This document provides an overview of cardiovascular anatomy and physiology and disorders. It begins by stating the objectives of describing the cardiovascular system and discussing related disorders. It then covers topics like heart anatomy, chambers and valves, blood supply, conduction pathway, and cardiac output calculation. Assessment methods are discussed including health history, physical exam of vital signs, skin, extremities and listening to heart and lung sounds. Common diagnostic tests like ECG, echocardiogram and blood tests are also summarized. Management of dysrhythmias and conduction problems is mentioned.

1. Cardio - vascular, circulatory
and hematology disorder
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2. Objectives
At the end of the session the students will be
able to:-
Describe the anatomical and physiological
aspect of the cardiovascular system
Discuss disorders of the cardiovascular system
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3. Anatomy and physiology over view
 The heart is a hallow muscular organ located in
the center of the thorax.
 It occupies the space between the lungs and rests
over the diaphragm.
 It is encased in the thin fibrous tissue (sac) called
the Pericardium containing two layers.
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4. Anatomy and physiology over view
• The visceral pericardium lies over the heart
and the parietal pericardium supports the heart
in the mediastinum by attaching with the
diaphragm, sternum, and the vertebral column.
• Mediastinum is the section of the chest
between the lungs, where the heart,
oesophagus and vagus nerves are situated.
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5. Chambers of the heart
The heart has four chambers.
 Left atrium and ventricles, right atrium and ventricles.
 The Left ventricle pumps oxygenated blood to the body
against systemic pressure and it is about 2-5 times
thicker than the right ventricle which pumps
deoxygenated blood from the lung against pulmonary
pressure.
 The left atrium receives oxygenated blood from the lung
and the right atrium receives deoxygenated blood from
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6. Valves of the heart
 They permit blood flow only in one direction
1. Atrioventricular valves- separate the atria from
the ventricles.
A. Tricuspid valve - separate the right atrium &
right ventricles
B. Bicuspid valve- separates the left atrium & left
ventricles
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7. Cont’d…
2. Semi lunar valve- separates the ventricles and
the large arteries draining blood from them.
(Right ventricle from pulmonary artery and left
ventricle from aorta)
A. Pulmonic valve- lies between right ventricle
& pulmonary artery.
B. Aortic valve-lies between the left ventricle
and aorta.
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8. Cardiac Muscles: -
Heart consists of three layer
1. The Endocardium - the inner part that lines the
inside part of the heart & valves.
2. The myocardium- middle layer that is made up
of muscles responsible for cardiac contraction.
3. The epicardium- the outer layer that lies
beneath the pericardium
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9. Blood supply to the heart
 The heart consumes about 70-80% of the body
oxygen for its metabolic demand.
 It is supplied by the coronary arteries.
 They bifurcate/separates from aorta just above
the aortic valve.
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10. Conduction pathway
 The SA node (primary
pacemaker) near the
junction of atrium &
superior vena cava is the
starting point of electrical
stimuli in the myocardial
tissue.
 Then it travels in the right
atrium through the
conduction path way
called the inter nodal
path way till it reach the
AV node near the tricuspid
valve in the atria wall.
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11. Cont’d…
 After a slight delay (giving
time for atrial contraction)
impulses travel from the
AV node to the ventricles
through a conduction path
way called the bundle of
his across the septum
separating the left and the
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12. Cont’d…
 The bundle of His separate in to left and right
side supplying both the left and the right
ventricles.
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13. Cont’d…
 The left bundle again
subdivides in to left
anterior & posterior
branches terminating in
fibers called purkunje
fibers which are the
terminal point of the
electrical conduction in
the heart.
 It is after the impulse
reach this point that the
ventricles will contract.
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14. Cont’d…
 Cardiac out put (CO)- is the amount of blood
pumped by the left ventricle during a given
period of time usually in one minute.
 Stroke volume (SV)-the amount of blood
ejected per heartbeat (by one heartbeat).
 The normal heartbeat is approximately about
70-beats/ min (60-80), and during each beat the
left ventricle pumps about 70 ml of blood.
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15. Cont’d…
 So cardiac out put (CO) can be Calculated as
CO = SV x HR = 70mlx72 beat/min = 5040
ml/min
 Pulse pressure: is the difference b/n systolic
and diastolic pressure which is usually
40mmHg.
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16. ASSSESSMENT OF THE CARDIOVASCULAR
SYSTEM
i. Health history.
 Patients with cardiovascular disorders
commonly have one or more of the following
signs and symptoms:
Chest pain or discomfort (angina pectoris, MI,
valvular heart disease)
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17. Assessment…
Shortness of breath or
dyspnea (MI, left
ventricular failure, HF)
Edema and weight
gain (right ventricular
failure, HF)
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18. Cont’d…
Palpitations (dysrhythmias resulting from
myocardial ischemia, valvular heart disease,
ventricular aneurysm, stress, electrolyte
imbalance)
 Fatigue (earliest symptom associated with
several cardiovascular disorders)
 Dizziness and syncope or loss of
consciousness (postural hypotension,
dysrhythmias, vasovagal effect,
cerebrovascular effect)
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19. Cont’d…
 Medication: -
Aspirin- prolongs clotting time.
Tricyclic antidepressant-cause arrhythmia
Phenothiazide-arrhythmia & hypotension
Oral contraceptive-increase risk of
thrombophlebitis.
Lithium-arrhythmia
Theophiline-tachycardiac & arrhythmia
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20. Cont’d…
 Surgery -past history of surgery
- whether ECG was taken or not
- Admission related to CVS problem.
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21. Cont’d…
ii. Physical Assessment: -
 This is to confirm information obtained from
history.
 The assessment area include pain
characteristic, vital sign, heart sound,
peripheral edema etc.
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22. Cont’d…
 General Appearance and Cognition
The nurse observes the patient’s level of
distress, level of consciousness, and thought
processes as an indication of the heart’s ability
to propel oxygen to the brain (cerebral
perfusion).
The nurse also observes for evidence of
anxiety, along with any effects emotional
factors may have on cardiovascular status.
The nurse attempts to put the anxious patient at
ease throughout the examination.
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23. Cont’d…
 Inspection of the Skin
Pallor- a decrease in the color of the skin is
caused by lack of oxyhemoglobin.
It is a result of anemia or decreased arterial
perfusion.
Pallor is best observed around the fingernails,
lips, and oral mucosa.
In patients with dark skin, the nurse observes
the palms of the hands and soles of the feet.
