MedSurg Test 1 - Cardiac
MedSurg Test 1 - Cardiac NURS 479
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This 47 page Study Guide was uploaded by Lexi P on Friday September 30, 2016. The Study Guide belongs to NURS 479 at Catholic University of America taught by Connor-Ballard, P. in Fall 2016. Since its upload, it has received 59 views. For similar materials see Adults in Health and Illness in NURSING at Catholic University of America.
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Date Created: 09/30/16
Cardiac Nursing Part 1 & 2: Cardiac Conditions and Nursing Care Coronary Arteries The heart and coronary arteries o Right coronary arteries Only blood to lungs o Left coronary artery Brings blood to ventricles that pumps to the whole body Provides blood to the thick strong muscle Circumflex branch of left coronary artery The part of the artery that wraps around the back of the heart muscle o Cardiac Conditions Associated with Poor Coronary Artery Perfusion Coronary Artery disease Results from reduction of coronary artery perfusion by blockage or vasospasm of the coronary artery o Reduced blood flow through coronary arteries but no chest pain Atherosclerosis and arteriosclerosis can contribute to blockage Atherosclerosis – obstruction of an artery from build up of fatty plaque In early age it is more severe Arteriosclerosis – stiffening of arterial wall Arterial wall should pulsate, but does not o Tends to happen together Clinical manifestations of stable angina pectoris (chest) Occurs over time o 20s from lack of activity, genetic, smoking, poor diet Rx for Coronary Artery Disease o Low calorie/saturated fat/salt diet with weight reduction as needed o No smoking, limited ETOH intake o Regular physical activity Walk inside of the mall because it has AC, flat surface, sitting areas o Assess CBC, fasting glucose, lipid panel, cardiac enzymes o Baseline and follow-up 12 lead EKG Serial EKG testing 12 lead Look at ST wave Every 4-6 hrs x 2 days o Consider cardiac echocardiography to assess LV function, and cardiac catheterization to assess coronary artery perfusion o Stress cardiac echocardiography to assess function under physical activity – or drug-induced stimulation Anyone at risk Have patient walk on the treadmill and observe how the LV muscle function o CXR as needed (eg S/S heart failure) Chest xray o Aspirin, O2, rest o Avoid smoking because it is a vasoconstrictor o Dye into heart to monitor flow Acute Coronary Syndrome Results from significant reduction in coronary artery perfusion Serious risk of myocardial damage (ischemia, infarction) Clinical manifestation of unstable angina v. acute myocardial infarction (AMI) Much more severe patients of instability Chest pain worse means the clot is worse o At rest it does not go away Stable Angina Pectoris Chest discomfort >15 minutes at rest stress or exertion; episodes increase in frequency and intensity; significantly affects activity, does not fully respond to rest and NTG Rx Takes a lot to bring it on Pain quickly goes away when stop action Acute myocardial infarction (AMI) (“heart attack”) Significant loss of perfusion (80-90%) to the ventricle due to coronary artery obstruction; un-perfused ventricular muscle area becomes ischemic then infected Shut down and causes ischemia – restore blood flow; if still ischemic, what was not perfused is permanently damaged What a heart attack feels like o Man Cold sweat Poor skin color SOB Pain can radiate to jaw neck, arms, back and stomach Chest pain or pressure Feeling sick or vomiting Rapid or irregular pulse o Woman Women do not always have substernal chest pain Fatigue, N/V, SOB Because of this, women are very underdiagnosed Light-headed or dizzy Unusual fatigue Short of breath Nausea Cold sweat Upper body pain, both arms, back, shoulders, neck, jaw Chest pain, pressure Myocardial infarction as a result of a blocked left anterior descending coronary artery o Zone of infarction – central area is the worst – will never come back o Zone of injury – under perfused/damage – recoverable if quick o Zone of ischemia – without blood flow usually has, if not fast it will progress o Re-perfuse ASAP NSTEMI Non ST elevation MI Myocardial infarction without obvious ST segment elevation; common in women STEMI ST elevation MI Myocardial infarction with obvious ST segment elevation in 2/12 EKG leads; more common AMI presentation EKG changes Months – after reperfusion – comes back to baseline o Deepening of Q wave is indicative of MI Develops later Cardiac Conditions Associated with Poor Cardiac Output Heart failure Can’t get to all parts of the body o Organs, tissues not getting perfused o LV is more serious because the O2 can’t go to the body o RV is when the blood can’t get to the lungs which causes pooling in all major arteries Go into respiratory distress Blood moves from: right heart lungs left heart body Right-sided heart failure RV unable to empty effectively, leading to venous system congestion Symptoms o Fatigue o Increased peripheral venous pressure o Ascites o Enlarged liver and spleen o May be secondary to chronic pulmonary problems o Distended jugular veins o Anorexia and complaints of GI distress o Weight gain o Dependent Edema Patients call their weight into the clinic o >3 lbs/day, >5 lbs/week up Lasix o Nurse will ask the patients questions about what they’re eating (potassium), meds, ankles, weight Peripheral organs/veins congested Left-sided heart failure (traditional congestive heart failure/CHF) LV unable to either relax enough to fill effectively (diastolic HF), or empty effectively (systolic HF), leading to pulmonary vascular congestion o Reduced EF% most significant (<40%) if systolic HF; similar S/S Symptoms o Paroxysmal nocturnal dyspnea o Elevated pulmonary wedge pressure o Pulmonary congestion Cough, crackles, wheezes, blood-tinged sputum, tachypnea o Restlessness o Confusion o Tachycardia o Orthopnea o Exertional dyspnea o Fatigue o Cyanosis Veins in lungs congested Signs of decreased cardiac output o Low blood pressure, dizziness, fatigue, cool/clammy hands, SOB, cyanosis, anxiety, diaphoresis, decreased