Table of contents:

Objectives……………………………………………………………..1
Methods……………………………………………………………….1
Anatomy and Physiology……………………………………………..2
History and Assessment………………………………………………5
Dysrhythmias and Conduction problems……………………………..6
Coronary Vascular Disease…………………………………………...11
Structural, Infectious and Inflammatory Disorders…………………..15
Acquired Valvular Disorders
Mitral valve prolapse
Mitral valve regurgitation
Mitral valve stenosis
Aortic regurgitation
Aortic stenosis
Cardiomyopathies
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Restrictive Cardiomyopathy
Complications from Cardiac Diseases………………………………..21
Heart failure
Cardiogenic Shock
Hypertension…………………………………………………………23
References…………………………………………………………... 26
Objectives:

The general objective of the module is to discuss the cardiovascular system and
disorders to the students.
Specifically, after being done with the module the students will be able to:

1. Discuss various cardiac disorders and their pathophysiology.

2. Enumerate various symptoms specific for each disorder.
3. Give the management options, medical and non-medical treatment of choice.
4. Formulate various nursing diagnoses specific for each disease and patient.
5. Create appropriate nursing interventions for each priority cardiac problems
identified, encountered or will be encountered in the future.

Methods:

This lecture module is intended to guide the discussion of the subject and
facilitate the learning experience of the students. The lecturers will facilitate, expound on
some topics and clarify unresolved issues and questions.
Evaluation of the effectiveness of teaching will be measured through the students
participation, quizzes, mastery test and/or examination.
 CARDIOVASCULAR SYSTEM
by
Ruby Ruth Roces

I. Anatomy and physiology review

The heart is a hollow, muscular organ that lies within the pericardium in the
middle mediastinum. It is pyramidal in shape, with the apex directed downward,
forward and to the left, usually lying in the 5th intercostals space left mid-
clavicular line. It is divided into four chambers by an vertical septa. It is
composed of 3 layers; the outer epicardium, middle myocardium and inner
endocardium.
The 4 chamber of the heart are the right atium, right ventricle, left atrium and
left ventricle. The right side of the heart receives deoxygenated blood from the
peripheral organs and distributes it to the lungs via pulmonary arteries for
oxygenation. The left side of the heart receives oxygenated blood from the lungs
through the pulmonary veins and distributes it to the peripheral organs through the
aorta.
There are 4 valves in the heart which permits blood flow in 1 direction. These
valves can be classified into atrioventricular and semilunar valves. There are 2 AV
valves; the tricuspid so named because of it has 3 cusps, divides the Right atrium
from the Right ventricle. The bicuspid or mitral valve on the other hand divides
the left atrium from the left ventricle. The semilunar valves- the pulmonic and
aortic valves are named according to the vessels they’re located in.
The blood supply of the heart is given by the right and left main coronary
arteries.
The peripheral vascular system
Conduction system
SA node--AV node--Left and Right Bundle of His--Purkinje fibers
Cardiac Cycle

Cardiac Output- is the amount of blood pumped by each ventricle during a given
period.

Stroke volume- is the amount of blood ejected per heartbeat.

Control of HR
Cardiac output is responsive to changes in metabolic demands of the
tissues. Changes in the heart rate are accomplished by reflex controls mediated by
autonomic nervous system. The parasympathetic slows the heart rate, the
sympathetic speeds it up. The heart rate is also influenced by the central nervous
system and baroreceptor activity.
I. History and PE
1. History
General data
- age and sex
History of present Illness
- symptoms of cardiovascular disease
- patients functional capacity
- history of febrile illness
- pregnancy
Past Medical history
- history of systemic diseases such as hypertension, DM, Dyslipidemia,
cerebrovascular disease, Peripheral vascular disease, Thyroid diseases, Bronchial
asthma or Chronic obstructive lung disease
- history of allergies and previous and present medications
Family history (up to 1st degree relative)
-Hypertension, ischemic heart disease, DM, dyslipidemia
Personal and social history
- cigarette smoking( more than 10 sticks/day is a risk factor)
- alcohol intake( approx 2 beers/day allowed)
- illicit drug use
- obesity
- athletic history(lack of exercise)
- dietary intake( Salt and fat)
- Type A personality( workaholic and obsessive compulsive type)
2. PE
- regional examinations
- JVP( best seen at 30-45 degree angle. Normal value is 4-8 cms)
- Arterial pulse
- Examination of precordium
- Apex beat palpation
- Heart sounds
II. Dysrhythmia and Conduction Problems
- These are disorders of the formation or conduction of electrical impulses within
the heart which can cause disturbances in the heart rate, heart rhythm or both.