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24. Cont’d…
Peripheral cyanosis a bluish tinge, most often
of the nails and skin of the nose, lips, earlobes,
and extremities suggests decreased flow rate of
blood to a particular area, which allows more
time for the hemoglobin molecule to become
desaturated.
This may occur normally in peripheral
vasoconstriction associated with a cold
environment, in patients with anxiety, or in
disease states such as HF.
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25. Cont’d…
Central cyanosis- a bluish tinge observed in
the tongue and buccal mucosa denotes serious
cardiac disorders (pulmonary edema and
congenital heart disease) in which venous
blood passes through the pulmonary
circulation without being oxygenated.
Reduced skin turgor occurs with dehydration
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26. Cont’d…
Normally the skin is warm and dry.
Under stress, the hands may become cool and
moist.
In cardiogenic shock, sympathetic nervous
system stimulation causes vasoconstriction,
and the skin becomes cold and clammy.
During an acute MI, diaphoresis is common.
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27. Cont’d…
 Blood Pressure
Systemic arterial BP is the pressure exerted on
the walls of the arteries during ventricular
systole and diastole.
 It is affected by factors such as cardiac output,
distention of the arteries, and the volume,
velocity, and viscosity of the blood.
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28. Cont’d…
BP usually is expressed as the ratio of the
systolic pressure over the diastolic pressure,
with normal adult values ranging from 100/60
to 140/90 mm Hg.
The average normal BP usually cited is 120/80
mm Hg.
An increase in BP above the upper normal
range is called hypertension, whereas a
decrease below the lower range is called
hypotension.
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29. Cont’d…
PULSE RATE
The normal pulse rate varies from a low of 50
bpm in healthy, athletic young adults to rates
well in excess of 100 bpm after exercise or
during times of excitement.
Anxiety frequently raises the pulse rate during
the physical examination.
 If the rate is higher than expected, it is
appropriate to reassess it near the end of the
physical examination, when the patient may be
more relaxed.
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30. Cont’d…
• Heart Inspection and Palpation
The heart is examined indirectly by inspection,
palpation, percussion, and auscultation of the
chest wall.
A systematic approach is the cornerstone of a
thorough assessment.
Examination of the chest wall is performed in
the following six areas.
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31. Cont’d…
1. Aortic area second intercostal space to the right
of the sternum.
2. Pulmonic area second intercostal space to the
left of the sternum
3. Erb’s point third intercostal space to the left of
the sternum
4. Right ventricular or tricuspid area fourth and
fifth intercostals spaces to the left of the sternum
5. Left ventricular or apical area the location on
the chest where heart contractions can be
palpated.
6. Epigastric area below the xiphoid process
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32. Cont’d…
 Inspection of the Extremities
The hands, arms, legs, and feet are observed for
skin and vascular changes.
The most significant changes include the
following:
Decreased capillary refill time indicates a
slower peripheral flow rate from sluggish
reperfusion and is often observed in patients
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33. Cont’d…
Capillary refill time provides the basis for
estimating the rate of peripheral blood flow.
 To test capillary refill, briefly compress the
nail bed so that it blanches, and then release
the pressure.
Normally, reperfusion occurs within 3 seconds,
as evidenced by the return of color.
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34. Cont’d…
 Peripheral edema -is fluid accumulation in
dependent areas of the body (feet and legs,
sacrum in the bedridden patient).
 Assess for pitting edema (a depression over an
area of pressure) by pressing firmly for 5
seconds with the thumb over the dorsum of
each foot.
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35. Cont’d…
 Clubbing of the fingers and toes implies
chronic hemoglobin desaturation, as in
congenital heart disease.
 Hypoxia causes an angle greater than
180° between the fingernail and nail
base; nail feels springy when palpated.
 Normal nail: Has an angle of
approximately 160° between the
fingernail and nail base; nail feels firm
when palpated.
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36. Cont’d…
LUNGS
Findings frequently exhibited by cardiac
patients include the following respiratory
system sign and symptoms:
Tachypnea
Hemoptysis
Cough
Crackles
Wheezes
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37. Cont’d…
ABDOMEN
 For the cardiac patient, two components of the
abdominal examination are frequently
performed.
Hepatojugular reflux
Bladder distention.
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38. Cont’d…
iii. Common Diagnostic procedure
 Radiography (x-ray)
 Echocardiogram:-
 Cardiac catheterization
 Hemodynamic Monitoring
 Electrocardiogram: -
 Magnetic resonance image
 Computed tomography
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39. Cont’d…
Echocardiography is a noninvasive
ultrasound test that is used to measure the
ejection fraction and examine the size, shape,
and motion of cardiac structures.
The Electrocardiography/ECG is a graphic
representation of the electrical currents of the
heart.
The ECG is obtained by placing disposable
electrodes in standard positions on the skin of
the chest wall and extremities
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40. Cont’d…
Blood Tests
 Blood urea Nitrogen (BUN) - end product of
protein metabolism indicate reduced renal
function in cardiac patient when elevated.
 Fasting blood sugar
 Lipid profile-cholesterol, triglyceride, and
lipoprotein - cholesterol >200dl/ mg indicates
risk of atherosclerosis.
 Serum electrolyte analysis- (Na, k; Ca, Mg) are
important for depolarization &
repolarization.
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41. Management of patient with dysarthymias and
conduction problems
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42. Arryhthmias/Dysrryhthmias
 Is the disorder of heart beat caused by the
disturbance in automaticity or conductivity
or more commonly both.
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43. Cont’d…
A/ Bradycardia
 A condition when SA node creates an impulse
at a slower rate (40-60 bpm or less) than
normal.
 It is because of decreased automaticity in the
SA node.
 All the other characteristics are normal except
its rate.
 It is more common in well-trained athletes, at
rest and during night.
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44. Associated situation-
 Sepsis
Vagal stimulation
Vomiting
After surgical damage to SA node
Acute myocardial infarction etc
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45. Management
Objective is to increase the rate to normal
 Identifying & removing cause
 Atropine blocks vagal stimulation thus
allow normal rate.
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46. B/ Tachycardia:
 Is a condition where the sinus node creates an
impulse at a faster rate than normal (Exceeding
100 bpm).
 It is in response to enhanced automaticity in the
SA node
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47. Cont’d…
It may be caused by: -
Exercise where O2 demand is high.
