CARDIOVASCULAR

SYSTEM

BY: MARC ANTHONY LIAO RN

Brief Review Heart Structure
ELECTRICAL HEART CONDUCTION
 PHYSIOLOGIC CHANGES OF AGING
 Less distensible
 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
 DIAGNOSTICS
1. ECG (Electrocardiography) – graphical recording of the
heart’s electrical activities; 1st diagnostic test done when
cardiovascular disorder is suspected
 Waves:
 P wave – atrial depolarization (contraction/stimulation)
 QRS complex – ventricular depolarization (changes are
irreversible)
 T wave– ventricular repolarization (changes are
reversible)
 PR interval (time for impulse to travel) = 0.12-0.20 s
 QRS = 0.10s or (<2squares)
Cont…
DYSRHYTHMIA
SINUS DYSRHYTHMIAS
A. SINUS TACHYCARDIA
The heart has >100beats per minute.
The cause may be Increased Sympathetic Nervous System
(SNS) stimulation or decreased Vagal stimulation.
Beta-Blockers, Calcium Channel Blockers, Digitalis, or to
treat the underlying cause.
SINUS TACHYCARDIA
B. Sinus Bradycardia
The heart has <60 beats per minute.
The cause may be Increased Vagal stimulation.
Atropine Sulfate, Dopamine or Dobutamine,
Epinephrine, Isoproterenol,
SINUS BRADYCHARDIA
ATRIAL DYSRYTHMIAS
A. PREMATURE ATRIAL CONTRACTION
Ectopic beat from atria rate faster than sinus node
No treatment
If increase Ca channel blocker
Quinidine
B. ATRIAL FLUTTER
The heart has 250-300 beats per minute and there is
no P wave and QRS complex.
F wave or saw tooth appearance
Digoxin, Calcium Channel Blockers, Quintidine,
Cardioversion
C. ATRIAL FIBRILLATION
The heart has >300-400 beats per minute and there is
no P wave and QRS complex.
The management can be Epinephrine, Beta-Blocker,
or Anti-coagulant, Cardioversion
VENTRICULAR DYSRYTHMIAS
A. Premature Ventricular Contraction ectopic beat faster
from ventricles than the sinus node
B. Ventricular Tachycardia. >100 beats per minute
C. Ventricular Fibrillation. >300-400 beats per minute
Management for Ventricular Dysrhythmia
Lidocaine
Procainamide
Magnesium Sulfate
Bretylium
Cardiopulmonary Resuscitation
Defibrillation
CONDCUTION/ HEART BLOCK
Primary Heart Block. The AV Node is affected.
There is no management.
Secondary Heart Block. It has two types:
Mobitz Type I (Wencheback Phenomenon). AV Node
affectation
Mobitz Type II. Purkinje Fibers are affected
Management for Heart Block
Atropine
Pacemaker
Antidysrhythmics
Sodium-Channel Blocker
Procainamide, Dipyridamine, Quinidine. The mode of action is it decreases Sodium
flow into the cell.
Tocainide, Phenytoin, Mexilitine, Lidocaine. Mode of action it inhibits ion fluxes and
conduction or impulses.
Propafenone. The mode of action is it decreases the influx of Sodium ions, causing
excitability.
Beta-Blockers – Propranolol, Esmolol, Acebutolol
Indicated for Supraventricular Tachycardia or Atrial Fibrillation
Potassium Channel Blockers – Bretylium, Sotalol, Amiodarone, Ibufilide
It is indicated for Tachydysrhythmias. Mode of Action is it decreases automaticity that
initiate electrical impulse conduction and decreases conductivity that transmits
electrical impulse.
Calcium Channel blockers
It is indicated for Ventricular Tachycardia and Ventricular Fibrillation. It’s mode of
action is that it decreases automaticity and AV node conductivity.
CPR
2010 American Heart Association Guidelines for CPR and Emergency
Cardiovascular Care
Make sure the scene is safe.
Shake the victim’s shoulders and shout to see if they respond.
COMPRESSIONS
Push hard and fast on the center of the chest 30 times, at a rate of at least
100 compressions a minute. Push down at least 2 inches with each
compression. If you haven’t been trained in CPR, continue to give
compressions until an AED arrives or trained help takes over.
AIRWAY
If you have been trained in CPR, continue CPR by opening the airway with a
head tilt–chin lift.
BREATHING
Pinch the victim’s nose closed. Take a normal breath a cover the victim’s
mouth with your mouth, creating an airtight seal. Give two breaths (one
second each). Watch for chest rise as you give each breath.
Keep giving sets of 30 compressions and two breaths
Cont…
2. Cardiac Enzymes (Cardiac Markers):
 1st: Myoglobin
a. urine = 0 – 2mg/dL (↑within 30mins – 2hrs after MI)
b. blood = <70mg/dL