level of consciousness, chest pain New York Heart Association Functional Classifications of Heart Failure o Class I Existing cardiac disease Asymptomatic at rest Asymptomatic with any routine physical activity – symptoms are not a problem during regular daily activities o Class II Existing cardiac disease Asymptomatic at rest Routine physical activity can result in fatigue, palpitations, dyspnea, or angina pain Ex) walking up stairs while carrying something, taking longer walks Palpitations – feel bounding in chest at increased HR o Class III Existing cardiac disease Asymptomatic at rest Slight physical activity can result in fatigue, palpitations, dyspnea, or angina pain Ex) going from couch to bathroom o Class IV Existing cardiac disease May be symptomatic at rest Any physical activity result in fatigue, palpitations, dyspnea, or angina pain Ex) just sitting there, couch to anywhere “Cardiac cripple” Cardiomyopathy o Hypertrophic cardiomyopathy – barely any blood going in or out o Dilated cardiomyopathy – blood pooling The normal fiber muscles are destroyed Remaining fibers are extended Walls are hard to move with so much muscle Need a heart transplant Hypertrophic Obstructive Cardiomyopathy / Mitral Valve Prolapse Genetic trait o Collapse on sports field o Can be associated with Marfan’s Syndrome Structural defects with aortic and mitral valve o Aortic – semi-closed/open o Mitral – leaky, oversized Left ventricle is poor at pumping blood Mitral valve swings and blocks blood from entering the aorta and the person can drop dead Cardiac Tamponade Compare the two pictures, usually the pericardial sac does not irritate or tub the heart o But in this condition, the sac fills with fluid that traps the heart from moving (left) Signs/Symptoms o Sudden deterioration o Neck veins bulging o Not a lot of breath sounds, can barely heart cardiac fluid muffles S1 and S2 o Patient in variable degrees of shock or in extremis o Decreased arterial and pulse pressures often exist but not pathognomonic o Venous pressure elevated Pericardial tap at Larrey’s point – diagnostic and decompressive Cardiac Valves Tricuspid Valve – between RA and RV Pulmonary valve – between RV and Pulmonary artery Mitral (Bicuspid) Valve – between LA and LV Aortic Valve – between LV and aorta Valve Stenosis vs Regurgitation Stenosis – stiff – stuck either fully closed or fully open usually o Can have minor regurgitation Regurgitation o No strength against any pressure Cardiac Conditions Associated with Irritation/Inflammation/Infection Endocarditis (inner) o Infection of the inner lining of the heart (endocardium) due to bacteremia, especially staph or strep Untreated strep – at risk for septic shock Bacteria build up – causes damage and regurgitation o Results in structural changes such as vegetative lesion and cardiac valve stenosis o High mortality rate o High risk among IV drug users o Sticks to the tissue of the valves o Treatment IV antibiotics for 6 weeks Antibiotics before dental care Pericarditis (outer) o Inflammation of the outer membrane enclosing the heart (pericardium) o Acute or chronic o Bottom left ventricle – contraction causes irritated part of the heart to rub on the sac Supposed to be the pericardial sac, then some space, then the heart o Symptoms Classic sign – hurts with deep breath and they lean forward Sharp and stabbing pain Pain increases when coughing, swallowing, deep breathing, lying flat Feel the need to bed over or hold your chest to breathe more comfortably Pain in the back, neck, left shoulder Difficulty breathing when lying down Dry cough Anxiety or fatigue o Must prepare the patient for some chest pain post operatively, if not they will be very anxious and scared / freak out Aortic Anuerysm Progressive, pulsating outward expansion of the aorta to 2+ X its baseline High risk of dissection or rupture of the aneurysm wall with life- threatening hemorrhage o Sac only gets bigger o If the bleeding occurs between the layers of the aorta, it buys time o If the bleeding is a full dissection, only have minutes to live Abdominal (AAA) or thoracic (TAA) cavity Etiological factors include congenital defect, trauma, HTN, atherosclerosis, smoking, syphilis or connective tissue disorder o Ex) Marfan’s syndrome, Ehlers-Danlos syndrome o Stiffness of wall is detrimental with constant pounding because it will reach a breaking point Abdominal Aortic Aneurysm o The important question is: are the renal arteries involved? If so, they have to clamp the arteries to save the patient Beyond a half hour of not clamping will lead to kidney detriments o If the aneurysm is very big and the patient is thin, you can see pulsations above the umbilicus that matches the pulse o Ruptured Abdominal Aortic Aneurysm The best case scenario would be below the renal arteries Blood pours into the abdominal cavity Signs and Symptoms o In the beginning, the symptoms can be easy to miss o AAA: Abdominal, flank, or back pain that is steady and gnawing regardless of body position. Atypical pulsation between xiphoid process and umbilicus. o TAA: Back or chest pain, dyspnea, hoarse voice, difficulty swallowing Voice changes if its big enough Clogging of the ears is also a possible symptom o AA rupture: Sudden onset of severe pain, hypovolemic shock, abdominal distention and flank hematoma/bruising (if AAA) Shock “Whole body” physiological crisis triggered by inadequate gas exchange for oxygenation and inadequate tissue/organ perfusion to meet cellular needs o the cells and organs can’t function ischemia Temporary compensatory measures o Temporary and tragic Can lead to life-threatening multiple organ dysfunction system (MODS) without timely and effective Rx o Start to die off without nutrients and O2 Categorized by cause: hypovolemia, cardiogenic, septic, neurogenic, or anaphylactic shock o Hemorrhage, dehydration, sepsis o Problems with the volume, the pump, or the arterial walls The longer it goes unfixed, the more at risk the patient is for permanent damage Signs and Symptoms (regardless of cause) o LOC: Anxious/weak/restless/thirsty then lethargic/coma