Emotional stress, pain
Stimulation / coffee, tea
Drugs (atropine, Catecholamine, alcohol etc---
)
Hypovolemia, Anemia, heart failure
All of its aspects are normal except its rate
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48. Increased heart rate
Decreased diastolic
filling time
Decreased Cardiac Out Put
Hypotension
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49. Management
 Objective is to decrease the heart rate to
normal
- Remove the cause
-Propranolol (blocks the effect of adrenergic
fiber- reduce rate)
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50. C/ Atrial Fibrillation:
 A rapid disorganized and uncoordinated
twitching of atrial muscle.
 It may occur over short time or chronically.
 The atrial rate is 300-600 bpm while
ventricular response is 100-160 bpm, because
the AV node is unable to conduct multiple
impulses.
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51. Cause:
Advancement in age, pulmonary disease
Valvular heart disease, hyperthyroidism
 Cardiomyopathy
Inflammation
Moderate to heavy ingestion of alcohol
Some times with out underlying characteristics
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52. Management
 Identify and remove the cause
 Vagal stimulation
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53. D/ Cardiac Arrest
Occurs when the heart ceases to produce an
effective pulse and blood circulation.
There is an immediate loss of consciousness
and an absence of pulse.
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54. Cont’d…
It can occur with:
Ventricular tachycardia
Ventricular fibrillation
Bradycardia
Av block
It may follow respiratory arrest
It may occur when there are impulses but
ineffective cardiac contraction & circulating
volume.
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55. Etiology:
 Hypovolemia
 Hypothermia
 Massive pulmonary emboli
 Acidosis
 Acute massive myocardial infraction
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56. Sign & Symptom: -
 Seizure may or may not occur
 Absence of carotid pulse
 Brain damage may occur within four minutes
Management –
 Remove the underlying cause
 Epinephrine or atropine
 Cardiopulmonary resuscitation
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57. Congestive Heart failure
 Heart failure refers to a collection of signs
and symptoms that result from the heart’s
inability to pump enough blood to meet the
body’s metabolic demands.
 It is a common clinical syndrome that results
from the impaired ability of the ventricle to fill
with or eject blood.
 The pump itself is impaired and unable to
supply adequate blood to meet the cellular
needs.
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58. Congestive Heart Failure (CHF)…
Causes of CHF
The causes of CHF are classified into two
major classes as
Underlying causes and
Precipitating (secondary) causes
In general, CAD is the cause in 60% of cases.
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59. Congestive Heart Failure (CHF)…
I. Underlying causes
It is the main pathological lesion that is
responsible for the heart not to pump
adequately. These include:
Myocardial lesions
- Cardiomyopathy
- Myocarditis
- Myocardial infarction
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60. Congestive Heart Failure (CHF)…
I. Underlying causes … cont’d
Valvular & Endocardial lesions
- Endocarditis
- Congenital valvular heart disease
- RHD (Rheumatic Heart Disease)
Pericardial lesions
- Pericarditis
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61. Congestive Heart Failure (CHF)…
II. Precipitating (secondary) causes
 Normally in the absence of precipitating
factors or causes, an individual heart with
those underlying lesions tries to compensate
by making multiple Pathophysiologic
changes.
 But when the precipitating causes come to
the picture the individual heart goes in to
full blown clinical signs and symptoms of
CHF.
 The precipitating causes are abbreviated by a
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62. Congestive Heart Failure (CHF)…
II. Precipitating (secondary) causes… cont’d
• H = Hypertension
• E = Infective Endocarditis
• A = Anemia
• R = Rheumatic fever (Recurrence)
• T = Thyrotoxicosis
• F = Fetus (pregnancy) -L-lung
problems/pathologies
• A = Arrhythmias -S-stress
• I = Infections Rahel N.ArsiU. 62
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63. Stages of HF depending on New York Heart
Association
 Class I (mild)- Ordinary physical activity does
not cause symptoms.
 Class II (mild)- Comfortable at rest but ordinary
physical activity results in symptoms
 Class III (moderate)- Comfortable at rest but less
than ordinary activity causes symptoms
 Class IV (severe)- Symptoms at rest
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64. Stages of HF depending on American Heart
Association
Stage A- Patients at high risk for developing
heart failure due to underlying conditions such
as systemic hypertension, coronary artery
disease, diabetes mellitus, or family history of
cardiomyopathy.
Stage B- Patients have structural heart disease
such as left ventricular hypertrophy or valvular
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65. Cont’d…
Stage C- Patients have current or prior
symptoms of heart failure associated with
underlying structural heart disease that
includes left ventricular systolic dysfunction.
Stage D- Patients with advanced structural
heart disease and marked symptoms of heart
failure at rest despite maximal medical
therapy.
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66. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure
• The onset of heart failure may be acute or
insidious
• It is often associated with systolic or diastolic
over loading and with myocardial weakness
• As the physiologic stress on the heart muscle
reaches a critical level, the contractility of the
muscle is reduced and cardiac output declines,
But venous input to the ventricle remains the same
or becomes increased which is responsible for
cardiac over load
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67. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure… cont’d
• When cardiac output is decreased; the body
undergoes alteration to compensate for the
failure.
• There are two types of compensatory
mechanisms for congestive heart failure:-
I. Systemic compensatory mechanisms
II. Cardiac compensatory mechanisms
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68. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure… cont’d
I. Systemic compensatory mechanisms
A. Reflex increase in sympathetic activity.
B. Release of renin from the kidneys.
C. Anaerobic metabolism by affected tissues.
D. Increased extraction of oxygen by the
peripheral cells.
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69. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure… cont’d
II. Cardiac compensatory mechanisms
A. Myocardial dilatation
B. Myocardial Hypertrophy
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70. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure… cont’d
Systemic compensatory… cont’d
A) Sympathetic response to heart Failure:-A
decrease in cardiac out put results in
decreased blood pressure, which causes a
reflex stimulation of sympathetic nervous
system (SNS).
• The SNS causes increased force and rate of
myocardial contraction.
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71. Congestive Heart Failure (CHF)…
Pathophysiology of Heart Failure… cont’d
Systemic compensatory… cont’d
A) Sympathetic response to heart Failure:-
• It also causes vasoconstriction of arterioles
throughout the body.
• These effects temporarily prolong the
patient’s life.
