Management of patients with

Coronary Vascular disorders

CORONARY ATHEROSCLEROSIS
 Coronary atherosclerosis

• It is the most common cause of heart disease

• Defined as an abnormal accumulation of lipid,
fat and fibrous tissue in the blood vessels that
supply the myocardium( coronary vessels).
• This blocks/narrows the coronary vessels and
leads to reduction in blood flow to heart
muscles.
Occurs progressively and can be reversed.
The anatomic structure of the coronary arteries
makes them susceptible to artherosclerosis as
they twist and turn as they supply the heart
creating sites for fat/lipid deposits development
 Pathophysiology
• Cholesterol/lipids/fats is deposited on the tunica
intima of major coronary arteries
• – these deposits interfere with absorption of
nutrients by endothelial cells lining the vessel, they
also obstruct blood flow
• vessel endothelium becomes injured and necrotic
due to decreased blood flow. Injury is worsened by
smoking and hypertension
• Inflammation occurs – WBCs, Macrophages attack
the site
• Macrophages also release chemicals that damage
the endothelium and initiate clot formation
• The combination of deposited lipids, clots and
fibrous tissue form a plaque(atheroma) that
protrude into the lumen and obstruct blood flow
• The plaque may rupture leading to thrombus
formation which completely obstructs blood flow
(thromboembolism). – Causes sudden cardiac death
or Myocardial infarction
Coronary atherosclerosis
Effects of atherosclerosis
•Narrows coronary vessels
•Obstructs coronary vessels due to ruptured
plaque
•Weakens the vessel(aneurysm)
 Coronary thromboembolism

