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Cardio2 Cardio2 Presentation Transcript

  • Management of Clients with Functional Cardiac Disorders
    • Also known as coronary HEART disease (CHD)
    • Describes heart disease caused by impaired coronary blood flow
    • Common cause: atherosclerosis
    • CAD can cause the following:
      • Angina
      • Myocardial Infarction (MI) = heart attack
      • Cardiac dysrhythmias
      • Conduction defects
      • Heart failure
      • Sudden death
    • Men are more often affected than women
    • Approximately 80% who die of CHD are 65+ y/o
  • Risk Factors Non-modifiable Modifiable Age, gender, race, heredity Endothelial injury Stress, diet, sedentary living, Smoking, Alcohol, HPN, DM, Obesity, Contraceptive pills, Hyperlipidemia/hypercholesterolemia Desquamation of endothelial lining (peeling off)
  • Increased permeability/ adhesion of molecules LDLs & platelets assimilate into the area Plaques begins to form Decreased coronary tissue perfusion Coronary ischemia Decreased myocardial oxygenation ANGINA PECTORIS MYOCARDIAL INFARCTION
    • Inspection:
      • Skin color
      • Neck vein distention (jugular vein)
      • Respiration
      • Peripheral edema
    • Palpation:
      • Peripheral pulses
    • Auscultation:
      • Heart sounds (presence of S 3 in adults & S 4 )
      • Murmurs – audible vibrations of the heart & great vessels produced by turbulent blood flow
      • Pericardial friction rub – extra heart sound originating from the pericardial sac
      • - may be a sign of inflammation, infection, or infiltration
      • - described as a short, high-pitched scratchy sound
    • Dyspnea
      • Dyspnea on exertion – may indicate decreased cardiac reserve
      • Orthopnea – a symptom of more advanced heart failure
      • Paroxysmal nocturnal dyspnea – severe SOB that usually occurs 2-5hrs after onset of sleep
    • Chest Pain – may be due to decreased coronary tissue perfusion or compression & irritation of nerve endings
    • Edema – increased hydrostatic pressure in venous system causes shifting of plasma resulting to interstitial fluid accumulation
    • Syncope – due to decreased cerebral tissue perfusion
    • Palpitations
    • Fatigue
    • ECG (Electrocardiography) – graphical recording of the heart’s electrical activities; 1 st diagnostic test done when cardiovascular disorder is suspected
      • Waves: P wave – atrial depolarization (contraction/stimulation)
        • QRS complex – ventricular depolarization (changes are irreversible)
        • ST segment – ventricular repolarization (changes are reversible)
        • U wave – hypokalemia
      • PR interval (time for impulse to travel) = 0.12-0.20s (3-5 squares) √ for AV block
      • QRS = 0.10s or (<2squares) √ for electrolyte &/or ventricular imbalance
    • Abnormalities:
      • absent P wave = atrial fibrillation
      • saw-tooth pattern = atrial flutter
      • elevated ST segment = MI
      • 3rd degree heart block = prolonged PR then progressively prolonged
  •  
  •  
    • Cardiac Enzymes (Cardiac Markers):
      • 1 st : Myoglobin
      • a. urine = 0 – 2mg/dL (↑within 30mins – 2hrs after MI)
      • b. blood = <70mg/dL
    • 2 nd : Troponin* - regulates calcium-mediated contractile process released during MI (Troponin T & I)
    • - blood = <0.6mg/dL - ↑ within 3-6hrs after MI & remains elevated for 21 days upon onset of attack
    • 3 rd : Creatinine kinase (CK) – intracellular enzymes found in muscles converting ATP to ADP
    • CK-MB – specific to myocardial tissue (↑within 4-6hrs & decreases to normal within 2-3days)
        • male = 12-70 mg/dL
        • female = 10-55 mg/dL
    • 4 th : LDH (specifically LDH 1 - most sensitive indicator of myocardial damage) = 45-90mg/dL - ↑within 3-4 days & remains elevated for 14 days
    • Stress Test / Treadmill Test (Treadmill Stress Test) – ECG monitoring during a series of activities of patient on a treadmill
      • Purposes: identify ischemic heart disease
      • evaluate patients with chest pain
      • evaluate effectiveness of therapy
      • develop appropriate fitness program
      • Instructions to patient: get adequate sleep prio r to test
      • - avoid: caffeinated beverages, tea, alcohol, on the day before until the test day
      • - wear comfortable, loose-fitting clothes & rubber-soled shoes on the test day