• But in the long run, it facilitates the
progress of pumping failure (cause cardiac
decompositions). Rahel N.ArsiU. 71
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72. Pathophysiology of Heart Failure
Renin Angiotensin Aldosterone system:-
Decreased perfusion of tissues/renal
tissues
Release of Renin from juxtaglomerular cells
of the kidney
Formation of Angiotensin I ( formed from
Angiotensinogen in the liver by the action
of renin )
Formation of Angiotensin II ( by enzyme
reaction in the pulmonary capillary bed )
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73. Pathophysiology of Heart Failure…
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74. Cont’d…
NB. * After load:- the arterial pressure
against which the ventricles must contract.
** Preload:-It is the pressure during filling of
the ventricles or tension on myocardium due
to congestion.
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75. Types
1. Left sided heart failure
 Results from left ventricular dysfunction,
which causes blood, back up through the left
atrium & in to the pulmonary vein.
 The increased pressure causes fluid
extravasations from the pulmonary capillary
bed in to the interstitial and the alveoli, which
is manifested as pulmonary congestion and
edema.
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76. Cont’d…
Causes
 Myocardial infarction, Systemic hypertension
 Cardiomyopathy, Rheumatic heart disease
 Aortic stenosis
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77. 2. Right sided heart failure:
 Failure of right ventricle to eject leading to
venous congestion in the systemic circulation.
 Congestive: - both left and right sided heart
failure
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78. Sign and symptom: -
Left sided
 Increased heat rate
 Left ventricular hypertrophy
 Poor oxygen exchange
 Dyspnea (32-40 shallow breath)
 Orthopnea –Dyspnea at lying flat
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79. Cont’d…
 Paroxysmal nocturnal dyspnea- Orthopnea at
night
 Dry cough, crackle
 Hemoptysis, fatigue
 Anorexia, restlessness
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80. Right sided
 Edema –peripheral- in the leg
 Liver – hepatomegally
 Abdominal cavity –Ascitis
 Spleen- splenomegally
 Anasarca- massive edema
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81. Right sided…
 Edema of dependent body parts – pedal,
Sacrum, labia
 Jugular vein distension
 Weight gain, Nausea,
 Anorexia, vomiting
 Weakness, fatigue
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82. Sign and symptom of CHF
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83. CHF
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84. Diagnosis: -
History and physical examination
 Determining of underlying cause
 Chest x-ray
 Echocardiography
 Blood urea nitrogen
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85. Complication: -
 Cardiogenic shock
 Pulmonary edema
 Renal failure
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86. Management: -
 Treating underlying cause
 Oxygen therapy to reduce dyspnea and fatigue
 Physical & emotional rest to conserve energy &
high oxygen demand.
 Digitalis – increase the force of myocardial
contraction
 Decrease the conduction speed – decrease heart
rate
 Diuretics –to mobilize edematous fluid
 Reduce pulmonary venous pressure and reduce
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87. Cont’d
Vasodilator
- To decrease systemic vascular resistance
- To decrease pulmonary & peripheral venous
pressure.
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88. PATIENT TEACHING
Salt restriction
Fluid restriction
Weight reduction
Position- high fowler to decrease pulmonary
edema.
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89. Rheumatic heart disease
Rheumatic fever
 Is an inflammatory disease of the heart
potentially involving all layers of the heart
(Endocardium, myocardium, and epicardium).
 The resulting damage to the heart from the
rheumatic fever is called rheumatic heart
disease.
 It is chronic disease characterized by scarring
and deformity of the heart valves.
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90. Cause
 Group A beta hemolytic streptococcal infection
of the URTI.
Predisposing factor
 Poor socioeconomic system.
 Crowded living condition
 Family tendency- may be related to altered
immune system.
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91. Pathophysiology
 The heart and other organs are not damaged
directly by the microorganism causing the
infection but rather by the toxin they release.
 In this speculation how the attack reoccur is
not well known.
 Another theory suggests that the antigens of
the streptococcal and human tissue are
remarkably similar.
 So, antibodies mistakenly destroy normal
tissue as antigen.
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92. Clinical manifestation & diagnosis
 The American heart Association provided a
logical basis for the diagnosis as the presence
of:-
 Two major criteria or
 One major + two minor criteria accompanied
by evidence of proceeding group A
streptococcal infection.
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93. Major criterion
A. Carditis (Inflammation of the heart) with: -
 Murmur
 Congestive heart failure with cardiac
enlargement
 Dysrhythmias
 Pericarditis
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94. Cont’d…
B. Polyarthritis – inflammation of more than one
joint
 Large joints (knee, elbow, ankle etc) are
mostly affected and almost always
migratory.
 Has dramatic response to salisylates (within
48 hrs).
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95. Cont’d…
C. Chorea – spontaneous, purposeless, rapid
jerking movement
 Mostly seen in girls
 It is self limiting within weeks to months
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96. Cont’d…
D. Erythema marginatum lesion
 Redness of the skin b/c of widening of blood
vessels.
 Bright pink macular lesion in the chest &
inner aspect of upper arm & thigh but never
in face.
 It is non pruiritic & non painful
E. Subcutaneous nodule
 Firm, hard, small painless swelling 1- 4cm
mostly over bony prominences
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97. Minor criteria
 Arthralgia- joint pain
 Previous reoccurrence of rheumatic fever or
heart disease
 Fever
 Prolonged PR interval on ECG
 Lab finding Positive throat culture
 - ESR increase (> 15 mm in male & 20 in
female)
 - Increased WBC count
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98. Management
No specific cure once it has occurred
 Benzanthine penicillin
 ASA and steroid to inhibit inflammatory
response
 Bed rest
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99. Nursing management
 Prophylaxis to prevent recurrence- monthly
Benzanthine injection
 Antipyretics
 Oral fluid- adequately
 Promoting optimal rest to decrease cardiac
work load
 Comforting pt- to relief joint pain
 Pt education
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100. Infective Endocarditis
 Infective endocarditis is an infection of the
valves and endothelial surface of the heart.
 Etiology - Bacteria
- Fungi
- Variety of invasive procedure allow
micro
organism to enter the blood stream
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101. Predisposing factor
 Cardiac conditions like valvular disease
 Congenital heart disease
 Cardiac surgery, severe burn
 Immuno suppressive conditions, cancer
 Invasive surgery- dental surgery
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102. Clinical manifestation
 Fever, chills, anorexia, weight loss, cough,
back & joint pain
 Splenomegally, murmur, CHF
 Headache.
 Lung, kidney, heart, brain manifestations)
Diagnosis-
 Determining the causative organism by blood
culture
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103. Management
 The anti biotic is usually given for 4-6 weeks.
 Penicillin is the drug of choice and for fungal
infection amphotricin B is used.