Brain is not being perfused o CARDIAC: Tachycardia, hypotension, low CVP, narrowed SBP/DBP pulse pressure, weak peripheral pulses, slow capillary refill Become pale and shunting begins Patchy light purple Fast, weak pulses o RESP: Tachypnea, shallow respirations, abn ABGs (elevated PaCO2, low PaO2), cyanosis of nail beds and lips Hypoxia, CO2 levels increase acidosis o NEURO: Sluggish pupil responses, decreased deep tendon reflexes o GI: Decreased BoS X 4Q, possible N/V The GI tract is not considered vital o DERM: Moist/clammy, cool, pale to mottled skin o URO: Low urinary output, increased urine specific gravity Initial Stage – Early signs o MAP decreases 10mmHG from baseline Around 70-80 The minimum needed to perfuse organs Causes vasoconstriction and tachycardia to maintain cardiac output and tissue perfusion o Tissue perfusion is still adequate to continue anaerobic metabolism No tissue damage yet o S/S May be minor but include Tachycardia, tachypnea, possible slight rise in DBP Non-Progressive Stage – Compensatory signs o MAP decreases 10-15 mmHg from baseline Causes release of renin, ADH, aldosterone, and catecholamines to maintain kidney function via increased H2O reabsorption and vasoconstriction o Tissue hypoxia of non-vital organs o S/S tachycardia, tachypnea, lower SBP and higher DBP, low UOP, cool skin, restless, thirsty, <5% decrease in SaO2%, low blood pH (acidosis), hyperkalemia, apprehensive, scared/anxious Blood pressure comes closer together PaO2 – arterial blood SaO2 – pulse ox – not reliable during shock o Reversible with timely and effective Rx – refill intervascular space Progressive Stage (intermediate) o MAP decreases 20mmHg from baseline More severe territory, golden hour begins Causes poor tissue perfusion regardless of compensatory measures o Tissue / vital organ hypoxia with anoxia/ischemia of non-vital organs o S/S Impending doom/anxiety, confusion, very thirsty, tachycardia, hypotension, cool/moist skin with pallor to cyanosis, minimal UOP, acidosis, hyperkalemia and high lactic acid, decreased urine (oliguria), weak rapid pulse o Effective Rx must be implemented within 1 hour of onset of progressive stage to avoid MODS If it cannot be done in the hour, it goes to irreversible stage Refractory Stage (irreversible) o Excessive cell/organ damage cannot be reversed by Rx even if causes of chock is corrected and MAP is restored o MODS in a viscous, downward spiral nature as destroyed cells release massive amounts of toxic metabolites and enzymes, causing further tissue damage and cellular death…repeat… repeat It is released by cell and organ death o Multi system organ failure o S/S Loss of LOC, non-palpable pulse, extreme hypotension, cold dusky extremities, extreme hypoxia per SaO2, slow shallow respirations if any, decreased pH Drug Rx in Shock o “Fill, Tighten, Pump, Ensure” o IVFs to provide volume first then… o Dopamine or Levophed improves MAP via vasoconstriction, increased venous return, and increased cardiac contractility o Dobutamine or Primacor improves MAP and CO via increased cardiac contractility o Nipride dilates coronary arteries for perfusion during increased cardiac contractility o INSERT TABLE HERE Hypovolemic Shock Inadequate circulating blood flow results in decreased MAP o Loss of fluid from intravascular space Due to excessive loss of intravascular volume due to hemorrhage, burn shock, extreme dehydration, inadequate fluid loss replacement, diuresis, diabetes insipidus, vomiting/diarrhea Rx: crystalloid IVF (RL, NS), colloid (albumin), blood products (PRBC, plasma), IV drug infusions (Dopamine (vasopressor), Dobutamine, Nipride), O2 Rx, correct cause o Hang IV – short, large catheter 1 inch, 18 gage In the largest vein you can Subclavian, jugular, inner arm, ankle o Avoid D5, use NS or Ringer’s instead Has crystals and protein Colloid – has protein – interstitial intravascular S/S o Systemic vascular resistance, poor skin turgor, thirst, oliguria, low systemic and pulmonary preloads, rapid heart rates Diagnosis made after a loss of 15% intravascular volume Cardiogenic shock “Pump failure” (class IV HF classification) Adequate intravascular volume but LV is unable to pump effectively for sufficient CO and tissue/organ perfusion Commonly due to massive AMI, or repeated AMIs, leading to 40%+ necrosis of the LV Challenging to Rx without further burdening the LV, IABP may be necessary o Intra-Aortic Balloon Pump Assist for cardiogenic shock Can be done in the OR Inserted in coronary care unit in emergencies Has to be timed perfectly with the beat of the heart The pump inflates/deflates the balloon – goes up between pumps Push blood to coronary artery, carotid arteries, and renal arteries Deflates during systole Inflated during diastole Promotes flow to the brain and heart Cardiac Associated Labs CBC (H/H, platelet #, bleeding time) Coagulation (PT, PTT, INR) Renal function (BUN/crea) Electrolytes (sodium, potassium, calcium, magnesium) Lipid panel (total lipids, cholesterol, triglycerides, HDL, LDL) Cardiac enzymes/markers (CK-MB, troponin, myoglobin) Drug levels (digoxin) Common Cardiac Drugs Anticoagulants – Coumadin – prevention of clot Vasodilators – both arteries and veins Beta blockers – reduce workload of heart Anti-arrhythmics – regulate heart rate Stimulants Vasoconstrictors – vessel walls tighten – usually arteries Chronotropic agents (see table below) Inotropic agents (see table below) Drug category Drug effect Drug Example + Inotropic Increases cardiac Digoxin, agent contractility Dobutamine - Inotropic agent Decreases cardiac Inderal contractility + Chronotropic Increases heart rate Atropine agent - Chronotropic Reduces heart rate Digoxin, Inderal agent Dopamine (Intropin) – name alert o Drug effect per dose…+ inotropic agent (5-15), vasoconstrictor (>15), renal vasodilation (1-5) o Mcg/kg/min IV gtt via CVC using IV pump o Administer after/with IVFs to restore volume o Monitor VS, EKG, UOP, pulses, and cap refill o Concern = drug infiltration, peripheral perfusion o Different doses for different things Levophed (Norepinephrine) o Intense vasoconstrictor o