      • - light breakfast on the day of the test
      • - inform physician of any unusual sensations during the test
      • - rest after the test
    • Pharmacologic Stress Test – use of intravenous injection of pharmacologic vasodilator (dipyridamole, adenosine, or dobutamine) in combination of radionuclide myocardial imaging
      • To evaluate presence of significant CHD for patients contraindicated in TST
      • Dipyradamole blocks cellular re-absorption of adenosine (endogenous vasodilator) & increases coronary blood flow 3-5x above baseline levels
      • If with CHD, the resistance vessels distal to the stenosis already are maximally dilated to maintain normal resting flow, thus, further vasodilatation does not produce increased blood flow
      • Dobutamine – used in patients with bronchospastic pulmonary disease
      • - increases myocardial O 2 demand by increasing cardiac contractility, HR, & BP
    • Cardiac Catheterization – involves passage of flexible catheters into great vessels & heart chambers under local anesthesia
    • - lab is equipped for viewing & recording fluoroscopic images & for measuring pressures in the heart & great vessels, cardiac output studies, & for obtaining ABG samples
    • - Epinephrine – to counteract possible allergic reactions
      • Right heart Catheterization – catheter inserted into peripheral veins (basilic or femoral) then advanced into the right heart
      • Left heart Catheterization – catheter inserted retrograde through peripheral artery (brachial or femoral) into the aorta & left heart
    • Coronary Angiogram – injection of radiographic contrast medium into the heart so that an outline of moving structures are visualized & filmed
    • Coronary Arteriography - injection of radiographic contrast medium into the coronary arteries permits visualization of lesions in these vessels
  •  
    • Before Procedure:
      • Check consent form
      • √ for allergies to seafood & iodine
      • NPO post midnight
      • Baseline V/S
      • Explain that warm or flushing sensation may be felt upon administr ation of the dye; “fluttering” sensation may be felt as catheter enters the heart
      • Administer sedatives as ordered
      • Have the client void prior to transport to cath lab
    • After Procedure:
      • Bed rest – upper extremity catheter = until stable v/s, HOB not more than 30 °
      • - lower extremity = 24hrs, flat on bed for 6hrs
      • Apply pressure (5lb-sand bag) over puncture site & monitor for bleeding
      • Monitor v/s q15 for 1 st 2hrs then q1 until stable v/s, esp. peripheral pulses
      • Immobilize affected extremity in extension for adequate circulation
      • Monitor for color & temperature changes of extremities
      • Instruct client to report tingling sensations
    • Swan-Ganz Catheterization – to determine & monitor cardiovascular status; inserted via antecubital vein into the right side of the heart & is floated into the pulmonary artery
    • 4 lumens:
    • 1. CVP – specific to right heart RA = 0-12 RV = 5-12
      • Indications: increased CVP = heart failure
    • -decreased CVP = hypovolemia
    • 2. Pulmonary pressures:
      • PAP (pulmonary artery pressure) = 20-30mmHg
      • PCWP (pulmonary capillary wedge pressure) = 8-13mmHg (√ for pulmonary edema)
    • 3. Specimen collection tube – also used for administering meds
    • 4. Balloon
    • Echocardiography – uses ultrasound to assess cardiac structure & mobility
    • Doppler U/S – to detect blood flow of artery & vein specifically of lower extremities (No smoking 1hr before the test)
    • Holter Monitoring – portable 24hr ECG monitoring which attempts to assess activities which precipitate dysrhythmias & its time of the day
    • MRI – magnetic fields & radiowaves are used to detect & define abnormalities in tissues (aorta, tumors, cardiomyopathy, pericardiac disease)
    • - shows actual beating & blood flow; image over 3 spatial dimensions
      • Secure consent
      • Assess for claustrophobia
      • Remove metal items (jewelries, eyeglasses)
      • Instruct client to remain still during the entire procedure
      • Inform client of the duration (45-60mins)
      • CI: clients with pacemakers, prosthetic valves, recently implanted clips or wires
  • CHD Chronic Ischemic Heart Disease Acute Coronary Syndrome Stable Angina Variant Angina Silent Myocardial Ischemia Non ST-segment Elevation MI (Unstable Angina) ST-segment Elevation MI
