NUR 120 (UNIT 4) CAD, CABG and CHF 5.1- 6.1

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Coronary Artery Disease is:
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an umbrella disorder that includes: – athereosclerosis – angina pectoris – acute coronary sndrome (can lead to MI if not resolved) – myocardial infarction – heart failure – pulmonary edema
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atherosclerosis is:
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abnormal accumulation of fat in the arteries and arteries walls lipid deposit and fibrous tissue build up in the wall which leads to plaques which cause a decrease in blood flow
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atherosclerosis is significant because:
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it is the most common caused of CAD
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atherosclerosis pathophysiology
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foam cells (macrophages that have become distended with lipid) begin to form fatty streaks, – fatty streaks build up to become fibrous atheromatous plaque – these lead to damage to artery walls which causes an inflammatory response in the artery – fibrous atheromatous plaque build up to become complicated plaques – the inflamm response then leads to plaque build up – the plaque build up slows blood flow – the plaque can dislodge and becomes an emboli and may move to the brain or lung and cause stroke or death
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Atherosclerosis clinical manifestations
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– Acute Coronary Syndrome – coronary ischemia – coronary infarction
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Angina and Coronary Artery Disease
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– clinical syndrome with episodes of pressure and pain in the chest as a result of lack of O2 in the heart muscles due to insufficient blood flow to the myocardial tissues – angina is progressive
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How does activity effect Angina?
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– it increases metabolic demands and O2 requirements which leads to exacerbation and angina caused by atherosclerotic disease
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What may lead to an exacerbation of angina?
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– significant obstrucution of major coronary artery – high BP (increases O2 demand) – cold weather (causes vasoconstriction) – heavy dinner: blood shunt to the GI and increase in O2 demand, decrease peristalsis
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Coronary Arteries and Angina
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– right coronary artery becomes –> posterior descending artery – left main coronary artery becomes –> circumflex and anterior descending arteries – coronary arteries are filled during diastole – if the coronary arteries are clogged and blood perfusion is decreased (along with diminished O2 supply) ischemia occurs and angina pain presents
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clinical management and tx of angina
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– decrease their O2 demand – REST (supine position) – increase their O2 supply – NTG (sublingual, 3 doses every 5 mins, no more then go to ER) – PCI/CABG – Surgery to reduce plaque formation **rest will resolve early angina, usually**
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pharmacological tx of angina
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– usually done in hospital – O2 administration (increases O2 sat) – Nitroglycerin admin (dilates coronary arteries and increases blood/O2) – Beta Blocker admin (decreases sympathetic stimulation of the heart) – Ca+ Channel Blocker admin (dilates blood vessels) – Antiplatelet/anticoag admin (ASA) (thins blood/reduces viscosity)
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Nursing Interventions for a pt with Angina
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– start with assessment of pain (usu COLD AAA acronym) – tx and prevent pain – reduce anxiety – teach self care
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Myocardial Infarction and CAD
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the left anterior descending (LAD) coronary artery is blocked with a blood clot causing damage to the heart muscle and reads with an irregular ECG/EKG
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MI’s may also be called
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– Acute Coronary Syndrome – Heart Attack – coronary infarction
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Myocardial Infarction (diagram)
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MI pathophysiology
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– the coronary vessel is clogged by plaque and clotting factors – the part of the muscle distal to blockage doesnt get blood or O2 – then the BP raises (sympathetic/parasym kicks in) increasing O2 demand – heart rate and respiratory rate increases – causes anaerobic environment which is ischemia – ischemia causes pain – no blood and no O2 causes infarction and necrosis of the tissue **not all MI are the same** **ask how bad was it?**
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Where do MI’s mostly occur?
