Unit -3-

Management of patients with

cardiovascular disorders

By Hailemichael kindie ( BSc.,MSc.)

1
 Objective
• At the end of this session, the students will be able to
 Identify anatomy and physiology of cardiovascular
system
 Describe the function of CVS
 Assess cardiovascular system

 Diagnose common cardiovascular system disorders.

 Describe nursing intervention for common cardiac

system disorders.
2
 Anatomy and physiology of CVS

• Three Major Elements of CVS – Heart, Blood

Vessels, & Blood
• The heart is a hallow, muscular organ located in the
center of the thorax
• Weight ~300gm but depends on age, gender, body
weight, and physical exercises
 Layers of the heart
 It composed of three layers
Endocardium (inner layer)
Myocardium (middle layer)
Epicardium (exterior layer)
3
 Layers of the heart…
o The heart is encased with a thin fibrous sac called
pericardium
o Visceral pericardium(inner, fibrous tissue attach to
great vessels, diaphragm, sternum, and vertebral
column and supports the heart in the mediastinum)
parietal pericardium (outer)
o The space b/n these two layers known as
pericardial space which is filled with about 25 to 30
ml of fluid
o The fluid is important in lubrication the surface of
the heart and reduce friction during systole .
4
 Cont---

 Chambers of the heart

• There are 4 chambers
• 2 atrium and 2 ventricle
A. Receiving chambers
- Right atrium
- Left atrium
B. Pumping chambers
- Right ventricle
- Left ventricle

5
 Cont.…

 The right sides of the heart distributes a venous

blood (deoxygenated blood) to the lungs via the
pulmonary artery (pulmonary circulation) for
oxygenation
 The right atrium receives blood
 The superior venacava (head, neck, and upper
extremities )
 Inferior venacava (trunk, and lower extremities )
coronary sinus (coronary circulation) 6
 Cont---

• The left side of the heart distributes oxygenated

blood to the reminder of the body via aorta
(systemic circulation)
Ventricles are the chambers that eject blood from
veins
• atria are to receive the incoming blood from veins

7
 Cardiac valves

• Permit blood flow only in one direction through the

heart
• There are two types of valves i.e. atrio ventiricular
valves (AV) and semi lunar valves
 Atrio ventricular (AV) valves :
• Composed of tricuspid and bicuspid valves
• Separates the atria from the ventricles
• Tricuspid valve : Separates the right atrium from
right ventricle
• Bicuspid or mitrial valve: Separates the left atrium
from left ventricle
8
 Cont---

 Semi lunar valves

• Are situated b/n each ventricle and its

corresponding artery
• The valve b/n right ventricle and pulmonary artery
is called pulmonic valve
• The valve b/n left ventricle and aorta is called aortic
valve

9
 Coronary arteries

• Are vessels that supply blood to the heart muscle

• The left side of the heart by left coronary artery and right

by right coronary artery

The pumping action of the heart is accomplished by the

rhythmic contraction and relaxation of its muscular wall.

 A normal resting adult heart beats approximately

60 to 100 times per minute.

 Each ventricle ejects approximately 70 mL of blood per

beat and has an output of approximately 5 L per minute.

10
Blood Flow Through Heart

11
 Functions of the Heart

• Generating blood pressure

• Routing blood
– Heart separates pulmonary and systemic circulations

• Ensuring one-way blood flow

– Heart valves ensure one-way flow
• Regulating blood supply

– Changes in contraction rate and force match blood

delivery to changing metabolic needs
12
 Cardiac Physiology

CO = SV x HR
HR: parasympathetic and sympathetic tone
SV: preload, afterload, contractility
Preload:-Passive stretch of muscle prior to
contraction
Afterload:-Force opposing/stretching muscle after
contraction begins
Contractility:-Normal ability of the muscle to
contract at a given force for a given stretch,
independent of preload or afterload forces

13
 Assessment of cardiovascular system

Health history
 A complete health history is obtained during the initial
contact
 The family history

 Current weight
 Factors that relieve or aggravate

14
 Risk Factors for Heart Disease
Non-modifiable risk
factors
 Positive family history for
premature coronary artery
disease
 Increasing age
 Gender (three times more
often in men than in
premenopausal women)
 Race (higher incidence in
African Americans than in
Caucasians)
Modifiable risk factors
o Hyperlipidemia
o Hypertension
o Cigarette smoking
o Elevated blood glucose level
(ie, diabetes mellitus)
o Obesity
o Physical inactivity
o Use of oral contraceptives
15
 Symptoms related to cardiac illnesses
Classic symptoms:
 Chest pain
 Dyspnea
 Orthopnea is the d/c???
 PND (paroxismal nocturnal dyspnea) 3 min
 Palpitation
 Easy fatigability
 Dizziness (pre-syncope)
 Syncope
 Body swelling (edema)
16
 Physical examination

• General exam
• Arterial pulse & BP
• Venous exam
• Precordial exam

17
 General exam
• Anemia
• Cyanosis_bluish discoloration of skin and mucus
membrane
peripheral cyanosis: vasoconstriction, skin & lips
central : desaturation, mucus membrane of the
mouth
• Clubbing: CHD, IE
• Edema
• Chest wall deformity
• Prominent chest wall and neck venous collaterals
• Peripheral signs of IE 18
 Arterial pulse

• Palpate arterial pulses bilaterally

– Radial
– Bracheal
– Carotid

– Femoral
– Popliteal

– Posterior tibialis

– Dorsalis pedis
19
 Pulse….
 Rate
 Character
Normal 60-100bpm
-Pulse volume
 If <60 bradycardia
-Wave form
 If >100 tachycardia - Slowly rising_AS (aortic stenosis)
 Rhythm - Rapidly rising which collapses _AR
(aortic regargitation)
Normally regular
- Biphasic/bisferens _ AS & AR
 Irregularly irregular_ atrial
- Pulsus alternans_ sever LV
fibrillation(arrhythmia) failure
 Regularly irregular_VPC,  Symmetry
APC (ventricular or atrial
premature contraction)
- Radiofemoral delay_COA(
coarctaion of aorta)

Blood pressure /BP/ -------Reading assignment

20
 Jugular venous pressure(JVP)

• Reflects atrial pressure

• Assessed at right internal jugular vein
• Best measured at 30-45 degree
• Normal <4 cm above sternal angle

21
 Precordial exam
• Inspection
– Active versus quiet precordium
– Position of apical impulse_ outermost and lowest
impulse
– Precordial bulge

22
Precordium_palpation

23
 Purcussion
• Not routinely used in cardiac examination

• Palpation has replaced in estimation of cardiac size

• If apical impulse is not palpable percussion can be
used to delineate the boarder of the heart

24
Precordium_ auscultation

25
 Heart sounds

– S1_mitral valve & tricuspid valve closure

– S2_aortic valve &pulmonary valve closure
– Normally splits in inspiration
– Laud P2 pulmonary hypertension

– S3 and S4 cause gallop

• S3 occur due to rapid ventricular filling
– Physiologic in children and young adults
– Occurs in high output states like anemia, thyrotoxicosis, fever,
pregnancy, left ventricular failure

• S4 occurs due to vigorous atrial contraction

– Occurs in hypertrophied non compliant ventricle 26
 Auscultation_murmurs

• Caused by turbulent flow through the valves or

blood vessels
• Can be innocent or can show underlying cardiac
disease
• Diastolic murmurs are almost always pathologic
• Should be well characterized

27
Auscultation_ murmurs

28
 Common diagnostic procedures

Serum Cardiac Markers

• Must be determined in all patients suspected of acute MI
• Normal components of the myocytes get released in to
circulation when myocardium undergoes necrosis and
their serum level rise
Cardiac Enzyme Analysis: Because different enzymes move
into the blood at varying periods after MI, enzyme levels
should be tested in relation to the time of onset of chest
discomfort or other symptoms. 29
 Cont…

 Creatine kinase (CK) and co – enzyme of CK is the

most specific enzyme analyzed in acute MI, and it is
the first enzyme levels to rise.
 Lactic dehydrogenase:- analyzed in patients who
have delayed seeking medical attention, because
these blood levels rise and peak in 2 to 3 days,
much later than CK levels

30
 Blood Chemistry
Lipid profile
Cholesterol, triglycerides, and lipoproteins are
measured to evaluate a person’s risk for developing
atherosclerotic disease
Cholesterol and triglycerides are transported in the
blood by combining with protein molecules to form
lipoproteins.
The lipoproteins are referred to as low-density
lipoproteins (LDL) and high-density lipoproteins
(HDL).

31
 Cholesterol
Normal level, less than 200 mg/dl
A lipid required for hormone synthesis and cell
membrane formation.
It is found in large quantities in brain and nerve
tissue.
Two major sources: diet (animal products) and the
liver, where cholesterol is synthesized.
Elevated cholesterol levels are known to increase
the risk for CAD.
Factors that contribute to variations in cholesterol
levels include age, diet, exercise patterns, genetics,
menopause, tobacco use, and stress levels 32
 Low density lipoprotein

LDLs (normal level, less than 130 mg/dL)

Are the primary transporters of cholesterol and
triglycerides into the cell.
 Harmful effect of LDL is the deposition of these
substances in the walls of arteries.
 Elevated LDL levels are associated with a greater
incidence of CAD.
In people with known CAD or diabetes, the primary
goal for lipid management is reduction of LDL levels
to less than 100 mg/dL.

