Nursing Lecture in Cardiovascular Nursing

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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

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

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)

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

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

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

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

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

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 http://nursinglectures.blogspot.com

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

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)

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Nursing Lecture in Cardiovascular Nursing

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Nursing Lecture in Cardiovascular Nursing Presentation Transcript