    • Ischemia – suppressed blood flow
    • Angina – to choke
    • Occurs when blood supply is inadequate to meet the heart’s metabolic demands
    • Symptomatic paroxysmal chest pain or pressure sensation associated with transient ischemia
  • Causes: Atherosclerosis, HPN, DM, Buerger’s Disease, Polycythemia Vera, Aortic regurgitation Reduced coronary tissue perfusion Decreased myocardial oxygenation Anaerobic metabolism Increased lactic acid production (lactic acidosis) Chest pain
    • Stable angina – the common initial manifestation of a heart disease
      • Common cause: atherosclerosis (although those with advance atherosclerosis do not develop angina)
      • Pain is precipitated by increased work demands of the heart (i.e.. physical exertion, exposure to cold, & emotional stress)
      • Pain location: precordial or substernal chest area
      • Pain characteristics:
        • con stricting, squeezing, or suffocating sensation
        • Usua lly steady, increasing in intensity only at the onset & end of attack
        • May radiate to left shoulder, arm, jaw, or other chest areas
        • Dura tion: < 15mins
        • Relie ved by rest (preferably sitting or standing with support) or by use of NTG
    • Variant/Vasospastic Angina (Prinzmetal Angina)
      • 1 st described by Prinzmetal & Associates in 1659
      • Cause: spasm of coronary arteries (vasospasm) due to coronary artery stenosis
        • Mechanism is uncertain (may be from hyperactive sympathetic responses, mishandling defects of calcium in smooth vascular muscles, reduced prostaglandin I 2 production)
      • Pain Characteristics: occurs during rest or with minimal exercise
      • - commonly follows a cyclic or regular pattern of occurrence (i.e.. Same time each day usually at early hours)
      • If client is for cardiac cath, Ergonovine (nonspecific vasoconstrictor) may be administered to evoke anginal attack & demonstrate the presence & location of spasm
    • Nocturnal Angina - frequently occurs nocturnally (may be associated with REM stage of sleep)
    • Angina Decubitus – paroxysmal chest pain occurs when client sits or stands up
    • Post-infarction Angina – occurs after MI when residual ischemia may cause episodes of angina
    • Dx: detailed pain history, ECG, TST, angiogram may be used to confirm & describe type of angina
    • Tx: directed towards MI prevention
      • Lifestyle modification (individualized regular exercise program, smoking cess a tion)
      • Stress reduction
      • Diet changes
      • Avoidance of cold
      • PTCA (percutaneous transluminal coronary angioplasty) may be indicated if with severe artery occlusion
    • Nitroglycerin (NTGs) – vasodilators:
      • patch (Deponit, Transderm-NTG)
      • sublingual (Nitrostat)
      • oral (Nitroglyn)
      • IV (Nitro-Bid)
    • Β -adrenergic blockers:
      • Propanolol (Inderal)
      • Atenolol (Tenormin)
      • Metoprolol (Lopressor)
    • Calcium channel blockers:
      • Nifedipine (Calcibloc, Adalat)
      • Diltiazem (Cardizem)
    • Lipid lowering agents –statins:
      • Simvastatin
    • Anti-coagulants:
      • ASA (Aspirin)
      • Heparin sodium
      • Warfarin (Coumadin)
    • Class I – angina occurs with strenuous, rapid, or prolonged exertion at work or recreation
    • Class II – angina occurs on walking or going up the stairs rapidly or after meals, walking uphill, walking more than 2 blocks on the level or going more than 1 flight of ordinary stairs at normal pace, under emotional stress, or in cold
    • Class III – angina occurs on walking 1-2 blocks on the level or going 1 flight of ordinary stairs at normal pace
    • Class IV – angina occurs even at rest
    • Diet instructions (low salt, low fat, low cholesterol , high fiber); avoid animal fats
      • E.g.. White meat – chicken w/o skin, fish
    • Stop smoking & avoid alcohol
    • Activity restrictions are placed within client’s limitations
    • NTGs – max of 3doses at 5-min intervals
      • Stinging sensation under the tongue for SL is normal
      • Advise clients to always carry 3 tablets
      • Store meds in cool, dry place, air-tight amber bottles & change stocks every 6months
      • Inform clients that headache, dizziness, flushed face are common side effects.
      • Do not discontinue the drug.
