CARDIOVASCULAR

CONDITIONS
PURPOSE
The purpose of this course is to enable
the learner acquire knowledge, attitude
to be able to promote health, prevent
illness, diagnose, manage & coordinate
rehabilitation of adults suffering from
common cardiovascular diseases.
CARDIOVASCULAR
CONDITIONS
MAIN OBJECTIVE
The learner will acquire knowledge, develop
skills & attitudes on cardiovascular
disorders in order to provide effective
care to patients
LEARNING OBJECTIVES
Upon completion of this course the learner
should be able to :
1. Recall the anatomy & physiology of the
heart & the blood vessels
2. Describe common cardiovascular
diseases/conditions
ASSESSMENT
PHYSICAL ASSESSMENT
1. General appearance
 Breathing-stiffness of the lungs
 Cyanosis-inadequate oxygenation of
the blood
 Pain-may appear pale,cold and
clammy.when from heart muscles,pt
prefer to lie on back
 Clubbing of fingers-congenital heart
disease
 Level of orientation & clarity of thinking
ASSESSMENT
 2.Evaluate Bp

Pulse pressure: difference between

systolic & diastolic pressure.
Assess for postural hypotension
Take BP sitting, standing, & lying if
having problems with pressure
changes.
ASSESSMENT
 Paradoxical BP. (paradoxical pulse) a
decrease of systolic BP of at least 10
mmHg that occurs during inspiration.
3. Evaluate quality & rate of pulse;
assess for dysrhythmia as
 Pulse deficit: radial pulse rate is less
than epical pulse rate. Occurs in atrial
fibrillation
 Pulsus alternans: regular rhythm but
quality
ASSESSMENT
Of pulse alternates with strong beats and
weak beats.
 Thready pulse: weak and rapid, difficult to
count.
4. Assess quality and pattern of
respirations and evidence of respiratory
difficulty.
5. Auscultation of the heart
a) Heart sounds heard during the cardiac
cycle
 S1: closure of mitral valve and tricuspid
valves
ASSESSMENT
 S2: closure of the aortic & pulmonary
valves.
 S3: represents rapid ventricular filling;
normal in children & young adults; in
adults older than 30 years, it may
an indication of ventricular dysfunction.
 S4: gallop sounds heard during atrial
contraction are abnormal; may occur in
tachycardia.
(b) Presence of murmurs created by
turbulent blood flow
ASSESSMENT
 Abnormal flow through diseased valves,
stenosis and insufficiency.
 Increased rate or velocity of flow of
blood.
 Abnormal flow of blood between cardiac
chambers(congenital heart disease)
(c) Presence of a friction rub; rubbing and
inflammation of the visceral and parietal
layers of the pericardium.
pericardial friction rubs are heard
throughout the respiratory cycle.
ASSESSMENT
6. Evaluate adequacy of peripheral
vascular
circulation and check for presence of
peripheral edema.
7. Evaluate for presence of chest
discomfort
 Location
 Intensity if pain
 Precipitating causes.
ASSESSMENT
HISTORY TAKING
1. Identify presence of risk factors for the
development of arteriosclerotic
disease
2. Coping strategies
3. Respiratory
a. History of difficulty breathing
b. Medications taken for respiratory
problems
c. Determine normal activity level
ASSESSMENT
4. Circulation.
a. History of chest discomfort
i. Precipitating factors;
 May occur without precipitating
factors
 Physical exertion
 Emotional stress
 Eating a large meal
ASSESSMENT
 Smothering-suffocate/obstruct
 Burning
 Severe pain
 Increases with movement

iii. Region & Radiation

 Substernal or retrosternal
 Spreads across the chest
 Radiates to the side of either or both
arms, the neck, the jaw, upper
abdomen.
ASSESSMENT
iv. Symptoms & Signs (Associated with)
 Diaphoresis, cold clammy skin
 Nausea, vomiting
 Dyspnea-difficulty in breathing
 Orthopnea
 Syncope-loss of consciousness due to fainting
 Apprehension
 Dysrhythmias-abnormality in the rate, regularity, or
sequence of cardiac activation. Also called cardiac
arrhythmia.
 Palpitations
 Auscultation of extra heart sounds
 Auscultation of crackles
 weakness
ASSESSMENT
v. Timing & Response to Treatment
 Sudden onset
 Constant
 Duration >30 min
 Not relieved with nitrates or rest
 Relief with narcotics
b. History of edema & weight gain
c. History of syncope
d. Medication taken for the heart or for
high blood pressure.
ASSESSMENT
INVESTIGATIONS (HOME WORK)
1. Doppler Ultrasound flow studies
2. Exercise Stress test (EST)
3. Computed Tomography (CT)
4. Duplex Ultrasound
5. CT angiography
6. Magnetic Resonance Angiography
7. angiography
ASSESSMENT
8. Lymphangiography
9. Lymphoscintigraphy
10. Contrast Plebography
11. Air Plethysmography
12. Chest X-ray
13. Electrocardiography
14. Cardiac catheterization
15. Echocardiogram
16. Lab tests; CBC, electrolytes, cardiac
enzymes, lipid profile, urine tests etc.
ARTERIOSCLEROSIS AND
ATHEROSCLEROSIS
ARTERIOSCLEROSIS refers to hardening of
the arteries through a diffuse process
whereby the muscle fibers and the
endothelial lining of the walls of small
arteries & arterioles thicken.
ATHEROSCLEROSIS is disease process
involving the accumulation of lipids,
calcium, blood components,
carbohydrates, & fibrous tissue on the
intimal layer of large or medium-sized
artery .
 Both develop over a long period (beginning
in early childhood). Rarely does one occur
without the other.
RISK FACTORS
Modifiable
 Nicotine use (i.e tobacco smoking or
chewing)
 Diet
 Hypertension
 Diabetes mellitus (thickens the basement
membranes of large & small vessels)
 Obesity
 Stress
 Sedentary lifestyle
 Elevated CRP-C-Reactive proteins
 Hyperhomocysteinemia

Non-modifiable
 Age (above 50 years)
 Gender
 Familial predisposition/ genetics
Arteries commonly affected by
atherosclerosis
1. Cerebral vascular arteries causing stroke
(CVA)
2. Coronary artery causing myocardial
infarction
3. Aorta causing aneurysm, peripheral vascular
disease.
4. Renal artery causing hypertension and renal
failure
5. Large peripheral arteries causing peripheral
vascular disease
PATHOPHYSIOLOGY
 Atherosclerosis affects the inner lining of
the artery. First there is injury to the
endothelial cells that line the walls of the
arteries.
 The injury causes inflammation & immune
reactions.
 Lipids, platelets & other clotting factors
accumulate. Scar tissue replaces some of
the arterial wall.
 An early indication of injury is a fatty streak
on the lining of the artery. This build-up of
fatty deposits is known as plaque.
 Plaque has irregular, jagged edges that
allow blood cells & other material to adhere
to the wall of the artery.
 Over time this build-up becomes calcified &
hardened (arteriosclerotic), causing the
turbulence that damages cells and
increases the build-up within the vessel.
 As the vessel becomes stenosed
(narrowed), partial or total occlusion of the
artery may occur, resulting in reduced
blood flow.
 The area distal to the occlusion may
become ischemic as a result.
SIGNS & SYMPTOMS
 Chest pain
 Dizziness
 Pallor in the nail beds
 Reddish-purple colour in the extremities
 Thickened nails
 Dry skin with loss of hair
 Diminished peripheral pulses
 Extremities skin temperature is cool
 Prolonged capillary refill
DIAGNOSTIC TESTS