A.ECG Interpretation:

Six Components (mnemonic)

R- Rate
R- Rhythm
A- Axis
H-Hypertrophy
I- ischemia and Infarction
 M- misc. findings
1. Rate
Formula:
HR= 1500________________________________
No. of small Squares between 1 R-R Interval

300_______________________________
No. of big squares between 1 R-R interval

Mnemonic
HR No.of big squares between R-R interval
300 1
150 2
100 3
75 4
60 5
50 6

Normal rate = 60-100

Bradycardia = < 60
Tachycardia = > 100

3. Rhythm
 Identify the P wave- sinus P
 Check relation of P to QRS complex
-should be before QRS (normal)
-if buried before or after QRS (SVT, complete heart block)
 Check PR interval (normal- 0.12-0.02 secs.)
-Short PR (WPW syndrome)
-Prolonged PR (1st or2nd degree AV blocks)
 Check QRS duration (normal- <0.10 sec.)
-wide QRS (bundle branch block)
 Check relation of R-R and P-P interval (normal- equal intervals)
-P-P interval is shorter than R-R (complete heart block)
-P-P interval is longer than R-R (AV dissociation)

4. Axis
a) normal
b) left axis deviation
c) right axis deviation
d) indeterminate axis
I AVF II Type of deviation
+ + normal
+ - + normal
- + Right axis deviation
+ - - Left axis deviation
- - Far right or left

5. Hypertrophy
a) LVH
- S wave in V1 + R wave in V5 or V6 > 35mm (commonly used)
b) RVH
- Right axis deviation or + 110 degrees or more, with any of the following:
Lead V1: R wave > S wave
Deep S wave in leads V5 and V6
ST depression and T wave inversion in V1-V3
c) LAE
- Any of the following:
In lead V1: wide terminal component of P wave which is ≥ 1mm wide (0.04 sec)
And ≥ 1mm deep
In any lead: P wave wider than 0.12 sec (> 3 small squares) or with a ≥ 1 mm
Notch in the middle
d) RAE
- Any of the following:
In lead V1: tall initial component of P wave which is ≥ 2mm wide (0.08 sec)
And ≥ 2mm deep
In any lead: P wave ≥ 2.5 mm tall
e) Biventricular hypertrophy
- Any of the following:
The ECG meets one or more of the diagnostic criteria for isolated left and right
ventricular hypertrophy
The precordial leads show signs of left ventricular hypertrophy, but the QRS axis
In the frontal plane is greater than + 90 degrees (RAD).
f) Biatrial Enlargement
- Any of the following:
In lead V1, the presence of a large diphasic P wave with initial positive
component ≥ 2 mm tall (RAE) and the terminal negative component
≥ 1 mm deep and ≥ 0.04 second in duration (LAE).
In any lead, an increase in both the amplitude which is 2.5 mm or greater (RAE)
and duration of 0.12 second or more of the P wave (LAE).

6. Ischemia and Infarction

a) Ischemia
At least 1 mm ST-segment depression
Symmetrically or deeply inverted T waves
Abnormally tall T waves
Normalization of abnormal T waves
Prolongation of the QT interval in addition to the above
Others: arrhythmias, bundle branch blocks, AV blocks, or electrical alternans
b) Infarction
- Any of the following:
ST elevation ≥ 2 mm in 2 or more chest leads or ≥ 1 mm in 2 or more limb leads
 Q waves ≥ 0.04 sec (1 small square)

7. Miscellaneous
a) Hypokalemia
U wave as tall as or taller than the T wave at leads V2 and V3.
b) Hyperkalemia
In the chest leads, height of T waves > 10 mm in most leads.
In limb leads, height of T waves > 5 mm in most leads.
c) Hypocalcemia
Prolonged Qt interval, i.e. longer than half of the RR interval by eyeballing.
d) Hypercalcemia
Shortened QT interval.

