NOTES ON CARDIOVASCULAR DISORDERS

Coronary Artery Disease (CAD)

Narrowing or obstruction of one or more coronary arteries as a
result of:
1. Atherosclerosis
2. Arteriosclerosis

Angina Pectoris
Chest pain resulting from myocardial ischemia; a symptom of an
existing disease; no necrosis.
Demand VS supply
Types:
1. Stable
2. Unstable
3. Prinzmetal
4. Intractable
Causes: 5 Es
Exertion
Emotion
Exposure to cold
Excessive smoking
Excessive eating
Assessment:
Pain pattern:
Mild moderate
Retrosternal choking, heartburn, pressing, burning, squeezing
Radiating to neck, jaw, shoulder, arms (L)
3 5 mins.
Relieved by rest and nitroglycerine
Manifested by:
Pallor, diaphoresis, dizziness, palpitation
ECG change- ST depression, T wave inversion
Cardiac enzymes- normal
Medications:
Vasodilators nitroglycerine, isosorbide
B-adrenergic blocking agents propanolol, metoprolol
Calcium-channel blocker verapamil, nifedipine, diltiazem
Platelet-aggregating inhibitors ASA, ticlopidine, clopidogrel
(Plavix)
Anticoagulants heparin Na, Warfarin Na (Coumadin)
Responsibilities for drug administration: Monitor PTT/ APTT / PT
Nursing Intervention in Drug Therapy:
Anticipate postural hypotension

C.D.S
 Take maximum of 3 doses at 5 min interval
SL prep has burning or stinging sensation
Avoid alcohol
Advise client to carry 3 tabs in his pocket; store nitroglycerine in
a cool, dry, dark place; replace stock q 3-6 months
Nitropatch applied OD in AM, rotating sites
Do not give NTG if pt took Viagra or any drug for erectile
dysfunction
Evaluate effectiveness (if not, MI)
Interventions:
Beta-blockers, Calcium channel blockers
Monitor the HR and BP
Bedrest with BRP
Low fat, low cholesterol diet
Regular exercise
Medical management:
Surgery:
a. PTCA
b. Atherectomy
c. CABG

Myocardial Infarction
Sudden decrease of oxygenation due to absence of coronary
blood flow that results to destruction of myocardial tissue in
regions of the heart
After 15 mins. = necrosis
Causes:
Thrombus
Emboli
Atherosclerosis
Location:
Left anterior descending artery anterior or septal wall MI or
both
Circumflex artery posterior wall MI or lateral wall MI
Right coronary artery inferior wall MI
Diagnostic studies:
1. Total CK levels
2. Cardiac enzymes elevated
3. AST
4. ECG
a. T wave inversion (zone of hypoxia)
b. ST elevation (zone of injury)
c. Pathologic Q wave (zone of infarction)
Assessment:

C.D.S
 Pain pattern: severe crushing substernal pain; knifelike, viselike
(May radiate to jaw, back & left arm)
Fever
Nausea & vomiting
Oliguria
Pallor / cyanosis / coolness of extremities

Nursing interventions:
a. Acute Stage:
Administer prescribed medications : M. O. N. A.
Lidocaine (Xylocaine)
Beta-blockers (propranolol, timolol)
Thrombolytics (streptokinase, urokinase)
Anticoagulants (heparin, warfarin/coumadin)
Oxygen @ 2 4 L/min
Stool softeners & soft diet
Diet: liquid / small frequent meals (low fat, cholesterol, sodium
diet)
Semi-fowlers
Emotional rxns: anxiety, denial, depression
Monitor thrombolytic therapy (used within 3-4hours after onset of
symptoms )
b. Following acute episode:
maintain CBR with BSC
provide ROM
progress to ambulation
c. Rehabilitation:
Early activity : 1 2 metabolic activity on task (MET)
Hospital Discharge: 14th day
ADLs : 6 wks after
Sex : 4 8 wks after
Guidelines:
Resume if able to climb 2 flights of stairs
Before: rest is impt. / avoid large meals / wear loose fitting
clothes / nitro before sex /
usual environment / sex at room temperature / foreplay
During: comfortable position
Female position: side lying
Male Position: sitting position
Complications of MI:
Cardiogenic shock- pumping ability of the LV severely impaired
Cardiac Arryhthmias- lack of oxygen causes conduction problems

C.D.S
 CHF

Cardiac Dysrhythmias
Abnormal cardiac rhythms that can be due to abnormal
automaticity or conduction, or both
Most common complication and major cause of death in MI
The most common dysrhythmia in MI is PVCs
PVC of >6/min is life threatening
Predisposing factors are tissue ischemia, hypoxemia, CNS & PNS
influences, lactic acidosis, hemodynamic abnormalities, drug
toxicities and electrolyte imbalances
Types are: sinus, atrial, ventricular and conduction defects