 Total cholesterol (often elevated)-high

LDL
 Blood glucose level-high
 Angiography-x-ray of blood vessels
 Doppler ultrasound-narrowed lumen
 Cardiac catheterization-high pressure
TREATMENT
 A healthy Lifestyle; avoid saturated fats,
to be exercising, & stop smoking.
 Cholesterol screening
 Frequent check-ups & medications i.e
statins, fibrates (to lower triglycerides),
niacin (prevents conversion of fats into
very LDL)
NURSING INTERVENTION
 Identify individuals at risk & provide diet
low in saturated fat
 Recommend testing again in 6 months.
 Identify specific areas of involvement &
give specific nursing care of that area.
 Treat underlying causes
i.e.HTN,DM,OBESITY
PERIPHERAL ARTERIAL
OCCLUSIIVE DISEASE
Involves narrowing & obstruction of the
arteries of the extremities, especially
the lower extremities.
RISK FACTORS
1. Age; generally occurs during the fifth
or sixth decade of life.
2. Familial tendency
3. Hypertension & diabetes accelerate
the process
CLINICAL MANIFESTATIONS
1. Intermittent claudication (ischemic pain
during exercise).
2. Ischemic pain at rest particularly at night
(increasing in severity)
3. Paresthesia(prickling) of the feet
4. Pallor when extremity is elevated
5. Dependent rubor: dusky, purplish
discoloration of extremity when in
dependent position
6. Decreased or absent peripheral pulses;
pedal, popliteal, & femoral.
7. Poor healing of injuries on the
extremities.
8. Changes in the skin; cool to touch.
shiny, fragile, poor turgor. Dry & scaly.
Loss of hair on lower leg.
9. Brittle, thick toenails.
10. Ulcerations & gangrane
DIAGNOSTICS
a) Arteriogram-x-ray of artery after
injecting with a radio opaque material
b) Plethysmography –measures changes
of blood volume
c) Exercise tolerance testing
d) Ankle-brachial index
TREATMENT
Medical
1. Antiplatelet agent-reduce clotting
2. Stop smoking-stop damaging the walls
of arteries
3. Decrease dietary cholesterol
intake(saturated fats)
4. Exercise program as tolerated
5. Decrease viscosity of blood-more fluidy
(anticoagulants)
Surgical: procedures are done when
intermittent claudication incapacitates the
client, or when circulation must be restored
to salvage a limb.
1. Peripheral atherectomy: removal of
plaque within the artery.
2. Bypass graft: bypass of an obstruction by
suturing a graft proximally & distally to
the obstruction.
3. Intravascular stent: placement of a stent
 within a narrowed vessel to maintain
patency.
Other methods
1. Percutaneous transluminal angioplasty:
use of a balloon catheter to compress the
plaque against the arterial wall.
2. Laser assisted angiography: a probe is
advanced through a cannula to the area
of occlusion; a laser is used to vaporize
the atherosclerotic plaque
NURSING INTERVENTION
 Assess & compare peripheral pulses.
 Evaluate skin of the affected extremity:
color & warmth, capillary refill, condition
of the skin & nail bed, presence of ulcers
or lesions.
 Assess level of exercise tolerance
 To prevent injury & infection.
 Avoid vigorous rubbing of the extremity-
emboli
 Prevent skin breakdown at pressure
sites.
 Use heel covers & bed cradle to prevent
pressure on the toes & heels.
 Visually inspect extremities for:
discolored areas, breaks in skin,& signs
of infection.
 Encourage moderate exercise e.g
walking but not for pts with ulcers or on
the leg.
 Promote blood flow to legs
 Elevate the foot of bed on blocks.
 Avoid standing in one position for
prolonged periods.
 Avoid crossing legs at the knees or at
ankles.
 Active postural exercises.
 Avoid clothes & bandages that restrict
circulation to the lower extremities
 Stop smoking
ARTERIAL THROMBUS
A thrombus is a blood clot that remains
attached to a vessel wall.
A detached thrombus is a
thromboembolus
Thrombi tend to develop wherever
intravascular conditions, cascade (e.g
intimal irritation, roughening,
inflammation, traumatic injury,
infection, low blood pressures or
obstructions that cause blood stasis &
pooling within the vessels).
CAUSES OF ARTERIAL THROMBUS
Activation of the coagulation cascade is
usually caused by;
1. Roughening of the tunica intima by
atherosclerosis.
2. Invasion of the tunica intima by an
infectious agent causes roughening
leading to adhesion of platelets readily.
3. Anatomic changes especially those
causing pooling of arterial blood can
stimulate thrombus formation
 Arterial thrombus may grow large enough
to occlude the artery, causing ischemia in
tissue supplied by the artery.
 Thromboembolus can occlude flow of blood
into a distal systemic vascular bed.
TREATMENT
1. Thrombolytics or heparin, warfarin
derivatives.
2. A balloon-tipped catheter can be used to
remove or compress an arterial thrombus.
 EMBOLISM
Embolism is the obstruction of a vessel by an
embolus.
Embolus is a bolus of matter circulating in
the blood stream.
 Systemic (or arterial) emboli most
commonly originates in the left heart & are
associated with thrombi after myocardial
infarction, valvular disease, left heart
failure, endocarditis, & dysrhythmias.
 Embolism causes ischemia or infarction in
tissues distal to the obstruction. Embolism
of a central organ causes organ dysfunction
& pain.
 Embolism of a coronary or cerebral artery is
an immediate threat to life if the embolus
severely obstructs a major vessel.
 Other vessels that are commonly blocked
by arterial thromboembolism are lower
extremities’ femoral & popliteal arteries.
CLINICAL MANIFESTATIONS
1. Acute severe pain
2. Gradual loss of sensory & motor function
3. Pallor & cold (poikilothermia)
4. Pulselessness
5. Parasthesia
6. Paralysis
7. Colapsed superficial veins
DIAGNOSTIC FINDINGS
1. Sudden & acute nature of the onset of
symptoms & apparent source of embolus
2. Transesophageal echocardiography.
3. Chest x-ray
4. ECG
5. Doppler ultrasound
MEDICAL MANAGEMENT
Depends on it’s cause.
 Acute embolic occlusion requires urgent surgery.
 Heparin therapy to prevent further development of
emboli & existing thrombi.
 Intra-arterial thrombolytic agent-
streptokinase/urokinase to dissolve the embolus.
Contraindications to thrombolytic therapy
include
 Active internal bleeding
 Stroke
 Recent major surgery
 Uncontrolled hypertension & pregnancy.
NURSING MANAGEMENT
BEFORE SURGERY
1. Bed rest with extremity level slightly (15
degrees) dependent.
2. Affected part is kept at room temperature
& protected from trauma (foot cradles to
protect leg )
AFTER SURGERY
1. Nurse collaborates with surgeon about
patient’s activity level based on pt’s
condition
2. Generally leg movement is encouraged to
stimulate circulation.
3. Anticoagulant therapy may be continued
4. Assess for evidence of hemorrhage (local &
systemic) including mental status changes.
5. Monitor pulses, sensory & motor functions,
Doppler signals hrly to note reocclusion.
6. Monitor for complications: metabolic
abnormalities, renal failure, & compartment
syndrome( muscle, nerves, & vessels are
restricted to a confined space [myofascial
compartment] within an extremity.
ANEURYSM
A localized dilation, out-pouching or sac
formation on the an arterial vessel or
cardiac chamber.
CLASSIFICATION
They are classified according to their
characteristics
True aneurysms involve all three layers of
the arterial wall & are best described as a
weakening of the vessel wall.
Most are fusiform (i.e tapering at both
ends) & circumferential. E.g dissecting,
Saccular.
False aneurysm or pseudo-aneurysm is an
extravascular hematoma that
communicates with the intravascular space.
A common cause of this type of lesion is a
leak between a vascular graft & a natural
artery.
RISK FACTORS OF ANEURYSM
1. Atherosclerosis
2. Hypertension
3. Smoking
4. Trauma
5. Congenital abnormalities
6. Familial tendencies
 TYPES OF ANEURYSMS
1. Abdominal aortic aneurysm: occurs
primarily in the abdominal aorta below the
renal arteries.
Clinical manifestations
Maybe asymptomic
2. Back, flank, or abdominal pain
3. Epigastric discomfort
2. Pulsating abdominal mass may be
palpable.
Signs of rupture
a) Shock, hypotension
b) Oliguria
c) Dysrhythmias-irregular brain waves
d) Abdominal distention
e) Hematoma formation in the flank region
f) Client describes a tearing or ripping
sensation
2. Thoracic aortic aneurysm: located in
the thoracic area.
Risk factors
 Atherosclerosis
 Tear grafting
 Age 50-70 yrs.

Clinical manifestations
Generally asymptomatic
1. Client may complain of severe chest pain
2. Pressure on the oesophagus may cause
dysphagia
3. Pressure on the vena cava may cause
edema
4. Dyspnea
Signs of rupture
a) Sudden excruciating(extreme) back &/or
chest pain
b) Hypotension progressing to shock
Dissecting aortic aneurysm
Characterised by bleeding between the
layers of the vessel.Thoracic area is the
most common site for dissection.
Clinical manifestation of dissecting
aneurysm
1. Constant intense pain
2. Drop in BP, rapidly leading to
hemorrhagic shock
3. In abdominal aortic aneurysm
dissection, the abdomen may remain
soft.
DIAGNOSTICS FOR ANEURYSMS
 X-ray films
 Aortography
 Sonography
 MRI
 Transesophageal echo cardiogram
 Duplex uls
 CT scan
COMPLICATIONS OF ANEURYSMS
 Rupture
 Emboli
 Haemorrhage
 Renal failure