33
 High density lipoprotein
HDL (normal range in men, 35 to 65 mg/dL; in women, 35 to
85 mg/dL)
 Has a protective action.
 Transport cholesterol away from the tissue and cells of the
arterial wall to the liver for excretion.
 An inverse r/p b/n HDL levels and risk for CAD.
Factors that lower HDL levels include smoking, diabetes,
obesity, and physical inactivity.
In patients with CAD, a secondary goal of lipid management
is the increase of HDL levels to more than 40 mg/dL.
34
 Triglycerides

normal range, 40 to 150 mg/dL, composed of free

fatty acids and glycerol
 Are stored in the adipose tissue and are source of
energy.
Triglyceride levels increase after meals and are
affected by stress.
 Diabetes, alcohol use, and obesity can elevate
triglyceride levels.
Have a direct correlation with LDL and an inverse
one with HDL.
35
 CBC
• As a base line laboratory test

• To get supportive data in infectious cardiac

disorders
• Anaemia can be cause for CHF and occasionally
anaemia causes anginal pain
• Polycythemia may cause stasis and thrombosis,
which is one of the risk factors for Inflammatory
heart disease 36
 Renal Function Test (RFT)

• Proteinuria
• BUN
• Creatinine
 Renal function may be impaired if there is
decreased renal perfusion
Serum glucose
• The serum glucose level is important to monitor,
because many patients with cardiac disease also
have diabetes mellitus.
• Stressful situation , mobilization of endogenous
epinephrine results conversion of liver glycogen to
glucose . 37
 Chest X-ray

To determine:

• Cardiac size
• Contour and position of heart
• Contour of big vessels
• Correct position of cardiac catheters and
pacemakers

38
 Electrocardiography
• The electrocardiogram (ECG) is a graphic record of
the electrical activity of the heart and it is recorded
by the electrocardiograph
• Gold standard for diagnosis of cardiac arrhythmias
The ECG is obtained by placing disposable
electrodes in standard positions on the skin of the
chest wall and extremities.
The heart’s electrical impulses are recorded as a
tracing on special graph paper.

39
 Echocardiography

Echocardiography is a noninvasive ultrasound test

that is used to examine the size, shape, and motion
of cardiac structures.
 It is a particularly useful tool for diagnosing
 Pericardial effusions
 Determining the etiology of heart murmurs
 Evaluating the function of prosthetic heart valves
 Determining chamber size
 Evaluating ventricular wall motion.

40
 Magnetic Resonance Imaging

Non invasive painless technique used to examine

both the physiological and anatomical properties of
the heart .
Use powerful magnetic field and computer generated
picture to imagine the heart and great vessel .
Its valuable in diagnosing disease of the aorta ,heart
muscle , pericardiun ,as well as congenital heart
lesion.
41
 Blood tests
Blood tests Normal values
Hemoglobin (Hgb) male :14.5 – 16 gm/100ml of blood

female: 13-15.5 gm/100ml of blood

Hematocrit (Hct) Male: 42-50 u/100ml of blood

Female : 40-48 u/100ml
ESR Male: 0-20/hr
Female: 0-15/hr
WBCs 5000-11000mm3
RBCs 4.2 -6.1 million
Platelets 150,000-450,000
Coagulation time 5-15 minutes
Blood glucose 80-120mg/dl 42
 Disorders conduction of the heart
Normal electrical impulse
• Starts sinus (SA) node, near the superior vena cava in
the right atrium quickly travels atrioventricular
(AV)
( atrial contraction) AV node
slows the electrical impulse
• (allows ventricle to relax)
the bundle of His to
the RT and LT ventricle muscles
• ( cause mechanical contraction is systole and this
electrical stimulation is depolirazation ) the
cell then relax ( repolarization ) 43
 ECG
• The ECG is composed of waveforms (P wave,
QRS complex, T wave, and possibly a U wave) and
segments and intervals (PR interval, ST segment, and
the QT interval)

44
 Reading assignment
Read the details of ECG Waves and segments
Small square large square

45
 Estimate heart rate by ECG
A. Ventricular and atrial heart rate determination with a
regular rhythm:
 1500 divided by the number of small boxes between
two P waves (atrial rate) or between two R waves
(ventricular rate). Or 300dived by large square
 In this example, there are 25 small boxes between
both the R waves and the P waves, so the heart rate
is 60 beats per minute.
B. Heart rate determination if the rhythm is irregular.
Thereare approximately seven RR intervals in 6
seconds, so there are about 70 RR intervals in 60
seconds (7 x10 =70 mini.).
46
 Disorders conduction of the heart

Arrhythmias/ dysarthymias

Definition : Arrhythmias/ dysarthymias (define ??2 minute)

 Is a disorder of the heart beat I.e. disturbance of the rate ,
rhythm or both
 Dysartymia is named according to the site of origin of
impulse , mechanism and conduction involved.

E.g,. disarrtyhimia that originate in the SA node and slow rate

is called sinus brady cardia
• Classification : It can be sinus, atrial ventricular, junctional
47
 Cont---

Sinus arrhythmia
Is an irregular heartbeat that’s either too fast or too slow.
A . Sinus bradycardia
• has a normal sinus rhythm, but the SA node fires at a rate less than
60 beats/minute and is referred to as absolute bradycardia.
Common causes
 Physiologic bradycardia
-Laborers and trained athletes
-Emotional states leading to syncope
-Carotid sinus pressure, eyeball pressure,

- Intracranial --pressure
- Sleep 48
 Cont….
• Systemic disease
-Obstructive jaundice
-Obstructive diseases of the intestine, kidney or
bladder
-During convalescence after some diseases -marked
by fever(e.g. influenza )
-Myxedema (hypothyroidism)
-Myocardial infarction(inferior wall or atrial
infarction)
-High intracranial pressure

49
 Cont…

c/ms
• Shortness of breath, Fatigue , Dizziness/ fainting
• Treatments
– Identification and correction of underlying causes
– Treatment consists of administration of atropine
given as IV (an anticholinergic drug) for the patient
with symptoms. It blocks vagal stimulation and
cause, thus allowing a normal rate to occur .
– catecholamine
– Occasionally oxygen supplementation may be
required
50
 Cont…

b. Sinus tachycardia
has a normal sinus rhythm, but the SA node fires at a rate
greater than 100 beats/minute as a result of vagal
inhibition or sympathetic stimulation.
Factors associated with Sinus Tachycardia:
Physiologic : Exercise , Strong emotion , Pain and
Anxiety states
Pathologic : Fever, Hyperthyroidism, Hemorrhage ,
Shock , Anemia , Infection Congestive heart
failure ,Myocarditis and Hypoxia
Other factors: Drugs, Epinephrine ,Atropine,
Tea ,Coffee , Alcohol and Tobacco 51
 Cont---

• Angina may result from sinus tachycardia due to the increased

myocardial oxygen consumption that is associated with an
increased HR.
• All aspects of sinus tachy cardia is the same as those of normal
sinus rhythm except the rate i.e. rate 100- 180b/m
 Rx
• Rx of the underlying cause
• Digoxin is given to control rate of impulse formation and
improves heart failure
• Propranolol is an alternative to digoxin 52
 CONT…
Ventricular Arrhythmias
a. Ventricular Tachycardia
•Ventricular tachycardia is a condition in which the SA node no longer
controls the beating of the ventricles.
Cause : coronary artery disease
c/m: fast heartbeat, skipping beats., severe shortness of breath,
dizziness, or fainting (syncope),
•Its an emergency if it is some times unresponsive and pulseless
Management
•Treat underline cause
•Drugs: Amiodarone drug of choice
•CPR
•Defibrillation( unconscious and without pulse)
53
 b. Ventricular Fibrillation
• Rapid but disorganized ventricular rhythm that
causes ineffective quivering of the ventricles
and with no atrial activity
• The irregularity is both in force and in rhythm
• There is no cardiac output and therefore there is
no cerebral, myocardial, or systemic perfusion.
• Because of this reason, this rhythm is fatal if
not successfully terminated within 3-5 minutes

54
Causes
- Acute MI - Digoxin or quinine intoxication
- Thyrotoxicosis - Electrical shock
- RHD - hypokalemia
Clinical Manifestation
• Palpitation & syncope are most common
• No pulse is felt in the peripheral arteries and BP is
unrecordable
• On auscultation of the precordium, no heart sound is
heard
• Respiration is absent
55
 Treatment

• Immediate defibrillation: use of electrical

stimulation to restore a chaotic heartbeat to a
rhythmical pattern.
• Digitalization and anticoagulation
• Supportive: bed rest, sedation of the patient,
and oxygen supplementation

56
 Pre-excitation syndrome

 Cardiac ventricles are activated too early

Abnormal electrical connection or accessory
pathway between or within the cardiac chambers
Cause : congenital abnormal accessory pass
• C/M: not cause any symptoms but may lead to
palpitations caused by abnormal heart rhythms
• Diagnosed: using ECG,
• Management : verapamil, digitals, catecholamine to
reduce refractory period

57
 cont…
a. atrial arrhythmias( Supraventricular Arrhythmias)

Begin in the areas above the heart’s lower

chambers, (the atria)
Not as serious as ventricular arrhythmias.
Sometimes, they do not even require treatment.
Cause : Can be caused by including tobacco,
alcohol, caffeine, and cough and cold medicines.
Also caused by rheumatic heart disease or an
overactive thyroid gland (hyperthyroidism).
c/m: shortness of breath, heart palpitations, chest
tightness, and a very fast pulse
58
 Cont…
b. Atrial Fibrillation
• The atrial rate is 400-600/min but most impulses are
blocked at the AV node and the ventricular response
is completely irregular (irregularly irregular)
ranging from 80-180/min in the untreated cases
• Causes:
• Rapid, disorganized, and weak twitching of atrial
muscle
• The commonest cause of chorionic arrhythmias

59
 Cont…
• Occurs most commonly in elderly patients
with systemic hypertension
• Rheumatic heart disease is the most common
cause.
• Other causes include dilated cardiomyopathy,
mitral valve prolapse, atrial septal defect, IHD,
HTN, and chronic constrictive pericarditis
• Thyrotoxicosis, excessive alcohol intake
and/or alcohol withdrawal, and pulmonary
embolism can cause this arrhythmia

60
 Cont…
Clinical Presentation

• palpitation & chest discomfort

• Malaise, fatigue, and syncope are common

• Patients may develop CHF

• Commonest complication is pulmonary embolism

61
 CONT…
Treatment

• Remove underling condition

• Drug treatment: Propranolol 10-40mg PO tid,
calcium channel blockers like verapamil, or digoxin
• Cardioversion: (the use of an electric shock to
convert a dangerously rapid, fluttering, and
ineffective heartbeat to its normal rhythm)
• Prophylactic: warfarin or aspirin are given to
prevent embolic events
• Cardiopulmonary Resuscitation
• Defibrillation: restoring the heartbeat
62
 Atrioventricular (AV) block

Are group of disorders which are categorized

as:

1. 1st degree AV block

2. 2nd degree AV block or partial heart block

3. 3rd degree AV block complete heart block

63
 1 st
degree AV block
• All impulses from SA node are conducted but
atrioventricular conduction is prolonged or
delayed i.e. Conduction is slow.
• ECG reveals prolonged PR interval greater
than 0.21 sec.