Mcg/min via CVC using IV pump 1 mcg/min then titrated upward per BP o Administer IVFs after/with IVFs to restore volume o Monitor VS, EKG, UOP, pulses, and cap refill o Concern = drug infiltration, peripheral perfusion o Vasoconstriction Dobutamine (Dobutrex) – name alert o + inotropic afent, often used in combination with Nipride o Mcg/kg/min via CVC using IV pump o 2.5 mcg/kg/min then titrated upward per BP Start low then titrate up slowly o Administer after/with IVFs to restore volume o Monitor VS, EKG, UOP, pulses, and cap refill o Concern = drug infiltration, peripheral perfusion Nipride o Vasodilator (including coronary arteries Can make it worse if it is used wrong o Often used in combination with Dobutamine or high dose of Dopamine o Mcg/kg/min via CVC using IV pump 3mcg/kg/min titrated upward per BP o Administer after/with IVFs to restore volume o Monitor VS, EKG, UOP, pulses, and cap refill, chest pain o Concern – cyanide toxicity (almond breath odor, neuro changes, wrap v light) Wrapped in tinfoil and use special tubing Common cardiac procedures Cardioversion v. defibrillation o Use of an electrical impulse to regulate or initiate an effective cardiac rhythm Electric jolt will bring heart back to normal o Synchronized cardioversion of lower voltage under IV sedation if existing rhythm Ex) poorly compensated atrial tachycardia of rapid rate Emergent or urgent and planned Client is awake and frequently sedated Synchronized with QRS 50-200 joules Consent form EKG monitor o Asynchronized defibrillation of higher voltage during cardiac arrest scenario if non-viable or absent rhythm Ex) ventricular fibrillation, ventricular tachycardia, asystole Emergency No cardiac output Begin with 200 joules – can go up to 360 Client unconscious EKG monitor o AED Used for defibrillation only Anyone can use it in crisis The quicker the patient is zapped out of the problematic arrhythmia, the better the chances As soon as you identify a patient that is unconscious and pulseless – defibrillate asap User friendly will tell you how to use it o Implantable cardioverter defibrillation Meant for long term coverage Not used for emergency stimulation Used for patient with consistent problems with arrhythmias Especially ventricular Looks like a pacemaker Subcutaneous pocket is created in chest above the ribs and below the clavicle The catheter itself that contains the wires is then inserted into the subclavian vein It is advanced to where you want it to discharge the impulse In many patients its down by the ventricle and the catheter has a hook so it can adhere to ventricle wall The device can determine when the patient has gone into an episode of, for example, tachycardia Identifies the rhythm and zaps the patient’s heart The patient can feel a jolt They can feel the arrhythmia too – get dizzy Then get an energy surge – feels like you got kicked in the chest o Cardioversion care Witness informed consent Code cart nearby Patient IV catheter with running IVFs during procedure Oxygen by NC or mask per MD Telemetry monitoring IV sedation prior to procedure with anesthesia present if facility-mandated In some hospitals the critical care nurse can administer the sedation Most commonly used sedation is verset – includes amnesia Protective gel/gel patch to paddle site…topical skin care prn afterwards (ex. steroid cream – lidocaine mixed with it) Vonductive medium (gel) – sometimes area may be burned Ensure that defibrillator is set to synchronized cardioversion with marked R wave on screen Make sure you hit the synchronized button and verify with other people o Look for a dot over the R wave Pacemaker o The use of a generated electrical impulse to initiate or regulate cardiac rhythm o Temporary or permanent/implanted Implanted transvenous pacemaker Minor surgical procedure Battery on pocket attachment under skin Temporary transvenous pacemaker Procedure is similar to a control line placement in subclavian except exiting from the skin isn’t an IV catheter but wires that are connected to a pacemaker device with dials that you preset o On demand pacing o Atrial or ventricular pacing o What rate o etc Depending on what kind of heart surgery, some patients come back from a heart surgery with the wires just in case you need to connect them to a box o Transvenous or transcutaneous Transcutaneous AED has pacing capabilities – cardioversion, pacer, shock all in one Quickest way to apply a pacemaker in an emergency situation Use the patches so that the pacing impulse is sent across the skin Parametics can use this Usually patient should be considered for transvenous or either of the implanted pacemakers o Single or dual chamber Atria or ventricle = single Atria and ventricle = double o “Demand” pacing is programmed to act after a pre-set interval without a natural cardiac impulse o Pacemaker “spike” Vfi b No P wide, large, bizarre QRS Either the vertical upward from baseline or vertical downward from baseline – depending on the leads used When spike is used to generate a QRS pacing, wire is placed in RV so that it will get that impulse slightly ahead of the LV so the QRS you see ill be large, bizarre, wide and notched When you see the spike and the weird QRS, you know it’s a ventricular pacemaker o Ventricular pacing Spike needed for every QRS There is not a demand set pacing o “On Demand” pacemaker Preset to tolerate pause for certain duration then impulse Preset to wait a certain amount of time to see if the heart can conduct an impulse before kicking in and generating an impulse On demand atrial pacemaker because the spike occurs before the P wave – impulse in atria is normal down into the ventricles and the QRS has normal appearance o Post pacemaker care Monitor LOC, VS, O2 sat % and telemetry if used Look for normal perfusion Telemetry Incision care Activity limitations (no heavy lift/push/pull or contact sports) Worried about tip of pacing wire in heart that hooks in place Limitations especially in effected shoulder Medic Alert ID Might be sensitive to some equipment that can mess up the impulse, plus it is metal MRI contraindications Metal