TREATMENT
Prevention of rupture;
A. Identify aneurysm & control blood pressure
B. Endovascular stent graft
C. Surgical resection & graft
NURSING INTERVENTION
To prepare client & family for anticipated
surgery.
 Pre-op. care
 Identify other chronic health problems
 Evaluate characteristics of pulses in the
lower extremities & mark for evaluation after
surgery.
 Do not rigorously palpate the abdomen
 Evaluate for indications of dissection
 Maintain BP at normal level to decrease risk
of rupture
To promote graft patency & circulation
 General post-op care
 Maintain adequate BP to facilitate filling of
the graft.
 Monitor for hemorrhage: assess for
increasing abdominal girth, back pain,
indications for hypovolemia or shock.
 Hourly check of peripheral circulation,
sensations, & movement for first 24 hours.
 Evaluate blood, urea & nitrogen & serum
creatinine levels to assess renal function.
To maintain adequate homeostasis & prevent
infection
 Monitor acid-base balance
 Maintain adequate body warmth in initial
post-op period
 NG suction in immediate post-op period
 Evaluate status of GI system
 Bowel sounds
 Distention
 Passage of flatus
 Diarrhea
 Teach activity restrictions: no heavy lifting
for 6 to 12 weeks
 CT scanning for client who have not
undergone surgical repair.
BERRY ANEURYSM
Occurs in intracranial arteries. Lesions are
small & balloon shaped. Problem occurs
because of location & encroachment on
brain tissue.
Risk factors
Age: 50-60 years old
Atherosclerosis resulting in weakness of the
vessel wall
Hypertension
Head trauma may increase the risk
Clinical manifestations
Severe headache
Intermittent nausea
Signs of rupture
a) Severe headache continues
b) Seizure
c) Nuchal rigidity(neck region)
d) Hemiparesis (paralysis of one side of the
body)
e) Loss of consciousness
f) Symptoms of increased intracranial pressure
 Severity of symptoms depend on the
site & amount of bleeding.
DIAGNOSTICS
 LP- revealing blood in CSF
 Cerebral angiogram
 CT scan
TREATMENT
 Osmotic diuretics
 Corticosteroids
 Anticonvulsants
 Fluids to maintain systolic BP at 100-150
mmHg ( increase in volume & pressure
increases blood flow through narrowed
vessels)
 Surgical intervention: ligation or clipping of
the aneurysm within the first three days to
decrease the swelling & minimize the risk
of rebleeding.
Nursing intervention
1. Immediate strict bed rest
2. Prevent valsalva maneuver-increases
pressure,tachycadia
3. Client should avoid straining, sneezing,
pulling up in bed, acute flexion of the neck.
4. Elevate head of the bed 30 degrees to 45
degrees
5. Quiet, dim, nonstimulating environment.
6. Constant monitoring of the condition to
identify occurance of bleeding by symptoms
of increasing intracranial pressure (ICP).
7. Administer analgesics cautiously: the
client should continue to be easily
aroused so that neurological checks can
be performed.
 Not hot or cold beverages or food, no
caffeine, no smoking
 Assess & implement measures to
decrease ICP
 Appropriate pre-op nursing interventions.
 To maintain homeostasis & monitor
changes in ICP after craniotomy
HYPERTENSIVE
DISORDERS(HBP)
Blood pressure -is the force exerted by
the blood against the walls of blood
vessels.
The magnitude of this force depends on:
 Cardiac output-increase
 Resistance of the blood vessels
 Viscocity of blood

Def-A persistent elevation of the systolic

blood pressure at a level of 140 mmHg
or higher & of diastolic pressure at level
of 90 mmHg or higher.
N/B Cardiac output is increased by
conditions that increase heart rate or
stroke volume, where as peripheral
resistance is increased by factors that
increase blood viscosity or reduce
vessel diameter, particularly of the
arterioles.
TYPES OF HYPERTENSION
1. Primary hypertension or essential or
idiopathic
 There is no identifiable cause, but several
interacting homeostatic forces are
generally involved concomitantly.
 Most cases of combined systolic & diastolic
elevation fall into this category.
 Severity increase as the blood pressure,
both systolic & diastolic, increases
2. Secondary hypertension
Results from an identifiable cause.
 Specific diseases
 Acute glomerulonephritis
 Renal artery stenosis

 Pheochromocytoma

 Brain tumor,

 Steroid medications,

 Arteriosclerosis

These causes can be corrected therefore, it is important

to isolate the root of the problem so that the most
appropriate treatment regimen can be prescribed
Severity depends on underlying causes, & duration of
concurrent disease states.
3.Isolated systolic hypertension (ISH)
Occurs when the systolic BP is 140 mmHg or
higher but the diastolic BP remains less
than 90 mmHg.
Causes
 Increased cardiac output
 Atherosclerosis -changes in blood
vessel
Occurs with advancing age
5. Malignant hypertension
Persistent severe hypertension
characterized by a diastolic BP above
110 to 120 mmHg. It results when
hypertension is left untreated or is
unresponsive to treatment & becomes a
truly severe emergency condition as the
pressure continues to rise unchecked.
RISK FACTORS FOR HYPERTENSION
Nonmodifiable risk factors
1. Family history
2. Gender: most higher in men than women
3. Age: incidence increases with age
4. Ethinicity: more in blacks than in white
people.(attributed to higher salt intake,
greater sensitivity to vasopressin, greater
environmental stress).
Modifiable risk factors
1. Stress: increases peripheral vascular
resistance & cardiac output & stimulates
sympathetic nervous system activity.
2. Obesity
3. Nutrients: high salt diet may induce
excessive release of natriuric hormone,
which may indirectly increase BP.
4. Substance abuse.
PATHOPHYSIOLOGY
 Hypertension results from arterial
vasoconstriction or an increase in
circulating blood volume or both.
 Prolonged vasoconstriction & high
pressures within these vessels, particularly
the arteries & arterioles stimulate
hypertrophy (enlargement) & hyperplasia
(cellular proliferation) eventually the lumen
of the tunica intima & tunica media narrow
permanently.
 Hypertensive injury of the vessel walls also
stimulates the biochemical mediators of
inflammation (histamine, leukotrienes,
prostaglandins) to increase the permeability
of the vascular endothelium.
 Sodium, calcium, plasma proteins & other
blood-borne substances enter vessel walls
causing further thickening & calcium
increases responsiveness to stimuli causing
smooth muscle contraction (i.e
vasoconstriction)
INVESTIGATIONS
1. Urine for protein, blood & glucose (renal
disorders)
2. ECG- may confirm left ventricular
hypertrophy
3. CXR- rib notching due to collateral arteries
that for as a result of
coarctation(narrowing) of the aorta,
pulmonary oedema
4. U/E/C- renal function before treatment is
started.
GENERAL CLINICAL MANIFESTATIONS
1. Sustained (2 elevated pressure readings
obtained at least 1 week apart) average
increase in systolic BP at 140 mmHg or
higher or increase in diastolic BP above 90
mmHg . For malignant hypertension
diastolic pressure above 110-120 mmHg.
2. Headache, dizziness, palpitations.
3. Epistaxis
4. Organ function damage with progression
i.e heart, brain, kidneys & retinas.
MEDICAL MANAGEMENT
 Used as single drug therapy or in
combination depending on severity of the
HTN
 Thiazide diuretics - hydrochlorothiazide (HCTZ)
 Loop diuretics - furosemide(Lasix)
 Potassium-sparing diuretics -
spironolactone(Aldactone), amiloride
 Beta-adrenergic blockers - atenolol,
propranolol, timolol, nadolol
 Beta-adrenergic blockers with intrinsic
sympathomimetic activity-pindolol, acebutolol,
penbutolol
 Combined alpha- and beta-adrenergic blockers
- carvedilol, labetalol
CONT,,,
 Angiotensin-converting-enzyme inhibitors -
captopril, enalapril, lisinopril, ramipril
 Angiotensin Receptor blockers- losartan,
candesartan, valsartan
 Calcium channel blocckers -
nifedipine,amlodipine, verapamil, diltiazem
 Alpha₁ blockers – prazosin,
doxazosin,terazosin
 Central alpha2-agonists and other centrally
acting drugs – clonidine,methyl dopa
(Aldomet), reserpine
 Direct vasodilators – minoxidil,
hydralazine(Apresoline
1. Diet
 Sodium restriction
 Weight reduction; client should be within
10% of ideal body weight.
 Decreased cholesterol & saturated fats
 Decrease caffeine intake
2. Regular exercise (avoid isometric
exercises, e.g, weight lifting)
3. Moderation of alcohol, & stop smoking
4. Assist client to cope effectively with
stress.
5. Antihypertensive medications; calcium
channel blockers, nitrates, Angiotensi –
Converting enzyme (ACE), beta-
adrenergic blockers, & centrally acting
sympatholytics (alpha agonists)
medications.
6. Diuretics to decrease circulation
volume
NURSING INTERVENTION
o Encourage participation in community BP
screening program.
o Educate public regarding risk factors &
identify health promoting behavior.
o Assess response to medication regimen.
o Proper evaluation of the BP; seated with
arm at heart level, appropriate cuff size,
two or more readings averaged, no
smoking 30 min before measurement of BP.
o Maintain low sodium, low cholesterol diet.
o Assess change in weight in regard to low
sodium intake & diuretics.
o When BP is initially reduced evaluate client’s
tolerance to decrease; postural hypotension,
urinary output, change in energy level,
change in mental alertness.
o Educate client on medication:

i. Regular times of taking medication.