 2nd: 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
 3rd: 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

 4th: LDH (specifically LDH1- most sensitive indicator of myocardial

damage) = 45-90mg/dL - ↑within 3-4 days & remains elevated for 14 days
 Cont…
3. Stress Test / Treadmill Test (Treadmill Stress Test) – ECG
monitoring during a series of activities of patient on a
treadmill

Nursing Intervention:
 Get adequate sleep prior to txr 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
Cont…
4. Pharmacologic Stress Test – use of intravenous injection of
pharmacologic vasodilator (dipyridamole, adenosine, or
dobutamine) in combination of radionuclide myocardial
imaging
 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 O2 demand by increasing cardiac
contractility, HR, & BP
Cont…
5. Cardiac Catheterization – involves passage of into great vessels &
heart chambers under local anesthesia
- 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 Arteriography/ Angiogram - injection of radiographic

contrast medium into the coronary arteries permits visualization
of lesions in these vessels
Cardiac Catheterization Illustration
 Nursing Interventions for Cardiac
Catheterization
 Before Procedure:  After Procedure:
 Bed rest – upper extremity catheter =
 Check consent form
until stable v/s, HOB not more than
 √ for allergies to seafood &
30°
iodine - lower extremity = 24hrs,
 NPO post midnight flat on bed for 6hrs
 Baseline V/S  Apply pressure (5lb-sand bag) over
 Explain that warm or flushing puncture site & monitor for bleeding
sensation may be felt upon  Monitor v/s q15 for 1st 2hrs then q1
administration of the dye; until stable v/s, esp. peripheral
“fluttering” sensation may be pulses
felt as catheter enters the heart  Immobilize affected extremity in
 Administer sedatives as extension for adequate circulation
ordered  Monitor for color & temperature
changes of extremities
 Instruct client to report tingling
sensations
 6. HEMODYNAMIC MONITORING
 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 SVC = 0-12 RA = 5-12
cmH20
Indications: increased CVP = heart failure
-decreased CVP = hypovolemia
2. Pulmonary pressures:
PAP (pulmonary artery pressure) = 20- 30mmHg
3. Thermistor
4. Balloon Inflation
PCWP (pulmonary capillary wedge pressure) = 8- 13mmHg (√
for pulmonary edema)
7. Echocardiography – uses 8. MRI – magnetic fields &
ultrasound to assess cardiac radiowaves are used to detect &
structure & mobility define abnormalities in tissues
(aorta, tumors, cardiomyopathy,
pericardiac disease)
8. Doppler U/S – to detect - shows actual beating & blood
blood flow of artery & vein flow; image over 3 spatial
specifically of lower dimensions
extremities (No smoking 1hr  Secure consent
before the test)  Assess for claustrophobia
 Remove metal items (jewelries,
eyeglasses)
9. Holter Monitoring –  Instruct client to remain still
portable 24hr ECG during the entire procedure
monitoring which attempts  Inform client of the duration
to assess activities which (45-60mins)
precipitate dysrhythmias &  CI: clients with pacemakers,
its time of the day prosthetic valves, recently
implanted clips or wires
 CORONARY ARTERY DISEASE (CAD)
 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
Pathophysiology
Types of CHD
 Angina Pectoris /
Myocardial Ischemia
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
Types
A. Stable angina – the common initial manifestation of a heart
disease
 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:
 constricting, squeezing, or suffocating sensation
 Usually steady, increasing in intensity only at the onset &
end of attack
 May radiate to left shoulder, arm, jaw, or other chest areas
 Duration: < 15mins
 Relieved by rest (preferably sitting or standing with support)
or by use of NTG
B. Variant/Vasospastic Angina (Prinzmetal Angina)
 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 I2 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
C. Nocturnal Angina - frequently occurs
nocturnally (may be associated with
REM stage of sleep)
D. Angina Decubitus – paroxysmal chest
pain occurs when client sits or stands up
E. 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 cessation)
 Stress reduction
 Diet changes
 Avoidance of cold
 PTCA (percutaneous transluminal coronary
angioplasty) may be indicated if with severe
artery occlusion
Drug Therapy
 Nitroglycerin (NTGs) –
vasodilators:
 patch (Deponit,
 Lipid lowering agents –
Transderm-NTG) statins:
 sublingual (Nitrostat)
 Simvastatin
 oral (Nitroglyn)
 IV (Nitro-Bid)  Anti-coagulants:
 Β-adrenergic blockers:
 ASA (Aspirin)
 Propanolol (Inderal)
 Atenolol (Tenormin)  Heparin sodium
 Metoprolol (Lopressor)
 Warfarin (Coumadin)
 Calcium channel blockers:
 Nifedipine (Calcibloc,
Adalat)
 Diltiazem (Cardizem)
 Classification
 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