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– anterior, inferior, lateral aspects of the heart –> right ventricle (ventricles) **ask where was the MI occurred**
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Typical causes of MI
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– vasoconstriction that is persistent – plaque – clot
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MI Chest pain is described as:
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Severe, crushing, constrictive, heavy pain **does not go away with rest or NTG**
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SNS Response during MI
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– GI distress, nausea, vomiting – Tachycardia (HR increases) and peripheral blood vessels will vasoconstrict (shunts blood to the heart) – Anxiety, restlessness (may be caused by hypoxia)
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MI may lead to:
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– following the SNS response, hypotension and possibly shock – if not treated can lead to cardiac arrest **the SNS response is a compensatory state and hypotension is a decompensatory state**
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MI Hx and Phys findings
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– take VS – take ekg (tells where, if and how bad MI is) – get CK, ISO and troponins from blood (these help to dx.) – do phys exam and take hx
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MI pt Tx goals
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– promote tissue perfussion (give O2 to treat hypoxia, ntg, ASA, beta blocker admin, thrombolytic therapy: clot busting tx = all of these are to reduce the size of the infarction) – relieve pain – reduce anxiety – prevent complications
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What are some complications of an MI
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– dysrhythmias (like complete heart block, tachy, brady) – cardiogenic shock – acute pulmonary embolism (potential) – cardiac failure – thrombo-embolytic episodes
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Nursing Responsibility for pt with MI
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– assessment dx (head to toe for cardiac signs) – Planning: tx and prevent pain – reduce anxiety – teach self care – probably in CCU **when writing pathophys of MI you had better mention how the inflamm process, edema, WBC, etc are involved**
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Acute MI Medical Treatment
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– Drugs – Percutaneous Coronary Intervention (PCI) – Coronary Artery Bypass Graft (CABG)
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Acute MI Thombolytic Tx:
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– if patient is Dx by symptoms and EKG, begin this therapy. – ideally begins within 3-6 hrs of infarction. – must get informed consent from pt. – contraindicated in pt with bleeding abnormalities or recent surgery. – tx is systemic, usu pressure dressings, sml needles, hold pressure (5-10mins) when inserting IV.
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Thrombolytic Tx is used to
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– increase blood flow – decrease size of infarction – cause re-perfusion **thrombolytic tx is called door to needle time. once throm tx occurs the patient must have access to PCI usu at cath lab.**
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Nursing Care for Pts with MI’s
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– ongoing assessment – dx – planning: (independent interventions and dependent interventions and collaborative interventions)
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Immediate tx of an MI
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M- orphine O- O2 (standing orders) N- NTG A- ASA **must watch respiratory rate, heart rate, LOC, etc** **MONA** **dependent and collaborative interventions**
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MONA (memory)
MONA (memory)
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Invasive Med Interventions for MI
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– Percutaneous Transluminal Coronary Angioplasty (PTCA) – Coronary artery stent – CABG – Heart Transplant
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Percutaneous Transluminal Coronary Angioplasty (PTCA) (diagram)
Percutaneous Transluminal Coronary Angioplasty (PTCA) (diagram)
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PTCA: Percutaneous Transluminal Coronary Angioplasty
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– used for pts who have had acute MI, helps reperfuse, – can use for angina and recurrent chest pains – done in cath lab – use angiography to locate of plaque – surgeon uses fem artery and inserts balloon cath – uses flouroscopy to place – balloon inflates to compress plaque against wall – insert stents to hold wall lumen open. – can have angioplasty without stent placement
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PTCA Nursing Considerations
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– may cause coronary artery rupture – may cause emboli from dislodged plaque to move to the brain – may cause bleeding – may cause hematoma formation – do 5 P assessment – with CABG you need to worry about clot, shock, impaired tissue perfusion – keep leg straight and secure (sandbag, restraints)
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Coronary Artery Stinting Pts Teaching
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– not permanent solution – must have lifestyle change to prolong lifetime of stent – stent is coated with anticoag drugs to prevent coag – risk of thrombus with stint – wire mesh
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Percutaneous Coronary Intervention (PCI)
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an invasive procedure in which a catheter is placed in a coronary artery, and one of several methods is employed to remove or reduce a blockage within the artery
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Complications of PCI’s
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– dissection – perforation – abrupt closure – or vasospasm of the coronary artery – acute MI – acute dysrhythmias (eg, ventricular tachycardia), and cardiac arrest.