Bradycardia Regular, slower rate <60

Tachycardia Regular, faster rate >100
Atrial flutter 160-350/min, less filling
time
Atrial fibrillation Rate >300, uncoordinated
muscle contractions; no
filling, no output-cardiac
standstill
PVCs May induce fibrillation
Bundle Branch block Delayed conduction to BB
1st degree HB Delayed conduction AV node
2nd degree HB Some beats go to AV, some
dont
3rd degree HB No conduction to AV node,
ventricles slowly contract,
some independent of atrial
contractions

Sinus Dysrhythmias
Types:
Sinus tachycardia
- Meds: Digitalis
Sinus bradycardia
- Meds: Atropine
Atrial Dysrhythmias
Types:
Premature Atrial Contraction (PAC)
Paroxysmal Atrial Tachycardia

C.D.S
 Atrial Flutter
Atrial Fibrillation
Meds: Quinidine, Ca channel blockers, cardioversion, pacemaker

Ventricular Dysrhythmias
Premature Ventricular Contraction
Ventricular tachycardia
Ventricular fibrillation: chaotic discharge,
rate > 300/min, may result to clinical death
TX: immediate defibrillation
Epinephrine

Summary of therapeutic modalities in cardiac

dysrhythmias:
Antidysrhythmic drugs
Artificial Cardiac Pacemaker
Cardioversion/Defibrillation
Cardiopulmonary resuscitation
Pacemakers:
Electronic device that causes cellular depolarization and cardiac
contraction
It initiate and maintains HR
Pacing modes
Demand
Fixed rate
Nursing interventions (for pacemakers)
Monitor ECG following implantation, include VS
Make sure all the equipments is the clients unit is grounded
Observe for signs of pacemaker failure
Dizziness, fainting, chest pain, palpitation,
Avoid going near electrical devices (EMI)
Wear loose fitting clothes
Avoid contact sports
Cardioversion/Defibrillation:
Cardioversion- synchronous application of shock during R wave
Defibrillation is asynchronized electric shock to terminate VF or
V-tac without pulse
Nursing Interventions (for defibrillators)
Client in firm, flat surface
Apply interface materials to the paddle
Grasp paddle only by insulated handles
Give command to STAND CLEAR

C.D.S
 Apply one of paddles at precordium, other R parasternal area 3rd
ICS
For defibrillation, release 200-360 joules; for cardioversion, lower
energy is required
Defibrillation is done prior to CPR

Cardiopulmonary resuscitation:
Indication is CP arrest/clinical death
(breathlessness/pulselessness)
CPR should be started <5 min after arrest
2 types
Basic Life Support use of mouth, hands
Advance Cardiac Life Support BLS and equipments

Techniques of BLS: When to Stop CPR?

When client is revived
When EMS has been activated
When rescuer is exhausted
When client is dead

Congestive Heart Failure (CHF)

Inability of the heart to maintain adequate circulation to meet
the metabolic needs of the body bec. of an impaired pumping
capability.

Causes:
a) Hypervolemia
b) Arteriosclerosis
c) MI
d) Valvular Problems
Types:
Right-sided CHF (Systemic symptoms)
Fatigue
Ascites
Cyanosis
Polyuria / wt. gain
Distended jugular veins
Pitting edema
Hepatomegaly
Left-sided CHF (Pulmonary symptoms)
Cardiomegaly
Cough

C.D.S
 Exertional dyspnea
Cyanosis
Orthopnea
Blood tinged sputum
Acute pulmonary edema
Management:
Rest
High-Fowlers or sitting
Decrease fluids & Na+
Medications: Cardiac Glycosides (+) inotropy / (-) chronotropy
digitalis / digoxin (Lanoxin) / digitoxin (Crystodigin) / lanatoside
(Cedilanid-C)

Guidelines:
1. check HR
2. ^ K+ intake
3. Normal level: 0.5-2ng/mL
4. Toxicity: (BANDAV or BANDAM)
5. Antidote: Digoxin Immune Fab (Digibind) antibodies that
bind to digoxin
6. Diuretics H2O & Na+ excretion
7. Loop diuretics Furosemide (Lasix)
8. Potassium sparing spironolactone (Aldactone)

Guidelines in administering K sparing meds:

Give in AM
Monitor IO
S/E: hypokalemia / hyponatremia / dehydration / hypotension

Rotating tourniquet (Principles)

apply 3 tourniquets
inflate cuff 10 mm above diastolic pressure
rotate q 15 mins.
check distal pulses
remove 1 at a time @ 15 mins. Interval

- Inflammatory diseases of the heart

Pericarditis
acute or chronic inflammation of the pericardium
Assessment:
precordial pain

