Unique Introduction ro Cardiovascular Nursing

Studying Cardiovascular nursing is not rocket science. You just need the proper mindset and material in order to excel in this subject.

1. • Aorta & arteries tend to become less distensible
   • Heart becomes less responsive to catecholamines
   • Maximal exercise heart rate declines
   • Decreased rate of diastolic relaxation ( ↑in BP is more pronounced for systolic BP than diastolic BP)
   • Note that hypertension is NOT a normal age-related process
   • Compensatory mechanism are delayed/insufficient = orthostatic hypotension is common
   • Thickness of LV wall may increase with age due to blood vessel changes
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2. • 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
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3. http://nursinglectures.blogspot.com 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)
4. http://nursinglectures.blogspot.com 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
5. • Inspection:
   • Skin color
   • Neck vein distention (jugular vein)
   • Respiration
   • Peripheral edema
   • Palpation:
   • Peripheral pulses
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6. • 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
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7. • 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
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8. • 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)>
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9. • Abnormalities:
   • absent P wave = atrial fibrillation
   • saw-tooth pattern = atrial flutter
   • elevated ST segment = MI
   • 3rd degree heart block = prolonged PR then progressively prolonged
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12. • 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>
    • 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
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13. • 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
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14. • 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
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15. • 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
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17. • 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
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18. • 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
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19. • 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
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20. http://nursinglectures.blogspot.com 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
21. • 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
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22. http://nursinglectures.blogspot.com 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
23. • 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: <>
    • Relie ved by rest (preferably sitting or standing with support) or by use of NTG
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24. • 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
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25. • 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
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26. • 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
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27. • 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)
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28. • 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
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29. • 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)
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30. • 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
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31. • 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
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32. • 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
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33. 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 http://nursinglectures.blogspot.com
34. http://nursinglectures.blogspot.com 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
35. • 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
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36. • Surgery :
    • Revascularization
    • PTCA
    • Coronary stent implantation
    • Coronary Artery Bypass Graft (CABG) – no response to medical treatment & PTCA
    • Resection – aneurysm
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38. • 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
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40. • 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
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41. • 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
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42. • 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
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43. • 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)
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44. • 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)
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45. • 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
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46. • 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)