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Post operative Complications of PCI’s
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– abrupt closure of the coronary artery – bleeding at the insertion site – retroperitoneal bleeding – hematoma – arterial occlusion – acute renal failure
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Periprocedure care for Pt’s receiving PCI
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– Patients who are not already hospitalized are admitted the day of the PCI. – Those with no complications go home the next day. – During the PCI, patients receive IV heparin or a thrombin inhibitor – are monitored closely for signs of bleeding – pt may receive medication tx for several hours following the PCI to prevent platelet aggregation and thrombus formation in the coronary artery. – sheaths where PCI was inserted will be replaced after blood studies confirm that heparin is inactive and clotting times are normal – The patient must remain flat in bed and keep the affected leg straight until the sheaths are removed and then for a few hours afterward to maintain hemostasis. – Because immobility and bed rest may cause discomfort, treatment may include analgesics and sedation. – Sheath removal and the application of pressure on the vessel insertion site may cause the heart rate to slow and the blood pressure to decrease (vasovagal response). – An IV bolus of atropine is usually given to treat this response – a pressure dressing is applied to the site
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Coronary Artery Bypass Graft (CABG) (diagram)
Coronary Artery Bypass Graft (CABG) (diagram)
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– A.K.A Coronary Artery Revascularization
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CABG procedure (diagram)
CABG procedure (diagram)
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CABG uses:
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– can be used to prevent MI – viable option pts with CAD – variant angina (prinzmetal angina) happens at rest – unstable angina – positive exercise stress test – pts not responding to NTG – pts that have blockages that arent treatable by angioplasty
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CABG Nursing Considerations
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– need to preped for OR: clean skin, prep for gen anesthesia – will use coronary artery bypass machine due to stopping heart – blood vessels taken from another part of body and used for the heart (leg, mammary artery) – pts will be on heparin – anticoagulated – will be hypothermic 82-89 degrees (slow body processes like metabolic rate to reduce O2 demand) – not permanent
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Complications of CABG
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– potential for death – when veins are used they don’t last as long, not as muscular, not as many layers as arteries, will fail due to arterial pressure – possible infection r/t long incision – possible edema from removal of vein in leg
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What veins are commonly used for CABG?
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– greater and lesser saphenous veins – mammary artery
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CABG preop care
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– preop teaching: IV meds – PCA – morphine, inc spiro, cough and deep breathe, splinting incision, – phys and psych assessment – pts who are less anxious do better postop – health hx – informed consent – nursing process
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Nursing Dx for CABG
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– impaired tissue perfusion – pain – risk for infection – impaired gas exchange r/t ineffective airway clearance – altered breathing pattern – anxiety – decreased cardiac output – activity intolerance – risk for injury
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CABG intraoperative care:
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– Holding: Assess, prepare for OR & PACU – IV lines are inserted – Anesthesia –> ETT –> Mechanical Ventilator – Periop RN: Assist with procedure and Ensure pt comfort and safety
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CABG Postoperative care
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– Hemodynamic stability (assess for pressures in and around the heart) – Recover from general anesthesia – Wound care (slow healing, dehiscence) – Fluid and Electrolytes – Progressive activity – Diet – D/C home in 3-5 days
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CABG Complications
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– MI – Dysrhythmias – Hemorrhage – Stroke – Infection
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“Congestive” Heart Failure is
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** r/t Inadequate Tissue Perfusion** – Evaluate cardiac, pulmonary and systemic congestion – when you have heart failure the heart is not able to provide sufficient O2 to meet tissue needs which results in inadequate tissue perfusion – is contributed to by coronary artery disease – can be acute or chronic (insidious-gradually occurring and moves from stage A to B to C to D) – can be left or right sided – A form of cardiac failure – A syndrome – not a disease
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CHF is usually a:
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lifelong issue (chronic) some symptoms may be able to be resolved.