Nursing Management
 Diet instructions (low salt, low fat,  Do not discontinue the drug.
low cholesterol, high fiber); avoid  For patches, rotate skin sites
animal fats usually on chest wall
 E.g.. White meat – chicken w/o  Instruct on evaluation of
skin, fish effectiveness based on pain
 Stop smoking & avoid alcohol relief
 Activity restrictions are placed  Propanolols causes
within client’s limitations bronchospasm & hypoglycemia,
 NTGs – max of 3doses at 5-min do not administer to asthmatic &
intervals diabetic clients
 Stinging sensation under the  Heparin – monitor bleeding
tongue for SL is normal tendencies (avoid punctures, use
 Advise clients to always carry 3 of soft-bristled toothbrush);
tablets monitor PTT levels; used for 2wks
 Store meds in cool, dry place, max; do not massage if via SC;
have protamine sulfate available
air-tight amber bottles & change  Coumadin – monitor for bleeding
stocks every 6months & PT; always have vit K readily
 Inform clients that headache, available (avoid green leafy
dizziness, flushed face are veggies)
common side effects.
 Acute Coronary Syndrome
 Unstable Angina/Non ST-Segment Elevation MI – a clinical
syndrome of myocardial ischemia
 Causes: atherosclerotic plaque disruption or significant
CHD, cocaine use (risk factor)
 Defining guidelines: (3 presentations)
1. Symptoms at rest (usually prolonged, i.e.. >20mins)
2. New onset exertional angina (increased in severity of at
least 1 class – to at least class III) in <2months
3. Recent acceleration of angina to at least class III in
<2months
 Dx: based on pain severity & presenting symptoms, ECG
findings & serum cardiac markers
 When chest pain has been unremitting for >20mins,
possibility of ST-Segment Elevation MI is usually
considered
Myocardial Infarction
 ST-Segment Elevation MI (Heart Attack)
 Characterized by ischemic death of myocardial tissue
associated with atherosclerotic disease of coronary 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
Cont.
 Manifestations:
 PLEASE PO
 Pain
 Leukocytosis
 ECG changes
 Anxiety
 Shock
 Elevated Cardiac Enzymes
 Pulmonary Edema
 Oliguria
 Complications: death (usually within 1 hr of onset)
 Heart failure & cardiogenic shock – profound LV failure from
massive MI resulting to low cardiac output
 Thromboemboli – leads to immobility & impaired cardiac
function contributing to blood stasis in veins
 Rupture of myocardium
 Ventricular aneurysms – decreases pumping efficiency of heart
& increases work of LV
Tissue Changes After MI

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)
8th week Complete scar tissue replacement
Management of MI
 Initial Management: OMEN
- O2 therapy via nasal prongs
- adequate analgesia (Morphine via IV – also has
vasodilator property)
- ECG monitoring
-sublingual NTG (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, propanolol
 Anticoagulants & antiplatelets: ASA, heparin
 Stool softeners
Surgery :
1. Revascularization
PTCA
Coronary stent implantation
Coronary Artery Bypass Graft
(CABG) – no response to medical
treatment & PTCA
2.Resection – aneurysm
 Nursing Management
 Promote oxygenation & tissue perfusion (place client on semi-fowler’s,
O2 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
 Alterations in Blood Flow
in the Systemic Circulation
Buerger’s Disease
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
Manifestations
 Pain – predominant symptom; R/T distal arterial
ischemia
 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
 Diagnosis & Treatment
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
 Raynaud’s Disease
 Mechanism: intensive vasospasm of arteries &
arterioles in the fingers
 Cause: unknown
 Usually affects young women
 Precipitated by exposure to cold & strong
emotions
 Raynaud’s phenomenon – associated with
previous injury (i.e.. Frostbite, occupational
trauma associated with use of heavy vibrating
tools, collagen diseases, neuro d/o, chronic
arterial occlusive d/o)
 Manifestations
Period of ischemia (ischemia due to vasospasm)
 change in skin color = pallor to cyanotic
 1st 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)
Diagnosis & Treatment
 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, Nifedipine,
Nicardipine) – decrease episodes of attacks
 Care Plan for Clients with Altered
Cardiovascular Oxygenation
A. Assessment: C. Goals:
1. Hx of symptoms (pain, 1. Relief of pain &
esp. chest pain; symptoms
palpitations; dyspnea) 2. Prevention of further
2. v/s cardiac damage
B. Nursing Dx: D. Nursing Interventions:
1. ineffective tissue 1. Pain control
perfusion
2. Proper medications
(cardiopulmonary)
3. Decrease client’s
2. Impaired gas exchange
anxiety
3. Anxiety due to fear of
4. Health teachings
death (clients with MI
or Angina) (meds, activities, diet,
exercise, etc)
 THANK YOU

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