 Surgical valve replacement for pts who
develop CHF as result of aortic or mitral valve
stenosis
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104. Management
 Penicillin prophylaxis for pts who undergo
procedures known to put the pt at risk like
-Tonsillectomy
-Vaginal hysterectomy
-Urethral catheterization
-Prostatic surgery
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105. Complication
CHF
Valvular stenosis
Myocardial damage
Mycotic aneurysms
Cerebral vascular complication
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106. PERICARDITIS
 Is inflammation of the pericardium the
membrane sac involving the heart.
 It leads to fluid accumulation in the
pericardial sac & leads to the thickening of the
heart that decreases its elasticity resulting in
cardiac failure.
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107. Etiology
 Idiopathic (unknown)
 Infection
Viral
Maycotic
Bacterial
Streptococcus, meningococcus
pneumococcus
Staphylococcus, mycobacterium TB
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108. Clinical manifestation
 Fever, sweating chills
 Dyspnea due to decreased cardiac out put
 Pain- in the anterior chest
- Aggravate with breathing turning in bed
twisting of body
- Relieved by sitting up
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109. Cont’d…
Diagnosis - clinical manifestation
- ECG record
Management
- Analgesia
- Corticosteroid
- Antibiotic
- Amphotercin B for mycotic
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110. Nursing management
 Encourage the pt on bed rest
 Encourage the pt to increase activity with
improvement
 Bed rest should be reassumed if fever, pain &
friction rub reoccurs
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111. Myocardial infarction
 Myocardial infarction -refers to the process
by which myocardial tissue is destroyed in
regions of the heart that are deprived of blood
supply because of reduced coronary blood
flow.
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112. Cause
 Hemorrhage & shock decrease coronary blood
flow
 Non-sclerotic coronary artery occlusion from
emboli, trauma, inflammation,
hypercoagubility disorder.
 Thrombus in coronary artery.
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113. Pathophysiology
 Angina due to ischemia causes sustained
reversible cellular injury but myocardial
infarction is the result of sustained ischemia.
 Cardiac cells can withstand ischemia for about
20 seconds before cellular death or necrosis.
 When oxygen supply severely decreases, cell
damage starts endocardially & slowly progresses
through the epicardium.
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114. Clinical manifestation
 Lower sternal chest pain
 It is severe immobilizing pain that relieves
neither by rest nor by nitroglycerin.
 May radiate to the neck, jaw down the arms to
fingers
 Pts prefer dying than experiencing such a pain
again
 Associated symptom- nausea, dizziness,
diaphoresis, dyspnea, extreme fatigue
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115. Diagnosis
Pts history
 ECG
 Cardiac enzymes analysis
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116. Management
 Vasodilators – nitroglycerines are drugs of
choice to increase blood in supply
 Anticoagulants- heparin delays the clotting
time & reduces thrombus formation
 Thrombolytics – dissolves the thrombus and
prevents vascular occlusion
 Analgesics morphine decreases the pain and
associated anxiety
 oxygien administrations
 Surgical coronary artery by pass.
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117. Management…
 * Diabetic pts may not feel the pain as such
because of a diabetic neuropathy which
interfere with neuroceptors thus dulling the
pain experience.
 * Elderly pts may not feel the pain too because
of the decrease in neurotransmission that
occurs with aging.
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118. Complications
 Dysrthythmia
 Cardiogenic shock
 Mitral valve insufficiency
 Ventricular aneurysm etc
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119. Angina pectoris
 Angina pectoris- Is a clinical syndrome
characterized by paroxysm of pain or feeling
of pressure on the anterior chest caused by
disruption of myocardial oxygen demand &
supply.
 It occurs when myocardial oxygen demands is
greater than the capacity of arteries to supply
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120. Cont’d…
Etiology
 Coronary artery disease
 Valvular heart disease
 Hypertension
 Any factor that increase 02 demand
 Anemia
 Exercise
 Emotional stress
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121. Clinical manifestation
Pain
 Varying from pressure to agonizing pain, which
can be described as heavy, Squeezing, pressing
burning crushing.
 Occurs behind the upper or middle third of
sternum
 It may radiate to the left shoulder down the
inner aspect of the arm to the elbow, wrist &
fingers
 Typically an attack lasts less than 3 seconds &
removed by avoiding precipitating factors, rest
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122. Clinical manifestation…
Precipitating factors
 Cold – constrict blood vessels
 Heavy meal - increase blood supply to the
mesentery
Relieving factors –rest, nitroglycerine
Associated factors (symptoms)
 Dyspnea, tachycardia
 Palpitation diaphoresis
 Nausea & vomiting
 Important feature of angina pain is that it
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123. Angina pectoris…
Diagnosis
• History
• Clinical manifestation
• ECG
Management
• Nitroglycerine
• Propronalol
• Nifidipine
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124. VASCULAR DISORDER
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125. Hypertension
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126. Ob j e c t i v e s
 On completion of this session, the learner will
be able to:
1.Define normal blood pressure and categories of
abnormal pressures.
2. Identify risk factors for hypertension.
3.Describe treatment approaches for hypertension,
including lifestyle and medication therapy.
4. Use the nursing process as a framework for care
of the patient with hypertension.
5. Describe hypertensive crises and their treatment.
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127. Hypertension…
 Hypertension is defined as a systolic blood
pressure greater than 140 mm Hg and a
diastolic pressure greater than 90 mm Hg
based on the average of two or more accurate
blood pressure measurements taken during two
or more contacts with a health care provider.
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128. Stages of hypertension
 Prehypertension is a warning sign that you may
get high blood pressure in the future.
 It is characterized by the systolic reading of 120
mmHg-139 mmHg, or the diastolic of 80 mmHg-
89 mmHg.
 It is a risk factor for high blood pressure in the
future.
 It can be treated with diet, lifestyle habits,
and medications.
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129. Cont’d…
High blood pressure increases your risk of
 Heart attack,
 Stroke,
 coronary heart disease,
 Heart failure, and
 Kidney failure.
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130. Cont’d…
 Mild hypertension diastolic blood pressure 90–
99 mmHg, systolic blood pressure 140–149
mmHg.
 Moderate hypertension diastolic blood
pressure 100–109 mmHg, systolic blood
pressure 150–159 mmHg.
 Severe hypertension diastolic blood pressure
110 mmHg or greater, systolic blood pressure
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131. Sign and symptoms of Hypertension
 People with hypertension is asymptomatic
and remain so for many years. i.e. It is a silent
killer.