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CHF Pathophysiology:
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– systolic or diastolic overloading & myocardial weakness –> – then as this physiological stress reaches critical level, contractility is reduced (pain is a late symptom) –> – Cardiac Output declines –> – Venous input to ventricles remains the same
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CHF Acute vs Chronic Patho
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– Acute – short term response (Ventricular muscle dilatation and increased force of contraction) – Chronic – ventricular hypertrophy
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CHF Etiology
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– damage to the heart muscle (affects afterload) – ventricular overload rt increased *preload*: 2° MI, IV fluid volume overload & kidney failure –> increased venous return – ventricular overload rt increased *aferload*: 2° uncontrolled chronic HTN, valve problems – constriction of the ventricles: r/t cardiac temponade
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Cardiac Reserve is:
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– the ability of the heart to compensate under stress
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Cardiac reserve is affected by:
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– increased sympathetic activity (fight or flight) – Na and water retention (ALD, RAAS can increase preload) – anaerobic metabolism of affected cells – increased uptake of O2 by peripheral cells **when these fail or overwork, cardiac reserve is affected negatively**
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CHF Compensatory Mechanisms include:
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– Tachycardia – Ventricular dilation – Cardiac Hypertrophy – Changes in Vasculature, Kidneys, and Liver
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CHF Compensatory Mechanisms (diagram)
CHF Compensatory Mechanisms (diagram)
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Right and Left Hear Failure (diagram)
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Left Sided Heart Failure (memory)
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– notice he is in tripod position to facilitate breathing
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Left Sided Heart Failure
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– decreased cardiac output and pulmonary congestion – from decreased Cardiac Output you see activity intolerance and signs of decreased tissue perfusion. – if left ventricle is congested –> blood backs up into the pulmonary vein –> then into the lungs –> then into the pulmonary artery causing pulmonary congestion – from pulmonary congestion you can have impaired gas exchange (alveoli and caps) which means the blood that moves through will have *less O2* which causes *decreased tissue perfusion* – decreased tissue perfusion leads to cyanosis and signs of hypoxia. – because of congestion in the lungs, capillary pressure in the lungs begins to change – protein rich fluids begin to seep out of the caps into the alveoli which presents as *crackles* –> which leads to pulmonary edema – pulmonary edema can show as a cough with frothy sputum (can be pinkish due to blood) – orthopnea (pop up in bed to breathe) – paroxysmal nocturnal dyspnea – dont worry about elevated pulmonary capillary wedge pressure **most of these symptoms are heart and lung related –> symptoms close to the heart**
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With left ventricular failure there is
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– a stroke volume problem – compromised stroke volume and decreased cardiac output
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Right Sided Heart Failure (memory)
Right Sided Heart Failure (memory)
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Right Sided Heart Failure
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– congestion is in the right ventricle – blood will back up into the right atria –> & then the superior and inferior vena cava –> which leads to congestion of peripheral tissue –> which leads to dependent edema and ascites (r/t portal HTN) and JVD – can cause liver congestion – from liver congestion may see signs r/t to impaired liver funx – can caused GI tract congestion – from GI you may see anorexia, GI disress and weight loss **Most of these symptoms extend to more peripheral systems –> away from heart and lungs**
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What is Systolic Heart failure?
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– the most common type – is when there is *alteration in ventricular contraction* remember *systolic* = *contraction*
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What is diastolic heart failure?
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– is char by stiff and non compliant heart muscle – wont relax enough to fill correctly – *doesnt relax and fill properly* (Preload problem in ventricle) remember *diastolic* = *relax*
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What is Ejection Fraction?