      • For patches, rotate skin sites usually on chest wall
      • Instruct on evaluation of effectiveness based on pain relief
    • Propanolols causes bronchospasm & hypoglycemia, do not administer to asthmatic & diabetic clients
    • Heparin – monitor bleeding tendencies (avoid punctu res , use of soft-bristled toot hbrush ); monitor PTT levels; use d for 2wks max; do not massage if via SC; have protamine sulfate available
    • Coumadin – monitor for bleeding & PT; always have vit K readily available (avoid green leafy veggies)
    • Unstab le Angina/Non ST-Segment Elevation MI – a clinical syndro me of myocardial ischemia
      • Causes: atherosclerotic plaque disruption or significant CHD, cocaine use (risk factor)
      • Defining guidelines: (3 presentations)
        • Symptoms at rest (usually prolonged, i.e.. >20mins)
        • New onset exertional angina (increased in severity of at least 1 class – to at least class III) in <2months
        • Recent acceleration of angina to at least class III in <2months
      • Dx: based on pain severity & presenting sympto ms , ECG findings & serum cardiac markers
      • When chest pain has been unremitting for >20mins, possibility of ST-Segment Elevation MI is usually considered
    • ST-Segment Elevation MI (Heart Attack)
      • Characterized by ischemic death of myocardial tis sue associated with atherosclerotic disease of coro nar y arteries
      • Area of infarction is determined by the affected coronary artery & its distribution of blood flow (right coronary artery, left anterior descending artery, left circumflex artery)
      • Dx: based on presenting S/Sx, serum markers, & ECG (changes may not be present immediately after symptoms except dysrhythmias; PVCs/premature ventricular contractions are common after MI)
        • Typical ECG changes: ST-segment elevation, Q wave prolongation, T wave inversion
      • Manifestations:
        • chest pain – severe crushing, constricting, “someone sitting on my chest”
        • - substernal radiating to left arm, neck or jaw
        • - prolonged (>35mins) & not relieved by rest
        • Shortness of breath, profuse perspiration
        • Feeling of impending doom
      • Complications: death (usually within 1 hr of onset)
        • Heart fail ure & cardiogenic shock – profound LV failure from massive MI resulting to low cardiac output
        • Thromboe mboli – leads to immobility & impaired cardiac function contributi ng to blood stasis in veins
        • Rupture of myocardium
        • Ventricul ar aneurysms – decreases pumping efficiency of heart & increase s work of LV
  • Causes: atherosclerotic heart disease, thrombosis/embolism, shock &/or hemorrhage, direct trauma Myocardial ischemia ↑ cellular hypoxia ↓ myocardial O 2 supply ↓ myocardial contractility ↓ cardiac output ↓ arterial pressure Stimulation of sympathetic receptors ↑ peripheral vasoconstriction ↑ myocardial contractility ↑ afterload ↑ myocardial O 2 demand ↑ HR ↑ diastolic filling ↓ myocardial tissue perfusion
  • Time after Onset Type of Injury & Gross Tissue Changes 0-0.5hrs Reversible injury 1-2hrs Onset of irreversible injury 4-12hrs Beginning of coagulation necrosis 18-24hrs Continued necrosis; gross pallor of infected tissue 1-3days Total necrosis; onset of acute inflammatory process 3-7days Infarcted area becomes soft with a yellow-brown center & hyperemic edges 7-10days Minimally soft & yellow with vascularized edges; scar tissue generation begins (fibroplastic activity) 8 th week Complete scar tissue replacement
    • Initial Management: OMEN
    • - O 2 therapy via nasal prongs
    • - adequate analgesia ( M orphine via IV – also has vasodilator property)
    • - E CG monitoring
    • -sublingual N TG (unless contraindicated; IV may be given to limit infarction size & most effective if given within 4hrs of onset)
    • Thrombolytic Therapy – best results occur if initiated within 60-90mins of onset (Streptokinase & Urokinase – promote conversion of plasminogen to plasmin)
    • Anti-arrhythmics: lidocaine, atropine, propano lol
    • Anticoagulants & antiplatelets: ASA, heparin
    • Stool softeners
    • Surgery :
      • Revascularization
        • PTCA
        • Coronary stent implantation
        • Coronary Artery Bypass Graft (CABG) – no response to medical treatment & PTCA
      • Resection – aneurysm
  •  
    • Promote oxygenation & tissue perfusion (place client on semi-fowler’s, O 2 via nasal cannula, monitor v/s changes, remind client on his activity limitations & restrictions)
    • Promote comfort & rest
    • Monitor the ff perimeters: v/s, ECG, rate & rhythm of pulse, effects of ADLs on cardiac status
    • Diet: low salt, low cholesterol, low calories, avoid alcohol & smoking
    • Take prescribe meds at regular basis
    • Stress management
    • Resume sexual activity after 4-6wks from discharge or when client can go up 2 flights of stairs without difficulty
      • Assume less tiring position (non-MI partner takes active role).
