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BEGINNERS GUIDE TO CCU
5 East
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Index
Page
Anatomy & Physiology of the Heart
Cardiac Anatomy
3-4
The Cardiac Cycle
5
Coronary Circulation
6-7
Electrophysiology
8-9
Cardiac Monitoring in CCU
Hardwire Monitoring
10
12 Lead ECG’s
11
The Normal ECG Complex
12-13
Acute Coronary Syndrome
Defining ACS/ nursing management
14-16
Chest Pain Management
17-20
Diagnostic testing in ACS
21-22
Interventional Procedure in ACS
23
Heart Failure
Heart Failure Basics
24-25
IABP
26-27
CPAP
28-29
Arrhythmias
Arrhythmia Recognition
30-31
Nursing Care of Patient with Arrhythmia
32-33
DCCV
34
TVPM
35
Appendix 1: Review of Cardiac Anatomy & Physiology
Appendix 2: How to record an accurate ECG
Appendix 3: What’s at the heart of your patients chest pain
Appendix 4: Common Cardiac Arrhythmias
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Anatomy and physiology of the heart
CARDIAC ANATOMY
The heart lies within the mediastinal cavity between the left and right lungs.
The lower point of the heart, the apex, lies on the diaphragm and points to the
left. Approximately two thirds of the hearts mass is to the left of the body’s
midline.
The primary function of the heart is to supply the body with enough blood to
meets its metabolic needs.
Cardiac Tissue:
The heart is arranged in three layers, the pericardium, myocardium, and
endocardium.
The pericardium is the outermost layer consisting of two parts. The fibrous
pericardium forms a loose fitting sac around the heart, and is in contact with
the pleura of the lungs. The serous pericardium consists of two fluid secreting
layers, one of which is in contact with the myocardium, which provide lubrication
around the heart enabling friction free movement.
The myocardium is the middle layer of the heart, which is muscular and
responsible for the pumping action of the heart. It contains contractile fibers,
along with the conduction system of the heart and its associated blood supply.
The endocardium is the inner layer that lines the valves and inner chambers of
the heart.
Heart Chambers:
The heart consists of four hollow chambers. The two upper chambers, the right
and left atrium, are divided by the interarterial septum. The lower chambers,
the right and left ventricles are divided by a thick muscular wall, the
interventricular septum.
These chambers compile the pumping system of the heart. The right side of
the heart receives deoxygenated blood from the body and pumps it into the
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lungs. The left side of the heart receives freshly oxygenated blood from the
lungs and pumps it into the systemic circulation.
The ventricles are thicker and more muscular than the tissue of the atria as
they must eject blood against higher pressures. The left ventricle is the most
muscular due to it having to eject against the pressure of the systemic arterial
circulation.
The Heart Valves:
Atrioventricular Valves:
 Mitral Valve – lies between the left atria and the left
ventricle and has 2 cusps
 Tricuspid Valve – lies between the right atria and right
ventricle and has 3 cusps
Semilunar Valves:


Aortic Valve – lies between the left ventricle and the
aorta
Pulmonary Valve – lies between the right ventricle and the
pulmonary artery
Both these valves consist of 3 half moon shaped cusps.
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CARDIAC CYCLE:
Relates primarily to pressure changes within the heart.
Ventricular filling:

When pressure in the atria is greater than that of the
ventricles, the mitral and tricuspid valves are forced
open, and blood moves passively from the atria to the
ventricles.

Atria contract in response to electrical stimuli from the
sinoatrial (SA) node.
Atrial contraction accounts for 20-30% of ventricular
filling volume
Ventricular pressure rises
Atrial Systole:


Ventricular Systole:
2 phases during which contraction occurs.
Isovolumetric contraction
 Ventricular contraction occurs in response to electrical
stimuli
 Immediately after contraction commences ventricular
pressure rises abruptly, causing mitral & tricuspid valves
to close
 As all valves are closed, pressure continues to rise and
muscular contraction is occurring without a change in
volume.
 Wall tension created as ventricle s work to overcome the
resistance of the systemic arterial circulation.
Ventricular Ejection Phase
 When pressure in ventricle exceeds that of systemic
circulation, aortic & pulmonary valves open
As pressure in the ventricles falls below systemic circulation, the aortic &
pulmonary valves close.
Isovolumetric Relaxation/ Ventricular Diastole:
 Ventricular Filling
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CORONARY CIRCULATION
The Coronary arteries provide oxygen and nutrition to the myocardium, or heart
muscle. Partial occlusion of these arteries can lead to chest pain,
breathlessness, and a reduction of movement in the area of heart muscle being
supplied. Total occlusion of an artery will lead to the death of the myocardium
(myocardial infarction) in the area supplied by the artery. Depending on the
size of infarction and the location of any damage, this can result in heart
failure, arrhythmias and/or death.
When the myocardium is hypoxic or ischaemic, the collateral circulation may
become disfunctional. Collaterals, present at birth are inter-arterial vessels
that connect two branches of a coronary artery, or the right and left coronary
artery systems. When stimulated collaterals may become functional within a
period of as little as nine days. When fully developed collaterals are able to
vasodilate in response to nitrates, and may be affected by vasoactive
substances produced by the body.
Much individual variation exists in the pattern of coronary artery branching,
however as a rule, the following anatomy applies.
The Left Main Artery (LM) supplies much of the left atrium and ventricle. It
originates in the aorta and branches into the Left Circumflex and the Left
Anterior Descending arteries. Total occlusion of the left main coronary artery
results in death, as the total left side of the heart is left with virtually no blood
supply. This may not be the case in the patient who has an extremely well
developed collateral blood supply.
The Left Anterior Descending Artery (LAD) supplies the anterior surface of
the heart. Areas supplied include the heart apex, intraventricular septum, and
parts of the left ventricular papillary muscle. With LAD vessel occlusion the
conduction system of the Bundle of His, Right Bundle Branch and the Left
Anterior Bundle may be affected.
The Left Circumflex Artery (LCX) supplies the lateral portion of the heart.
Areas supplied include the left atrium and parts of the left ventricle. In 45%
of the population the LCX supplies the conduction system of the Sino Atrial
Node (SA node), and that of the Atrioventricular Node (AV node) in 10% of the
population.
The Right Coronary Artery supplies the inferior portions of the heart. Areas
supplies include the anterior and posterior portions of the right ventricle. The
conduction system of the SA node and the AV node, in 55% of the population,
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and the Left Posterior Fascicle and Bundle of His in 90% of the population are
all supplied by the RCA.
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ECG Region & Vessel Identification:
The 12 lead ECG directly correlates to the myocardium and the vessels that
supply it with blood. When looking at an ECG we can define which vessel is likely
to be the culprit lesion in a person suffering from a myocardial infarction, by
knowing which vessels correspond to what regions on the ECG.
ELECTROPHYSIOLOGY:
Cardiac cells
The cells of the heart possess 5 distinct characteristics, which differentiate
them from other skeletal muscle cells.

Automaticity: the ability of a cell to generate an
electrical impulse

Excitability: the ability of a cell to respond to an
electrical impulse

Conductivity: the ability of a cell to transmit an electrical
impulse from one cell to another

Contractility: the ability of a cell to shorten and lengthen
its muscle fibers

Extensibility: the ability of a cell to stretch
Electrical Conduction System of the Heart:
The heart contains a specialized electrical conduction system that generates
electrical impulses along a specific pathway resulting in Atrial and ventricular
contraction.
The Sino Atrial Node (SA node) is the pacemaker of the normal heart. It
discharges impulses at a rate of 60-100bpm. As its intrinsic rate is greater
than any other cells in the heart, it is primarily the hearts pacemaker.
As impulses leave the SA node they are conducted through the left atria by the
Bachmann's bundles, and through the right atria by the intranodel tracts. The
impulse then arrives at the Atrio Ventricular Node (AV node).
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The AV Node delays the impulse transiently, awaiting the completion of
ventricular filling and atrial contraction. The AV node then conducts the
impulse to the ventricles via the Bundle of His. As a pacemaker the AV node can
generate impulses at a rate of 40-60bpm.
The Bundle of His rapidly conducts the impulse prior to it splitting into the
Right and Left Bundle Branches.
The Right Bundle Branch conducts the impulse throughout the right ventricle.
The Left Bundle Branch divides into the anterior and posterior fascicles,
conducting the impulse through the left ventricle.
The Purkinjee fibers then conduct the impulse deep within the muscle cells,
resulting in ventricular depolarization and contraction.
As pacemaker cells, ventricular cells have an intrinsic rate of 30-40bpm.
Please read Appendix – A review of cardiac anatomy
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Cardiac Monitoring
HARDWIRE MONITORING
All beds within the CCU are able to be hardwire monitored. This involves the
patient being directly connected to a monitor located next to their bed.
Generally patients requiring monitoring can be divided into three groups.