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– % of blood volume in the ventricle at end of diastole that is ejected during systole – measure of contractility – an indicator of severity of CHF **% of blood volume in the ventricles that can be squeezed from the ventricles at the end of systole.**
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What is normal ejection fraction
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– we want it to be greater than 55%
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CHF signs and symptoms:
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– fatigue and tiredness – hypertrophy (XRAY) – lower ejection fraction (ECHO) – SOB
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CHF Dx studies
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**help evaluate cardiac, pulmonary and systemic congestion** – CXR – Echocardiogram: shows = ejection fraction which is an indicator for severity of disease – pulse ox (not diagnostic but indicator) – hemodynamic monitoring
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Lab Tests for CHF
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– BNP – shows LVH (normals are 100 and under-usually) – CK-MB – shows cardiac muscle stress
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Stage A of Heart Failure
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– Stage A Patients at high risk for developing left ventricular dysfunction but without structural heart disease or symptoms of heart failure – pts can usu have pretty normal lives with limited symptoms
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Stage B of Heart Failure
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– Stage B Patients with left ventricular dysfunction or structural heart disease who have not developed symptoms of heart failure – pts have slight limitations with ADL, symptoms with activity
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Stage C of Heart Failure
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– Stage C Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart failure – pts have marked limitiation in ADL, comortable at rest
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Stage D of Heart Failure
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– Stage D Patients with refractory end-stage heart failure requiring specialized interventions – pts can’t breath or manage themselves at rest (usu tx is heart transplant)
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UNLOAD FAST for CHF
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U – pts will be in *upright position* to help breathing – tripod N – give *Nitrates* to vasodilate and increase tissue perfusion L – give *lasix* (loop diuretic) to loose fluids (will loose K too) O – give *O2* A – give *ACE-Inhibitors* (chronic cough and angioedema can become hypotensive) D – admin *digoxin* F -* fluid restriction* (caution c IV fluids, 1500-2000ml of H2O or less) A – decrease *AFTERLOAD* S – *Sodium restriction* (less than 2g) T – *Test* (ABG’s, digoxin level, potassium levels) **will need to give potassium supplement due to lasix**
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Treating Congestive Heart Failure (memory)
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Clinical Mgt of CHF
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– Decrease preload – Decrease afterload – Improve contractility
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Conditions that decrease preload
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– tachycardia (ventricles cant fill properly- effects stroke volume) – venous stasis – dehydration (either cellular or vascular): high temp, diarrhea, diuretics, heat
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Things that affect Afterload:
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– vascular tone (constricted vessels increase afterload and dilated vessels decrease afterload) –> System Vascular Resistance –> vasodilators and vasoconstrictors **after load is is the pressure that the ventricles must overcome to eject the blood during systole**
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Things that affect contractility:
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– think Starling’s Law: the greater the stretch the greater the force of ejection until the muscle is overstretched then there is hypertrophy and weakened force of contraction ** it is the force generated by the heart muscles**
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Nursing Care for CHF
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– Nursing Process – Assessment – Promote Activity Tolerance – Manage Fluid Volume – Control Anxiety – Be aware of conditions that affect preload/afterload – Interventions that increase venous return which increase preload (foot pumps, massage – distal to proximal, elevate the lower extremities) – fluid retention is a big deal (1500-2000 fluid per day or less) – weight daily – teach to weigh daily at home – pt call md if more than 3 lbs of weight gain in one day – need occup therapist to check to see if home is okay for activity level – teach about diet – may be on home health care – may be on transplant list – may have pacemeaker
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Nursing Interventions for CHF
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– Promote Activity Tolerance – Reduce Fatigue – Manage Fluid Volume – Control Anxiety – Minimize Powerlessness – Promote Home and – Community Based Care
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Digoxin and CHF
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– cardiac glycoside, PO, 0.25 – 0.125 mg, once daily – decreases heart rate and increase contractility to decrease blood pressure – Therapeutic serum digoxin levels range from 0.5-2 ng/mL – be aware for Digoxin overdose – antidote = digifab – check apical and must be 60 or above – pts are “digitalized” = at therapeutic level of drug
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Digoxin overdose S/S:
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EENT: Blurred vision, Halos around objects (yellow, green, white) * Skin: Allergic reaction (see: Stevens-Johnson syndrome), Hives, Rash GI: Diarrhea, Loss of appetite*, N/V, Stomach pain, CV: Irregular heartbeat (or slow), Weakness CNS: Confusion, Depression*, Disorientation, Drowsiness Fainting, Hallucinations*, Headache, Lethargy Psychological: Apathy (not caring what happens) *are usu only seen in chronic toxicity
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Dopamine drip and CHF
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– vasodilator to increase tissue perfusion

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