 However, when specific signs and symptoms
appear, they usually indicate vascular damage,
with specific manifestations related to the
organs served by the involved vessels.
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132. Cont’d…
 Retinal change such as hemorrhages,
exudates(fluid accumulation), arteriolar
narrowing, and small infarctions occur.
 In severe hypertension, papilledema (swelling
of the optic disk) may be seen.
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133. Cont’d…
 Coronary artery disease with angina and
myocardial infarction are common
consequences of hypertension.
 Left ventricular hypertrophy occurs in
response to the increased workload placed on
the ventricle as it contracts against higher
systemic pressure.
 Heart failure
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134. Reading assignment on the Pathophysiology
of Hypertension
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135. Investigations
 Urinalysis
 Blood chemistry potassium, sodium,
creatinine/estimated glomerular filtration rate
 Fasting blood glucose
 Fasting total cholesterol, high-density
lipoprotein (HDL) cholesterol, low-density
lipoprotein (LDL) cholesterol, triglycerides
 Electrocardiogram (ECG)
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136. Management of Hypertension
Non pharmacology
Pharmacological
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137. Treatment Objectives
 Detection and management of other
cardiovascular risk factors
 Detection and management of target organ
damage
 Prevention of target organ damage
 Decrease the side effects of medications
 Achieve target blood pressure (<
140/90mmHg, in patients having diabetes with
proteinuria and chronic kidney disease (<
130/80 mmHg)
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138. Non pharmacologic
Smoking cessation
Complete cessation of smoking
Physical activity: At least 30 minutes of
moderate intensity activity 5-7 days per week
Weight reduction: BMI 18-24kg/m2
Dietary recommendations
Reduce salt intake: about1 tsp of table salt.
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139. Cont’d…
 Alcohol consumption: limited to two drinks or
less per day (one standard drink)
 1 bottle (341 mL) of 5% beer or,
 1 glass (150 mL) of 12% wine or,
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140. Hypotension
 It is diminished tension, lowered B/P, systolic
< 90 mm of Hg & Diastolic less than 60 mm
Hg.
 An extremely low B/P is occasionally
symptoms of a serious condition which can
result in shock.
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141. Types of Hypotension
 Orthostatic (postural) hypotension
Associated with dizziness, Syncope, & blurred
vision occurring up on standing or when standing
motionless in fixed position.
 Hypotensive hypotension
Characterized by abnormal low B/P due to
decreased volume.
 Hypotens or hypotension
Occur because of substance that lowers the B/P
Example Antihypertensive drugs when taken in
large dose.
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142. Causes of Hypotension
Blood loss
 Dehydration (diaphoresis, diarrhoea,
vomiting, not taking fluids)
High dose of anti hypertensive drugs (diuretic,
vasodilators)
 Systemic disease (Malaria & Septicaemia)
 Hormonal (Addison’s disease), & Poison
(snake bite & orally taken poisons).
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143. Clinical Manifestations
Dizziness, Syncope & even shock, tachycardia.
Diagnosis
• Physical examination (Measuring B/P & Pulse
rate).
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144. Management
The objective is to increase the B/P to the normal
level.
Treat the patient based on the identified problem,
Remove the cause; Blood loss should be
transfused if severe.
Dehydration should be replaced with IV or oral
fluid.
If drug over dose withheld it & correct B/P
If hormonal example Addison’s increase salt &
Sugar intake.
If poison Adrenalin or hydrocortisone may be
used.
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145. Nursing Care
Take B/P on regular base
 Measure intake & out put
Educate the patient how to prevent &
Educate the patient on the adherence to
treatment
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146. DISEASE OF THE ARTERIES
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147. Arteriosclerosis
It is the hardening of the arteries.
It is a diffuse process where the muscle fibres
& endothelial lining of the wall of small
arteries & arterioles become thickened.
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148. Atherosclerosis
• It affects the intimae of the large & medium
sized arteries.
• These changes consists the accumulation of
lipids, calcium, blood components,
carbohydrate & fibres tissue in the intimae
layer of the artery.
• These accumulations are referred to us
Atheromas or plaques.
• ECG interpretation
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149. Aneurysm
• Aneurysm is a sac formed by localized dilation
of an artery or vein.
• The most common affected are renal artery,
abdominal artery, subclavian artery & most
frequently poplitial artery.
Cause
• Congenital, Traumatic & infections (usually
localized infections).
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150. Cont..
Clinical manifestations
Mass & pulsation with disturbance of peripheral
circulation
Pain & swelling because of pressure on adjacent
nerve.
Diagnosis
x-ray
Management
 Surgical repair with replacement graft.
The prognosis of ruptured aneurysm is poor so it
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151. Complications
• Rupture & bleeding if there is coexisting
hypertension & thrombi formation.
Nursing care
• Encourage the patient to move the legs to
prevent stasis & increased circulation
• Anticoagulant after surgery, & assess after
surgical incision frequently for evidence
haemorrhage.
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152. Disorders of the veins
Phlebitis
• It is an inflammation of the vein related to both
chemicals and mechanical irritation,
characterized by reddened warm area around
the insertion site or a long the path of the vein
& swelling.
• Incidence – Length of the IV line, composition
of fluid (medication) especially it’s PH,
tonicity, size & site of cannula, improper
anchoring of the line & introduction of micro
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153. Treatment
• Discontinue the IV line & start on other site.
• Apply warm & moist compress.
• The prevention is avoiding the incidence
factors.
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154. Phlebothrombosis
• When a clot develops initially in veins as a
result of stasis or hypercoagulability with out
inflammation.
• Three factors play a significant role in its
development.
Stasis of blood
vessel wall injury &
altered blood coagulation.
• Presences of at least two of these factors are
necessary for thrombus to occur.
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155. Thrombophlebitis
It is the inflammation of the wall of the veins
& is frequently accompanied by formation of a
clot or presence of a clot plus inflammation in
the veins.
 Vein thrombus can occur in any vein but
occurs most frequently in deep veins of the
lower extremities (but both superficial & deep
veins thrombus can occur).
All surgical patients are at risk for deep vein
thrombosis.
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156. Deep Vein Thrombosis
Produces oedema & swelling, of the extremities
because venous blood flows is inhibited.
Other sign & symptom includes warm skin,
prominent superficial vein & tenderness.
Superficial Veins
 The risk of superficial vein thrombi become
dislodge is very rare because most of them
dislodge spontaneously.
The sign & symptom includes localized pain
(tenderness), redness & warmth.