• Thromboembolism refers to obstruction of a

blood vessel by a blood clot that has become
dislodged from another site in the circulation.
• Decreased mobility of a patient with cardiac
disease and impaired circulation contribute to
intracardiac and intravascular Clots e.g Are
detected by Echocardiogram and treated by
anticoagulants – heparin and warfarin and
antiplatelets -asprin
Embolism
Pulmonary embolism
•Most common in patients with heart failure.
•Clots may form deep in the veins of the leg and
embolize in pulmonary vessels. Emboli block vessels
cutting off blood supply to parts of the lung.
•Characterized by dyspnea, tachypnea, chest pain,
hemoptysis.. Can lead to respiratory failure.
•Managed by anticoagulants(heparin, warfarin)
 Risk factors For Coronary
atherosclerosis
These are conditions that accompany onset of
coronary atherosclerosis disease
Non-modifiable risk factors – individual has no
control
• Family history,
• Increasing age,
•Gender – more in men,
•Gace – higher in African Americans than Caucasians
Modifiable risk factors – controlled by changing
lifestyle or habit
• High cholesterol, lipids, triglycerides
•HBP,
•Smoking,
•High blood glucose,
•Obesity- BMI, waist above 35Inches(F), 40inches(M))
• inactivity,
•stress,
•use of COCs,
•personality – aggressive, ambitious
 Clinical Manifestation Of Atherosclerosis
• Symptoms caused by narrowing of coronary vessels
and obstruction of blood flow to heart
• Inadequate blood flow (ischemia) to the heart
deprives cardiac cells with nutrients and oxygen. This
results in symptoms of ischemia which are:
 Angina pectoris - Chest pain due to myocardial
ischemia (reversible)
 myocardial infarction – Death of myocardial cells due
to ischemia
 Heart failure – Death/injury of myocardial cells
generates scar tissue that prevents proper pumping
(contraction) of the heart
 ECG changes, Dysrrhythmias
 Sudden death
 Prevention
This is by identifying and reducing risk factors . it
includes
• Reduce cigarette smoking – active or passive.
Cigarretes increase blood carbondioxide and
deprive heart of oxygen, nicotine causes arterial
constriction reducing oxygen, increases platelet
adhesion thus higher chance of thrombus
• Control blood pressure – it is asymptomatic –
increases the heart workload and oxygen demand
as the heart has to pump through high pressured
vessels (Heart failure) and also stains vessels
leading to injury and atherosclerosis.
• Control cholesterol/lipid levels with diet, exercise
and drugs to lower cholesterol. Test for fasting lipid
profile every 5 years (>20years) and every 6weeks if
risk factors are present.
• Exercise – lowers LDL (harmful as it sticks to artery
walls) and raises HDL (Cardio protective), controls
BP and weight
• Lower blood sugar – hyperglycemia fosters
increased platelet aggregation and dyslipidemia
• Lower stress and control behavior ( competitive,
aggressive, urgency, hostile – coronary prone)
NB – aging also produces changes in vessel walls that
 Management of Coronary
atherosclerosis
Manage risk factors by:
• Diet – Healthy heart diet(Low in fats and
cholesterol, high in vegetables and fruits)
• Physical activity (30 min moderate activity daily –
10000 steps/day)
• Smoking Cessation
• Stress management
• Hypertension (High blood pressure) management
• Manage high blood sugar (Diabetes Mellitus)
• Drugs to lower cholesterols, triglycerides and
LDL (antilipemic drugs) – In many cases, diet
alone does not lower the lipid levels
• Bile sequestrants – Cholestyramine,
• HMG-CoA inhibitors – Atorvastatin, Lovastatin
Apart from controlling risk factors, management
depends on whether it is angina pectoris or
myocardial infarction or heart failure
ANGINA PECTORIS
 Angina pectoris
• It is a clinical syndrome characterized by
episodes of feeling pain or pressure on the
anterior chest.
• It is caused by insufficient coronary blood flow
(Ischemia) resulting in inadequate oxygen supply
to the myocardium
 Causes of Angina Pectoris(AP)
Caused by coronary atherosclerosis (obstruction to
coronary vessels) or conditions that increase
myocardial oxygen demand.
A number of factors can trigger angina pain
• Physical exertion – increases oxygen demand of the
heart.
• Exposure to cold
• Eating a heavy meal
• Stress or emotions – increase adrenaline, increase
workload on heart
 Assessment of Angina Pectoris
Clinical features
•Chest pain – characteristics of angina pectoris chest
