AF 48 hours old (needs Coumadin) o Shorter diastole time reduces coronary artery perfusion; can cause myocardial ischemia o Erratic atrial contraction promotes formation of thrombus within atria ▪ Increases risk of thrombotic event ▪ 2-5 fold increase in risk of stroke • Coumadin (3-4 weeks prior to cardioversion) • TEE: check for mural thrombus/Heparin prior to cardioversion if no thrombus • Loss of AV synchrony (the atria and ventricles will contract at a different rate) • We have a loss of atrial kick – which will impair cardiac output • Decreases ventricular filling  reduce stroke volume • Since the atria ARE NOT contracting, we will worry ABOUT CLOTS • Patient is at risk for HF, MI, and stroke. This rapid and irregular response reduces the time for ventricular filling, resulting in a smaller stroke volume. PAC Have the following characteristics: o Ventricular and atrial rate: Depends on the underlying rhythm (e.g., sinus tachycardia) o Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval that is shorter than the others. This is sometimes followed by a longer-than-normal PP interval, but one that is less than twice the normal PP interval. This type of interval is called a noncompensatory pause. o QRS shape and duration: The QRS that follows the early P wave is usually normal, but it may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC). o P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent. o PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20 seconds. o P:QRS ratio: Usually 1:1 Etiology: caffeine, nicotine, alcohol, anxiety, hypokalemia, stretched atrial myocardium (hypovolemia), hypermetabolic states, atrial ischemia such as injury or infarction Clinical Manifestations: Skipped beat, pulse deficit Management: o Reducing stress o Reducing/eliminating stimulants o Treat CHF o Correcting electrolyte imbalances PVCs *HAPPENING WAY TOO EARLY- NO S/S* Impulse that starts in ventricle and is conducted through the ventricle before the next normal sinus impulse o Bigeminy: every other complex is a PVC o Trigeminy: every third complex is a PVC o Quadrigemy: every fourth complex is a PVC Have the following characteristics: o Ventricular and atrial rate: Depends on the underlying rhythm (e.g., sinus rhythm) o Ventricular and atrial rhythm: Irregular due to early QRS, creating one RR interval that is shorter than the others. The PP interval may be regular, indicating that the PVC did not depolarize the sinus node. o QRS shape and duration: Duration is 0.12 seconds or longer; shape is bizarre and abnormal. o P wave: Visibility of the P wave depends on the timing of the PVC; may be absent (hidden in the QRS or T wave) or in front of the QRS. If the P wave follows the QRS, the shape of the P wave may be different. o PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds. o P:QRS ratio: 0:1; 1:1 Etiology: o Can occur in healthy patients (intake of caffeine, alcohol, and nicotine) If a patient stops this and the problem still occurs, we would go to medication o Cardiac ischemia or infarction, Digitalis toxicity, Hypoxia, Acidosis, Electrolyte imbalance such as hypokalemia Clinical Manifestations: patient may be asymptomatic, “my heart skipped a beat” o Stable  correct the use o Unstable  medications such as amiodarone and sotalol • This is a heartbeat! You would say sinus rhythm with PVC • RHYTHM IS IRREGULAR • QRS SHAPE IS BIZARRE AND ABNORMAL • P: QRS RATIO IS 0:1 OR 1:1 AV Nodal Reentry Tachycardia (SVT) Impulse conducted in the AV node that causes the impulse to be rerouted back into the same area over and over again very fast • Considered greater than 160 BPM (165-170) Have the following characteristics: - THIS IS NOT V-TACH o Ventricular and atrial rate: Atrial rate usually 150 to 250 bpm; ventricular rate usually 120 to 200 bpm o Ventricular and atrial rhythm: Regular; sudden onset and termination of the tachycardia o QRS shape and duration: Usually normal, but may be abnormal o P wave: Usually very difficult to discern o PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds. o P:QRS ratio: 1:1, 2:1 Etiology: caffeine, nicotine, hypoxemia, stress, CAD, and cardiomyopathy Clinical Manifestations: • Reduced CO – having a fast HR can affect this and perfusion o Restlessness, Chest pain, SOB, Pallor, Hypotension, Loss of consciousness Management: The goal is to alleviate s/s and improve quality of life – it is usually a benign dysrhythmia • Treatment aimed at breaking reentry of impulse • Vagal maneuvers  this can LOWER HR o Carotid sinus massage, Gag reflex, Breath holding • Adenosine • Cardioversion • HR IS OVER 150 BPM • REGULAR RHYTHM • P WAVE IS DIFFICULT TO SEE • P: QRS RATIO IS 1:1 OR 2:1 Coronary Vascular Disorders Atherosclerosis (this causes CVD) -PLAQUE BUILD UP THAT CAUSES NARROWING OF THE ARTERIES -An abnormal accumulation of fatty substances, and fibrous tissue in the lining of the arterial blood vessels • These substances block and narrow the lumen of the coronary vessels and will reduce blood flow to the heart • Repetitious inflammatory response to the injury of the vessel wall Angina Not enough oxygen going to the heart due to the atherosclerotic build up. This is a syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest secondary to insufficient coronary blood flow • Physical exertion or emotional stress increases myocardial demand for oxygen and the coronary blood vessels are unable to supply the increased heart’s needs ▪ Since oxygen supply is LESS TO HEART; this will result in pain when the patient is stressed or with physical activity since there is less blood flow to the heart and these activities will increase myocardial oxygen demand Risk factors: • Modifiable- Smoking, diet, alcohol, HTN, physical inactivity, obesity, depression, stress, oral contraceptives, substance abuse • Non-modifiable- Race, gender, age, family hx (men more likely) Clinical Manifestations: o Feels like pt is having a heart attack – but it’s just insufficient oxygen not a HA o Pain varies - mild to severe o Tightness, choking, or a heavy sensation-chest, frequently retrosternal and may radiate to the neck, jaw, shoulders, back or arms (usually left) o Anxiety frequently accompanies the pain o Possible other symptoms: dyspnea/sob, dizziness, n/v o With stable Angina the pain subsides with rest or nitroglycerin o The symptoms and complications are due to the myocardial ischemia, this is related to the location and degree of vessel obstruction Complications Angina pectoris, MI, HF, sudden cardiac death Stable Angina Unstable Angina Pain will subside with rest of nitroglycerin Pain characterized by increased frequency and severity and is not relieved by rest and nitroglycerin REQUIRES MEDICAL INTERVENTIONS ARTERY IS NOT COMPLETELY OCCLUDED CAN TURN INTO AN MI CALL 911 after 1st nitroglycerin Nursing Mx Assessment • Assess all symptoms carefully and compare to previous and baseline data to detect any changes or complications • Monitor ECG o If patient starts complaining of chest pain, LOOK AT THIS. It will tell us several things going on in the heart o Can reveal a current diagnosis BUT IT IS NOT A DIAGNOSTIC o Performed on anyone who is c/o chest pain Diagnosis • Ineffective Cardiac Perfusion, Risk for fluid imbalance, Risk for ineffective peripheral tissue perfusion, Death Anxiety, Knowledge Deficit Plan/Goal • Pain relief and resolution of ischemic signs • Prevention of further myocardial damage • Absence of respiratory difficulties • Adequate tissue perfusion • Decrease Anxiety • Self-care adherence • Absence or early recognition of complications – OUR GOAL Treatment • Nitroglycerin given to pt, they usually take 3 and they are 5min apart (call 911 after 1st nitro) • Have patient stop all activity and rest • Assess the patient while performing other necessary interventions • Administer Oxygen & Meds per protocol Anxiety – DO NOT LEAVE THE PATIENT • Use a calm manner • Use stress reduction techniques – such as breathing • Educate patient • Assess and meet both patient and family needs How would we decrease anxiety? Do not leave the patient and talk with the patient. Sit them up and have them deep breath (this can calm the patient) Patient Teaching • Educate regarding when to seek emergency treatment • Recognize and adapt behaviors that produce episodes • Educate regarding disease process, meds, and stress reduction Patient Education • Smoking cessation • Balanced diet – limit intake of fats and sodium • Check BP and cholesterol regularly • Engage in physical activity Myocardial Infarction An area of the myocardium is permanently destroyed. The area in the heart becomes necrotic and ischemic. There is no oxygen going to this area and there is decreased flow • IN MI THE ARTERY IS COMPLETELY OCCUDLED due to plaque rupture and subsequent thrombus formation • Usually caused by decreased blood flow to a coronary artery due to an atherosclerotic plaque rupture and subsequent occlusion • Acute coronary syndrome includes unstable angina and MI (they are considered the same process but at different points in time) o Unstable angina plaque ruptures but it is NOT completely occluded Diagnostics: MUST BE PERFOMED WITHIN 