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157. Risk Factors for Deep Vein Thrombosis
Endothelial damage-leg trauma, surgery,
central venous catheters & local vein damage.
Venous Stasis– immobilization, bed rest,
obesity, history of varicosities & over 65 yrs.
 Coagulopathy– malignancy, pregnancy, OC,
polycythemia, leukocytosis, thrombocytosis
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158. Cont’d
Preventive Measures– Elastic stocking for
patient with venous insufficiency
,administration of subcutaneous heparin for
surgical patient.
Body position & exercise (elevate feet & lower
leg periodically above the level of the heart,
active & passive leg exercise & early
ambulation).
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159. Cont’d….
Management – active application of the
preventive measures should be applied.
Contraindications to Anticoagulant therapy –
bleeding from GI, GU, & Respiratory, severe
hepatic or renal disease.
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160. Varicose Veins
Varicose vein (Varicosities) are abnormal
dilated tortuous superficial vein caused by
incompetent venous valves.
Commonly occurs in lower extremities.
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161. Pathophysiology
Primarily (with out involvement of deep veins)
& Secondary (resulting from obstruction of
deep veins).
When superficial veins are affected the person
may have no symptoms but may be troubled
by cosmetic appearance of the dilated veins.
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162. Cont’d…
 If symptoms present it includes dull pain;
muscle cramps & increase muscle fatigue.
 When deep vein obstruction oedema, pain,
pigmentation, ulceration, & increase
susceptibility to infection.
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163. Management
Surgery, Sclerotherapy (irritating chemicals
such as 0.5 % Na tetradecyl sulphates is
injected in to the vein, elastic bandages
application, elevating the lower extremities &
avoid long standing.
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164. Hematologic disorders
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165. Anaemia
It is a condition in which the haemoglobin
concentration is lower than normal.
 It reflects the presences of fewer RBCs than
normal in the circulation.
As a result the amount of oxygen delivered to
the tissue is decreased.
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166. Cont’d…
 There are many kinds of anaemia;
Some are due to inadequate production of RBC
Premature excessive destruction of RBC
 Blood loss
Deficit in nutrients eg.vit
 Heredity factor (unknown origin) &
Chronic disease.
 Iron deficiency anaemia is the most common
anaemia in the world.
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167. Aetiology & Classification
1. Hypoproliferative anaemia - is a deficiency of
RBCs because of their defect in their
production.
These are:
A. Iron deficiency anaemia - because of decreased
iron
B. Megaloblastic anaemia - because of decreased
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168. Cont’d…
C. Foliate deficiency anaemia - because of
decreased or deficiency of folic acid.
D. Aplastic anaemia- Anaemia due to bone
marrow failure. When the bone marrow is
depressed (e.g. by medication, tumours, toxin).
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169. Cont’d…
2. Haemorrhagic Anaemia - is anaemia due to
excessive bleeding potentially occurring from any
major source such as GIT, uterus, nose
(epistaxis), wound etc.
2.1. Acute post haemorrhagic anaemia – It is
anaemia resulted from an immediate haemorrhage
example Accidents, Gunshot etc.
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170. Cont’d…
2.2. Normocytic Normochromic Anaemia
( Normal size of RBC & normal color of RBC)
 It develops following large loss of blood.
The sign & symptom of normocytic anaemia is
RBC < 1000, 000/mm3, Leukopenia (<
2000/mm3), & Thrombocytopenia (<
300,000/mm3).
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171. Cont’d…
2.3. Chronic Blood Loss Anaemia – Anaemia
due to chronic bleeding (Epistaxis, bleeding
from cancerous lesion).
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172. Cont’d…
3. Haemolytic Anaemia – it may occur because of
over active reticulo endothelial system(RES) or
other problems. These can be:-
3.1- Sickle cell anaemia - cell lyses occurs because
of the abnormal shape of RBCs.
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173. Cont’d…
 It is a chronic hereditary disorder characterized
by the presence of RBC that contains
abnormal haemoglobin (Hgb).
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174. Cont’d…
3.2- Hypersplenism anaemia- RBCs cell lysis
occurs because of hyperactive RES.
3.3. Anaemia b/c of haemolytic transfusion
reaction –
It is anaemia due to clumping of RBC
(haemolysis).
 Example Erythroblastosis fetalis.
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175. Cont’d…
 Two types of haemolytic anaemia;
Intracorpusular (haemolysis in the cell) example
enzympathy (G6Pd) deficiency; fragile RBCs <
120 days
Extracorpusular (haemolysis out side the cell)
example trauma, & Protozoal infections (malaria).
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176. The three-hall marks of haemolytic anaemia
are
Decreased RBC life span (90-120 days),
Increase number of RBC destroyed &
Failure of the bone marrow to compensate for
the vast number of RBC destroyed.
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177. Pathophysiology
When anaemia occurs because of the above
different reasons, the demand of oxygen will
increase stimulating the heart to increase its
out put.
When this condition continues for longer
period of time the heart finally fails to pump
the required blood.
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178. Sign & Symptoms-
 Retculocytosis (formation of immature RBCs),
 Jaundice,
 Cholelithiasis (Gallstone),
 Hepatomegally,
 Hyperbilirubinemia with high urinary & faecal
uribilinogen) &
 Haemoglobinemia,
 Haemoglobinuria (especially with haemolytic),
tachycardia, fast breathing, dyspnea, fatigue and
edema.
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179. Management
 Eliminate the cause e.g. Malaria
 Fluid & electrolyte balance, Maintain renal
function
 Blood transfusion & Spleenectomy for
autoimmune disorder.
 Remove steroids, Antibiotics & vitamins to
activate the bone marrow.
 Oxygen, rest, maintain renal function,
 Iron, folic acid, vitamin B 12 supplements.
 Fluid and electrolyte balance.
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180. Nursing management-
 Correct medication administration.
 Monitoring the pt if the pt is taking fluid,
blood, oxygen etc.
 Pt educations on diet, avoidance of bare foot,
prevention of hook warm related anaemia
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181. HEMORRHAGIC DISORDER
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182. HEMORRHAGIC DISORDER
1. Purpura – is a bleeding in the skin, mucous
membrane or the subcutaneous tissue.
These hemorrhagic spots do not disappear on
pressure.
2. Ecchymosis – larger purpuric haemorrhage
3. Pitachiae – these are tiny purpuric
haemorrhage of pinpoint or pinhead sized
purpura.