pain are:
mild or moderate
 located in substernal region,
crushing/squeezing/choking/strangling pain.
May radiate to the neck, jaw , inner arm and
shoulder
Pain intensity not affected by breathing
Lasts 5-15 minutes
Relieved by Nitroglycerine and rest
• Dyspnea
• Pallor, sweating
• Palpitations, tachycardia,
• Hypertension
• Numbness of upper limbs
• A feeling of impending death
• Elderly patients may not show pain due to altered
perceptions – may just be weak and faint, dyspnea,
restless. Women may also present with dyspnea
and palpitations (Silent Angina)
NB – angina pain subsides when the cause is
removed. If angina attacks increase in frequency and
intensity, it could be sign of impending myocardial
infarction
Investigations
•ECG – Normal at rest, Abnormal during pain episode
(ST depression, T wave inversion)
•Cardiac Markers – CK-MB, Troponin are normal in
angina
•Cardiac catheterization – Done to check on patency
of vessels
 Management of AP
Goal
• To provide relief from acute attack
• To decrease oxygen demands of the myocardium
• To increase oxygen supply.
• To prevent progression to Myocardial infarction
 Immediate Management
• Assess chest pain and verify it is angina pain
• Administer oxygen by nasal cannula or mask
• Place the client in bed in semi-fowlers position
and stay with the client
• Continuous cardiac monitoring
• Obtain a 12 lead ECG
• Insert an IV line
Drugs
Nitroglycerin
• drug of choice for angina. Reduces myocardial
oxygen consumption which decreases ischemia and
relieves chest pain.
• Does this by dilating both veins and arteries.
• Given sublingually or on the cheeks and alleviates
pain in 3 minutes.
• Angina patients should always have nitroglycerine
and note how long it takes to relieve the
discomfort. If pain is not relieved, it could be an
impending MI. Side effects are headache,
hypotension, tachycardia.
Other drugs –
• Beta adrenagic blockers – propranolol is the drug
of choice – lowers heart rate and force of
contraction
• Calcium channel blockers ( calcium influences
contraction of all muscles and electrical stimulation
of the heart, they dialate vessel smooth muscles,
reduce BP and reduce heart workload) eg
nifedipine, Amlodipine
• Antiplatelet drugs – Asprin is the drug of choice.
Inhibits platelet aggregation and reduces risk of MI
 Follow up care
• Identify angina precipitating events
• Instruct the client if pain occurs again, he
should rest immediately and take
nitroglycerine and to seek emergency services
if pain is not relieved
• Surgery
Surgery can be done to open blocked coronary
arteries and revascularize the heart – coronary
artery bypass surgery / coronary angioplasty
( enters the vessel with a catheter and guiding wire
and cracks the plaque) and or use of laser to
vaporize the plaques
Control risk factors
Reduce smoking, diet, exersice, control blood sugar,
avoid oral contraceptives e.t.c (refer to Mx. Of
atherosclerosis)
 Myocardial infarction (also called
Acute coronary syndrome)
• Refers to the process which myocardial tissue are
destroyed in regions of the heart that are deprived
of adequate blood supply because of reduced
coronary blood flow.
• Caused by narrowing of coronary vessels due to
artherosclerosis or complete occlusion of vessel by
thrombus or embolus. Shock can also cause MI
• Heart attack and myocardial infarction (MI) are
used synonymously, preferred term is MI.
Pathophysiology – discussed in coronary
artherosclerosis
CLINICAL MANIFESTATION OF MI
• Studies show patients with MI have coronary
artherosclerosis and arterial hypertension. Also
women on oral contraceptives and smokers are at
high risk.
• Chest pain – suddenly, continues without relief over
lower sternum and upper abdomen is the main sign
• Pain continues to increase, may radiate to the left
shoulder and arm, jaw or neck
• Unlike angina – pain begins spontaneously – not
triggered. Continues for hrs or days, not relieved by
nitroglycerine or rest.
• Pain accompanied by shortness of breath(gasp),
diaphoresis, dizziness, nausea and vomiting
Diagnosis
• Patients history – present illness, family history
• ECG – provides information on the conducting
system of the heart. Can show size and location
of MI. 1st choice, done bed side and non
invasive
• Echocardiogram
• Serum cardiac enzymes – Creatinine kinase and
lactic dehydrogenase are elevated
 Medical management of MI