C.D.S
 pain (inspiration, coughing & swallowing)
pain worse when supine
pericardial friction rub
fever & chills
elevated WBC
Pericardial effusion
Dresslers syndrome
Management:
Position: side lying, high Fowlers, upright & leaning forward
Admin. analgesic, corticosteroids, NSAIDs
Avoid aspirin & anticoagulants
Antibiotics
Diuretics & digoxin
Monitor for complications: Cardiac Tamponade

Cardiac Tamponade
pericardial effusion occurs when the space bet. the parietal &
visceral layers of the pericardium fill with fluid.
Etiology:
stab wound
effusion
heart Sx
Assessment:
Becks triad: distended neck veins / muffled heart sounds /
hypotension
Chest pain
Cardiogenic shock
Increased CVP
Management:
CCU for hemodynamic monitoring
PERICARDIOCENTESIS
Admin. IV fluids as prescribed

Myocarditis
acute / chronic inflammation of the myocardium
Etiology:
Bacterial : staphylococcus / pneumococcal
Viral : mumps / influenza
Parasitic : Toxoplasmosis
Radiation / Lead
Assessment:
fever

C.D.S
 pericardial friction rub
gallop rhythm
murmur
S/S of HF
Chest pain
Management:
Position: Bed rest / sitting up or leaning forward
Monitor pulse rate & rhythm
Admin. NSAIDs / analgesics / salicylates for fever & pain
Limit activities
Admin. digoxin / antidysrhythmics / antibiotics as prescribed

Endocarditis
Inflammation f the inner lining of the heart
Assessment:
fever, anorexia, wt loss, fatigue
cardiac murmurs
Janeways lesions
Osslers nodes
Petechiae, splinter hemorrhages in nailbeds
Splenomegaly

Management:
Rest
Antibiotics
Prophylactic ATB prior to dental procedures (6months)
Anti-embolic stockings
Monitor for emboli:
Splenic sudden abd. pain radiating to L shoulder
Renal flank pain radiating to groin, hematuria & pyuria

Cardiomyopathy
Myocardium around left ventricle becomes flabby, altering
cardiac function > decreased CO
Increased HR and increased muscle mass compensate in early
stage but later stage > HF
Types:
Dilated (congestive)- dilated chambers contract poorly causing
blood to pool and reducing CO

C.D.S
 Hypertrophic (Obstructive)- hypertrophied LV cant relax and fill
properly
Assessment:
Chest pain, dyspnea, cough, crackles, enlarged heart, dependent
pitting edema, enlarged liver, jugular vein distention, murmur, S3
S4 sounds, syncope
Treatment:
Low sodium diet
Dual chamber pacing
Surgery: heart transplant or cardiomyoplasty

Valvular Heart Disease

3 types of mechanical disruption from VHD
1. stenosis or narrowing-doesnt open the valve
2. insufficiency- incomplete closure of the valve
3. prolapse of the valve
can result from endocarditis and inflammation > HF
Forms:
Aortic insufficiency
Mitral insufficiency
Mitral stenosis
Mitral valve prolapse
Tricuspid insufficiency
Assessment:
Aortic insufficiency- dyspnea, palpitations, angina, fatigue,
cough, pulmonary congestion, orthopnea
Mitral insufficiency- same + peripheral edema
Tricuspid insufficiency- R sided HF
Treatment:
Sodium Restrictions
Open heart surgery using CP bypass for valve replacement
Medications: Anticoagulants
Nursing Management:
Monitor for signs of HF or pulmonary edema and monitor for
adverse reactions from drug therapy
Place in upright position to relieve dyspnea
Maintain bed rest
If patient undergoes surgery, watch for hypotension, arrhythmias
and thrombus formation. Monitor VS, I&O, labs weight to detect
post-op complications

C.D.S
 PERIPHERAL VASCULAR DISEASES

Arterial Diseases
1) Buergers Disease
Occlusive disease of the median & small arteries & veins
accompanied by clot formation.
Etiology:
unknown
smoking
males
Assessment:
intermittent claudication
ischemic pain occurring in the digits while at rest
cool, numb, tingling sensation
diminished pulse at distal extremity
ulceration
Management:
Instruct to stop smoking
Monitor pulses
Avoid injury to extremities
Admin. vasodilators as prescribed

2) Reynauds Disease
vasospasm of the arterioles & arteries of extremities.
Etiology:
cold
stress
smoking
Assessment:
blanching of ext. followed by cyanosis
reddened tissue
numbness, tingling, swelling & coldness of extremities
Management:
stop smoking
Vasodilators
avoid precipitating factor
warm clothing
avoid injuries to hands & fingers

Venous Diseases
1. Thrombophlebitis clots lead to vein inflammation

C.D.S
2. Phlebothrombus a thrombus w/o inflammation
3. Phlebitis vein inflammation usu. assoc. w/ invasive procedures
4. Deep Vein Thrombosis
pain (calf or groin tenderness)
(+) Homans sign
warm skin tender to touch
5. Varicose veins distended protruding veins that appear
darkened & tortuous; vein walls weaken & dilate, the valves
become incompetent
Etiology:
prolonged standing
pregnancy
obesity
Congenital
Incidence:
Female
35 40 y. o.