ii. Know names & common side effects
iii. Do not stop taking medication call health
care provider for clarification.
iv. Cost of medication
v. Avoid hot baths, steam rooms, & spas bcoz it
increases vasodilating effect of medications.
vi. Wake up slowly, sit at bed side to regain
equilibrium, then stand slowly.
vii. Lie or sit when dizziness occur.
viii. If a sexual problem or impotence develops,
contact physician without stopping
medication.
COMPLICATIONS
 Coronary artery disease.
 Congestive heart failure
 Cerebral vascular disease; transient ischemic
attack, stroke, peripheral vascular disease
 Nephrosclerosis
 Retinopathy
 Hypertensive crisis
HYPERTENSIVE
CRISIS(HYPERTENSIVE EMERGENCY)
 It is a severe type of hypertension
characterized by rapid progressive
elevations in BP with diastolic values
above 110mmHg.
 BP has to be lowered immediately to
prevent damage to the target organs
Hypertensive urgency is a situation in
which BP must be lowered within a few
hours e.g severe preoperative
hypertension.
RISK FACTORS
 Untreated hypertension
 Drug & diet defaulters
 Stopping medication abruptly
 Preeclampsia & eclampsia
 Head injury
SIGNS & SYMPTOMS
 Morning headaches
 Blurred vision
 Dizziness
 Nose bleeding
 Dyspnea
 Diminished LOC
 Weakness
 Paralysis
 Palpitations
 Chest pain
MANAGEMENT
 Admission in the critical care unit.
 IV vasodilators eg Nitroprusside- onset of action
is about seconds to minutes.
 Other medications are IV ACE inhibitors, IV
adrenergic drugs.
 The patient’s BP should be checked every 2-3
minutes during initial administration of the
drugs.
 The rate of drug administration is
titrated(adjusted)
according to the level of Mean Arterial Pressure
 MAP -average blood pressure in an individual
during a single cardiac cycle.
 Control hypotension in this person whose
body system has adjusted to high blood
pressure as it may result to stroke, MI, or
visual changes.
 Continual ECG monitoring is done
frequently to observe for cardiac
dysrrhythmias.
 Hourly urinary output should be measured
to assess renal perfusion & the
effectiveness of these drugs & pt’s
response to therapy.
 Frequent neurologic checks, include LOC,
pupillary size & reaction, movement of
extremities & reactions to stimuli to detect
any changes to pt’s condition.
 Cardiac, pulmonary & renal systems should
be monitored for decompensation caused
by the severe elevation in BP (e.g
pulmonary edema, heart failure, angina,
renal failure)
 Once crisis is solved identify the cause &
deal with it to avoid another episode in
future.
N/B In hypertensive emergencies, the
mean arterial pressure (MAP) is often
used instead of systolic & diastolic
readings to guide & evaluate therapy.
MAP= (SBP + 2DP)
3
Normal MAP is between 70 to 110 mmHg
VENOUS CONDITIONS
VENOUS THROMBOEMBOLISM
 Thrombus formation in veins is the same
as that of arteries.
 Venous thrombi are more common than
arterial thrombi because of low flow &
pressure in the veins.
RISK FACTORS
1. Aging
2. Long-term bed rest
3. Constricting clothing
4. Genetic predisposition
TYPES OF EMBOLI
1. Venous thromboemboli: Dislodged
thrombus; source is usually from the
lower extremities; obstructs branches of
pulmonary artery.
2. Air embolism: A bolus of air displaces
blood in the vasculature, source is usually
room air entering circulation through IV
lines; trauma to the chest also may allow
air from lungs to enter vascular space.
3. Amniotic fluid embolism: A bolus of
amniotic fluid; extensive intra-abdominal
pressure attending labor & delivery can
force amniotic fluid into bloodstream of
mother; introduces antigens, cells & protein
aggregates that trigger inflammation,
coagulation, & immune responses.
4. A bacterial embolism: Aggregates of
bacteria in bloodstream, source is subacute
bacterial endocarditis of abscess.
5. Fat embolism: Globules of fat floating
in the bloodstream associated with
trauma to long bones; the lungs in
particular are affected.
6. Foreign matter: Small particles or
fibers introduced during trauma or
through an IV or intra-arterial line;
coagulation cascade is initiated &
thromboemboli form around the
particles.
VENOUS THROMBOSIS
Thrombophlebitis is the formation of a
thrombus that is associated with inflammation
also venous thrombosis
Phlebothrombosis is a thrombus without
inflammation .
Deep venous thrombosis is a thrombus in
the deep vein, usually a calf vein or a pelvic
vein.
DVT is associated with a high risk for
development of pulmonary embolus.
RISK FACTORS
3 (Virchow’s triad).
 Venous stasis (surgery, pregnancy,
obesity, long trips, heart disease)
 Increased coagulability of the blood
(malignancy, dehydration)
 Damage to the endothelial wall of
the vessel. (intravenous therapy, blunt
trauma, fractures & dislocation,
atherosclerosis)
PATHOPHYSIOLOGY
 A venous thrombus is made of platelets,
RBCs, WBCs, & fibrin.
 Platelets attach to a vein wall & then a
tail forms as more blood cells & fibrin
collect.
 As the tail grows, it drifts in the blood
flowing past it.
 The turbulence of the blood flow can
cause parts of the drifting thrombus to
break off & become emboli that travel to
the lungs.
SIGNS & SYMPTOMS
Superficial thrombophlebitis
 Tender to touch
 Reddened
 Warm
 Swollen
 Induration (firm cordlike feeling)

Deep venous thrombosis

 Tenderness
 Pain
 Oedematous area
 Warm
DIAGNOSTICS
 Venous duplex scan
 D-dimmer assay; global marker for
coagulation activity.
 Coagulation profile
MANAGEMENT
Medical management
 Bedrest 5-7 days
 Elevate extremity
 Anticoagulant & anti-inflammatory
medications
 Warm moist packs
 Elastic stocking on unaffected leg during
period of bedrest
 Do not use pillow under the knee or
allow foot to hung independent.
Surgical intervention
Done to prevent formation of pulmonary
embolism
 Venous thrombectomy; incision is made
on the vein.
 Umbrella filter device in the vena cava;
filter is placed in inferior vena cava
through the femoral or right internal
jugular vein.
NURSING INTERVENTION
 Obtain history including recent IV
therapy or use of contrast dye, surgery,
extremity trauma, childbirth, bed rest,
recent long trip, cardiac disease, recent
infections, & current medications.
 Physical assessment noting pain, fever,
tenderness & positive Homan’s sign,
redness, warmth, swelling, edema, & a
firm cordlike vein in the affected
extremity.
 Daily measurements of bilateral thighs
& calves to monitor swelling.
 Coagulation tests are monitored.
 Relief of pain by giving analgesics (NSAIDs)
 Legs are elevated to reduce edema
 Observe for any signs of complicationsi.e