B. Types of dysrhythmias
1. Sinus node dysrhythmias
a) Sinus bradycardia- occurs when the sinus node creates an impulse at lower than
normal.
b) Sinus tachycardia- occurs when the sinus node creates an impulse at faster than
normal.
c) Sinus arrhythmia- occurs when the sinus node creates an impulse at an irregular
rhythm.The rate usually increases with inspiration and decreases with expioration.
2. Atrial dysrhythmias
a) Premature atrial complex- is a single ECG complex that occurs when an electrical
impulse starts in the atrium before the next normal impulse of the sinus node.
b) Atrial flutter- occurs in the atrium and creates impulses at an atrial rate between
250 and 400 times per minute. Due to the faster atrial rate than the AV node can
conduct, all atrial impulses are conducted into the ventricle causing a therapeutic
block.
3. Junctional dysrhythmias
a) Premature junctional complex- is an impulse that starts in the AV nodal area before
the next normal sinus impulse reaches the AV node.
b) Junctional rhythm- occurs when the AV node instead of the SA node becomes the
pacemaker of the heart.
d) Atrioventricular nodal reentry tachycardia- occurs when an impulse is conducted to
an area in the AV node that causes the impulse to be rerouted back into the same area
over and over again at a very fast rate.
4. Ventricular dysrhythmias
a) Premature ventricular complex- is an impulse that starts in a ventricle and is
conducted through the ventricles before the next normal sinus impulse.
b) Ventricular tachycardia- is defined as 3 or more PVCs in a row occurring at a rate
exceeding 100 beats per minute.
c) Ventricular fibrillation- is a rapid but disorganized ventricular rhythm that causes
ineffective quivering of the ventricles. There is no atrial activity seen on ECG.
d) Ventricular asystole- commonly called flatline is characterized by absent QRS
complexes, although P waves may be apparent for a short duration in 2 different
leads.

5. Conduction abnormalities
a) First-degree AV block- occurs when all the atrial impulses are conducted through
the AV node into the ventricles at a rate slower than normal.
b) Second-degree AV block, type 1- occurs when all but one of the atrial impulses are
conducted through the AV node into the ventricles.
c) Second-degree AV block, type 2- occurs when only some of the atrial impulses are
conducted through the AV node into the ventricles
d) Third-degree AV block- occurs when no atrial impulse is conducted through the AV
node into the ventricles.

C. Nursing Diagnoses:
- Decreased cardiac output
- Anxiety related to fear of the unknown
- Knowledge deficiency about dysrhythmia and its treatment

D. Adjunct modalities and management

Pacemaker Therapy
- Pacemakers are electronic devices which provide electrical stimuli to the heart. It
can be permanent or temporary.
Cardioversion and defibrillation
- Are treatments for tachydysrhythmias. They are used to deliver electrical current
in order to depolarize a critical mass of myocardial cells.
- Cardioversion involves the delivery of a “timed” electrical current to terminate a
tachydysrhythmia.
- Defibrillation is used in emergency situations aas the treatment of choice for
ventricular fibrillation and pulseless VT. Defibrillation depolarizes a critical mass
of myocardial cells at once; when they repolarize, the sinus node usually captures
its role as the pacemaker.
III. Coronary Vascular Diseases
1. CAD
It is the most prominent type of cardiovascular disorder.
a. Coronary Atherosclerosis
- It is the most common heart disease in U.S.A.
- It is due to an abnormal accumulation of lipid on fatty substances and fibrous
tissues in the vessel wall creating blockage or narrow the vessel in a way that
reduces blood flow to the myocardium.
- Risks factors:
Major risk factors;
 Age
 Male sex
 Hypertension
 DM
 Dyslipidemia
 Smoking
 Family history of ischemic heart disease
Minor risk factors
 obesity
 decrease physical activity
 Type A personality
 Diet high in cholesterol

Pathophysiology (Coronary diseases)