Goal – minimize myocardial damage and reduce

complications. Managed by
• medications
• oxygen - to increase oxygen supply to heart
• Rest - to reduce heart workload
Medication
3 classes of drugs are used to increase oxygen
supply to the heart:
• Vasodialators – nitroglycerine - given IV
• Anticoagulants – they reduce probability of
thrombus formation – heparin
• Thrombolytics – they dissolve any thrombus
formed in the coronary artery, minimizing
blockage of the artery. They need to be
administered at the onset of chest pain
Oxygen
• Initiated at the onset of chest pain. increases
oxygen in blood. Observe rate and rhythm of
respiration for effectiveness
Analgesics
• Used for those who nitroglycerines and
anticoagulants do not relieve pain. IV morphine is
the drug of choice. Morphine reduces workload on
heart. Pt needs to be monitored for hypotension
which is a side effect.
 Assignment
• Describe the differences between angina
pectoris and myocardial infarction
• Make a nursing care plan for a patient with
myocardial infarction
( Do this in your note books)
HEART FAILURE (CONGESTIVE
CARDIAC FAILURE)
 Cardiac failure – congestive cardiac
failure (CCF) – heart failure
• This is inability of the heart to pump sufficient
blood to meet the needs of tissues for oxygen
and nutrients
Pathophysiology
• Impairment of contractile properties of the heart –
leads to lower than normal cardiac output
NB: Cardiac Output = SV *HR
• HR increased by sympathetic N.S to compensate
• Stroke volume is the amount of blood pumped with
each contraction and depends on
I. Amount of blood filling the heart
II.Contractility( force of cardiac muscle contraction)
III.Arterial blood pressure
In CCF any of these 3 factors is altered such that
cardiac output is impaired
Cause of CCF
Caused by cardiac muscle disorders that impairs
contractile properties of the heart. These are:
• Coronary artherosclerosis – leads to hypoxia and
acidosis that results in myocardial cell death(MI).
Results in impaired heart contraction and CCF
• Hypertension – increases work requirement of the
heart leading to hypertrophy of myocardial muscle.
Hypertrophied cardiac muscle do not function
normally
• Inflammatory diseases of the myocardium – lead to
direct damage of heart muscle and decreased
contractility
• Other heart disorders – disorders of the heart
valves, heart compression
• Systemic factors – increased metabolic
rate(thyroxoxicosis), hypoxia, anemia,
acidosis, electrolyte abnormalities, cardiac
dysrrhythmias
 Clinical manifestations of CCF
• Dominant feature – increased intravascular volume
due to decreased cardiac output
• Increased pulmonary vessel pressure results in
pulmonary edema characterized by cough and
shortness of breath
• Congestion of blood results in peripheral edema
and weight gain
• Because of decreased CO, not enough blood
reaches tissues and organs resulting in :
• dizziness,
• fatigue,
• exercise intolerance
• Reduced urine output(oliguria leads to
aldosterone secretion – sodium and water
retention and increased intravascular volume
 CCF can be:
• Left sided heart failure
• Right sided heart failure
 Left Sided cardiac failure

• Pulmonary congestion predominates left sided

CCF as the LV is unable to adequately pump
adequate blood coming from the lungs.
• Increased pulmonary pressure causes
pulmonary edema manifested by.
Pulmonary signs seen in Left sided CCF include:
•dyspnea(orthopnea – difficulty breathing when
flat),
•cough (dry, moist, large quantities of frothy
sputum),
•fatigue( low oxygen and difficulty breathing),
•tachycardia, heart murmurs
•Anxiety(impaired oxygenation and difficulty
breathing)
 Right sided cardiac failure

• When the right ventricle fails, congestion of

organs and peripheral tissues dominates.
• The right side of the heart is unable to empty
its blood volume thus cannot accommodate
all the blood coming from venous circulation.
Clinical manifestations seen in systemic
circulation are:
• Edema – begins in feet and ankles and can spread
to legs and thighs then genitalia, sacrum and trunk
• Hepatomegally – tenderness of the right upper
abdominal quadrant from engorgement of hepatic
veins. High pressure within portal veins causes fluid
to be forced into abdominal cavity – ascites. This
puts pressure on diaphragm and worsens
respiratory distress
• Anorexia – due to engorgement of abdominal
vessels
• Nocturia – improved renal perfusion with rest
• Weakness – due to reduced CO, impaired
circulation, increased wastes
Diagnosis
• Evaluating clinical manifestation of pulmonary and
systemic congestion
• Measuring pulmonary artery pressure (CVP)
Management of CCF
Objectives are:
• Promote rest and reduce workload on heart
• Increase force and efficiency of myocardial
contractions through drugs
• To eliminate excessive accumulation of body water
by diuretics, diet and rest
Drugs
• Cardiac glycosides – increase force of heart
contraction and slow the heart rate. This increases
cardiac output, decreases venous pressure and
increases dieresis which removes fluids and relieves
edema. Relief of signs and symptoms is noted – less
dyspnea, edema. DOC – digitalis, digoxin, they are
toxic and need to be monitored. They Can cause
dyrrhythmias. Apical heart rate is assessed before
giving digoxin, if HR is lower than 60beats/min, drug
is withheld and physician notified.
• Diuretics – promote excretion of water and sodium.
Should be administered in the morning,
input/output should be monitored, should be
monitored for resolving congestion – weighed daily,
skin turgor checked and pulse rate monitored. DOC
– furosemide. NB can cause hyponatremia and
hypokalemia( causes weakening of cardiac
contractions – leads to dysrrhythmias) and pt needs
to be monitored for serum electrolytes
• Vasodialators – relax blood vessels and reduces
resistance to LV ejection of blood relieving
pulmonary congestion. DOC – IV nitroglycerine.
Patient monitored for arterial BP
Diet
• The diet should cause the heart least possible
work. Sodium is restricted to prevent edema,
HTN and cardiac failure. – explain to patient
sources of sodium
Conclusion
Nursing process management of
patient with CCF