10 MINUTES OF ED ADMIT • ECG, CK-MG, myoglobin, and troponin o Troponin is more indicative that something is going on with the heart o Inverted T wave: zone of ischemia. This will tell the patient had a heart attack o Elevated ST: zone of injury. Standing up more and is very pronounced. This means injury occurred in the heart o Well pronounced Q wave: zone of infarction. you will see appearance of Q waves Clinical Manifestations: chest pain with possible radiation (which can go to the jaw) • S/S are on the LEFT side of the heart Interventions/Treatment: Labs w/in 10minutes MONA ▪ Morphine ▪ Oxygen ▪ Nitroglycerin ▪ Aspirin o ACE inhibitor within 24 hours o Beta blockers such as metoprolol o Evaluate for PCI (to go to cath lab) or thrombolytic therapy such as a cardiac cath which should be done within 90 minutes o As indicated, IV heparin, LMWH, clopidogrel or ticlopidine o Best rest  to decrease workload of heart o Medications: nitro, beta blocker, calcium channel blocker, antiplatelet and anticoagulant, clopidogrel and ticlopidine Nursing Process: MI Assessment • Patients symptoms & Activities that precede the attack • Risk factors-lifestyle/family history Nursing Diagnosis • Ineffective cardiac tissue perfusion (Nursing dx for MI), Death Anxiety, Knowledge deficit, Noncompliance Planning/Goal – ABSENSE OF ANY COMPLICATION • Immediate and appropriate angina treatment, prevention, decrease anxiety, awareness of the disease process, understanding of prescribed care, adherence to the self-care program, and absence of complications PCl (percutaneous coronary intervention) Cath lab within 90minutes • What they do • Put stent in, inflate balloon, cell will open up once balloon is blown up and then the pt will have oxygen flow through the heart (fixes the blockage) • Pt will have perfusion, blood flow, oxygenation CABG Next thing they do • Done when nothing in the cath lab could be performed • This is OPEN heart surgery • They take a vein from another part of the body (legs or mammarys from heart, wrist) and put it in the heart Chapter 28- Inflammatory cardiac disorders Valvular disorders: Mitral Valve prolapse Mitral valve leaflets balloon back into atrium during systole – blood will then regurgitate back from left ventricle into left atrium • CM: asymptomatic, SOB, fatigue, lightheaded, dizziness, syncope, palpitations, chest pain, anxiety – may hear SYSTOLIC click. • Tx: Antiarrhythmic meds, no antibiotics prior dental tx, nitrates, CCB, beta blockers, valvuloplasty, valve replacement • Avoid: caffeine, alcohol, tobacco • Complications: infective endocarditis (may need antibiotic therapy) Mitral regurgitation  Blood backflow from left ventricle into left atrium – get hypertrophy & systolic HF • Etiology: mitral valve prolapse & rheumatic heart disease • CM: asymptomatic, HF, dyspnea, fatigue, weakness, palpitations, SOB, cough, systolic murmur, pulse deficit • Mx: afterload meds (ACE, ARBS, beta blockers) • Diagnostic: echocardiogram can determine if condition is progressing • Complication: HF Mitral Stenosis  Opening issue- valve narrows and blood has difficulty moving forward – decrease C.O and increased HR *RISK for clots* • Etiology: rheumatic endocarditis • CM: risk for clots, dyspnea, cough, wheezing, fatigue, hemoptysis, palpitations, orthopnea, PND, repeated respiratory infections • Diagnostic: echo, ECG, exercise testing, cardiac catherization • Mx: anticoagulants, cardioversion (if afib), control HR with beta, digoxin, CCB, avoid activities that increase HR Aortic regurgitation  Closing problem- blood back into LV from aorta during diastole • Etiology: inflammation, infective or rheumatic endocarditis • CM: asymptomatic, forceful HB, visible palpitations, orthopnea, PND, pulse pressure • Mx: avoid streneous activity, tx of dysrhtythmia/ HTN, restrict sodium and fluid volume overload • Prevent bacterial infections Aortic stenosis  opening issue- orifice is narrowing blood is having trouble moving forward • Etiology: Degenerative calcifications (progressive narrowing of valve) • CM: dyspnea, orthopnea, PND, pulm edema, dizziness, angina, syncope, systolic murmur and S4 Cardiomyopathy  disease of heart muscle • Dilated- issue with altered valve functioning • Hypertrophic- Autosomal dominant disorder caused by ischemia • Restrictive/constrictive- amyloidosis can be sometimes associated with this condition • Arrhythmogenic right ventricular • Unclassified cardiomyopathy • Mx: improve C.O and perfusion (rest, position, O2, meds, low NA diet, avoid dehydration) • Increase activity tolerance + improve gas exchange, Reduce