Fatty streaks, lipids

deposited

intimal wall of arteries

Infiltration of T lymphocytes and monocytes

Ingest lipids then die

Vascular smooth muscles then proliferate + formation of fibrous cap over

the fatty core

Atheroma
rupture
 Thrombus emboli

Occlusion of coronary artery(s/sxs of ischemia)

Conversion to anaerobic metabolism (dec. pH)

Conduction system disorders

Dysrhythmias
Decreases cardiac contractility

Myocardial cells will necrose (check for enzyme markers- these enzymes
will be introduced to the blood stream at this time)

Clinical manifestations:
- produces symptoms and complications according to the location and degree of
narrowing

b. Angina Pectoris
- clinical syndrome usually characterized by episodes or paroxysms of pain or
pressure in the anterior chest
- Cause is usually insufficient coronary blood flow resulting in decrease O2 supply
not enough to meet the myocardial demand for O2 esp. during physical exertion
or stress.
- Types:
1. Stable
2. Unstable- with new or worsening symptoms.
3. Refractory angina- with severe incapacitating chest pain
4. Variant or Prinzmetal’s angina- with pain at rest

c. Myocardial infarction
- Refers to the process by which areas of myocardial cells in the heart are
permanently destroyed.
Clinical presentation:
- severe chest pain usually > 30 mins. Unrelieved by nitroglycerin, may radiate as
high as occipital area but not lower than the umbilicus.
- May be painless (25%)
Assessment and Diagnosis:
- by a typical rise and gradual fall (troponin) and /or more rapid rise and fall (CK-
MB) of biochemical markers of myocardial necrosis with at least 1 of the following
myocardial symptoms: ischemic symptoms, pathologic Q waves on ECG, ECG
findings indicative of ischemia.
- Or a pathological finding of an acute myocardial infarction.
Management:
- Objectives of treatment are to reduce the O2 demand and to increase O2 supply to
the myocardium
 Pharmacologic:
1. Nitrates- mainstay of treatment. Acts as vasodilators and decrease myocardial O2
demand in turn decreasing ischemia and relieving pain.
2. B-blockers- decrease myocardial O2 consumption by blocking B-adrenergic
stimulation, resulting in decrease HR, BP and contractility.
3. Ca channel blocking agents- have different effects. Some decrease HR and
strength of contractility, others increase O2 supply by relaxing blood vessels.
4. Antiplatelet and anticoagulant medications- administered to prevent platelet
aggregation which impedes blood flow. (e.g. aspirin, Clopidogrel, Ticlopidine
and Heparin)
5. Thrombolytics
• The first four medications are also used as treatment of angina except
thrombolytics.
Non pharmacologic
1. Invasive Interventional procedures
> Percutaneous Transluminal Angioplasty- used to treat patients who do not
experience angina but are at risk for a cardiac event. Its’ purpose is to improve blood
flow within the artery by cracking the atheroma. Possible complications during the
procedure are dissection, perforation abrupt closure and vasospasm of the coronary
artery. Post procedure care involves monitoring for bleeding since patients received
large amounts of heparin during the procedure.
> Coronary artery stent- placed to overcome the risks that the coronary artery may
recoil and the tissue will remodel and form restenosis.
> Transmyocardial revascularization- those who have ischemia and are not candidates
for CABG may benefit from this procedure.
2. Surgical Procedures
> Coronary artery revascularization
Coronary artery bypass graft- a surgical procedure in which a blood vessel from
onother body part is grafted to the occluded coronary artery so that blood can flow
beyond the occlusion. The coronary artery must have at least 70% occlusion for this
procedure to be considered. Complications of this procedure include Mi,
dysrhythmias and hemorrhage.
- Goals of the Plan of care after procedure are: restoration of cardiac output to
maintain/ attain desired lifestyle; to achieve adequate gas exchange; to improve fluid
and electrolyte balance; to reduce symptoms of sensory perceptual imbalance and
prevention of postcardiotomy psychosis; to promote relief of pain and to be able to
perform self-care.