Reportable S/S to include those of low CO, chest pain, palpitations, and infection May indicate pacemaker isn’t working well S/S o Palpitations, dizziness, return of chest pain CP could mean coronary arteries aren’t getting perfused Follow-up to ensure pacemaker function Cardiac catheterization o Diagnostic test Sometimes combined with threatment o Strategy – angioplasty or stent placement o Interventional radiology needed – IV access/fluids, oxygen o They are sedated – incision in either anticubital vein of mid arm or femoral vein of the groin Catheter is inserted up the vena cava into RA then dye is injected watch the dye travel from RA RV pulmonary artery lungs LA LV then as it goes into coronary arteries o Used to identify any obstruction of coronary arteries o Can be elective/planned – family history, cpmplaints of chest pan o Acutely – worried might be having acute MI Can be very stable or very unstable Angioplasty and stent placement o Only used for partial occlusion, it won’t work for total occlusion o Inflate the balloon and flatten the obstruction (plaque) – pull balloon out but leave in place a wire coil stent Coronary artery bypass graft (CABG) o Taking the vein from another part of your body and using it as a detour Donor vein is attached to aortic root – get fresh oxygenated blood The other side is swung below the obstructed coronary artery so there is a detour and oxygenated blood comes from the aortic root to the under perfused myocardium o Procedure to Re-profuse myocardium when there is an obstruction of coronary arteries When the coronary artery obstruction can be relieved by angioplasty When more than one coronary artery is obstructed If you have to stent more than 3 places of coronary artery system then you need to open the patient up and take a look at what is going on o Concern – may sure the patient is not allergic to iodine because the dye used contains it Can be irritating to the kidneys, want to flush it out of the body ASAP o Watch I’s and O’s, BUN, creatinine Valve replacement o Surgery done when the valve is stenotic or regurgitive in nature, or the patient is showing signs of HF Aortic/mitral stenosis, aortic/mitral regurgitation o Kinds Metal prosthete valve Biological non metal valve – Boluire cattle Biological valve porcine – pig Combo of metal and bone o Biological – cow or pic – less need for anticoagulation o Metal valve – requires anticoagulant for the rest of the patients life so they don’t get a clot in the valve Left ventricular assist device (LVAD) o Similar treatment option to IABP used for cardiogenic shock or end stage CHF o A version of an artificial heart Can be in the hospital or ambulatory – can be used at home o Primary use – buys some time o Moves blood in LV to aorta union then delivers oxygenated blood through the body Pumps the blood and circulates it – keeps the heart going when it is too weak o LVAD includes: Connection to LV Inflow case Outflow case Some type of pumping device – external to LV May be a rotary pump A catheter that exits the torso that is attached to some type of energy source Most are battery operated o Recharge and check often Cardiac transplant o Treatment – done a lot o Leaving majority of RA, vena cava, aortic arch, and pulmonary veins in place and sewing on lower part of the heart o Post op Patient needs antirejection drugs Many need biopsy of heart through cardiac catheterization to make sure it isn’t rejecting Under transplant service and cardiology Thrombolytic/Fibrinolytic Rx for STEMI o “Clot bluster” to restore coronary artery perfusion during ACS with chest pain refractory to NTG Rx o TPA (Alteplase) by IVB via pump o Combined with anti-coagulant and anti-platelet agents o Most effective when started within 6 hrs of chest pain onset and within 30 minutes of ED admission (“door to needle” time) o Initiate bleeding precautions o Contraindicated if recent OR, trauma or CVA o Watch for re-perfusion ventricular arrhythmias Post-op for all Heart Surg Patients Will have chest tubes, initially intubated and ventilated, will have swan line for hemodynamic monitoring, foley, arterial line, peripheral catheters Will go home under cardiac surgeon supervision – enter into cardiac rehab Monitor LOC, VS, O2 sat%, pulses, capillary refill, breath/bowel sounds, drain output, UOP, I/O, weight, and labs (CBC, chemistry, coagulation) Oxygen Rx o Must use incentive spirometer to prevent atelectasis and pneumonia IV fluids, pain management, antibiotic Rx, electrolyte replacement, and blood products as ordered o May need more blood products o Watch I+Os because received a ton of fluid during surgery Wound assessment and care Drains to gravity or suction (self, wall) Resumption of diet and activity over time Discharge planning o Cardiac rehab Pain management is important o Don’t want to give too much narcotics that it interferes with cardiac function and breathing Monitor potassium Monitor chest tube drainage NURS 479 – Adults in Health and Illness – Hemodynamics Preload Total amount of blood presenting to the RA/LA from the vena cava and pulmonic vein Afterload Resistance to CO from LV what LV faces when trying to produce cardiac output Increases with hypertension Heart rate (HR) # LV contractions per minute Stroke volume Amount of blood pumped out of LV per (SV) contraction Ejection % blood pumped out of LV fraction (EF) Cardiac output Amount of blood pumped out of LV per minute (CO) (SV X HR) Cardiac index CO per body size (CO divided by body surface (CI) area) Diastole Relaxation and filling of the atria and ventricles Systole Contraction and emptying of the atria and ventricles Primarily ventricles Mean arterial Minimal BP to ensure perfusion to coronary pressure arteries and major organs Diastole Filling Blood enters heart and goes to ventricles Systole Pumping o RV pulmonary system o LV arterial system with O2 blood to organs/tissues Preload Volume entering ventricles RA from SVC and IVC LA through pulmonary/vascular system post oxygenation Ideally the preload in the right = the preload in the left o There are times where there are structural deficits