anxiety, decrease sense of powerlessness, promote home/community based care (educate about lifestyle, educate family of AED and CPR) • Complications: HF, dysrhythmias, cardiac conduction defects, pulm/cerebral embolism, valvular dysfunction Infectious diseases of the heart: Rheumatic endocarditis  occurs in school age child’s- a beta hemolytic streptococcal pharyngitis Infective endocarditis  develops in prosthetic heart valves or structural cardiac defects (bacterial infection) • Risk factors: IV drug users, diseases, catheters, prolonged IV therapy • CM: prosthetic heart valve, temperature, osler nodes on fingers, new onset murmur, janeway lesions, roth spots, splinter hemorrhages in nail beds Pericarditis  inflammation of pericardium • Complications: pericardial effusion and cardiac tamponade • CM: friction rub (left lower sternal border), renal failure, new heart murmur Myocarditis  inflammation of myocardium • VIRAL • Complications: cardiomyopathy, HF • CM: fever, dyspnea, syncope, palpitations, chest pain CM in infectious diseases fever, cardiomegaly, splenomegaly, HF, tachycardia • Diagnostic tools blood cultures, echocardiogram, CBC, rheumatoid factor, ESR, CRP, urinalysis, ECG, cardiac catheterization, CMR imaging, TEE, CT scan • Prevention antibiotics prior dental procedure, oral hygiene, NO IUDS, immunizations Chapter 30: Peripheral Vascular disease — Peripheral Vascular disease — PVD, PAD, PVI ● Peripheral venous disease can include  DVT, Chronic venous insufficiency, Varicose veins, Superficial venous thrombosis PVD Assessment- • HX of HTN, lipidemia, DM – these pt can develop PVD (PVD is a mini MI of legs) • Pain  intermittent claudication (PAD), dull pain (PVD) • Skin inspection pallor, rubor, loss of hair, brittle nails (PAD), gangrenous changes (PAD), dry scaling skin (PVD), atrophy, ulcerations (round is PAD) (irregular is PVD) • Risk factors modifiable (smoking cessation, diet), nonmodifiable (age, gender, hereditary, genetics) • Diagnostic doppler, ABI (ankle brachial index, 0.9-1.3 normal, under 0.4 is severe obstruction is occuring), exercise testing, ultrasonagraphy, CT, angiography, MRA, venography, pymphoscintigraphy • Medical mx: 6 P’s**** • Surgical mx: bypass, anastomosis, STENT (CABG) • Radiologic procedures: arteriogram, angiography • Nursing Mx: improve PAC (for PAD, dangle legs), promote vasodilation & prevent vascular compression, for PVD (8 safety C’s), relieve pain, maintain tissue integrity, assess skin daily, hydration • PVD- 8 safety C’s  careful with hot temps, cautious foot trauma, avoid constriction, do not cross legs, no smoking, no caffeine, beware cold temps (constriction) Arteriosclerosis  hardening of the arteries (most common) – lining of walls of artery vessels become thickened Atherosclerosis Accumulation of lipids, calcium, carbohydrates and fibrous tissue (plaque) on the intimal layer of the artery. • Risk factors: diet, sedentary lifestyle, HTN, Dm, hyperlipidemia, stress, elevated C-reactive Protein (sensitive marker of cardiovascular inflammation) hyperhomocysteinemia (homocysteine protein that promotes coagulation) • Mx: decrease risk factors, improve blood supply • Prevention: reduce fat in diet, exercise, reduce lipid levels (LDL 100) (Cholesterol 200) (Tri 150), statins, niacin, questran, zetia, manage HTN Peripheral Arterial disease occlusive disease- arterial insufficiency of extremities, legs most frequently affected • CM intermittent claudication • Diagnostics/Assessment cool, pale, ruddy, cyanotic, bruits present, unequal pulses • Med/Surgical Mx exercise, walking, cessation smoking, endarterectomy, bypass grafts • Pharm tx anticoagulants, antiplatelets, cholesterol lowering drugs • Nursing Mx: Maintain circulation, frequent check for pules, color, cap refill, temp, 6 P’s**, compare legs, monitor urine output, mental status, CVP (elevated BUN with normal creatinine is volume problem aka dehydration), pulse rate, no leg crossing, no prolonged leg dependence, lifestyle modifications Aneurysms  localized sac or dilation formed at a weak point in wall of an artery (types: sacular, fusiform, dissecting) • Life threatening- rupture leads to hemorrhage and death • Dx: Chest XRAY • Thoracic aortic aneurysm wall is so stretched out that it breaks o Risk factors: 85% caused by atherosclerosis, 50-70yrs, common site for dissecting aneurysm, 1/3 die due to rupture o CM: asymptomatic, dyspnea, cough, hoarseness, stridor, aphonia, large veins in chest compressed (become dilated) o Diagnosis: chest XRAY, CTA, TEE o Medical MX: BP control (SBP 90-120) (MAP 60-7