Nursing Diagnoses:
1. Ineffective myocardial tissue perfusion secondary to CAD, as evidenced by chest
pain
2. Anxiety related to fear of death
3. Potential ineffective air exchange related to fluid overload
4. Potential ineffective peripheral tissue perfusion related to decreased cardiac
output.
IV. Structural, Infectious and Inflammatory cardiac disorders
1. Acquired Valvular disorders
a) mitral valve prolapse
- is a deformity which usually produces no symptoms
- In this disorder, a portion of the mitral valve leaflet balloons back into the atrium
during systole, blood then regurgitates from the left ventricle back into the left
atrium.
Clinical Manifestations:
- fatigue, shortness of breath, light-headedness, dizziness, syncope, palpitations, chest
pain and anxiety. May also be asymptomatic.
Assessment and Diagnostics-
- On physical exam – extra heart sound referred to as Mitral click
Management- symptomatic relief and control. In advance cases mitral valve repair
and replacement may be necessary.

b) Mitral Regurgitation
- involves flowing back from the let ventricle to the left atrium
- Maybe caused by problems in one of more leaflets, chorda tendinae, annulus or
the papillary muscles. Regardless of the cause, blood regurgitates back into the
atrium during systole.
Assessment and diagnostics:
- (+) systolic murmur, high pitched blowing sound at the apex. Echocardiography is
used to diagnose and monitor progression of mitral regurgitation.
Management:
-medical management used is the same as those used for congestive heart failure.
Surgical interventions consist of mitral valve replacement or valvuloplasty.

c) Mitral stenosis
- It is an obstruction of blood flowing from the left atrium to the left ventricle.
- It is most often caused by the rheumatic endocarditis, which progressively
thickens the leaflets and chorda tendinae. Leaflets often fuse together narrowing
the orifice and progressively obstructing blood flow into the ventricle.
Clinical manifestations
- first symptom often is difficulty breathing on exertion. They may expectorate blood,
cough and with repeated respiratory infections due to venous pulmonary
hypertension.
Assessment and Diagnosis:
- PE-weak, irregular pulse, low pitched rumbling diastolic murmur heard at the
apex. - Echocardiography is used to diagnose.
- ECG and cardiac catheterization are used to determine severity.
Management:
- antibiotic prophylaxis use to prevent recurrence of infections. Anticoagulants may
be given to decrease risk for developing atrial thrombus. Surgical interventions
consist of valvuloplasty.

d) Aortic Regurgitation
- It is the flow of blood back from the aorta back into the left ventricle during
diastole.
- It maybe caused by inflammatory lesions that deform the leaflets preventing them
from closing the orifice.
Clinical Manifestations:
- develops without symptoms usually. Some may have forceful heartbeat in the head
and neck, visible or palpable temporal pulsations, followed by exertional dyspnea and
fatigue.
Assessment and Diagnostics
- (+)high pitched, blowing sound diastolic murmur heard at the 3rd to 4th intercostals
space at left sternal area.(+) widened pulse pressure, water-hammer pulse.
- Diagnosis confirmed by echocardiography, radionucleide imaging, ECG, MRI
and cardiac catheterization.
Management:
- use of antibiotic prophylaxis prior to any invasive and dental procedure. Heart
failure treatment will be discussed in the next topic. Dysrhythmias will be treated as
previously described. Surgery is recommended for any patients with left ventricular
hypertrophy regardless of the presence or absence of symptoms.

e) Aortic Stenosis
- It is the narrowing of the orifice between the left ventricle and the aorta. In adults,
stenosis may involve congenital leaflet malformation or abnormal number of
leaflets or it may result from rheumatic endocarditis or cusp calcification of
unknown cause.
Clinical manifestations:
- Many are asymptomatic. After symptoms developed, patients usually first have
exertional dyspnea caused by left ventricular failure. Other s/sxs are dizziness,
syncope due to reduced blood flow to the brain, angina pectoris results from increased
O2 demand of a hypertrophied left ventricle.
Assessment and diagnostics:
- PE- loud, rough systolic murmur heard at the aortic area (systolic crescendo-
decrescendo).
- Echocardiography is used to diagnose and monitor progression.
Management:
- Antibiotic prophylaxis to prevent endocarditis. Dysrhhythmia medications ma also
be required. Definitive treatment for aortic stenosis is valve replacement.
Pathophysiology of the acquired valvular defects and their complication:
2. Cardiomyopathies:

a) Dilated cardiomyopathy
- It is the most common form of cardiomyopathy. It is distinguished by significant
dilation of the ventricles without concomitant hypertrophy. The microscopic
examination of the muscle tissue will show diminished contractile elements and
diffuse necrosis of myocardial cells resulting in poor systolic function. These
changes decrease the amount of blood ejected from the ventricle in systole,
increasing the remaining blood in the ventricle after contraction. Less blood is
then able to enter the ventricle during diastole, increasing the end-diastolic
pressure and eventually increasing the pulmonary pressure. Echocardiography and
ECG are used to diagnose DCM.