64
 2nd degree AV block

• Some atrial impulses are blocked i.e. Some atrial

impulses fail to conduct the ventricle
• Type 1: occurs when there is a repeating pattern in
which all but one of a series of atrial impulses are
conducted through the AV node into the ventricles (eg,
every four of five atrial impulses are conducted).Each
atrial impulse takes a longer time for conduction
than the one before, until one impulse is fully blocked.
• Type 2: occurs when only some of the atrial impulses
are conducted through the AV node in to the ventricles

65
 3rd degree AV block
• No atrial impulse propagates to the ventricles
• The ventricles are depolarized independently by a
second pacemaker
• May predispose to cardiac arrest causing ventricular
tachycardia, ventricular fibrillation or asystole.
• It is regarded as a dangerous rhythm
• ECG reveals ventricular QRS complexes are
independent of atrial P-waves
• PP and RR intervals are regular but they are not
equal to each other

66
 Treatment of AV-blocks

• Asymptomatic 1st degree & 2nd degree type 1 do not need

therapy
• In symptomatic 1st & 2nd degree AV block and all patients
with 2nd degree type 2 block patients, the nurse administers
oxygen and atropine as prescribed

• Acute termination of the AV blocks can be achieved with

IV administration of atropine 0.5-2mg

• Other antiarrhythmic drugs that may be used include

amiodarone , lidocaine , and magnesium sulfate

67
 Coronary Artery Diseases/CAD/

 Arthrosclerosis and arteriosclerosis

 Angina pectoris

 Myocardial infraction

68
 Arteriosclerosis and atherosclerosis

Differentiate Arteriosclerosis and atherosclerosis? 2min

Arteriosclerosis:- is the most common disease of the arteries
(hardening of the arteries).
 It is a diffuse process whereby the muscle fibers and the
endothelial lining of the walls of small arteries and
arterioles become thickened.

69
 Atherosclerosis
 The accumulation of lipids, calcium, blood
components, carbohydrates, and fibrous tissue on
the intimal layer of the artery.
These are referred to as atheromas/plaques.
Affects the intima of the large and medium sized
arteries.
Because atherosclerosis is a generalized disease of
the arteries, when it is present in the extremities,
atherosclerosis is usually present elsewhere in the
body.

70
71
 Pathophysiology

The most common direct results of atherosclerosis

in arteries include: narrowing (stenosis) of the
lumen, obstruction by thrombosis, aneurysm,
ulceration, and rupture.
Indirect results: subsequent fibrosis of the organs
that the sclerotic arteries supply with blood.
All actively functioning tissue cells require an
abundant supply of nutrients and oxygen and are
sensitive to any reduction in the supply of these
nutrients.
72
 Cont…

If such reductions are severe and permanent, the cells

undergo ischemic necrosis and are replaced by fibrous
tissue, which requires much less blood flow.
Atherosclerosis can develop at any point in the body,
but certain sites are more vulnerable, typically
bifurcation or branch areas.
 There is no single cause or mechanism for the
development of atherosclerosis; rather, multiple
processes may be involved. 73
 Cont---

• Blood clot can partially or completely block the

blood flow.
• when coronary arteries are narrowed or blocked
oxygen rich blood can’t reach to the heart muscle
• This can cause angina and heart attack.
• Over time CAD can weaken the heart muscle and
lead to heart failure and arrhythmias.

74
Fig. A. shows a normal artery with normal blood flow,
Fig. B. shows an artery with plaque buildup.
75
 Cont..

Phatophysiology
• accumulation of lipids, or fatty substances →
narrowing of arterial lumen → obstruction of blood
to myocardium → inadequate blood supply to
myocardial cells → angina and or cell damage (MI)

Epidemiology
• CAD is the most common cause of death
• Incidence increases when age increases
• The prevalence is ~30% in developed and ~ 3% in
developing countries
76
 Risk factors of CAD
Non modifiable Modifiable risk factors
risk factors • High blood cholesterol/
• Family history hyper lipidimia
• Cigarette smoking and
• Age
alcoholism
• Gender • Elevated BP/ HPN
• Race • Elevated blood glucose
• Pre existing • Obesity /over weight
• Physical inactivity
coronary heart
• Stress etc
diseases

77
 Angina Pectoris

• Is a clinical syndrome characterized by episodes of

pain or feeling of pressure in the anterior chest.
 Causes:
• The cause is usually insufficient coronary blood flow.
• The insufficient flow results in a decreased oxygen
supply to meet an increased myocardial demand for
oxygen in response to physical exertion or emotional
stress.
• In other words, the need for oxygen exceeds the
supply.

78
 Cont..

• Angina is usually caused by atherosclerotic disease

and or significant obstruction of a major coronary
artery.
• The severity of angina is based on the precipitating
activity and its effect on the activities of daily living.

79
 Precipitating factor
Physical exertion(increases myocardial oxygen
demand)
Exposure to cold (cause vasoconstriction and an
elevated BP, with increased oxygen demand)
Eating a heavy meal (increases the blood flow to
the mesenteric area for digestion, thereby reducing
the blood supply available to the heart muscle
Stress/emotion-provoking situation (release of
adrenaline and increasing BP),which accelerate
heart rate and increase myocardial workload.

80
 Types of angina

Stable angina: predictable and consistent pain that

occurs on exertion and relieved by rest
Unstable angina:- symptoms occur more frequently
and last longer than stable angina
- The threshold for pain is lower, and pain may occur at
rest
Intractable or refractory angina: severe
incapacitating chest pain
Variant angina: pain at rest with reversible ST-
segment elevation (stent thrombosis)
Silent ischemia: objective evidence of ischemia ECG
changes), but patient reports no symptoms 81
 Clinical manifestation
Pain varying in severity from a feeling of
indigestion to a choking or heavy sensation in the
upper chest that ranges from discomfort to
agonizing pain .
Pain is often felt deep in the chest behind the
upper/middle third of the sternum (retrosternal)
Accompanied by severe apprehension and a feeling
of impending death
Typically, the pain or discomfort is poorly localized
and may radiate to the neck, jaw, shoulders, and
inner aspects of the upper arms, usually the left
arm. 82
 Cont…
The patient with DM may not have severe pain with
angina
- the neuropathy that accompanies diabetes can
interfere with neuroreceptors, dulling the patient’s
perception of pain.
 A feeling of weakness/numbness in the arms,
wrists, and hands may accompany the pain
Shortness of breath, pallor, diaphoresis,
dizziness/lightheadedness, nausea and vomiting
 Anxiety may accompany angina.
 An important characteristic of angina is that it
subsides with rest or nitroglycerin. 83
 Assessment and Diagnostic Findings
Evaluating the clinical manifestations of ischemia and the
patient’s history
Echocardiograph
ECG
C-reactive protein(CRP) measure inflammation of
vascular endothelium
An elevated blood level of homocysteine (an intermediary
amino acid formed by the conversion of methionine to
cysteine ) and an amino acid
Medical Management
The objectives of management:-
 To decrease the oxygen demand of the myocardium
 To increase the oxygen supply. 84
 Pharmacologic therapy

A. Nitroglycerin:-remain the mainstay for treatment of angina

pectoris
 Vasoactive agent reduces myocardial oxygen consumption,
which decreases ischemia and relieves pain
 Dilates primarily the veins and, in higher doses, also dilates
the arteries
 It helps to increase coronary blood flow by preventing
vasospasm and increasing perfusion through the collateral
vessels.
 It usually is not given if the systolic blood pressure is 90 mm
Hg or less.
 Administer based on the patients symptom while avoiding the
side effect such as hypotension. 85
 Cont…

B. Beta-blockers:- reduce the incidence of recurrent

angina, infarction,& cardiac mortality.
Propranol ,metoprolol,and Atenolol .
Decreased HR, slow conduction of impulse through
the heart, decrease BP and myocardial contractility .
After administering ECG, HR and BP must be closely
monitored
Diabetic patient must be monitored closely
The dose can be titrated to achieve a resting heart
rate of 50 to 60 beats per minute
 Contraindicated in patients with significant
pulmonary constrictive diseases (asthma) 86
 Cont…

Patients taking beta-blockers are cautioned not to

stop taking them abruptly, because angina may
worsen and MI may develop.
C. Calcium Channel Blocking Agents.
 Decrease the workload of the heart
Decrease SA node automaticity & Av node
conductivity
Decrease HR and contraction
 Relax the blood vessels, causing a decrease in blood
pressure and an increase in CA perfusion
 Increase myocardial oxygen supply by dilating
smooth muscle wall of the coronary arterioles 87
 Cont…
Decrease myocardial oxygen demand by reducing systemic
arterial pressure and the workload of the left ventricle.
D. Antiplatelets:- administered to prevent platelet
aggregation, which impedes blood flow.
Aspirin: prevents platelet activation and reduces the
incidence of MI &death in patients with CAD.
 One of the most important medications in the treatment
of CAD
Patients should be advised to continue aspirin
 Aspirin may cause gastrointestinal upset and bleeding,
treatment of Helicobacter pylori and the use of H2-blockers
should be considered to allow continued aspirin therapy.
88
 Cont…

E. Anticoagulants (Heparin)
 Prevents the formation of new blood clots
Use of heparin alone in treating patients with
unstable angina reduces the occurrence of MI.
F. Oxygen
 Usually initiated at the onset of chest pain in an
attempt to increase amount of oxygen delivered to
the myocardium and to decrease pain
The therapeutic effectiveness of oxygen is
determined by observing the rate and rhythm of
respirations.
89
 Myocardial infarction (MI)

• MI is the death of a portion of heart muscle in area

where there is sudden loss of blood supply due to
occlusion of a major coronary artery or one of its
branches.
• MI some times called a heart attack or coronary
thrombosis.
• Because unstable angina and acute MI are
considered to be the same process but different
points along a continuum, the term acute coronary
syndrome (ACS) may be used for these diagnoses.