in the pulm/vasc system where it is not equal Afterload Resistance left ventricle must overcome to circulate blood o Pump blood into the arterial system via the aorta Stroke volume A. right sided preload from vena cava, left side heard from pulmonary vein B. left ventricle per minute, hopefully equal between right and left In reference to hemodynamics, usually talk about output as coming out of LV o Blood is dispersed through the body to major organs Ejection fraction When LV pumps, it does not completely empty o The majority of the blood is pushed out, but not 100% of it Cardiac output Increased HR – drugs, exercise, positive chronotropic drugs o To decrease use a negative chronotropic agent Increased SV – positive inotrobic agents o Pumps stronger, contracts longer stronger CO Increased CO by increased preload o IV fluids increased preload increased blood in heart increased cardiac output Example values in a healthy 70 kg man (average adult) SV – blood out of left ventricle with each contraction Ef – % of blood that the left ventricle is ejecting o ~35% of blood left in the LV which is pumped out in the next contraction o End stage HF, EF less than or equal to 20% CO – L/min – 75% to vital organs (heart, liver, kidney, brain, lungs) Cardiac Index CardiacIndex=CardiacOutput÷BodySurface Area o Individualized to each particular patient Mean Arterial Pressure (MAP) Range = 70-110 mmHg The average pressure of the arteries M AP= (2×diastoli)+Systolic 3 MAP is multiplied by 2 because diastolic phase last longer than the systolic phase Minimal BP that’s necessary to keep vital organs perfused CVP monitoring Monitor that goes into the heart to monitor the pressure the chambers are experiencing Central venous pressure = when the monitory is in right atrium ~5-7 Right ventricular pressure waveform – not a lot of emphasis on it because it is assumed that if the CVP/right atrium pressure is normal, the RV is too Swan Ganz Pulmonary Artery Catheter Yellow catheter with multiple lumens at the end Usually in the neck/jugular or subclavian vein heart Cortis introducer – large diameter IV catheter o It adds an additional 2 ports o Yellow catheter is pushed through this 4 specific values o Reflecting pressure in the different parts of the heart o 1. RA pressure – CVP Average 5-7, hydration will increase or decrease it o 2. RV pressure Changes based on systole/diastole Systolic 20-30 mmHg; Diastolic 0-8 mmHg o 3. Pulmonary artery pressure Systole # divided by diastole number Systolic 20-30 mmHG; Diastolic 8-15 mmHg o 4. Pulmonary artery wedge pressure 8-12 mmHg Closest indicator we have of preload coming into the Left side of the heart Once you get this number, immediately deflate the balloon Cant put a catheter into the left side of the heart because it is too dangerous, so put it as close to the left side as you can by using “wedge pressure” Balloon at the tip – inflate for a very short amount of time, the pulmonary artery will pull the balloon as far as possible and it will get lodged in a branch of the pulmonary artery Reading provided is pulmonary artery wedge press o When deflated, it will float back to just the pulmonary artery itself Pulmonary Artery wedge (PAOP) Only get it when you inflate the balloon briefly Pulmonary artery waveform slowly inflate pulmonary artery wedge deflate pulmonary artery waveform 2 3 1 4 Afterload and MAP – Direct monitoring via A-line Catheter positioned in artery Radial artery – direct BP reading o Connected to hemodynamic line, connected to continuous flushing with heparinized saline under pressure, connected to transducer Cuff bag to provide pressure Transducer quantifies pressure reading Appears on wave screen as waveform and number Typical arterial waveform o Dicrotic notch – opening/closing of aortic valve and LV Nurs 479 Adults in Health and Illness – Cardiac Nursing – A/P Review and EKG Interpretation EKG’s have been around for about 50 years Coronary Care Units Coronary Care units were primarily for patients with AMI o Cardiac Care = Coronary Care 1962 – Bethany Hospital in Kansas City, KS – first CCU 1963 – Presbyterian Hospital in Philadelphia 1965 – NY Hospital-Cornell Medical Centre in NYC Holy Cross Hospital was the 4 in Silver Spring (1965) In just 4 years (1962-1966), the US went from 0 250 CCUs o This was made possible by technology EKG interpretation, mechanical ventilators, further advancement in cardiac drugs 1964-1965 – CCU guidelines were published The 7 essentials for the ideal CCU o Cardiac arrest team o Quiet, peaceful environment o Adequate space for resuscitation in each patient cubicle o Adequate and specialized training for nurses This was difficult to implement because nurses were being educated in 3-year hospital programs 1966 – nurse educators and cardiologists had a meeting to devise the “Criteria and Guidelines for Nurse Training Courses in a Coronary Care Unit” 1967 – there were 13 SONs funded to offer short-term training courses to CCU RNs o CUA was one of them – part of our SON legacy is in cardiac 1960s CCU o ward-like setting o main telemetry screens were at the nurses’ stations o at the bedside there was: O2, suction, and outlets In the 1960s they also created ICUs for medical and surgical patients 1965 CCU there was a one distinct nurse every shift that would just monitor the screens Heart Anatomy There are 4 chambers of the heart – atria and ventricles Blood goes to the heart by the IVC and the SVC In the wall of the left ventricle, there is more muscle because this ventricle has to pump blood to the body Travelling with the blood o Right atrium tricuspid valve Right ventricle lungs for O2 oxygenated blood to Left atrium bicuspid valve Left ventricle aorta Body The coronary arteries branch off of the aortic root and supply the heart itself with oxygenated blood o The aortic root is the very beginning of the aorta, where it first comes out of the heart The left coronary artery goes down the left anterior of the heart and descends to the back o The back part of the left coronary artery is called the “circumflex branch of the left coronary artery” Key