Assignment
 Nursing responsibilities

• Assess – respiration – dyspnea, resp. rate, spo2,

dyspnea, fatigue, knowledge, self management,
urine output, fluid balance-daily weights
• Manage fatigue – mild physical activity with rest
periods
• Manage fluid volume – Daily weights, restrict
sodium, diuretics- Furrosemide, monitor input
and output, elevate extremities to relieve
edema
• Manage dyspnea – rest, semi fowlers position,
oxygen therapy
• Medications – Digoxin, diuretics, Angiotensin
converting enzyme inhibitors
• Monitor lab results – Electrolytes, renal
function tests, ECG
• Manage anxiety and powerlessness- inform
them about their care, help client verbalize
concerns, participate in care and decisions
Make 5 priority nursing diagnosis of a patient
with CCF
 PERICARDIAL EFFUSION AND
CARDIAC TAMPONADE
Pericardial effusion – accumulation of fluid in the
pericardial space. Caused by heart failure,
pericarditis, metastatic cancer, heart surgery or
trauma. This fluid raises pressure in the pericardial
sac and compresses the heart. This result in
• Increased pressure in all chambers of the heart
• Decreased venous return – compressed atrium
• Inability of ventricles to distend and fill adequately
resulting in reduced cardiac output ( compression
of the heart( cardiac tamponade)
• Manifestation – fullness of chest, dull pain, ,
chest pressure, engorged neck veins(jugular
venous distension), shortness of breathe,
labile weak systolic BP, narrowing pulse
pressure, distant heart sounds
• Diagnosis – Chest Xray and Echo
Management
• Pericardiocentesis – puncture of pericardial space
to aspirate fluid. ECG monitored during the
procedure and should be ready for CPR
• Pericardiotomy – portion of pericardium is cut off to
allow pericardial fluid to drain in lymphatic system (
cardiac surgery). Done for recurrent pericardial
effusion due to cancer
Dysrrhythmias
 Dysrrhythmias (arrhythmias)
• These are disorders of conduction of electric
impulses of the heart.
• They cause disturbances in heart rate and heart
rhythm.change in heart rhythm also causes a
change in blood pressure.
• Dysrrhythmias are named according to the site
of origin and the effect e.g. SAN, ventricular
• Dysrhythmias are diagnosed by ECG
NB: Diagnosis of the patient must include both
ECG and clinical assessment
Normal Electrical conduction
 The Electrocardiogram
• Electrical impulses that travel through the
heart can be viewed by means of ECG
• Electrodes are placed on the skin. Number
depends on types of machines( usually 2-5
and placed on the limbs and chest).
• The conduction of impulse in the heart is
reflected as a wave (PQRST complex). the
wave and intervals can then be interpreted
Electrocardiogram (ECG) can trace conduction
of electrical signals through the heart
• P – shows impulse from the SA node spreading
through the atria(atrial depolarization)
• QRS – spread of impulse through AV node to the
Bundle of HIS in the ventricles causing ventricles to
contract(ventricular depolarization). There is a
delay between the P wave and QRS complex
• T – relaxation of ventricular muscles (ventricular
repolarization)
• Heart rate can also be assessed from the wave
 Normal rhythm
Normal heart has a sinus rhythm - electrical
impulse starts at the SAN (P wave) at regular
rate(60-100) and rhythm and travels through
the normal conduction pathway
Electrocardiogram (ECG) can trace conduction
of electrical signals through the heart
 Types of Dysrrhythmias