Assessment (in comparison w/ arterial diseases)
ARTERIAL VENOUS
Intermittent claudication Heaviness & leg cramps
Cyanosis Redness
Coldness Warmth
Absent pulse Unpalpable pulse due to
edema
Loss of sensation No loss of sensation
Gangrene ulcers Venous stasis ulcers
Decreased capillary refill (+) Trendelenburg test

Aortic Aneurysms
abnormal dilation of the arterial wall, caused by localized
weakness & stretching in the medial layer or wall of the artery.
Types:
a. According to morphology or form:
b. Fusiform
c. Saccular
d. Dissecting
e. False (Pseudoaneurysm)
According to location:
Thoracic Aortic Aneurysm
S/S:
pain

C.D.S
 syncope
dyspnea
increased pulse
cyanosis
weakness

Abdominal Aortic Aneurysm

S/S :
pulsating mass in abdomen
systolic bruit over the aorta
tenderness on deep palpation
abdominal or lower back pain

Cerebral Aneurysm
S/S:
headache
vomiting
^ ICP
Interventions:
Prevent rupture:
antihypertensive drugs
modify risk factors
Surgery:
Resection of aneurysm with Teflon/Dacron Graft
Post-op
monitor hemorrhage
Flat position / Avoid SF position
O2 as ordered
Coughing / breathing exercise
Check distal pulses
Avoid hip-knee flexion

Hypertension
Abnormal elevation of BP above 140/90 mmHg based on at least
2 readings on same conditions.
Types:
Primary / Essential / Idiopathic
90% - 95% of cases
unknown cause
Secondary - with known cause
Endocrine

C.D.S
 Cardiovascular
Renal
Pregnancy
Labile
intermittently elevated BP

Malignant
severe, rapidly progressing & sustained -> leads to rapid end
organ complication
White Coat
elevation of BP only during clinic visits
Assessment:
headache
depression
dizziness
nocturia
unsteadiness
tinnitus
blurred vision
memory loss

Hypertension s/s:
Asymptomatic
L ventricular hypertrophy
Cerebral ischemia
Renal failure
Visual disturbances including blindness
Epistaxis
Diagnostic Elevation:
Increased BUN, creatinine, Na and cholesterol levels
Sustained BP readings of 140/90 mm Hg
CXR show cardiomegaly
ECG shows LVH
Management:
Step-Care Approach
(Joint Committee on Detection, Evaluation and Treatment of High
Blood Pressure)
a. Lifestyle modification:
sodium restriction
weight reduction
alcohol restriction

C.D.S
 smoking cessation
regular exercise

JNC VII Classification of BP for adults aged 18 or older

BP SBP DBP
CLASSIFI mmHg mmHG
CATION
Normal <120 & <80
Prehypert 120-139 Or 80-89
ension
Stage 1 140-159 Or 90-99
HPN
Stage 2 160 Or 100
HPN
b. Single Drug Therapy
Mild hypertension Diuretics (Thiazide)
c. Beta-Blockers
c. Multi-Drug Therapy
Add: ACE Inhibitors
^ dosage of Beta-Blockers
Add Beta-Blocker to Diuretics (Thiazides)
Substitute Vasodilators
AII receptor blockers (sartans)
Anti-lipemics (statins)
d. Add: Vasodilator or slow Calcium Channel Blocker to
current regimen
e. Add: Sympatholytic / Antiadrenergic
guanethidine sulfate (Ismelin sulfate)
methyldopa (Aldomet)
clonidine (Catapres)
prazosin (Minipress)
reserpine (Serpasil)
d.
e. Major side-effects of antihypertensive drugs:
Orthostatic hypotension
Dizziness
Cardiac rate alteration
Sexual disturbances
Drowsiness
f. Health Teachings:
Emphasize compliance
Therapy is usually for life

C.D.S
 Monitor BP
Do not increase or decrease dose w/o doctors order
Do not abruptly discontinue meds
g.
h.
i.
j.
k.
l.
m.
n.
o.
p.
q.
r.
s.
t.
u.
v.
w.
x.
y.
z.
aa.
ab.
ac.
ad.
ae.
af.
ag.
ah.
ai.
aj.
ak.
al.
am.
an.
ao.
ap.
aq.
ar.
as.
at.
au.
av.

C.D.S
aw.

C.D.S
ax.