elements of EKG assessment Heart rate R-R interval (rhythm) o The distance between 2 R’s in 2 back-to-back QRS waves = rhythm P/QRS, T waves…U when present o U wave = abnormal PR and QT intervals ST segment depression or elevation Is the cardiac rhythm tolerated by the patient? Is there adequate tissue/organ perfustion? o Tolerated = the patient is continuing to be perfused Look at: BP, color, pulses, pain, etc Electrical current o 1. Sinoatrial (SA) Node o 2. Atrioventricular (AV) node o 3. Atrioventricular bundle (Bundle of His) o 4. Left and right bundle branches o 5. Purkinje fibers This pattern creates the wave on the EKG EKG Strip P – impulse goes through the atria o Should be above baseline QRS – impulse through ventricles o Should be above baseline o Tall, thin, spiked, taller than P T – electrical recovery, rebooting system, heart settling to get ready for the next impulse o Should be above baseline PR interval – want it to be less than 0.2 seconds ST segment – should be at baseline EKG Definitions Heart Rate (HR) – 60-100 bpm at rest o Regular even spaces between the R’s o Based on # ventricular contractions (QRS) per min Heart Rhythm – consistency of P-P and R-R intervals Repolarization – recovery Depolarization – stimulation P wave (atrial depoloarization) o Want one before each QRS o Consistent shape and size o Deflected from baseline PR interval (atrial depolarization/impulse delay by AV node) o Consistent 0.12-0.20 seconds in length on EKG QRS wave (ventricular depolarization) o 0.4-0.10 seconds in length o Consistent size/shape, deflection from the baseline QT interval (both ventricular de- and repolarization) o 0.10 seconds or less in length o Ventricles active, stimulation and recovery o Note if prolonged – risk for ventricular arrhythmias T wave (ventricular repolarization) o Preparation for next impulse o 1 post QRS, consistant size/shape o note peaking or inversion U wave (hypokalemia v. unconducted P wave?) o Occurs after and is smaller than T wave ST segment (estimated time of ventricular muscle contraction) o Flat at baseline o Note depression below or elevation above baseline Reduced Cardiac output can result from: Bradycardia Tachycardia Irregular heart rate Loss of atrial “kick” o Happens in the Right atrium, blood should flow from RA to RV o The last 1/3 of blood in the RA gets pushed into the RV with a little contraction but when this doesn’t happen, the blood can pool atrial fibrillation/flutter Signs and symptoms the patient is not tolerating the arrhythmia Skin pallor Altered LOC Hypotension Slow capillary refill Weak/thread peripheral pulses Reduced urine output – with ongoing arrhythmias Dizziness, weakness Palpitations – feel own heart racing Angina pain o Chest pain = serious o This means that coronary arteries are not getting sufficient blood and the myocardia is not getting what it needs Leads, Placement, and Results 12-perspective view of impulses o chest, peripheral W B W R W BBrown B G G R R o An example of a continues EKG format o Best to monitor p wave Telemetry lead placement hints o White on the Right o Clouds (white) above the grass/trees (green) o Smoke (black) above fire (red) o Dirt (brown) in the middle of the garden White = RU chest Green = RL chest Black = LU chest Red = LL chest Brown = middle Telemetry data collection system – 24 hour Holter EKG Monitoring NS and Arrhythmias Normal Sinus Rhythm (NSR) o 60-100 bpm o Regular rhythm (R-R wave), normal QRS complexes at rest, PQRST Sinus Tachycardia (ST) o 100-150 bpm o Regular rhythm, normal QRS complexes at rest o Often due to pain, fever, stress, and exercise o Gradual onset and gradual termination Sinus Bradycardia o Less than 60 bpm o Regular rhythm, normal QRS complexes o Extremely athletic – heart is at this point but not a problem Sinus Dysrhythmia (formerly sinus arrhythmia o NSR but with an irregular rate correlating to respirations o Increase HR on inspiration, decrease on exhalation NSR vs. ST = HR NSR vs. SB = HR NSR vs. SD = HR when you breathe in, and HR when you exhale Rhythm Strip Examples Normal Sinus rhythm o Black marker at the top, is the “3 second marker” used to help calculate the rate Sinus tachycardia o (Compare to the 3 second marker from slide 23) o R-R interval is normal but shorter o P and T waves can almost be blended if the heart is beating fast enough Sinus Bradycardia o R-R interval is longer Sinus Arrhythmia / Dysrhythmia o The first three beats are on inhalation, so they are faster o The second two are on exhalation and they are slower Common Atrial Arrhythmias o has something to do with the AV node or Bundle of His Premature Atrial Contraction o Underlying sinus rhythm with a premature beat o Abnormal or absent P wave o The heart beats so quickly Atrial Tachycardia o 150-200 bpm o impulse from somewhere around the atrial node o “Narrow complex (QRS) tachycardia” o AT vs Sinus Tachy = rate is much faster and AT is not tolerated for very long Paroxysmal Atrial Tachycardia o Sudden (paroxysmal), abnormal P waves Atrial Fibrilation o 60 (controlled) to >100 (uncontrolled) irregular rhythm o Heart is quivering – usually requires digoxin o Not one impulse is in control of the system Instead of a P wave, there is a wavy baseline without the presence of P Atrial Flutter o “Sawtooth” = atrial flutter (F) wave at 250-350 flutter bpm Count the F waves per QRS Reported as a ratio o Lacks single control, multiple sparks with atria trying to respond No real baseline More F before QRS, worse, impulse not dropping into ventricles Norm Norm Norm premature pause There is a compensatory pause – before it falls back into rhythm Impulse is short, smaller P wave on the premature beat Flips switch to normal Cound the QRS between 3 seconds and multiple by 20 to get a full minute (bpm) First 3 seconds – short R-R and blended P+T waves 4 flutter – blocking 4 waves until one is accepted A flutter – no flat baseline wavy, sawtooth baseline o Varying flutter to QRS ration is concerning A fib – wavy baseline o Determinable QRST, no P; Irregular rhythm between R-R Premature Ventricular Contractions (easier to