Dysrrhythmias can be
•Sinus dysrrhythmias
•Atrial dysrrhythmias
•Junctional dysrrhythmias(A-V node)
•Ventricular dysrrhythmias
 Sinus Node dysrrhythmias
• Sinus bradycardia – occurs when the sinus node
creates an impulse at a slower than normal rate. ECG –
Atrial and ventricular rhythm regular, Rate is lower
than 60beats/min
Mx- Required if the patient has signs of decreased cardiac
output. Management involves giving Oxygen, drugs-
Atropine and application of a Pacemaker(non invasive
or permanent)
• Sinus Tachycardia – sinus node creates impulse at a
faster than normal rate (100-180beats/min). Caused by
physical stress, shock, hypervolemia, fever sympathetic
stimulation. ECG similar to a normal sinus rhythm
except the rate.
MX- Treat underlying cause
Sinus arrhythmias – occurs when the SAN
creates an impulse in an irregular rhythm.
Caused by heart disease. ECG – rate is normal
but rhythm is irregular
Atrial Dysrrhythmias
• Atrial flutter – occurs due to conduction defects in
the atrium and causes rapid, regular atrial rate(250-
400/min).
• Atrial fibrillation – Rapid, disorganized and
uncoordinated impulses depolarizing the atrial
muscle. The atrial kick absent, atrial quiver can lead
to formation of clots.
Occurs in heart failure and valve disorders
ECG – atrial rhythm 300-600b/min, ventricle rhythm
100-200b/min. P wave is not visible.
Mx- Give Oxygen, Give anticoagulants (Heparin),
Antidysrhythmia drugs and Cardioversion
(synchronized countershock to convert undesirable
rhythm to desirable rhythm)
Junctional Dysrrhythmias
• Junctional Rhythm – Occurs when the AV node
instead of SAN becomes the pace maker.
• Occurs when the SAN slows down or when impulses
are blocked and cannot be transmitted through the
AV node. Causes signs of reduced Cardiac output.
ECG –reduced HR (40-60), p wave not seen).
• Caused by digoxin toxicity, heart failure, coronary
artery disease
Ventricular dysrhythmias
Premature ventricular contraction (PVC) – impulse
starts in the ventricle and is conducted to the
ventricles before the next sinus impulse.
• ECG – atrial and ventricular rhythm irregular,.
Caused by cardiac ischemia, MI, heart failure,
MX- Check for hypoxemia and give oxygen, Check
Potassium levels (Hypokalemia), Antidysrhythmia
drugs, Notify doctor if client has chest pain and PVC
increase in frequency
• Ventricular tachycardia (VT) – Ventricular rate at
140-250 beats/min and is regular. it is an
emergency because the patient can go into cardiac
arrest. ECG – no P waves, more QRS complex, and
regular
• Patient presents in 3 ways:
1.Stable- VT with pulse and no signs of decreased
Cardiac output (Oxygen and antidysrhythmics)
2.Unstable- VT with pulse and signs of decreased CO
(Oxygen, antidysrhythmics, cardioversion)
3.Pulseless VT- client is in coma (CPR and
defibrillation (asynchronous countershock to
terminate VT rhythm)
Ventricular fibrillation – is the most common
dysrrhythmia in patients with cardiac arrest.
•This is rapid, disorganized ventricular rhythm.
Caused by coronary artery disease, MI, valvular
heart disease, electrolyte imbalance and electric
shock.
•ECG – ventricular rate is over 300/min, ventricular
rhythm irregular, QRS –no recognizable complex.
• Patient will have no heartbeat, palpable pulse and
respiration. Immediate CPR and defibrillation
required for survival. Antiarrhythmia medication
may also be used
• Ventricular asystole – commonly called flat line.
ECG – QRS complex absent. Patient has no
heartbeat, no pulse, no respiration. It is usually
fatal. Management is by CPR, defibrillation,
antiarrhythmia drugs and managing the cause.
• Caused by hypoxia,, electrolyte imbalance,
hypovolemia, coronary thrombosis, trauma. Has
a poor prognosis, if patient does not respond, it
leads to death.
 Management of dysrrhythmias
Dysrhythmias are managed by