dyspnea, tachycardia, tachypnea,

bloodstained sputum, chest pain, changes in
LOC & report immediately.
GOAL: to prevent thrombophlebitis, DVT
 Prophylactic measures for patients who
have undergone surgery.
 Prevent complications of immobilition.
 Prophylactic anticoagulants may be used for
the high risk clients (hip & prostate surgery)
 Use nursing measures to reduce venous
stasis.
GOAL: education for patients already
having DVT
 Teach about the disease & treatment to
reduce anxiety about complications &
enhance compliance
 Avoid oral contraception
 Stop smoking
 Use methods to reduce venous stasis
 Exercise regularly
 Decrease weight if possible
 Reduce sodium in the diet if edema is
present
 Understand need for follow-up
COMPLICATIONS
 Pulmonary embolism
 Chronic venous insufficiency.
VARICOSE VEINS
Occur when veins in the lower trunk &
extremities become congested & dilated
as a result of incompetent valves in the
vessels & loss of elasticity of the vessel
walls.
RISK FACTORS
 Congenital weakness of the vessel walls.
 Obesity
 pregnancy
CLINICAL MANIFESTATIONS
 Dilated tortuous subcutaneous veins.
 Pressure or pain after prolonged
standing
 Pain is generally relieved by elevating
the extremity.
DIAGNOSTIC
 Positive trendelenburg’s test result.
TREATMENT
Medical
 Encourage mobility
 Elastic stockings
 Teach to elevate legs for 20 min. every 4
or 5 hrs.
 Avoid prolonged sitting or standing ;
walk around every 1 to 2 hrs.
 Don’t cross legs when sitting or lying in
bed.
 Do not wear restrictive clothing
 Maintain good fluid intake; avoid
dehydration
 Use pneumatic compression devices to
Surgical
Sclerotherapy: injection of sclerosing
agent into the affected vein.
Surgical ligation of the veins; may be
combined with vein stripping as well.
ACUTE RHEUMATIC FEVER
Rheumatic fever is a diffuse,
inflammatory disease caused by a
delayed immune response to infection
by the group A beta hemolytic
streptococcus in genetically predisposed
individuals.
 In its acute form, rheumatic fever is a
febrile illness characterized by
inflammation of the joints, skin, nervous
system, & heart.
 If untreated, rheumatic fever can cause
scarring & deformity of cardiac
RISK FACTORS
1. Children between age 5 to 15 years
old.
2. 3% in pharyngeal streptococcal
infection
3. Crowding & poor hygienic conditions.
PATHOPHYSIOLOGY
Acute rheumatic fever affects the heart,
joints, central nervous system, & skin
through an abnormal humoral & cell-
mediated immune response to group A
streptococcal cell membrane antigens
called M-proteins.
This antigens can bind on the receptors
of the heart, muscle, & brain cells &
have an affinity for membrane receptors
within synovial joints, where they trigger
an autoimmune response.
Diffuse, proliferative, & exudative
inflammatory lesions develop in the
connective tissues, especially in the
heart, joints & skin. The inflammation
may subside before treatment, leaving
behind damage to the heart valves &
increasing the individuals susceptibility
to the recurrent acute rheumatic fever
after any subsequent streptococcal
infections.
Repeated attacks of acute rheumatic
fever cause chronic proliferative
changes in the previously mentioned
organs as a result of scarring,
granulomas & thrombosis.
 A proximately 10% of patients will
develop rheumatic heart disease (RHD),
cardiomegally & left heart failure may
occur during episodes of untreated
acute or recurrent rheumatic fever.
CLINICAL
MANIFESTATIONS
1. Fever
2. Lymphadenopathy
3. Arthralgia
4. Nausea, vomiting
5. Epistaxis
6. Abdominal pain
7. Tachycardia
Specific manifestations include;
8. Carditis
9. Polyarthritis
10. Chorea
11. Erythema margnatum
 Carditis: is the earliest manifestation.
Undetected murmur caused by mitral or
aortic semilunar valve dysfunction. Chest
pain is caused by pericardial inflammation.
Extra heart sounds, heart block, atrial
fibrillation, & a prolonged PR interval often
are associated with chronic rheumatic heart
disease.
 Migratory polyarthritis: is the inflammation
of more than one joint. Large joints are
more often affected. Two or more joints of
the extremities are usually involved
simultanously or in succession. Exudative
synovitis causes heat, redness, swelling,
severe pain & tenderness but no
permanent disability.
DIAGNOSTIC FINDINGS
 Positive throat culture for group A beta-
hemolytic streptococci
 Elevated Antistreptolysin O (hemolytic
factor produced by hemolytic
streptococcus). Produces antibodies which if
greater than 250 Todd units in adults & 333
Todd units in children are considered
elevated & diagnostic.
 Doppler echocardiogram to confirm acute
rheumatic carditis
 Elevated WBC, CRP-(C reactive protein
produced by the liver during inflammation),
ESR.
 Sydenham chorea/ st. vitus dance:
disorder of the central nervous system
characterized by sudden, aimless,
irregular, involuntary movement. May
occur several months after the
streptococcal infection. Chorea is self
limiting.
 Erythema marginatum: a distinctive
truncal rash that often accompanies
acute rheumatic fever. It consists of
nonpruritic, pink, erythematous macules
that never occur on the face or hands.
 Subcutenouos nodules: often develop
over bony prominences & along
extensor tendons. They do not interfere
with joint function.
TREATMENT
1. a) 10 days regime of oral penicillin or
erythromycin.
b) Nonsteroidal antiinflammatory
drugs (carditis & arthritis)
c) Serious carditis may require cardiac
glycosides, corticosteroids, diuretics, &
bedrest.
2. Surgical repair of damaged valves may
be needed in chronic recurrent
rheumatic fever/carditis.
Active disease is considered resolved
when
i. Murmur has disappeared or cardiac
status becomes stable.
ii. Major manifestations are no longer
present
iii. Individual is afebrile
iv. ESR is normal or stablized
This can take 1 to 6 months.
RHEUMATIC HEART
DISEASE
Is an inflamatory disease, primary affecting
connective tissue, especially cardiac valves.
Usually follows/ preceded by a group A beta-
hemolytic streptococcal.
N/B prevention & adequate treatment of
streptococcal infections prevent the
development of rheumatic fever.
Tissue damage is believed to be related to an
autoimmune process.
Antibodies produced in response to
streptococcal infection react with
connective tissue (cardiac tissue joints)
Myocardial involvement is characterized
by inflammation of the endocardium,
myocardium, & pericardium.
Endocarditis produces scarring of the
cardiac valves mitral & aortic valves are
most commonly affected, either by
valvular stenosis or valvular
insufficiency.
RISK FACTOR
Previous infection by betahaemolytic
streptococcus.
CLINICAL MANIFESTATION
Symptoms vary with no specific
manifestations to diagnose rheumatic
fever
DIAGNOSIS
 Carditis
 Migratory polyarthritis
 Chorea
 Erythema marginatum
 Subcutaneous nodules
TREATMENT
1. Adequate treatment of streptococcal
infection
2. Bed rest until tachycardia subsides
3. Salicylates to control inflammatory
process.
4. Prophylactic treatment
 Initiated after immediate therapy
 Monthly administration of penicillin
over extended period of time,
depending on extent of cardiac
involvement
 Administration of prophylactic
penicillin before & after medical
procedures that increase risk factor of
NURSING INTERVENTION
Child is generally cared for in the home
environment.
 Decrease activity: bed rest if pulse rate
is increased or if child is febrile.
 Friends may visit for short periods. Child
is not contagious.
-Maintain adequate nutrition
-Maybe anorexic during the febrile phase
-provide soft or liquid foods as tolerated
-Assist child with feeding if choreic
movements are severe.
-Maintain adequate hydration
 Administer analgesics for arthralgia
 Reassure child that chorea & joint
involvement are only temporary & there will
be no residual damage.
 Assist parents to understand need for
longterm prophylactic antibiotic therapy.
-Importance of preventing recurring infections
-Include child in planning, especially when
numerous injections are involved
-Importance of prophylactic therapy before
invasive medical procedures
-Continued medical follow-up for the
development of valvular problems as child
grows.
COMPLICATIONS
Severe valvular damage precipitates the
development of congestive heart failure
& may require open heart surgery for
replacement of diseased valve.
CARDIAC VALVE
DISORDERS
 Causes of valve disease
 Congenital heart disease
 Rheumatic heart disease
 Bacterial endocarditis
 Arteriosclerotic heart disease
 Mitral valve is the most commonly
involved, followed by the aortic valve.
`

Valvular stenosis: A narrowing of the valve

opening & progressive obstruction of blood
flow; increase in workload of the cardiac
chamber pumping through the stenosed
valve.
Valvular insufficiency(incompetency,
regurgitation): impaired closure of the
valve allows blood to flow back into the
cardiac chamber, thereby increasing the
workload of the heart.
DISORDERS OF THE MITRAL VALVES
1. Stenosis : Increases workload on the left
atrium as it attempts to force blood
through the narrow valve.
2. Mitral insufficiency (regurgitation):
with each cardiac contraction, the left
ventricle forces blood back into the left
atrium.
With both conditions the left atrium dilates &
hypertrophies because of an increase in
workload. This causes an increase in
pulmonary pressure & subsequent
development of congestive Heart Failure.
RISK FACTORS
Associated with history of rheumatic fever &
endocarditis.
CLINICAL MANIFESTATIONS
a) Exertional dyspnea, orthopnea.
b) Progressive fatigue caused by decrease in
cardiac output.
c) Narrow pulse pressure
d) Cardiac murmur (diastolic)
e) Systemic embolization
f) palpitations
g) Develop congestive heart failure (CHF).
h) Atrial fibrillation
DIAGNOSTICS
 Echocardiogram
 Cardiac catheterization