b) Hypertrophic Cardiomyopathy
- It is a genetic disease. In this disorder, the heart muscle increase in size and mass
especially along the septum. The increased thickness reduces the size of
ventricular cavity causing longer relaxation time. This makes it difficult for the
ventricles to be filled with blood during the 1st part of diastole and making them
more dependent on atrial contraction for filling.

c) Restrictive cardiomyopathy
- It characterized by diastolic dysfunction caused by rigid ventricular walls that
impair ventricular stretch and diastolic filling. The systolic function is usually
normal.The cause for this disorder is usually unknown in most cases but in others
can often be attributed to amyloidosis and other infiltrative disease.
Clinical manifestations:
- Usually asymptomatic for years, may have s/sxs of heart failure, exertional
dyspnea, orthopnea, fluid retention, peripheral edema, cough, poor perfusion to
git(nausea), chest pain, dizziness and syncope with exertion.
Assessment and Diagnostics:
- PE- tachycardia and extra heart sounds in early stages, symptoms of CHF(
pulmonary crackles, vein distention, pitting edema)
- Echocardiogram
- ECG
- CXR
- Endomyocardial biopsy
Management:
- Determine and manage cause, correction of heart failure with medications, low
salt diet and exercise.
- Surgical management includes heart transplantation when medical management
fails. A left ventricular assistive device may be used pending the transplant.
Nursing Diagnoses:
- Decreased cardiac output related to structural disorders caused by
cardiomyopathy or to dysrhythmia from the disease process and medical
treatments.
- Ineffective CP, cerebral, peripheral and renal tissue perfusion related to decreased
peripheral blood flow.
- Impaired gas exchange related to pulmonary congestion caused by myocardial
failure
- Activity intolerance related to change in health status
- Powerlessness related to disease process
3. Infectious diseases of the heart
a) Rheumatic Endocarditis
- It occurs most often in school children following a streptococcal pharyngitis.
- Occurs as a result of sensitivity reaction occurring in response to the Streptoccal
infection.
Clinical manifestations:
- Signs and symptoms of valvular regurgitation as previously discussed.
Assessment and diagnostics:
PE- findings will depend on which side of the heart is involved; severity depends on
the size and location of the lesion, presence of murmur.
Management;
- eradicate microorganism through long term antibiotic regimen( Penicillin).

b) Infective Endocarditis
- It occurs as a direct invasion of the microorganisms to the endocordium.
- Its presentation is similar to the rheumatic endocarditis with the addition of
influenza-like symptoms prior to the valvular damage manifestations.

c) Myocarditis
- It is an inflammatory process involving the myocardium.
- Myocarditis results from Viral, bacterial, mycotic, protozoal, spirochetial
infection. It may also be caused by an Allergic reaction. The degree of myocardial
involvement determines the degree of hemodynamic effect and resulting signs and
symptoms.