1.Antidysrhythmic Medication
2.Electrical therapy – emergency defibrillation,
cardioversion
3.Pacemaker – Temporary or Permanent
Nurses roles = Monitor patients response to
medication, document and ensure patient has
ability to manage medication, Assess patients
understanding of implants and self management
abilities and Help patient live an active and
productive life
 Antidysrhythmic drugs
They inhibit abnormal electrical conduction in the
heart therefore eliminate abnormal rhythms
1.Sodium Channel blockers – Quinidine,
Procainamide, Lidocaine
2.Beta (ᵝ) Blockers – (Block beta adrenal receptors) –
Atenolol, propranolol, acebutolol
3.Potassium channel blockers (delay repolarization) –
Amiodarone
4.Calcium channel blockers – Nifedipine, Amlodipine,
Verapamil
5.Others – Adenosine, digoxin
For all – Monitor BP, Pulse, ECG, cardiac output effect
 Cardioversion and defibrillation
• Used to treat dysrrhythmias that cause
tachycardia. An electric current is delivered that
causes depolarization of cardiac muscles. When
the cells repolarize, the SAN is usually able to
recapture its role as pace maker.
• Cardioversion – delivery of electric current
synchronized with patients electric event. The
current is timed to synchronize with an ECG on
monitor so that the impulse is delivered during
ventricular contraction (QRS-depolarization).
Considered successful if sinus rhythm, BP and pulse
are restored. Continuous ECG monitoring required
after the procedure.
• Defibrillation – delivery of current is immediate and
unsynchronized – for pulseless patients
• Implanted cardioverter-Defibrillator (ICD) – Leads
Placed on heart, monitors rhythm and terminates
VT and VF
 Nursing care in cardioversion/
Defibrillation
• Proper placement of electrodes on clean dry skin
• Stop oxygen when delivering the shock – risk of
fire
• No one should touch bed or client when delivering
the shock
• Post procedure – Monitor rhythm, pulse, BP, LOC,
airway and burns on chest from the pads
 Pacemaker
• A pacemaker – an electronic device that
provides stimuli to the heart muscle and sets
the heart rate. Used for patients with slow
cardiac impulse formation (bradycardia) that
don’t respond to drugs e.g after MI or heart
surgery
• Can be temporary ( used in hospital) or
permanent (lead wires usually placed in the
apex of the left ventricle).
• Pace makers have an electric impulse
generator. Complications – local infection and
bleeding at insertion site, dislocation of lead,
• Patients with pacemakers are taught to check
on battery, check pulse, avoid electric
transmitters and MRI
Cardiac surgery
Surgery can be done to open blocked coronary
arteries and vascularize the heart
•Coronary artery bypass grafting surgery - Occluded
artery is bypassed with the patients own vein/ artery
(saphenous vein, internal mammary artery)
It is an open heart surgery
Coronary bypass graft surgery
• coronary angioplasty – enter coronary vessel
with a balloon catheter to crack and flatten
the plaque, This opens the vessel and
improves blood flow. A metal stent may be
used to support vessel
• Atherectomy - catheter with cutting chamber
or laser to remove plaques in coronary artery
Coronary Angioplasty
• Heart transplant – From compatible donor
within 6 hrs. Risk of rejection
 Cardiac Surgery- Pre op
• Client education – what to expect (sternal
incision, arm/leg incision, chest tube, IVF,
pain, Mechanical ventilation
• Informed consent
• check allergy to iodine
• NPO- 6-8hrs
• Premedication
 Cardiac Surgery- Post op
Patient initially nursed in cardiac unit/ICU
•Monitor HR, BP, Pulse, Cardiac output, Urine
output, continuous ECG
•Fluids and electrolytes
•Mechanical ventilation
•Pain management
Transferred to ward for further care- - Vitals, ECG,
infection monitoring, wound care, activity
tolerance