TREATMENT
1. Prevention of CHF
i. Digitalis
ii. Diuretics
iii. Beta-blockers to decrease cardiac rate
2. Prophylactic anticoagulation to prevent
thrombus formation.
3. Prophylactic antibiotics.
4. Open heart surgery for valve
replacement when there is evidence of
progressive cardiac failure.
DISORDERS OF THE
AORTIC VALVE
 AORTIC REGURGITATION
(INSUFFICIENCY)
 Is the flow of blood back into the left
ventricle from the aorta during diastole.
There is incomplete closure of the aortic
valve orifice.
 RISK FACTORS
 Idiopathic
 Inflammatory lesions that deform the
leaflets of aortic valves
 Infective endocarditis
 Congenital abnormalities
 Syphilis
 Dissecting aneurysm (dilation or tearing
of the ascending aorta)
 Blunt chest trauma
 Detolerating aortic valve replacement
PATHOPHYSIOLOGY
Blood from the aorta returns to the left
ventricle during diastole, in addition to the
blood normally delivered by the left atrium.
The left ventricle dilates in an attempt to
accommodate the increased volume of
blood. It also hypertrophies in an attempt
to increase muscle strength to expel more
blood with above-normal force, thus
increasing systolic BP. The arteries
attempts to compensate for the higher
pressures by reflex vasodilation;
 the peripheral arterioles relax, reducing
peripheral resistance & diastolic BP.
CLINICAL MANIFESTATION
 Asymptomatic in most patients
 Forceful heartbeat especially in the head or
neck.
 Marked carotid or temporal arteries
because of increased force & volume of the
blood ejected from the hypertrophied left
ventricle.
 Exertional dyspnea & fatigue.
 Left ventricular failure- progressive
orthopnea
DIAGNOSTICS
 Doppler echocardiogram to confirm the
diagnosis.
 Physical examination- diastolic murmur &
wide pulse presure, water hammer/corrigan’s
pulse (pulse strikes the palpating finger with a
quick, sharp stroke & then suddenly collapses.
 MRI
 ECG
TREATMENT
 Prophylactic antibiotics before invasive
procedures.
 Avoid physical exertion, competitive sports
& isometric exercise.
 Treat dysrrhythmias & heart failure
 Vasodilators- calcium channel blockers
(nifedipine) & ACE inhibitors (captopril).
 Surgery- valvuloplasty or valve
replacement (left ventricular hypertrophy)
AORTIC STENOSIS
Narrowing of the orifice between the left
ventricle & the aorta. In adults, stenosis is
often a result of degenerative calcification
from years of normal mechanical stress.
RISK FACTORS
 DM
 Hypercholesterolemia(high ammounts of
cholesterol in blood)
 Hypertension
 Low levels of high-density lipoprotein
cholesterol
 Congenital leaflets abnormalities
PATHOPHYSIOLOGY
Progressive narrowing of the valve orifice
occurs, usually over several years to
several decades. The left ventricle
overcomes the obstruction to circulation by
contracting more slowly but with greater
energy than normal; forcibly squeezing the
blood through the smaller orifice. The
obstruction to left ventricular outflow
increases pressure on the left ventricle.
The ventricular wall thickens, or
hypertrophies. When this compensatory
mechanisms of the heart begin to fail,
clinical signs & symptoms develop.
CLINICAL MANIFESTATION
 Many patients are asymtomatic.
 Exertional dyspnea
 Orthopnea
 Pulmonary edema
 Angina pectoris
 Dizziness & syncope
 Low pulse pressure because of diminished
blood flow
DIAGNOSTICS
 Physical exam- loud systolic murmur
over aortic area, S4 sound
 Doppler echocardiography for diagnosis
& 6 monthly for symptomatic patients
 ECG- left ventricular hypertrophy.
 Left sided heart catheterization
TREATMENT
 Antibiotic prophylaxis for invasive
procedures to prevent endocarditis.
 Aortic valve replacement is the
definitive treatment
 Symptomatic patients can benefit from
one or two balloon percutaneous
valvuloplasty procedures.
NURSING INTERVENTION FOR VALVULAR
HEART DISORDERS
1. Assess for manifestations of heart failure,
dysrhythmias, dizziness,syncope,
increasing weakness or angina.
2. Develop medication schedule with patient
& teach about medication.
3. Teach about daily weight monitoring &
report a gain of 2 pounds in 1 day or 5
pounds in a week.
4. Help client plan activities & rest
5. For surgery (valvuloplasty or valve
replacement patient).
CORONARY ARTERY
DISEASE (CAD)
Commonly:
1. Coronary atherosclerosis
2. Angina pectoris
3. Myocardial infarction
 ANGINA PECTORIS
Chest pain resulting from myocardial
ischemia.
A clinical syndrome characterized by
episodes of paroxysms of pain or pressure
in the anterior chest.
Cause: insufficient coronary blood flow,
resulting in a decreased O2 supply when
there is increased myocardial demand for
O2 in response to physical exertion or
emotional stress. The severity of angina is
based on the precipitating activity & it’s
effect on activities of daily living.
TYPES OF ANGINA
 Stable angina: Predictable & consistent
pain that occurs on exertion & is relieved
by rest.
 Unstable angina: symptoms occur more
frequently & last longer than stable angina.
The threshold for pain is lower, & pain may
occur at rest.
 Intractable/refractory angina: severe
incapacitating chest pain.
 Variant/prinzmetal’s: Pain at rest with
reversible ST-segment elevation; thought
to be caused by coronary artery
vasospasm.
 Silent ischemia: objective evidence of
ischemia (such as ECG changes with a
stress test), but patient reports no
symptoms.
 Several factors are associated with typical
anginal pain.
 Physical exertion
 Exposure to cold
 Eating a heavy meal
 Stress or any emotion

N/B atypical angina is not associated with

the listed factors it may occur at rest.
PATHOPHYSIOLOGY
When an increased workload is placed on
the heart, as in exercise or strenuous
activity, there is an increased demand for
oxygen. Normally, when the heart needs
more oxygen, the coronary arteries dilate
to carry more blood. However, with CAD,
the narrowed vessels are unable to dilate &
supply the heart with this extra blood &
oxygen. This inability to supply more blood
& O2
 causes myocardial ischemia. Chest pain
results from the ischemia but usually
lasts only for a few minutes, especially if
activity is stopped. If adequate blood
supply to the myocardium is restored
with rest, no myocardial damage usually
occurs.
CLINICAL MANIFESTATIONS
 Chest pain radiating to the shoulder left
arm, neck, jaw.
 Pain is squeezing, pressing or sensation of
heaviness.
 Shortness of breath
 Pallor
 Diaphoresis
 Dizziness or lightheadedness
 Nausea & vomiting
 Anxiety
 Pain subsides with rest or nitroglycerin
DIAGNOSIS
 History, signs & symptoms
 ECG
 Blood laboratory values (CRP, Lipid profile,
cardiac enzymes, Troponin 1, CKMB)
 Stress test (exercise or pharmacological)
 CXR
 Myocardial perfusion scan
 Coronary angiography
MEDICAL MANAGEMENT
Objective: decrease O2 demand of the
myocardium & increase O2 supply.
1. Control of risk factors
2. Reperfusion procedures maybe used to
restore the blood supply to the
myocardium e.g percutaneous
transluminal coronary angioplasty (PTCA),
intracoronary stent, and atherectomy,
Coronary Artery Bypass Graft (CABG).
3. Pharmacological therapy.
a) Nitroglycerin (Vasodilator)
b) Beta- adrenergic blocking agents
(decrease workload on the heart)
c) Calcium channel blocking agents (relax
muscular smooth muscles)
d) Antiplatelets (reduce platelet
aggregation) & anticoagulant
medication
4. Oxygen therapy: to increase the
amount of oxygen delivered to the
myocardium & to decrease pain.
NURSING CARE
1. Allay anxiety – reassure
2. Ensure patient gets O2 & medication&
observe for side effects
3. Monitor the vital signs
4. Ensure investigations are done
5. Evaluate the general condition after
interventions
6. Patient education
i. Understanding the disease
ii. Self administration of nitroglycerin
PRN
iii. Proper diet-low cholesterol, high fibre
iv. Control hypertension
v. If smoking to quit
vi. If obese, weight reduction
vii. Other stressers like cold, coffee
drinking, strenuous exercises.
NOTE
All clients with chest pain get MONA
treatment
M – morphine sulfate
O - oxygen
N - nitroglycerin
A - asprin
Give subligual nitroglycerin tablet/spray. If
the pain is not relieved after three
nitroglycerin tablets each taken 5 minutes
apart or after morphine, notify physician.
Oxygen to ensure adequate oxygenation &
asprin for antiplatelet activities.
MYOCARDIAL INFARCTION
Or coronary occlusion or heart attack is a
total occlusion of a portion of a coronary
artery. After the occlusion myocardial
ischemia, injury, or death occurs.
Infarction commonly occur in the left
ventricle. The change (destruction) is
permanent.
The severity of the situation depends on
the area of the heart involved, as well as
the size of the infarct.
CAUSES
1. Reduced blood flow in a coronary artery
due to rupture of an atherosclerotic
plague & subsequent occlusion of the
artery by a thrombus.
2. Vasospasm (sudden constriction or
narrowing) of coronary artery.
3. Decreased oxygen supply (e.g from acute
blood loss, anemia or low blood pressure)
4. Increased demand for oxygen (e.g
increased heartrate, thyrotoxicosis, or
ingestion of cocaine)
N/B in each case there is a profound
imbalance between oxygen supply &
demand.
PATHOPHYSIOLOGY
The area of infarction develops over
minutes to hours. As the cells are
deprived of oxygen, ischemia develops,
cellular injury occurs, & the lack of
oxygen results in infarction (the death of
the cells).
The expression ‘time is a muscle’ reflects
the urgency of appropriate treatment to
improve patient outcome.
 Various descriptions are used to further
identify an MI.
 The type of MI (ST-segment elevation,
non-ST segment elevation)
 The location of the injury to the
ventricular wall (anterior, inferior,
posterior, or lateral wall)
 The point & time within the process of
infarction (acute, evolving or old)
CLINICAL MANIFESTATIONS
1. Cardiovascular: Chest pain/ discomfort,
palpitations,
DYSRHYTHMIAS/
ARRHYTHMIAS
Are disorders of the formation or
conduction (or both) of the electrical
impulse within the heart.
 These disorders can cause disturbances
of the rate, the heart rhythm, or both.
NORMAL SINUS RHYTHM
Characteristics of normal sinus rhythm
Rate: 60 to 100 beats/min
Rhythm: regular
P wave: present, precede each QRS complex.
P-R interval: 0.12 to 0.20 seconds
QRS complex: present and under 0.10 second
Relationship of conducting pathways to
the electocardiogram
1. P-wave:indicative of the impulse
generated from the sinoatrial node:
initiates atrial depolarization.
2. PR interval: delay of the impulse at the
atrioventricular node & bundle of His to
promote ventricular filling.
3. QRS complex: passage of impulse through
the bundle branches through the purkinje
fibres; depolarization of the ventricles
occurs
4. T-wave: ventricular repolarization &
return to the resting rate.
5. S-T segment: reflects the time from
completion of a contraction
(depolarization) to recovery
(repolarization) of myocardial muscle
for next impuse.
6. U-wave: not usually present. It is seen
in patients with hypokalemia. Appear
shortly after T-wave & distorts it.
 Dysrhythmias may be classified
according to rate- either bradycardia or
tachycardia.
 They are also classified according to
their origin- atrial or ventricular.
 Ventricular dysrhythmias are more life
threatening than atrial dysrhythmias.
Types of dysrhythmias
i. Sinus dysrhythmias (from sinus (SA)
node)
ii. Atrial dysrhythmias (from atria)
iii. Junctional dysrhythmias (from
atrioventricular (AV) node or junction)
iv. Ventricular dysrhythmias (from
ventricles)
CAUSES
1. Conditions like heart diseases, COPD,
anemia, myocardial infarction
2. Some medications e.g digoxin
3. Cardiac catheterization
4. Electrolyte imbalance
SIGNS & SYMPTOMS
1. Syncope
2. Lightheadedness
3. Dizziness
4. Fatigue
5. Chest discomfort
6. Palpitations
7. Engorged neck veins
8. Crackles & wheezes
9. Pale & cool skin
10. Decrease/increased pulse rate & rhythm
SINUS BRADYCARDIA
 These are slow heart rhythms, which
may arise from disease in the heart’s
conduction system (such as SA node, AV
node or HIS-Purkinje system).
SINUS BRADYCARDIA
SINUS TACHYCARDIA
It’s a heart rate greater than 100 beats
per minute.
It has same components as a normal
sinus rhythm except the heart rate is
faster
SYNUS TACHYCARDIA
HEART BLOCK
A delay or complete block of the electrical
impulse as it travels from the sinus node
to the ventricles. The level of the block
or delay may occur in the AV node or
HIS-Purkinje system. The heart may
beat irregularly and, often, more slowly.
HEART BLOCK
Premature atrial contractions (PACs)
Early extra beats that originate in the
atrial (upper chamber of the heart)
ATRIAL FIBRILLATION