90
 Cont…

Causes
• Like unstable angina, MI is usually caused by
reduced blood flow in a coronary artery
 This may be due to
• Critical narrowing of a coronry artery due to
atherosclerosis or
• Complete occlusion an artery due to embolus
or thrombus.
• vasospasm (sudden constriction or narrowing of
a coronary artery )
91
 Cont…

Other causes
• decreased oxygen supply (e.g. from acute
blood loss, anemia, or low blood pressure)and
• increased demand for oxygen (eg, from a
rapid heart rate, thyrotoxicosis, or ingestion of
cocaine).
• N.B. In each case, a profound imbalance exists
between myocardial oxygen supply and
demand.

92
 Pathophysiology

• Thrombosis => blocks a blood flow to a part of

the heart => tissue ischemia I.e. w/n the blood
flow is acutely reduced by 80-90% => cellular
damage and necrosis (ischemia lasting 30-45
minutes ) => impaired ability of cardiac muscle
to contract and pump blood.
• N.B. 10 % reduction in serum cholesterol/LDL
leads to 30% reduction in CAD.

93
 Cont…
 Epidemiology
• MI is common in men than women at all ages
especially male age > 40 and has history of
atherosclerosis and hypertension
• But also common in women who take oral
contraceptives, smoking and postmenopausal
women i.e. pre menopausal women appear to be
protected from atherosclerosis
• The average incidence of MI for those age b/n 30-
69 years is about 600 per 100000 men and 200 per
100,000 for women
94
 Clinical Manifestations
• Chest pain that occurs suddenly and continues
despite rest and medication is the presenting
symptom in most patients with an MI.
• The pain may be radiated to shoulders arms neck
and jaw.
 Unlike the pain of angina pains of MI
• begins spontaneously/not after effort or emotional
upset
• Persists for hours or days
• Not relived by neither by rest nor by nitroglycerin.

95
 Cont…

 The pain is acompained by

• Shortness of breath - pallor
• Nausea and vomiting - diaphoresis
• Dizziness or light headness
• Patients may also be anxious and restless.
• They may have cool, pale, and moist skin.
• Their heart rate and respiratory rate may be
faster than normal.

96
97
 Diagnosis
• History and c/ms
• ECG
• Laboratory tests/serum enzymes- creatine kinase
(CK), with evaluation of isoenzymes (CK-MB)(CK
myoglobin) and lactic dehydrogenase (LDH) levels.
• CK-MB is a cardiac specific isoenzmes that is found
only in cardiac cells and rises only w/n there is a
damage to cardiac cells
• Is the most specific and sensitive indicator for the
diagnosis of MI. is always increased in acute MI (AMI).

98
 Cont…
 Lactase dehydrogenase /LDH and its iso enzymes
• Is not a reliable indicator of acute MI b/c it peaks later
and is elevated longer than other cardiac enzymes.
• LDH is useful in diagnosing MI In patients who may
have sustained AMI but have delayed admission to
the hospital
 Time of cardiac enzymes following AMI
• CK-MB: onset (2-4hrs) peak 12-20 hrs) return to
normal (48-72hrs)
• LDH: onset (24hrs) peak (48-72 hrs) return to normal
(7-10days)
99
 Mgt
 Goal

• Minimize myocardial damage

• Reduce complication
Minimizing myocardial damage is accomplished
by reducing myocardial oxygen demand and
increasing oxygen supply with medications,
oxygen administration, and bed rest
100
 Cont…

 Drug mgt
• Vasodilators /specifically nitrates i.e. IV nitroglycerin
• Anti coagulants to reduce probability of thrombus.
• Beta blockers
• Thrombolytic (e.g. streptokinase, antistreplase ) to
dissolve any thrombus
• Analgesics for pain (motrpine sulfate)
• Oxygen (to increase oxygen supply
• Bed rest (to reduce oxygen demand)

101
 Inflammatory and infectious cardiac diseases
• Rheumatic fever
• Endocarditis
• Myocarditis Reading assignment
• Pericarditis

102
 Rheumatic fever
 Is an inflammatory diseases related to streptococcal
infection affecting mostly the heart and joints.
• The major complication of RF is heart damage
especially scaring of mitrial valve.
• The heart damage secondary to RF is termed as
Rheumatic Heart Diseases/RHD
• It occurs mostly in children.

103
 Cont---
 Etiology-
• Group A beta hemolytic streptococcus.
• Usually follows infection of the upper
respiratory system infection with streptococci.
(2-6weeks )
• Pathogenesis: is due to abnormal immune
response to bacterial infection with group A
streptococcus.

104
 Cont---
 Antibodies produced against the streptococci
antigen cross react and cause immunologic
damage to the:
• Heart valves
• Heart muscle  
• Pericardium
• Joint synovium ( arthritis)
• Nervous tissue (chorea)
• Subcutaneous tissue (subcutaneous nodule)
105
 C/ms
 Carditis
• Occurs in 40-80% of patients.
• It presents as breathlessness, fever and cough.
• Tachycardia, murmur and cardiac enlargement.
• In severe cases there are signs of heart failure

106
 Cont---
  Arthritis : painful swelling in one or more
main joints.
• It is the commonest manifestation.
• Is polyarthralgia and involves several larger
joints (knee, ankle, elbow and wrist).
• The affected joint is swollen, red, warm and
exquisitely tender. 
• Those signs disappear within 24 hours if anti-
inflammatory drug is given.

107
 Cont---

 Sydenham chorea : purposeless jerky

repetitive movements of muscle( particularly involving
hands and face) and possible altered speech.
• CNS involvement may manifest late after the initial
infection (6  months or more)
 Erythema marginatum: is non-pruritic a rash over the
chest and trunk.
• Occurs in 10-20 % of children.
• It starts as red macules which fade in the center but
remain red at the edges.
• It disappears in hrs or days
108
 Cont---
 Subcutaneous nodules :
• Small painless nodules which occur more
frequently on the extensor surface of large joints
(elbow, wrist & knee) and spine.
 4 minor criteria
 Arthralgia
 Fever
 Elevated acute phase reactants [erythrocyte
sedimentation rate (ESR), C-reactive protein (CRP)]
 Prolonged PR interval 109
 Diagnostic evaluation
• Evidence of a systemic illness (non- specific):
Leucocytosis /increased WBC, Raised ESR.
• Evidence of preceding streptococcal infection
(specific):
 Throat swab culture, Group A B-hemolytic
streptococcus, Anti streptolysine o antibodies
elevated titers.
• Evidence of carditis: Chest radiograph
( Cardiomegaly, Pulmonary congestion) , ECG
(Features of pericarditis).
110
 Diagnosis
• No single clinical feature or test is diagnostic of
acute rheumatic fever.
• Modified Jones criteria for the diagnosis of
rheumatic fever: (5 major and 4 minor criteria's)
• 1 major , 1 minor c/ms plus evidence of preceding
streptococcal infection (+ throat culture) OR
• Chorea plus evidence of preceding streptococcal
infection

111
 Management
 Objectives
• Eradication of hemolytic streptococci
• Prevention of the recurrence
• Prevention of permanent cardiac damage
• Prevention of symptoms

N.B. except carditis all manifestation subside

w/o residual effect.

112
 Drug mgt

 Antistreptococcal therapy:
• Ten- days’ course of Amoxicillin or a single IM injection of
Benzanthin penicillin. (50,000IU/kg/day) or for 1wk
• Aspirin – usually relieves symptoms of arthritis rapidly. Starting
60-100mg/kg/ body weight per day into 4-6 divided doses for 4
weeks (arthritis w/o carditis)
• Anti inflammatory drugs- to control the clinical features:
 Corticosteroids: Prednisolon 2mg/kg/day for 2-4 weeks . These
produce more rapid symptomatic relief than aspirin, and are
indicated in cases with carditis or severe arthritis.
• Digoxin and diuretic for the heart failure
• Chorea: Chlorpromazine and Phenobarbital (usually recovered
with out Rx)
113
 Cont---

 Nursing management
• Bed rest and supportive therapy.
• The bed rest should be continued for 2-6 weeks
after the ESR and temperature have returned to
normal.

114
 Prevention

• Primary prevention early (with in 1 week): Treatment of

streptococcal pharyngitis to prevent an initial attack of acute
rheumatic fever. (Amoxicillin for 10 days or B.P single IM
injection.
• Secondary prevention: Prevent recurrence so as to reduce the
damage to heart valves and the risk of chronic rheumatic heat
disease.
• Secondary prophylaxis with monthly single IM benzatine
penicillin or daily oral penicillin is recommended for all people
with a history of ARF or RHD.
• Prophylaxis should continue for at least 10 years from the last
episode of acute thematic fever

115
 Cont---

 Complications
Chronic valvular heart disease.
• Mitral valve
• Aortic valve
• Tricuspid valve
• Pulmonary valve
Intractable heart failure.
Serious dysrhythmia.
 Embolism.
116
 Valvular heart disease

Assignment
Mitral valve
 MVP (mitral valve prolapse )
 MR (mitral regurgitation)
 MS ( mitral stenosis )
 Aortic disorder
• AR (aortic regurgitation
• AS (aortic stenosis )
 Tricuspid disorder
TR ( tricuspid regurgitation)
117
 Heart Disease
• Heart failure
• Acute pulmonary edema
• Cardiac arrest assignment reading
• Cardiomyopathy

118
 Heart Disease

Heart failure
• Is the inability of the heart to pump sufficient
blood to meet the needs of the tissues for
oxygen and nutrients.
• HF often referred to as congestive heart
failure (CHF) b/c many of pt with HF manifests
pulmonary or systemic congestion.