      • Perform sexual activity in a cool, familiar place.
      • Take prescribed NTG before sexual activity
      • Refrain from sexual activity after a large meal or during a tiring day.
      • Moderation should be observed if palpitations, dizziness or dyspnea is observed
  •  
    • Also known as Thromboangiitis obliterans
    • Usually a disease of heavy cigarette smoker/tobacco user men, 25-40y/o
    • Inflammatory arterial disorder that causes thrombus formation often extends to adjacent veins & nerves
    • Affects medium-sized arteries (usually plantar & digital vessels in the foot or lower legs)
    • unknown pathogenesis but it had been suggested that:
      • tobacco may trigger an immune response or
      • unmask a clotting defect;
      • -> these 2 can incite an inflammatory reaction of the vessel wall
    • Pain – predominant symptom; R/T distal arterial i schemia
      • Intermittent claudication in the arch of foot & digits
    • Increased sensitivity to cold (due to impaired circulation
    • Absent/diminished peripheral pulses
    • Color changes in extremity (cyanotic on dependent position; digits may turn reddish blue)
    • Thick malformed nails (chronic ischemia)
    • Disease progression ulcerate tissues & gangrenous changes may arise; may necessitate amputation
    • Diagnostic methods – those that assess blood flow (Doppler ultrasound & MRI)
    • Tx: mandatory to stop smoking or using tobacco
      • Meds to increase blood flow to extremities
      • Surgery (surgical sympathectomy)
      • amputation
    • Mechanism: intensive vasospasm of arteries & arterioles in the fi ngers
    • Cause: unknown
    • Usually affects young women
    • Precipitated by exposure to cold & strong emotions
    • Raynaud’s phenomenon – associated with previous injury (i.e.. Frostbite, occupation al trauma associated with use of heavy vibr ating tools, collagen diseases, neuro d/o, chro nic arterial occlusive d/o)
    • Period of ischemia (ischemia due to vasospasm)
      • change in skin color = pallor to cyanotic
      • 1 st noticed at the fingertips later moving to distal phalanges
      • Cold sensation
      • Sensory perception changes (numbness & tingling)
    • Period of hyperemia – intense redness
      • Throbbing
      • Paresthesia
    • Return to normal color
    • Note: although all of the fingers are affected symmetrically, only 1-2digits may be involved
    • Severe cases: arthritis may arise (due to nutritional impairment)
      • Brittle nails
      • Thickening of the skin of fingertips
      • Ulceration & superficial gangrene of fingers (rare occasions)
    • Dx: initial = based on Hx of vasospastic attacks
      • Immersion of hand in cold water to initiate attack aids in the Dx
      • Doppler flow velocimetry – used to quantify blood flow during temperature changes
      • Serial Computed thermography (finger skin temp) – for diagnosing the extent of disease
    • Tx: directed towards eliminating factors causing vasospasm & protecting fingers from injury during ischemic attacks
      • PRIORITIES: Abstinence in smoking & protection from cold
      • Avoidance of emotional stress (anxiety & stress may precipitate vascular spasm)
      • Meds: avoid vasoconstrictors (i.e.. Decongestants)
      • -Calcium channel blockers (Diltiazem, Nifedip ine , Nicardipine) – decrease episodes of attacks
    • Assessment:
      • Hx of symptoms (pain, esp. chest pain; palpitations; dyspnea)
      • v/s
    • Nursing Dx:
      • ineffective tissue perfusion (cardio pulmonary)
      • Impaired gas exchange
      • Anxiety due to fear of death (clients with MI or An gina)
    • Goals:
      • Relief of pain & symptoms
      • Prevention of further cardiac damage
    • Nursing Interventions:
      • Pain control
      • Proper medications
      • Decrease client’s anxiety
      • Health teachings (meds, activities, diet, exercise, etc)
  • Thank You for Listening!