Extremely rapid incomplete contractions

of the atria result in fine rapid, irregular,
& uncoordinated movements.

Cannot identify P waves or P-R interval on

ECG.
ATRIAL FIBRILLATION
Paroxysmal supraventricular
tachycardia (PSVT)
A rapid, usually regular rhythm,
originating from above the ventricles.
PSVT begins and ends suddenly.
VENTRICULAR ARRHYTHMIAS
V-TACH
Ventricular tachycardia (V-tach). A
rapid heart rhythm originating from the
lower chambers (or ventricles) of the
heart.
The rapid rate prevents the heart from
filling adequately with blood; therefore,
less blood is able to pump through the
body.
This can be a serious arrhythmia,
especially in people with heart disease,
and may be associated with more
symptoms.
PREMATURE VENTRICULAR
CONTRACTION
Is a too-early heartbeat that originates in
the ventricles and disrupts the heart’s
normal rhythm.
The pattern is a normal beat, an extra
beat (the PVC), a slight pause, then a
stronger-than-normal beat.
The heart fills with more blood during the
pause following the PVC, giving the next
beat extra force. This pattern may occur
randomly or at definite intervals.
Ventricular fibrillation (VF).
An erratic, disorganized firing of impulses
from the ventricles.
The ventricles quiver and are unable to
contract or pump blood to the body.
This is a medical emergency that must be
treated with cardiopulmonary
resuscitation (CPR) and defibrillation as
soon as possible
Asystole
Or the silent heart is the absence of
activity in the cardiac muscle.
It is referred to as arrest.
A straight line appears on an ECG strip.
MANAGEMENT OF DYSRHYTHMIAS

The method of cardiac rhythm

management depends firstly on whether
or not the affected person is stable or
unstable.