119
 Phatho -physiology
• For number of reasons cardiac out put is
inadequate to meet oxygen and nutrient
requirements of vital organs
• Decrease Stroke volume and CO leading to
the following compensatory mechanisms
A) Stimulate sympathetic system reflex =
increase release of catecholamine's from
adrenal medulla leading to tachy cardia

120
 Cont---
B) Increase activity of rennin- angotensin – aldostrone
system leading to vasoconstriction of blood vessels ,
sodium and water retention
C) Increase release of ADH (vasopressin) from posterior
pituitary gland leading to vasoconstriction and
decrease diuresis =>This lead to more edema
D) Decrease renal blood flow due to vasoconstriction
and congestion of renal vessels leads to increase the
release of vasodilators prostaglandin as a
compensatory mechanisms to maintain renal blood
flow and renal function
121
 Cont---
• Cardiac out put /CO decrease further as the
compensatory mechanism fail , impairment of
calcium influx => decrease myocardial
contractility => decrease CO => decrease
blood supply => increase over load of heart =>
heart failure.

122
123
124
 Etiology
It can be caused by either
• Decrease cardiac out put (CO)
• Increase metabolic demand OR
• Decrease contractility w/c contributes to
increase heart load

125
 Etiology …
Risk factors

• H- Hypertension (systemic)

E- Endocarditis (infections)

A- Anemia

R- Rheumatic fever and myocarditis

T- Thyrotoxicosis and pregnancy

F- Fever (infections)

A- Arrhythmia

I- infarction (myocardial)

L- Lung infection

E- Embolism (pulmonary)

S- Stress (emotional, physical, environment, dietary, fluid excess)

126
 Cont---
 Types
• It can be classified as right side and left side
heart failure
A) Right side heart failure
• The right side of the heart unable to empty
its blood volume adequately
• The right ventricle unable to pump the blood
coming from the lower and upper body .

127
 Cont---
• When the right ventricle fails, congestion of
the viscera and the peripheral tissues
predominates.
• Superior vein = distention of neck vein
• Inferior vein = congestion of vein of the liver,
GI vein etc

128
 S/sx of right side HF
• edema of the lower extremities (dependent
edema),
• hepatomegaly (enlargement of the liver),
• Distended jugular veins/JVD,
• ascites (accumulation of fluid in the peritoneal
cavity),
• anorexia and nausea, and paradoxically,
weight gain due to retention of fluid.

129
Fig. JVD

130
 left side heart failure
• Left ventricle unable to pump the blood
coming from the lungs=> back flow of the
blood => increase pressure in the lungs and
pulmonary vein => congestion and rupture of
vein around the lung alveoli => fluid
accumulation in the lung tissue.

131
 Clinical manifestations
- Cough - Paroximal nocturnal dyspnea
- Orthopenea - Tachypnea
- Dyspnea - Cerebral hypoxia
- Anxiety and restless due to dyspnea
S/Sx can present in both cases
• Tachycardia
• Heart gallop
• Cardio megally
• weakness
132
• Symptom classification/NYHA grading system

133
 STAGES

• Stage A: Patients at high risk for developing HF in

the future but no functional or structural heart
disorder.
• Stage B: a structural heart disorder but no
symptoms at any stage.
• Stage C: previous or current symptoms of heart
failure in the context of an underlying structural
heart problem, but managed with medical
treatment.
• Stage D: advanced disease requiring hospital-based
support, a heart transplant or palliative care
134
 Dx
• C/m
• Physical examination
• X-ray
• ECG

135
 Major and minor criteria's for CHF
 Major Criteria  Minor Criteria
• Cardiomegally • Edema of extremities
• Gallop/murmur • Tachycardia
• Neck vein distention • Cough
• Acute pulmonary • Hepatomegally
edema
• Nocturnal dyspnea
N.B. to establish a clinical Dx of CHF
at least 1 major and 2 minor criteria
is required
136
 Mgt

 Objective
• To increase the efficiency of myocardial
contraction
• To decrease excessive accumulation of water
and Na
• To remove the precipitating factors
• To reduce workload on the heart

137
 Pharmacological therapy
I) Digitalis /cardiac glycosides e.g. Digoxine and
digitoxine
• To increase myocardial contractility (main action)
it has also a diuretic effect
II) Diuretics : are effective alone in mild cases of
CHF and in combination with digitalis in sever
cases
• The role of diuretics in CHF is to promote
excretion of Na and water => relives edema =>
reduction of heart load
138
 The following diuretics can be used
A) Thiazide diuretics e.g. chlorothiazide ,
benzthiazide and hydrochlorothiazide
B) Potassium sparing diuretics: e.g.
spironolactone (aldactone)
C) Loop diuretics e.g. furosemide /Lasix
N.B. prolonged use of diuretics can cause
hyponatrimia, hypokalimia, magnesimia

139
 Cont---
III) vasodilators: to promote peripheral
vasoconstriction e.g. sodium nitroprusside,
nitroglycerine, hydralizine
IV) angotensin converting enzyme/ACE
inhibitors e.g. captopril, enalapril
V) positive intropic agents E.g. dobutamine ,
amrinone,
VI) KCL

140
 Vascular disorders
 Arteries disorder
 Hypertension
Veins disorder
 Phlebothromboisis
 Thrombophlebitis
 Deep vein thrombosis
 Varicose vein

141
 Hypertension /HPN

• Is a persistent increase in the level of blood

pressure ≥140/90 mm Hg.

Factors Determining Blood Pressure

• Cardiac output (CO)
• Peripheral vascular resistance (PVR)
• Blood viscosity
• Circulating blood volume
• SNS overstimulation /leading to vasoconstriction/
• Increases in hormones (i.e., aldosterone)
• Changes in kidney function 142
 Cont---
 BP = CO X PR (peripheral resistance)
 CO = SV X HR
So; High blood pressure, known as
hypertension, can result from a change in
cardiac output, a change in peripheral
resistance, or both.

143
 Phatophysiology

• It is understood that hypertension is a

multifactorial condition
• Vasomotor center w/c is situated in the
medulla of the brain controls the constriction
and relaxation of blood vessels
• Due to variety of causes e.g. fear, anxiety,
emotion, stress etc there is an increased
sympathetic nervous system activity = leading
to stimulation of adrenal gland.

144
 Cont-----

1) Adrenal medulla secretes epinephrine =>

vasoconstriction => reduce blood flow to the
kidney => releasing rennin => formation of
angotensin I => ACEZ => Angotensin II (potent
vasoconstrictor and also causes Na and water
retention ) = HPN
2) Adrenal cortex => secretes cortisol and other
steroids => enhance vasoconstriction /causes
Na and water to be retained by the kidney
tubules and also reduce blood flow to the
kidney => increased intravascular volume =>
HPN 145
 Classification

Category SBP DBP Follow up

Optimal <120 < 80 Recheck 2 yrs
Normal <130 < 85 Recheck 2 yrs
High normal 130- 139 <85-89 Recheck 1yr

Hypertension SBP DBP Follow up

Stage 1 140 -159 90 – 99 Confirm with in
(Mild HPN) months
Stage 2 >160 > 110 Evaluate within 1
(Moderate) month

146
 Types of HPN
• HPN can be classified as primary and secondary
• Primary /idiopathic
- 90% and 95%
• Secondary /with the identifiable causes
- the remaining 5-10%
 The real causes of primary HPN is unknown but risk
factors for developing primary HPN are
- Emotional disturbance (increase sympathetic Ns
activity)
- Over weight
- Excessive alcohol intake

147
 Cont---
- Over stimulation with coffee and stimulatory drugs =
increased catecholamine release
- Smoking = nicotine causes vasoconstriction
- Genetic /family history/
- Age
- Sex
- Excessive Na intake
- Elevated serum lipids
- Lack of exercise and etc

148
 Causes of secondary HPN
• Reno-vascular narrowing= renal diseases
• Certain drugs e.g. catecholamine's /NSAIDS ,
OCPs
• Tumors of the adrenal medulla
• Pregnancy
• Thyrotoxicosis
• Organ dysfunction (renal diseases, endocrine
diseases, coartartion of aorta)

149
 Risk Factors

Non modifiable Modifiable/

/unchangeable/ changeable/
• Family history of  Stress
hypertension  Weight
• Age  Diet
• sex  Alcohol use
• Race and ethnicity  Smoking
• Diabetes mellitus  Lack of exercise

150
 Signs and Symptoms
• HPN also called : “Silent Killer” b/c symptoms
do not occur until it advanced.
• Rare: Headache, bloody nose, blurred vision,
palpitation, dizziness
• Late signs: Target organ disease: Damage to
blood vessels of heart, kidney, brain, eyes

151
 Diagnosis of Hypertension

• History
• Signs/symptoms
• Kidney or heart disease
• Medications
• Take a simple B/P - may see slight differences
in each arm (take the B/P with the arm at
about heart level)

152
 Other Tests

• ECG
• Blood glucose
• Hematocrit
• Serum K
• Ca
• Lipoprotein profile (HDL& LDL)
• Triglyceride levels
• Urinalysis or serum creatinine level

153
 Management of hypertension
Treatment help to
• 35-40% decline in stroke
• 25% decline in CAD/MI
• >50% decline in HF

154
 A) Life style modification
• Regular exercise e.g. walking
• Weight reduction
• Dietary salt restriction
• Promote relaxation
• Avoidance of stress, emotions, alcohol&
smoking
• The DASH (Dietary Approaches to Stop
Hypertension) Diet

155
The DASH (Dietary Approaches to Stop Hypertension) Diet

 Food group & Number of serving per day

• Grains and grain products 7–8
• Vegetables 4–5
• Fruits 4–5
• Low fat or fat-free dairy foods 2-3
• Meat, fish, 2 or fewer
• Nuts, seeds, and dry beans 4-5 weekly