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183. 4. Thrombocytopenic purpura – purpura that
occurs because of failure of the coagulation
process.
This may be due to deficiency of circulating
blood platelets.
 The reduced number of the thrombocytes may
be primary or secondary.
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184. 5.Thrombocytopenia– is a condition in which the
number of platelets is decreased because of
decreased production by the bone marrow,
increased destruction by the autoimmune
reaction or increased consumption.
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185. Cause –
A/ Primary or idiopatic thrombocytopenia – with
unknown cause
B/ Secondary thrombocytopenia – occurs as a
result of depressed bone marrow activity that is
associated with radiation exposure, drug
sensitivity and anticancer drugs.
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186. Clinical manifestation.
Pitachiae, nasals and gingival bleeding, heavy
menses in women.
Excessive bleeding after procedures,
intracranial or intestinal hemorrhage.
The purpuric area may appear on the skin (dry
purpura) or on the mucous membrane (wet
purpura) from the nose, GIT, GUT, lung.
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187. Management
Platelet transfusion
Rest,
Corticosteroids
Remove the medications that prolong the
clotting time e.g. aspirin, quinine etc.
Splenoctomy if more severe.
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188. 6. Haemophilia (Clotting Factor Defects)
 It is a hereditary disease caused by deficiency
of a clotting factor VIII (Haemophilia A) and
factor IX (Haemophilia B)
 Factor VIII deficiency is about 3 times more
common.
 Males are affected mostly.
 Females are also affected but mostly they are
asymptomatic.
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189. Clinical Presentations
Spreading bruises & bleeding in to muscle,
joint & soft tissues.
Haemorrhage after minimal trauma
Joint pain (joint haemorrhage in sever case),
haematuria & GI bleeding.
Pain, swelling and limited motion of the joints.
Spontaneous hematuria, GIT bleeding.
Many patient die before they reach adult hood.
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190. Management –
IV administration of clotting factor VIII & IX.
Never administer ASA (b/c it prolong the clotting
time)
 IM injections are contraindicated
Complications
Bleeding episodes.
Ankylosis (fixation) of joint from haemorrhage
Spontaneous haematuria & GI bleeding
Risk of blood born infections due to repeated
transfusion e.g. HIV, hepatitis virus.
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191. Nursing management –
• Educate pt to avoid conditions that induce
bleeding e.g. drugs (Aspirin, NSAIDs) &
procedures.
• Assist the pt to cope with the disease.
• Avoid hazardous practice that cause injury
• Cold compress to avoid joint pain, assess and
quantify bleedings.
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192. POLYCYTHEMIA
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193. POLYCYTHEMIA
• Polycythemia refers to an increased volume of
RBCs. It is a term used when the hematocrit
is elevated (to more than 55% in males, more
than 50% in females).
• Dehydration (decreased volume of plasma) can
cause an elevated hematocrit, but not typically
to the level to be considered polycythemia.
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194. Pathophysiology of Polycythemia
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195. • Normal hematocrit at FMLH:
–Male 47  5 percent
–Female 42  5 percent
• Normal hemoglobin at FMLH:
–Male 15  2 gm/dl
–Female 13.5  1.5 gm/dl
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196. Classification
Polycythemia is classified as either
• Primary polycythemia/ polycythemia vera
• Secondary polycythemia
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197. A. Primary polycthemia
 Is a proliferation disorder in which all the
marrow cells that produce RBCs seem to have
escaped from the normal control mechanism.
 Here the myeloid cells from which RBCs are
produced become out of the normal control
mechanism.
 The bone marrow is hyper cellular and
consequently the number of the RBCs,
platelets increase but the RBCs count is highly
predominant.
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198. B. Secondary polycythemia
Is caused by excessive production of
erythropoetin.
This may occur in response to a reduced
amount of oxygen, which acts as a hypoxic
stimulus as in COPD, or cyanotic heart
disease.
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199. Clinical manifestation
Hepato or splenomegally,
Headache, dizziness, and pruiritis
Complications
 Thrombolytic disorder.
 Excessive bleeding because of abnormal
functioning platelets
 CHF, hypertension, death
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200. Management
Phlebotomy (removal of blood from the vein).
Treating the primary cause
 Antihistamines for the pruiritis
Suppressing the function of the bone marrow
by radioactive phosphorous etc.
Fluid replacement
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201. Nursing Care
Prevent complications (CHF);
Avoid infections,
Oral & skin care
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202. Leukaemia
Leukaemia is a persistent unregulated and
abnormal proliferation or accumulation of
WBC in the bone marrow.
There is also proliferation abnormally in the
liver, spleen & lymph node & invasion of non-
haematologic organs such as Meninges, GIT,
Kidney, & Skin.
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203. Cause
 unknown but genetic predisposition
 radiation exposure
viral pathogenesis and
chemicals as benzene play a major role in the
predisposition.
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204. classification
Two types are there: -
• Acute leukaemia
• Chronic leukaemia
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205. Acute leukaemia
 It may be lymphocytic (is the most common
variety and common in children), granulocytic
or monocytic.
It is the most common cause of death from
malignant disease in children.
Clinical Manifestations
– Acute onset with fever, general malaise,
epistaxis.
- Gum bleeding, muscular and joint pain.
- Spleeno or hepathomegally.
- Increased WBC count (as much as 20-50,000/
mm3
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206. Cont’d…
• Complication
–Bleeding
–infection
–death
• Diagnosis
– CBC shows decrease erythrocyte &
platelets
–Bone marrow specimen shows excess
immature blast cells.
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207. B/ Chronic leukaemia
 It is uncontrolled proliferation of immature
WBCs from the bone marrow, spleen and liver.
Clinical Manifestations
 Many pts are asympyomatic but some may
develop:
Shortage of breath
Confusion
spleeno or hepatomegally
Malaise
Anorexia
weight loss.
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208. Management
• Chemotherapy and
• Radiotherapy .
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209. Supportive Care
 Administering blood products treat infections
 Bone marrow transplantation after destruction of
leukemic marrow by chemotherapy.
 Rest and prevention of unnecessary expenditure
of energy
 Assisting the pt in turning and moving.
 Increase fluid intake.
 Encourage the pt on high calorie and high
vitamin diet.
 Advise the pt on oral hygiene and skin care.
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210. Prognosis
With treatment survive an average of only one
year.
 The cause for death is infection or
haemorrhage.
 Untreated patients survive only about 2 –5
months.
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211. 5/30/2023 211
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212. The end
THANK YOU
THANK YOU FOR
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