Treatments may include physical

maneuvers, medications, electricity
conversion, or electro or cryocautery.
Physical maneuvers
A number of physical acts can increase
parasympathetic nervous supply to the
heart, resulting in blocking of electrical
conduction through the AV node.
This can slow down or stop a number of
arrhythmias that originate above or at the
AV node.
Parasympathetic nervous supply to the heart
is via the vagus nerve, and these
maneuvers are collectively known as vagal
maneuvers
Antiarrhythmic drugs
 There are many classes of antiarrhythmic
medications.
 Although the goal of drug therapy is to
prevent arrhythmia, nearly every
antiarrhythmic drug has the potential to
act as a pro-arrhythmic, and so must be
carefully selected and used under medical
supervision
 Other drugs
 There are drugs can be used to "rate
control" a fast rhythm and make it
physically tolerable for the patient.
 Some arrhythmias promote blood
clotting within the heart, and increase
risk of embolus and stroke.
Anticoagulant medications such as
warfarin and heparins, and anti-platelet
drugs such as aspirin can reduce the
risk of clotting.
 Electricity
Dysrhythmias may also be treated electrically,
by applying a shock across the heart — either
externally to the chest wall, or internally to
the heart via implanted electrodes.
 Cardioversion is either achieved
pharmacologically or via the application of a
shock synchronised to the underlying
heartbeat. It is used for treatment of
supraventricular tachycardias. In elective
cardioversion, the recipient is usually sedated
or lightly anesthetized for the procedure.
 Defibrillation differs in that the shock is
not synchronised. It is needed for the
chaotic rhythm of ventricular fibrillation
and is also used for pulseless ventricular
tachycardia. Often, more electricity is
required for defibrillation than for
cardioversion. In most defibrillation, the
recipient has lost consciousness so
there is no need for sedation.
 cardiac pacing. Temporary pacing may
be necessary for reversible causes of
very slow heartbeats, or bradycardia,
(for example, from drug overdose or
myocardial infarction). A permanent
pacemaker may be placed in situations
where the bradycardia is not expected
to recover.
 Electrical cautery
In specialised catheter laboratories, they use
fine probes inserted through the blood vessels
to map electrical activity from within the
heart.
This allows abnormal areas of conduction to be
located very accurately, and subsequently
destroyed with heat, cold, electrical or laser
probes.
AV nodal reentrant tachycardia is often curable.
Atrial fibrillation can also be treated with this
technique.
 Catheter ablation
During an ablation, high-frequency electrical
energy is delivered through a catheter to a small
area of tissue inside of the heart that causes the
abnormal heart rhythm.
This energy "disconnects" the pathway of the
abnormal rhythm.
Ablation is used to treat most PSVTs, atrial flutter,
and some atrial and ventricular tachycardias.
It can also be used to disconnect the electrical
pathway between the atria and the ventricles,
which may be useful in people with atrial
fibrillation.
Ablation may be combined with other procedures
to achieve optimal treatment.
Heart surgery
Heart surgery may be needed to correct
heart disease that may be causing the
arrhythmia ( valve surgery or
coronary artery bypass surgery)
Nursing care
 Regular evaluation of patients BP, pulse
rate & rhythm, rate & depth of respirations,
& breath sounds to determine the
dysrhythmias hemodynamic effect.
 Ask about lightheadedness, dizziness or
fainting as part of on going assessment.
 12-lead ECG monitoring continuously on
track dysrhythmias.
 Monitor administeration of medications
carefully to maintain a constant serum
blood level
 6 minute walk to identify the patient’s
ventricular rate in response to exercise.
 Assist patient eliminate contributing factors
to dysrhythmia (e.g caffeine, stress,
nonadherence to medication regimen)
 Assist pt in developing a plan to make
lifestyle changes that eliminate or reduce
these factors.
 Family education, on manifestations,
emergency access & continuous care.
 Minimize anxiety.
PACEMAKER
A specialized cell or group of cells that
automatically generate impulses that
may spread to other regions of the
heart.
The normal pacemaker is the sinoatrial
node, a group of cells in the atrium near
the entrance of the superior vena cava
into the right atrium.
An artificial pacemaker is an electrical
device that can substitute for a
defective natural
 pacemaker & control the beating of the
heart by a series of rhythmic electrical
discharges.
 If the electrodes that deliver the
discharges to the heart are placed on the
outside of the chest wall, the device is
called an external pacemaker.
 If the electrodes are placed within the
chest wall, the device is called an internal
pacemaker.
 These devices are powered by batteries
that last 16 years or longer.
ARTIFICIAL PACEMAKER
ARTIFICIAL PACEMAKER
INDICATIONS FOR ARTIFICIAL
PACEMAKER
1. To maintain an adequate heart rate
because the heart's natural pacemaker
is not fast enough
2. If there is a block in the heart's
electrical conduction system.
Insertion
 A pacemaker is typically inserted into the
patient through a simple surgery using
either local anesthetic or a general
anesthetic.
 The patient may be given a drug for
relaxation before the surgery as well.
 An antibiotic is typically administered to
prevent infection.
 In most cases the pacemaker is inserted in
the left shoulder area where an incision is
made below the collar bone creating a small
pocket where the pacemaker is actually
housed in the patient's body.
 The lead or leads (the number of leads
varies depending on the type of
pacemaker) are fed into the heart through
a large vein using a fluoroscope to monitor
the progress of lead insertion.
 The Right Ventricular lead would be
positioned away from the apex (tip) of the
right ventricle and up on the inter
ventricular septum, below the outflow tract,
to prevent deterioration of the strength of
the heart.
 The actual surgery may take about 30 to 90
minutes.
 The most basic preparation is that
people who have body hair on the chest
may want to remove the hair by clipping
just prior to surgery or using a
depilatory agent (preoperative shaving
has been on the decline as it can cause
skin breakage and increase infection
risk of any surgical procedure) as the
surgery will involve bandages and
monitoring equipment to be a fixed to
the body.
 Since a pacemaker uses batteries, the
device itself will need replacement as the
batteries lose power.
 Device replacement is usually a simpler
procedure than the original insertion as it
does not normally require leads to be
implanted.
 The leads are removed from the existing
device, the leads are attached to the new
device, and the new device is inserted into
the patient's body replacing the previous
device.
Pacemaker patient identification card
International pacemaker patient
identification cards carry information
such as patient data (among others,
symptom primary, ECG, aetiology),
pacemaker center (doctor, hospital),
rate, mode, date of implantation,
manufacturer, type) and lead.
Periodic pacemaker checkups
-Once the pacemaker is implanted, it is
periodically checked to ensure the device
is operational and performing
appropriately.
-Routine pacemaker checks are typically
done in-office every six (6) months, though
will vary depending upon patient/device
status and remote monitoring availability.
-The device will be interrogated to perform
diagnostic testing. These tests include:
 Sensing: the ability of the device to "see"
intrinsic cardiac activity (Atrial and
ventricular depolarization).
 Impedance: A test to measure lead
integrity. Large and/or sudden increases in
impedance can be indicative of a lead
fracture while large and/or sudden
decreases in impedance can signify a
breach in lead insulation.
 Threshold: this test confirms the minimum
amount of energy (Both volts and pulse
width) required to reliably depolarize
(capture) the chamber being tested
Lifestyle considerations
A patient's lifestyle is usually not modified
to any great degree after insertion of a
pacemaker. There are a few activities that
are unwise such as full contact sports and
activities that involve intense magnetic
fields.
Turning off the pacemaker
It is legal and ethical to honor requests by
patients, or by those with legal authority to
make decisions for patients, to deactivate
implanted cardiac devices.
Privacy and security
Security and privacy concerns have
been raised with pacemakers that allow
wireless communication.
Unauthorized third parties may be able
to read patient records contained in the
pacemaker, or reprogram the devices,
as has been demonstrated by a team of
researchers
NOTE:
 Modern pacemakers are externally
programmable and allow the cardiologist to
select the optimum pacing modes for
individual patients.
 Some combine a pacemaker and
defibrillator in a single implantable device.
Others have multiple electrodes
stimulating differing positions within the
heart to improve synchronisation of the
lower chambers (ventricles) of the heart.
Methods of pacing
a) Percussive pacing
 Percussive pacing, also known as
transthoracic mechanical pacing, is the use
of the closed fist, usually on the left lower
edge of the sternum over the right
ventricle in the vena cava, striking from a
distance of 20 – 30 cm to induce a
ventricular beat.
 This is an old procedure used only as a life
saving means until an electrical pacemaker
is brought to the patient.
b) Transcutaneous pacing
 Also called external pacing, is
recommended for the initial stabilization
of hemodynamically significant
bradycardias of all types.
 External pacing should not be relied
upon for an extended period of time. It
is an emergency procedure that acts as
a bridge until transvenous pacing or
other therapies can be applied.
c) Epicardial pacing (temporary)
 Temporary epicardial pacing is used
during open heart surgery should the
surgical procedure create atrio
ventricular block. The electrodes are
placed in contact with the outer wall of
the ventricle (epicardium) to maintain
satisfactory cardiac output until a
temporary transvenous electrode has
been inserted.
d) Transvenous pacing (temporary)
 Transvenous pacing, when used for temporary
pacing, is an alternative to transcutaneous
pacing.
 A pacemaker wire is placed into a vein, under
sterile conditions, and then passed into either
the right atrium or right ventricle. The pacing
wire is then connected to an external
pacemaker outside the body.
 Transvenous pacing is often used as a bridge
to permanent pacemaker placement. It can
be kept in place until a permanent pacemaker
is implanted or until there is no longer a need
for a pacemaker and then it is removed.
e) Permanent pacing
 Permanent pacing with an implantable
pacemaker involves transvenous
placement of one or more pacing
electrodes within a chamber, or chambers,
of the heart.
 The procedure is performed by incision of
a suitable vein into which the electrode
lead is inserted and passed along the vein,
through the valve of the heart, until
positioned in the chamber.
 The procedure is facilitated by fluoroscopy
which enables the physician to view the
passage of the electrode lead.
 After satisfactory lodgment of the
electrode is confirmed, the opposite end of
the electrode lead is connected to the
pacemaker generator.
 There are three basic types of permanent
pacemakers, classified according to the
number of chambers involved and their
basic operating mechanism
i. Single-chamber pacemaker. In this type,
only one pacing lead is placed into a
chamber of the heart, either the atrium
or the ventricle.
 Dual-chamber pacemaker. Here, wires are
placed in two chambers of the heart. One
lead paces the atrium and one paces the
ventricle. This type more closely resembles
the natural pacing of the heart by assisting
the heart in coordinating the function
between the atria and ventricles.
 Rate-responsive pacemaker. This
pacemaker has sensors that detect
changes in the patient's physical activity
and automatically adjust the pacing rate to
fulfill the body's metabolic needs.
Hi, please write the nursing care of this
clients preoperatively & post
operatively.
THANKYOU
Complications
 A possible complication of dual-chamber
artificial pacemakers is pacemaker-
mediated tachycardia (PMT)
Treatment of PMT typically involves
reprogramming the pacemaker.
 “pacemaker-tracked tachycardia," where a
supraventricular tachycardia is tracked by
the pacemaker and produces beats from a
ventricular lead
THE FIRST IMPLANTABLE
PACEMAKER
IN 1958, ARNE LARSSON (1915-2001)
BECAME THE FIRST TO RECEIVE AN
IMPLANTABLE PACEMAKER
CARDIAC SURGERY
TYPES OF PROCEDURES
1. Open heart surgery (refers to the chest
not the heart). Is performed with the
use of the cardiopulmonary bypass.
This machine allows for full
visualization of the heart while
maintaining perfusion & oxygenation.
surgery involves the heart, either the
myocardium itself, coronary artery, or
heart valves.
2. Closed heart surgery is performed
without the use of the bypass machine.
The most common closed heart
procedure is the mitral commissurotomy
(surgery on dividing space btn mitral
orifice).
NURSING INTERVENTION
PRE-OPERATIVE
GOAL: prepare patient psychologically &
physiologically for surgery.
1. Evaluate client’s history for other
chronic health problems.
2. Establish baseline data for post-op
comparison.
3. Provide appropriate pre-op. teaching
according to age level frequently
involves a visit to ICU. (If child, in
company of parents)
4. Discuss immediate post-op. nursing care
& anticipated nursing procedures.
5. Correct metabolic imbalance.
6. Establish & maintain adequate hydration.
7. Anticipate adjustments in medication
schedule before surgery.
a) Digitalis dose is usually decreased.
b) Diuretic maybe discontinued 48 hrs
before surgery.
c) Long-acting insulin will be changed to
regular insulin.
d) Antihypertensive medication dosage
maybe modified
8. Eliminate all possible sources of
infections.
POST-OP
GOAL: to evaluate & promote
cardiovascular function after surgery.
 Maintain adequate blood pressure.
 Evaluate for dysrrhythmia; document &
treat accordingly.
 Maintain client in semi-fowler’s position.
 Evaluate fluid & electrolyte balances.

a) Record daily weight & compare with

previous weight.
b) Evaluate electrolyte balance especially
potassium levels.
c) Assess for adequate HB & hematocrit
values.
d) Evaluate hemodynamic levels for
adequate volume.
e) Measure urine output hourly to
evaluate adequacy of renal perfusion.
f) Administer IV fluids, as indicated
 Observe for hemorrhage: most often
identified by increase in chest drainage.
 Mediastinal chest tubes are frequently
placed in the pericardial sac to prevent
tamponade. These tubes are cared for
in the same manner as pulmonary
chest tubes.
 Bedside hemodynamic monitoring as
indicated.
GOAL: to evaluate & promote respiratory
function.
 Mechanical ventilation via endotracheal
tube maybe used for approximately 12
to 24 hrs after surgery. Generally
children are extubated sooner than
adults.
 Maintain UWSD for mediastinal/ chest
tubes.
 Pulmonary hygiene via endotracheal
tube carefully assess pulse oximetry
during suctioning.
 Promote good respiratory hygiene after
extubation (fluids, incentive spirometry,
activity)
 Evaluate arterial blood gases for
adequate oxygenation as well as acid-
base balance.
 Encourage activity as soon as possible.
Client should be out of bed on the first
post-op day.
 Monitor pulse oximetry levels.

GOAL: evaluate neurological status for

complications after surgery.
 Recovery from anaesthesia within
appropriate time frame.
 Able to move all extremities equally.
 Appropriate response to verbal
command.

 Careful explanation of all procedures
 Prevent sensory overload
 Promote uninterrupted sleep
 Administer pain medications as appropriate.

COMMON COMPLICATIONS AFTER

CARDIAC SURGERY
1. Dysrhythmias
2. Hypovolemia
3. Embolism
4. Cardiac tamponade
5. Psychosis (common in adults)