156
 The effect of Life style modifications on reduction of blood pressure

- Decrease weight: lowers BP 5-20mmHg/10 Kg

- DASH diet: 8-14 mmHg
- Low Na diet: 2-8 mmHg
- Aerobic exercise: 4-9 mmHg
- Decrease EtOH: 2-4 mmHg

157
 B) Drug mgt
1) Diuretics : Reduce the body of excess fluids and
salt
– thiazide (hydrochlorothiazide)
– loop (lasix)
– Potassium-sparing (sprinolactone)
2) Sympatholytics: Reduce the heart rate and the
work of the heart
– adrenergic neuron blockers e.g. reserpine,
guannethedine)
– alpha adrenergic blockers e.g. prazosin
– beta adrenergic blockers
158
 Cont ---

3) Vasodilators: allowing the vessel to dilate (widen)

hydralizine,
sodium nitroprusside
4) Angiotensin converting enzyme inhibitors
captopril,
enalapril,
 lisinopril
5) Calcium channel blockers: Reduce heart rate and relax
blood vessels
 Verapamil
 Nifedipine
 Diltiazem
159
 Selection of antihypertensive drugs
Mild case : usually respond to a single drug e.g.
diuretics, beta blockers, ACE inhibitors or
calcium channel blockers
Moderate cases: diuretics +one of the above
drugs ( if not responding to a single drug)
- if 3 drug required diuretics + sympatolytics
+ ACE inhibitors or calcium channel blockers

160
 Cont ---

Sever HPN: loop diuretics ,vasodilators (sodium

nitopruside , hydralazine)
• In elderly : thiazides and Ca blockers
• Renal vascular disease: avoid ACE inhibitors
• Pregnancy : Beta blockers should be avoided
• Angina Beta-blocker
• Acute coronary syndrome Beta-blocker+ ACE
inhibitor
• MI ACE inhibitor + Beta blocker +Aldostrone
antagonist
• Heart failure ACE inhibitor + Beta blocker +
Aldostrone antagonist + Loop diuretic
161
 Complications of Hypertension
If not treated early it leads to end organ damage
• CVS damage/ CAD, MI, angina, CHF, Left ventricular
hypertrophy,
• CNS damage / decrease cerebral blood flow=
hypoxia, stroke
• Renal diseases /nephrosclerosis, acute renal failure
• Eye damage

162
 Hypertensive Crises
• Occur in patients whose hypertension has
been poorly controlled or in those who have
abruptly discontinued their medications
• Include
 Hypertensive emergencies and
 Hypertensive urgencies

163
 Hypertensive emergency
• is a situation in which blood pressure must be
lowered immediately (not necessarily to less
than 140/90 mm Hg) to prevent damage to
the target organs.
• life threatening blood pressure elevations that
require prompt treatment .

164
 Rx of hypertensive emergency
• The medications of choice in hypertensive
emergencies are those that have an immediate
effect.
• Intravenous vasodilators, including:
 sodium nitroprusside
 nicardipine hydrochloride
 nitroglycerin have an immediate action that is
short lived (minutes to 4 hours),

165
 Hypertensive urgency
• is a situation in which blood pressure must be
lowered within a few hours.

Treatment of hypertensive urgency

Hypertensive urgencies are managed with oral doses
of fast-acting agents such as loop diuretics.
Furosemide [Lasix],
beta-blockers (propranolol)
Metoprolo
bumetanide [Bumex)
166
 Prevention

• What Can Do?

– Loose weight if overweight
– Get regular physical activity
– Avoid excessive alcohol
– Stop smoking
– Manage stress
– Decrease salt intake
– Eat for heart health
– Discuss the use of oral contraceptives with your
doctor
– Discuss the use of some medications with your doctor

167
 Nursing Interventions
• Increasing knowledge about the disease,
medication , diet, life style change etc
• Promoting home and community-based care

• Teaching Patients Self-Care

• Continuing Care: Regular follow-up care

• Monitoring and managing potential complications

168
 Disorders of the vein

 Venous thrombosis/phlebothrombosis
 thrombophlebitis,
• They can be used interchangeably
• Phlebitis: is an inflammation of the vein due to
some causes e.g. injury, pressure, infection etc
• Thrombophlebitis: is an inflammation of the wall
of the vein frequently accompanied by the
formation of clot.

169
 Phlebothrombosis/venous thrombosis:
Is formation of blood clot with in the vein without
inflammation.
• can occur in any vein but occurs more in the veins
of the lower extremities.
• The superficial and deep veins of the extremities
may be affected.
• w/n the thrombus dislodges and migrate =
thrombo embolism.

170
 Cont…

• Clot formation may occur and obstruct deep

vein = deep vein thrombosis (DVT) or
superficial vein = superficial vein thrombosis
• Superficial veins (such as the greater
saphenous, lesser saphenous, cephalic, basilic,
and external jugular veins) are thick-walled
muscular structures that lie just under the
skin.
• Deep veins are thin walled and have less
muscle in the media.
171
 Cont…

Causes
Unclear but may be due to
• Stasis of the blood : occurs w/n heart failure,
shock, veins are dilated, medication, immobility,
extremity paralysis, anesthesia etc.
• Vessel wall injury: direct trauma e.g. fracture
/dislocation, diseases of the vein, chemical
irritation of vein from IV medication etc.
• Altered blood coagulation : increased blood
coagulopaty (may be due to abrupt withdrawal of
anticoagulant medications, blood abnormalities)
172
 c/ms

• Varies according to the sites and extent of

involvement
Superficial veins
• pain/ tenderness, redness, warmth in the
involved area
Deep vein thrombosis/DVT: is the most common
and serious than superficial vein thrombosis
• extremely swollen extremities , pain, warm,
cyanotic skin, calf pain on dorsi-flexion
/Homan’s sign/
173
 Management
• Superficial vein thrombosis: can be treated at home
with bed rest, elevation of the leg, analgesics, and
possibly anti-inflammatory medication
• The objectives of treatment for deep vein
thrombosis are to prevent the thrombus from
growing and fragmenting (risking pulmonary
embolism) and to prevent recurrent thrombo -
emboli.
• Anticoagulants
• Elastic stocking; exerting sustained evenly
distributed pressure over the entire surface of calves
174
 Mgt….

 Body position and exercise

• If the pt on bed the feet and lower legs should be
elevated above the heart level
• Active and passive leg exercise.
 Surgical mgt: thromboctomy (removal of
thrombosis).
• is necessary for deep vein thrombosis w/n
anticoagulant or thrombolytic therapy is
contraindicated .

175
 Varicose veins
 Varicosities are abnormally dilated, twisted,
superficial veins caused by incompetent venous
valves
 Most commonly occurs in the lower extremities,
the saphenous veins, or the lower trunk
However, it can occur elsewhere in the body,
such as esophageal varices.
The condition is most common in women and in
people whose occupations require prolonged
standing

176
 Varicose…
Sales people, hair stylists, teachers, nurses, and
construction workers are commonly affected
A hereditary weakness of the vein wall may
contribute to the development of varicosities.
Varicose veins are rare before puberty
The leg veins dilate during pregnancy because
of hormonal effects related to distensibility,
increased pressure by the gravid uterus, and
increased blood volume which all contribute to
the development of varicose veins.
177
 Pathophysiology

Varicose veins may be considered

 Primary (without involvement of deep veins)
Secondary (resulting from obstruction of deep
veins).
A reflux of venous blood in the veins results in
venous stasis.
 If only the superficial veins are affected, the
person may have no symptoms but may be
troubled by the appearance of the dilated
veins.
178
 Clinical Manifestations

 Symptoms, if present, may take the form of

Increased muscle fatigue in the lower legs

Feeling of heaviness of the legs

Dull aches

Muscle cramps

Ankle edema

Nocturnal cramps
179
 C/M
 When deep venous obstruction results in
varicose veins
Patients may develop the signs and symptoms
of chronic venous insufficiency:
 Edema, pain, pigmentation, and ulcerations.
 Susceptibility to injury and infection is
increased

180
 Management

 Surgery for varicose veins requires that the deep

veins be patent and functional.
Sclerotherapy/closing the unwanted vein/:- a
chemical is injected into the vein, irritating the
venous endothelium and producing localized
phlebitis and fibrosis, thereby destroy the lumen of
the vein.
Sclerosing is palliative rather than curative.
 After the sclerosing agent is injected, elastic
compression bandages are applied to the leg and
are worn for approximately 5 days.
181
 Mgt…
Elastic compression stockings are then worn for an
additional 5 weeks.
After sclerotherapy, patients are encouraged to
perform walking activities as prescribed to maintain
blood flow in the leg.
Bed rest is maintained for 24 hours, after which the
patient begins walking every 2 hours for 5 to 10
minutes.

182
 Mgt…

The nurse assists the patient to perform exercises and

move the legs.
The foot of the bed should be elevated
Standing still and sitting are discouraged.

Analgesics are prescribed to help patients move

affected extremities more comfortably.
Dressings are inspected for bleeding.
183
 Prevention

 Avoid activities that cause venous stasis (wearing tight

socks or, crossing the legs at the thighs, and sitting or
standing for long periods).
Changing position frequently, elevating the legs when
they are tired, and getting up to walk for several
minutes of every hour
Walking up the stairs rather than using the elevator is
helpful in promoting circulation.
Swimming is good exercise for the legs
Elastic compression stockings, especially knee-high
stockings, are useful.
 Weight reduction of overweight 184
Disorders of the lymphatic system
• Lymphadenitis
• Lymphangitis
• Lymphatic obstruction Reading assignment

185
 Shock
 objectives
At the end of the session student able to:
 Define shock
 List down type of shock
 Describe cause /risk factor of shock
 Identify Clinical feature shock and its diagnosis
methods
 Describe medical and nursing management of shock

186
 Shock

Definition what is shock ? Brainstorming 2min

• Is the acute disruption of circulatory function
leading to inadequate delivery of nutrients to the
tissues.
• a significant, systemic reduction in tissue perfusion,
resulting in decreased tissue oxygen delivery

187
 Shock ….

 Shock can have three progressive stages

 (discuses and reflect 5 min )
 Compensation,
Vasoconstriction, increased heart rate, and increased
contractility of the heart and normal BP
 Decompensate,
d/c BP, hypoperfusion
 Irreversible states.
Organ damage ,not responded to treatment

188
 Con…

Clinical features
 early, compensated state by easily detectable
clinical signs {Tachycardia, decreased capillary
refill, and altered mental status.}
 Generalized cellular hypoxia (prolonged oxygen
deprivation)
 Increases pulse, respiratory rate, d/c blood pressure
are key in diagnosis for adults
 Show signs of organ dysfunction, failure and die.