understand with pictures) PVC o Underlying EKG rhythm, the impulse comes from the ventricular tissue o Irregular rhythm due to the premature beat o Beat will cause irregularity of rhythm, no P wave or PR interval, large and wide QRS o It is isolated in the EKG and surrounded by normal beats, not a constant arrhythmia Unifocal o PVCs share the same QRS shape Multifocal o PVCs with differing QRS shapes, each representing different ventricular foci Each different one comes from a different place in the ventricle When there are multiple sites, there is more to worry about Interpolated o PVC between 2 normal EKG complexes, usually without a compensatory pause Couplet o 2 consecutive PVCs Triplet o 3 consecutive PVCs (3-beat run of V tach) Bigeminy o Every other beat is a PVC Trigeminy o Every third beat is a PVC R on T o PVC occurs on the proceeding T wave, triggers Vtach or Vfib o This is very concerning T wave = recouping period of irritability; when R on T occurs, it can trigger Vtach or Vfib – both are deadly PVC with compensatory pause N N o These PVCs look the same, so they have the same foci (UNIFOCAL) – there is one area of irritation o It looks negative, but it is only because of the lead that was used, it helps to visualize it upside down Unifocal PVCs o Another view of the same sort of PVC, but just right side up o These QRS intervals are wide, large and bizarre on the PVCs o These QRS intervals are wide, large and bizarre on the PVCs Multifocal PVCs o They have different sizes and shapes; they are coming from two different irritated places in the ventricles Slide 35 Interpolated PVCs – occurs between sinus beats without a compensatory pause N N o System reboots without a pause o There is supposed to be a pause between these two normal waves, but instead there is an extra beat PVC couplet o Concerning because two beats can lead to three beats, and three beats can lead to Vtach o These PVC beats are unifocal – coming from the same irritated part of the ventricle PVC triplet N N Pause o Unifocal o 3 beats in a row can lead to tachycardia, need to act on this PVC Bigeminy N N o Unifocal but concerning o Singular area but taking over the impulse system o The longer it goes on, the more symptomatic the patient is o Over time (minutes) the heart and body stop tolerating this, the patient gets dizzy, light headed, CP, decreased BP, pulses weaker Ventricular trigemini N N N N o Unifocal but concerning o The longer it goes on, the more symptomatic the patient is o Over time (minutes) the heart and body stop tolerating this, the patient gets dizzy, light headed, CP, decreased BP, pulses weaker PVC “R on T” Phenomenon QRS P T o PVC on descent Common Ventricular Arrhythmias o Very serious – untreated = life threatening – short term only Premature Ventricular Contraction (PVC) Idioventricular ventricular rhythm o “last resort paymaker” – SA failed, AV failed ventricular tissue o 20-40 bpm o Absent P wave and PR interval o Wide, bizarre QRS o 3 degree AV heart block (complete) Ventricular Fibrillation (Vfib) o Entire EKG complex is replaced by a coarse or fine wavy baseline o Cardiac arrest situation Ventricular tachycardia (VT) o >100 bpm o Wide bizarre QRS o Cardiac arrest situation o PVC after PVC, ventricular tissue controls Torsade de pointes o VT with “twisting” of the QRS complexes o Rare Asystole o “Flat line” o Complete absence of EKG complexes Common Ventricular Arrhythmia Strips Idioventricular Rhythm o Pause with nothing coming so the ventricles step in o No P, No QRS o 20-40 bpm o *The body can only be sustained on this rhythm for a short amount of time Ventricular Fibrillation Best time for defibrillation – shocks them out of this; more electric activity; starts as this Quickly flattens (minor quivering); harder for defibrillation o Loss of impulse, no impulse through ventricles o Electrical flickering o No adequate outflow Ventricular Tachycardia (R on T?) N N o So fast, the intervals between R’s is short o No P or T o Possible R on T first beat of Vtach o During this display of VT, the patient is probably semi-conscious Ventricular Tachycardia Run N N N o Rapid beats from ventricle, goes away as quickly as it came; may or may not be conscious Torsades de Pointes (rare) o High risk for people who have a long QT segment (more than usual) o Twisting appearance o It is dangerous because it is hard to get out of o Prevented if monitored V-fib – lack QRS, wavy baseline, course fine V-tach – impulse by ventricular tissue, fast rate, not sustainable, no cardiac output Asystole – complete flat line AV heart block o Heartblock gets worse over time 1 degree heart block o Underlying heart rhythm and normal EKG wave except for prolonged PR interval (> 0.20 seconds) o Impulse generated but held at AV node/bundle of His area 2 nddegree Mobitz Type 1 AV heart block (“Wenckebach”) o Progressively increasing PR intervals until a non-conducted P wave occurs (No QRS), then a pause, then the cycle restarts o P wave keeps getting longer then dropped 2 nddegree Mobitz Type 2 AV heart block o More P waves than QRS complexes due to unconducted P waves o PR interval remains normal and consistent o Unconducted P, no QRS behind it 3 degree AV heart block o “complete” heartblock complete wall between atria and ventricles SA AV ventricles Ventricles are creating their own impulses o Usually HR slows to 20-40 bpm o 2 completely separate rhythms atria and ventricles Heart Block Strips st 1 Degree AV Heart Block o PR interval longer than 0.2 seconds 2 nddegree AV Heart Block Type 1 (Mobitz 1) P P P P Pause, did not go down to ventricles o “Wenckebach” nd 2 Degree AV Heart Block Type 2 (Mobitz 2) Dropped P 3 Degree AV heart block R P T P P o Consistent, 20-40 bpm rate of ventricular pace maker what pulse is like o Wall between atria and ventricles Impulse does not go from one to the other Two rhythms occurring without regard of the other Junctional Arrhythmias o Pulse occurs at the junction of all four chambers Impulse generated by the AV node, with simultaneous impulse transition up to
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