d) Pericarditis
- refers to inflammation of the pericardium( membranous sac enveloping the
heart).. It maybe a primary illness or caused by a variety of medical and surgical
disorders.
- It can lead to pericardial effusion and increased pressure on the heart leading to
cardiac tamponade. Frequent or prolonged episodes may also lead to thickening
and decreased elasticity that restricts the hearts ability to fill properly (constrictive
pericarditis).
Clinical manifestations:
- Chest pain-most characteristic symptom, usually constant but may worsen with
inspiration or when lying down or turning.
- Friction rub- most characteristic sign
- Dyspnea and other signs of heart failure may occur as a result of pericardial
compression.
Assessment and Diagnostic findings:
- Echocardiogram
- ECG
V. Complications from heart disease
1. Heart Failure
- It is the inability of the heart to pump sufficient blood to meet the needs of the
tissues for oxygen and nutrients.
Etiology:
- most often caused by coronary artery disease, cardiomyopathy or valvular
disorders.
Pathophysiology:
Clinical Manifestations:
Left-sided heart failure
-pulmonary congestion, dyspnea, shortness of breath, cough, crackles, lower than
normal O2 saturation levels
Right-sided heart failure
-congestion of viscera and peripheral tissues, distended neck veins and bi-pedal
edema.
*Most common cause of right sided heart failure is left-sided heart failure
Assessment and Diagnostic tests:
- PE- s/sxs of left or right-sided heart failure
 - ECG- non-specific findings
- CXR-cardiomegaly and signs of congestion and effusion
- Echocardiogram
- Cardiac catheterization- for selected patients to detect presence of CAD
Management:

Nursing Diagnoses:
- Activity intolerance related to imbalance between O2 supply and demand
- Excess fluid volume related to excess fluid intake or sodium intake and retention
of fluid due to HF and its medical therapy
- Anxiety related to breathlessness and restlessness from inadequate oxygenation
- Powerlessness related to inability to perfoem role responsibilities because of
chronic illness and hospitalizations

2. Cardiogenic shock
- Occurs when the heart can not pump enough blood supply to the amount of oxygen
needed by the tissues.
Pathophysiology of cardiogenic shock

P
Clinical manifestations:
- Tissue hypoperfusion manifested as cerebral hypoxia, low BP, rapid weak pulse,
cold and clammy skin, increased crackles, hypoactive bowel sounds and
decreased urinary output.
Assesment and Diagnostics:
- PA catheter to measure left ventricular pressure and CO.
Mangement:
- correct underlying problems
- intubation and ventilation
- High concentration O2
- Inotropic agents e.g. dopamine, dobutamine, norepinephrine
- Vasodilators and diuretics as BP permits
- Use of intra-aortic balloon pump

VI. Hypertension
- It is defined as a systolic BP of 140 mmHg and diastolic BP of 90 mmHg over a
sustained period, taken in 2 separate occasions.

Primary hypertension
- also called essential, is hypertension without a known cause
Secondary hypertension
- also called the non-essential is a result of a known or definable cause
Classification:

Pathophysiology:

Clinical Manifestations:
- elevated BP
- Retinal changes and papilledema, LVH, pathologic changes in the kidney, stroke
or TIA, all of which are complications of hypertension.
Assessment and diagnostics:
- BP monitoring
- CBC, serum K, Ca, FBS, Creatinine, Lipid profile and 12-lead ECG
Management:
- Pharmacologic therapy involves use of beta-blockers, Ca channel blockers, alpha-
blockers, ACE inhibitors, diuretics.
- Lifestyle modifications involved diet, cessation of smoking and alcohol intake,
exercise, lose weight if over weight and minimize stress
Nursing Diagnoses
- Knowledge deficiency regarding treatment regimen and control of disease process
- Non compliance to therapeutic regimen related to side effects of prescribed therap
or financial constraints
• monitoring for complications should be emphasized

Hypertensive Crises;
2 types:
1. Hypertensive emergency- is a situation in which the BP must be lowered
immediately to halt or prevent damage to target organs. These are acute life-
threatening elevation in BP that requires prompt treatment. Medications of choice are
those with immediate effects such as IV venodilators.
2. Hypertensive urgency- on the other hand is a situation in which the BP must be
lowered in a few hours. These are usually managed with oral doses of fast-acting
agents such as loop-diuretics, beta-blockers and ACE inhibitors.

References:

o Richard S. Snell. Clinical Anatomy, an illustrated review with questions

and explanations. 2nd edition,1996
o Ong, Willie, Patacsil,Gregorio. Cardiology blue book. 3rd edition, 2004
o Bare, Brenda, Smeltzer, Suzanne. Brunner and Suddarth’s Medical-
Surgical nursing. 10th edition, 2004
o Guyton, A., Hall,J. Pocket companion to Textbook of Medical physiology.
10th edition2001
o Ferry, David. Basic Electrocardiography in Ten Days. McGraw-hill,
Singapore, 2001