189
 Types of shock
 Shock classification
list and discuses ( 5 minute )
 Cardiogenic
 Hypovolemic
 circulatory /distributive shock
 Septic
 Neurogenic
 Anaphylactic

190
 Cont…

1. Cardiogenic shock
- is a clinical condition of inadequate tissue
perfusion due to the inability of the heart to
contract and pump an adequate amount of blood.
- This results in decreased oxygen and nutrient
delivery to the tissues and, if prolonged,
potentially end-organ damage and multi-system
failure.
- All forms of shock, will present with poor or low
urine output.

191
 Cont…
- Patients with cardiogenic shock have a low
cardiac index (<2.2 L/min/m 2 ), elevated filling
pressures of the left, right, or both ventricles,
and a decreased mixed venous oxygen
saturation.
- The systemic vascular resistance is often high,
but it may be in the normal or low range.
- Cardiogenic shock is the leading cause of
death in patients with acute MI, with hospital
mortality rates approaching 50 percent .

192
 Con…

2) Hypovolemic Shock
• Is caused by a reduction in the volume of circulating
blood due to
– Blood loss (in case of hemorrhage)
– Plasma loss (in case of sever burns )
– Fluid loss e.g. sever vomiting, diarrhea, or polyurea (DKA)
 3 Phases to hypovolemic shock
• Compensated
• Decompensated and
• irreversible phase

193
 Con….
 Compensated phase
• Tissue perfusion is maintained and cardiac output is
adequate (increase HR ) although blood flow may be
mal-distributed.
• Blood flow to vital organs is directed from non-
essential organs.
 Decompensated: Compensatory mechanisms are unable to
maintain organ perfusion and alterations
 Irreversible:
• Cell damage is so extensive that cell death occurs
precipitating a devastating physiologic cascade that is
refractory even with the most aggressive treatment.
194
3) Septic Shock
• Inflammatory response to invading
microorganisms and the toxins they produce,
resulting in clinical, metabolic, and
homodynamic dysfunction.
•  Systematic vascular resistance is decreased

195
4) Neurogenic Shock
• Results from the disruption of autonomic nervous
system control.
• Produces an impairment in vasomotor tone in
arteriolar and venous system leads to
- decrease in systemic vascular resistance
- large increase of venous capacity
- decrease in venous return to the heart and
- decrease in cardiac output.
• Veins and arteries immediately dilate, causing
sudden drop in BP.
196
• Neurogenic shock is caused by: vasodilatation
occurs as a result of reflex stimulation of
parasympathetic system due to :
– Severe head injury
– Spinal cord injury
– Sever pain, burn, bone fracture;
– Pharmacologic sympathetic block
– High spinal anesthetic
– fear

197
5) Anaphylactic Shock
• Occurs when a patient is exposed to a
substance to which the body is particularly
sensitive.
• The most severe form the body goes into
instantaneous violent reaction.
• Severe edema affects body parts and the
respiratory system.
• Blood pressure drops and fainting or coma
may occur.

198
 Circulatory shock

 Risk factors

199
 Treatment
 General management
• Put the patient in the recumbent position
• Raise the foot of the bed
• Keep airways open by putting the patient on
side or on abdomen and pull his tongue forward
• Aspiration of bronchial secretion
• Artificial respiration or oxygen inhalation if
required
• Tracheotomy if there is laryngeal edema
• Avoid sedatives or CNS depressants
200
 Specific management
Neurogenic shock
• Morphine for sever pain
• Vasoconstrictor ( Dopamine is preferred b/c it
produces renal vasodilatation & maintain
renal function)
• anaphlytic shock
• Hydrocortisone & antihistaminic
• Aminophiline if there is bronchospasm
• septic shock :Antibiotics for

201
2) Hypovolaemic shock
– Replace the lost fluid
– Blood transfusion in case of blood loss
– Plasma transfusion in case of plasma loss
– Fluids e.g. saline & 5% glucose solutions for
dehydration
3) Cardiogenic shock
• Positive inotropic drugs (cardiac stimulants) e.g.
dopamine, Dobutamine, Amrinone , Atropine….
N.B Delays in diagnosis or treatment can be fatal.

202
 Hematologic disorders

• Blood is a specialized organ that defers from other

organs is that it exists in a fluid state.
• The volume of blood in humans is 7-10% of the
normal body weight and it is around 5-6Lts.

Blood consists of 3 primary cell types

• Red blood cells/RBC or erytrocytes
• White blood cells (WBC) or leukocytes (basophiles,
eosinophils, monocytes, lymphocytes, neutrophils.)
• Platelets or thrombocytes

203
 Cont----

• Mature RBC primarily consists of hemoglobin

(Hgb).
• Hgb is an oxygen caring blood.
• The whole blood normally contains about 15gm
of Hgb per 100ml of blood.
• Normal amount of RBC is (4.7-6.1 million in
male and 4.2-5.4 million in female)
• WBC: protects the body from invasion by
bacteria and other foreign entities
• Normal value: 4.5-11,000/mm per cub
204
 Cont---
• Iron is one of the most important element in the blood
• normally 0.5 to 1mg of Iron is absorbed per day
• The concentration of Iron in blood is 80-180ug/dl in
male and 60-160ug/dl in female), total~ 3gm
• Vit B12 and folic acid: are another the most important
elements for erythropoiesis.
• Both derived from diet
• Vitam B12 combines in intrinsic factor produced in
stomach
• Folic acid absorbed in the proximal of small intestinal.

205
 Anemia

• A condition in which the amount of

hemoglobin or hematocrit concentration is
lower than normal.
• Reflects the presence of fewer than normal
RBCs within the circulation.
• As a result, the amount of oxygen delivered
to body tissues is also diminished

206
 Causes

 It occurs w/n
• marrow failure/ decrease production: reduced
erythropoiesis
• increased destruction of RBCs or
• excessive red cell lost

207
 Cont---
• Loss of RBCs—occurs with bleeding, potentially from any
major source, such as the gastrointestinal tract, the uterus,
the nose, or a wound.
• Decreased production of RBCs—can be caused by a
deficiency in cofactors (including folic acid, vitamin B12, and
iron) required for erythropoiesis;
• RBC production may also be reduced if the bone marrow is
suppressed (eg, by tumor, medications, toxins) or is
inadequately stimulated because of a lack of erythropoietin
(as occurs in chronic renal disease).
• Increased destruction of RBCs—may occur because of an
overactive RES (including hypersplenism) or because the bone
marrow produces abnormal RBCs that are then destroyed by
the RES (eg, sickle cell anemia).
208
 Types of anemia

• Anemia may be classified in several ways.

• The physiologic approach is to determine
whether the deficiency in RBCs is caused by
A defect in their production (hypoproliferative
anemia),
 by their destruction (hemolytic anemia), or
by their loss (bleeding).

209
 Cont---

 Generally anemia can be classified by 4 types

based on the cause
• Nutritional deficiency anemia
• Hemorrhagic anemia
• Aplastic anemia
• Hemolytic anemia

210
 A) Nutritional deficiency anemia
• It occurs w/n lack of important elements of
blood (including folic acid, vitamin B12, and
iron) required for erythropoiesis
 It includes
• Iron deficiency anemia
• Vitamin B12 deficiency anemia
• Folate /folic acid deficiency anemia

211
 Iron deficiency anemia

• Iron deficiency anemia typically results when the

intake of dietary iron is inadequate for hemoglobin
synthesis.
• The body can store about one fourth to one third of its
iron, and it is not until those stores are depleted that
iron deficiency anemia actually begins to develop.
• Iron deficiency anemia is the most common type of
anemia in all age groups, and it is the most common
anemia in the world; where inadequate iron stores can
result from inadequate intake of iron or from blood
loss

212
 Cont---
 Causes
• Inadequate iron intake
• Mal absorption
• Excessive menstrual bleeding
• Bleeding (from ulcers, gastritis, GI tumors,
wound, epitasis etc)
• from blood loss (eg, from intestinal hookworm).
• Increased metabolic demand (pregnancy,
infection )-------

213
 Clinical manifestations and diagnosis
• Fatigue,
• Pallor
• Anorexia
• Feeling of finiteness
• Decreased RBCs, Hgb and Hct
• Decrease serum iron level

214
 Management
• Treating the causative agents
• Administration of extra Iron /ferrous sulfate
0.3 gm TID
• Iron rich diet

215
Pernicious/Vitamin B12 deficiency anemia (Cobalamin)
• a nutritional deficiency anemia in w/c the
body is unable to absorb the needed Vit B12
from the food.
• Is due to absence of intrinsic factors normally
secreted by the cells of stomach due to
abnormality in the gastric mucosa /i.e. is not
usually due to deficiency of intake)
• Intrinsic factor binds with Vit B 12 and travel
with in ileum were Vit B12 is absorbed.

216
 Cont---

• The deficiency can also occur if there is a disease

involving the ileum or pancreases that impairs
absorption
 c/ms and Dx
• Abnormal RBCs
• Sore tongue and mouth
• Digestive disturbances
• Diarrhea
• Personality change ( Irritable, confused, depression)
• Decrease (Hct, Hgb, and RBC count)

217
 Cont---

 Mgt
• Vitamin B12 100mcg once a month oral or IM
(dose can be adjusted)
• Treatment of the underlying causes

218
 Folic acid deficiency anemia

• Folic acid is another vitamin necessary for the

normal red blood cell production
• It results fro either due to inadequate dietary
intake of folate (as malnutrition, malnutrition
and the like) or from disorders of the small
intestine were the folate is absorbed
• Folic acid deficiency anemia and vit. B12
deficiency anemia also called megaloblastic
anemia.

219
 Cont---
 c/ms
• Similar to vit B12 deficiency anemia in the
abscess of neurologic manifestation
 Mgt
• Oral dose of folic acid (0.1 to 0.2 mg )daily for
1-2 weeks
• Well balanced diet
• Correction of the probable causes

220
 B) Hemorrhagic anemia
• Anemia resulting from blood loss (acute or
chronic)
• Acute blood loss due to trauma, complication
of surgery etc
• Chronic blood loss: uterine tumors,
hemorrhoids, abnormal menstrual blood loss
etc
 c/ms : the same

221
 Cont---
 Mgt
• Replacement of the lost of blood = if not may
lead to shock
• Identify the source of hemorrhage and
stopping blood loss
• IV fluids
• Iron supplement (during each 2ml of blood
loss approximately 1mg of Iron is lost)

222
 III) Aplastic anemia

• Is deficiency of circulating red blood cells b/c

of failure of the bone marrow to produce
these cells
 This may be due to
• Long term exposure of the bone marrow to
toxic substances such as infection, radiation,
certain drugs (for Rx of CA),
• Hereditary or idiopathic

223
 Cont---

• Aplatic anemia is usually occurs with

leukopenia (reduction of WBCs) and
thrombocytopenia (reduction in platelets)
 c/ms
• s/sx of anemia
• Decrease WBCs and platelets
• Fatigue/ weakness
• Lower resistance to infection and bleeding
tendency etc

224
 Cont---

 Mgt
• Blood transfusion
• Bone marrow transplantation
• Administration of immuno suppressive
therapy.
- Antithymocyte globulin (ATG) alone
- ATG and cyclosporine
- Methylprednisolone
- cyclosporine

225
 IV) Hemolytic anemia

• Is anemia results from abnormal destruction

of red blood cells leading to reduce the
number of RBCs in the circulation.
 Causes
• Can be acquired (extrinsic problems) or
• Congenital (intrinsic problems)

226
 Cont----
 Causes of acquired hemolytic anemia
• Burns
• Snake venom
• Use of incompatible blood transfusion
• Infection (malaria, toxoplasma, streptococcus
etc)
• Exposure to certain heavy metals and organic
compounds

227
 Cont----

 Congenital hemolytic anemia/ inherited

• It is caused by defect resulting in the formation
abnormal RBCs = this are fragile and easily
ruptured.
• Sickle cell anemia: is results from inheritance of
sickle hemoglobin (defective Hgb molecule
known as S(HgS) w/c is less oxygen carrying
capacity in place of normal A (HgA) hemoglobin.
• In sickle cell anemia the mean red cell survival
time is about 10-15 days.

228
 Cont----
 c/ms
• All manifestations of anemia in sever form.
• Clinical findings of hemolysis (jaundice,
increase bilirubin , hepatomegally)

229
 Management
 For acquired causes
• Eliminate the causes
• Corticosteroids
• Antibiotics for infection and
• blood transfusion
 For congenital once
• Blood transfusion and Bone marrow
transplantation

230
 Poly cytemia

• Is the presence of increased number of

circulating erythrocytes (i.e. RBC > 6 million)
• Blood circulation is impaired due to increased
blood viscosity and blood volume
 Causes: unknown
 Incidence: not common
 Mgt: reduce blood volume , viscosity and bone
marrow activity.
• Phlebotomy until desired Hct is achieved
 Complication: thrombosis
231
 Thrombo cytopenia/
platelet deficiency

• Is reduction of platelet from the normal range(150,000-

450,000mm3)
 Causes
• Idiopathic or acquired (either from decrease production
or increase destruction of platelets)
• Tumors of the bone marrow
• Aplastic anemia
• Alcohol
• Toxins/ infection /antibodies
• Drugs (CAF, heparin, thiazides)
232
 Cont---
 c/ms
• Presence of bruises ,or hemorrhage up to 1cm
in diameter
• Ecchymosis /bleeding in the soft tissue
• Dizziness
• Hypotension
• Fainting /weakness

233
 Cont--

 Diagnosis
• Hx and PE
• Platelet count
• Hct and hgb study
• Bleeding time
• Reduction bellow 150,000 may be termed as
thrombocytopenia ;however bleeding does not
usually occur until the platelet count are ,50,000
• If it drops below 20,000 serious bleeding

234
 Cont---
 Mgt
• Managing the underlying causes
• Corticosteroids
• Platelet transfusion

235
 Assignment
Lymphoma and Thrombocythemia

236
 Hemophilias

• Hereditary bleeding disorders caused by reduce

clotting activity of specific coagulation factors.
• Two inherited bleeding disorders—hemophilia A/
classic hemophilia and hemophilia B—are clinically
indistinguishable, although they can be
distinguished by laboratory tests.
• Hemophilia A is caused by a genetic defect that
results in deficient or defective factor VIII;
hemophilia B (also called Christmas disease) stems
from a genetic defect that causes deficient or
defective factor IX.
237
 Cont---
• Hemophilia is a relatively rare disease; hemophilia A,
which occurs in 1 of every 10,000 births, is three times
more common than hemophilia B.
• Both types of hemophilia are inherited as X-linked
traits, so almost all affected people are males; females
can be carriers but are almost always asymptomatic.
• The disease is recognized in early childhood, usually in
the toddler age group. However, patients with mild
hemophilia may not be diagnosed until they
experience severe trauma (eg, a high-school football
injury) or surgery.

238
 Clinical Manifestations

• Slow, persistent, prolonged bleeding from

trauma and small cuts
• Delayed bleeding arrest after minor injures
• Epitasis
• Hematuria from GUT trauma
• GI bleeding from ulcers and gastritis
• Hemarthrosis etc

239
 Mgt
• Fresh frozen plasma until the Dx is confirmed
• Then factor VIII or IX
• N.B. never give IM injection

240
 Leucopenia
• Refers to a decrease in the total WBC count
(leukocyte count <5000/mm3)
 Causes
• Leukemia
• Aplastic anemia
• Drug induced condition
• Nutritional deficiency (Vit B12, folic acid)
• Secondary to diseases (sever sepsis, bone
marrow malignancies, diseases of spleen)
241
 Cont----
 c/ms
• Frequent infection
• Diminished phagostic responses / the classic signs of
infection i.e. redness, heat, swelling are not manifested
 Mgt
• Identify the cause and Rx
• Granulocyte transfusion
• Rx of infection
• N.B decrease in all cells RBC,WBC, and platelets is
called pan cytopenia.

242
 Leukemia
• Is an unregulated/uncontrolled proliferation of
WBCs {granulocytes (neutrophils, basophils,
eosinophils) , monocytes, lymphocytes, } in the
bone marrow.
• Is an increase number of immature abnormal
WBCs in the blood.
• As a result the bone marrow becomes
overcrowded with immature non functional cells
and production of normal cells is greatly
decreased.
243
 Cont---
• This cells are abnormal and their excessive
production in the bone marrow stops normal
bone marrow production of red blood cells,
platelets and mature leukocytes leading to
anemia, thrombocytopenia, and leucopenia.
• Leukemic cells can also be found in the spleen,
liver, and lymph nodes of CNS.

244
 Causes
 The exact cause is unknown
• Genetic factor/abnormal chromosomes
• Environmental factors /Bone marrow damage
- Ionizing radiation
- Environmental irradiation e.g. atomic bomb,
nuclear accident
• Immunologic factors

245
 Cont---
 Incidence
• Leukemia accounts for 2% of all new cases of
cancer and 4% of all deaths from cancer.
• Leukemia can be acute (with sudden onset and
short duration or chronic (with a slow onset and
symptoms that persists for a period of years)
• The leukemia's are commonly classified
according to the stem cell line involved, either
lymphoid or myeloid.

246
 Cont---
I) acute myeloid leukemia/AML: most common
form of adult leukemia
II) acute lymphocytic leukemia/ALL: constitutes
about 10% of adult leukemia but most
common in children
III) chronic myeloid leukemia/CML: constitutes
about 20% of adult leukemia
IV) chronic lymphocytic leukemia /CLL: rare
type and common in people > 50 years.

247
 Clinical manifestations
• Leukemia affects all blood cells = influences
the health and functions of all organs and
systems
• CVS changes: Increase HR, decrease BP,
murmurs, anemia, etc
• Respiratory change: related to anemia and
infection (increase RR, dyspnea)
• Skin manifestation: pale skin/pallor, petechia,
ecchymosis,

248
 Cont---
• GIT manifestations: bleeding gums, anorexia,
weight loss, enlarged liver and spleen,
constipation
• CNS change: Headache, seizure, comma, fever
(due to infection)
• Renal manifestation: hematuria, oliguria
• Musculoskeletal : bone pain, joint swelling,
and pain.

249
 DX/lab findings
• Decrease Hgb, Hct level and platelet count
• Abnormal WBC count (20-100,000)
• Definitive test: examination of cells obtained
from bone marrow aspiration and biopsy

250
 Mgt

• Infection is the major cause of death in client

with leukemia (skin, Respiratory tract, and
intestinal tract are the most common sites of
infection)
 Drugs for infection
• Antiviral (ganciclovir, foscarnet, steroids),
• Antifungal (amphotersin B, ketoconazole,
Nystatin)
• Antibacterial (gentanmycin and penicillin)

251
 Cont---
 Chemotherapy (aggressive IV Drugs) e.g.
cytosine arabinoside for 7 days, daunorubicin
for 3 days, retinoic acid, aspiriginase,
prednisone
 Radiotherapy
 Bone marrow transplantation.

252
• Thank you in advance

Thank you in advance

253