Patients who are risk of developing an arrhythmia following an acute
event. These patients are monitored for a selected period of time, until
the major risk of arrhythmia development has passed.

Patients who have presented with symptoms of, or who have a
documented arrhythmia. These patients are monitored until the
arrhythmia is diagnosed and treated.

Post surgical patients Cardiothoracic and Interventional
It is a medical responsibility to document patients at high risk of arrhythmia,
and select the appropriate protocol for monitoring.
It is essential that all monitoring alarms be assessed, and appropriate action
taken.
Electrode Placement for Cardiac Monitoring:
Skin Preparation for Electrode Application

Choose site for electrode away from large muscle groups

Wipe skin with an Alco swab if diaphoretic

Lightly abrade the area with the emery dot on the electrode

Attach the electrode to the patient

Attach lead wire to electrode
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
V lead for monitoring is placed in accordance with region in which
monitoring required. (e.g. post PTCA / AMI lead is placed to correspond
with region of insult)
12 LEAD ELECTROCARDIOGRAMS
A 12 lead ECG gives a more complete view of the heart than a rhythm strip. It
is most frequently used to diagnose myocardial Ischaemia or infarction.
How to Perform a 12 lead ECG:
1.



Position Patient
Explain procedure and ensure privacy
If possible position at 45degree angle
Check patient is relaxed i.e. Hands/feet not clenched or flexed




Electrode Application
Shave patient if very hairy
Wipe skin with Alco swab if diaphoretic
Position limb leads away from large muscle groups
Ensure chest electrodes are measured and positioned correctly



Reducing Interference
Check patient is relaxed as above
Relieve pain if possible prior to ECG
Minimize shivering


ECG Machine
Enter patients name and MRN
Note indication for ECG on top of page e.g. Chest pain


On completion of ECG
Ensure leads are not kinked or twisted
Plug machine into power to recharge
2.
3.
4.
5.
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THE NORMAL ECG COMPLEX:
P wave:
 atrial depolarization
 precedes every QRS complex
 rounded and upright
PR Interval:
 duration: 0.12 – 0.20 seconds
 short duration indicates impulse originating elsewhere than the AV node
in the atria
 prolonged duration indicates conduction delay
QRS






Complex:
ventricular depolarization
falls after the p wave
duration: 0.06 – 0.10 seconds
Q wave: first negative deflection after P wave, before R wave
R wave: first positive deflection after P wave
S wave: first negative deflection after R wave
J point:
point marking the end of the QRS complex, beginning of ST segment
ST Segment:
 represents the end of ventricular depolarization and beginning of
repolarisation
T wave:
 ventricular repolarisation
 follows S wave, typically rounded and upright
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QT Interval:
 ventricular depolarization and repolarisation
 duration: 0.36 – 0.44 seconds
 duration varies according to heart rate
U Wave:
 recovery of purkinjee fibers
 not always present
 rounded and upright
QRS Variations:
Remember:



Q wave – first negative deflection after the P wave
R wave – first positive deflection after the P wave
S wave – first negative deflection after the R wave
Large deflections are labeled with an upper case / capital letter, small
deflections are labeled with a lower case letter.
Please read Appendix 2: How to record an accurate ECG
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Acute Coronary Syndromes (ACS):
DEFINING ACS
Acute Coronary Syndromes (ACS) is a term used to group three of the
presentations of coronary artery disease. The term ACS encompasses Acute
ST Elevation Myocardial Infarction (STEMI), Non-ST Elevation Myocardial
Infarction (NSTEMI), and Unstable Angina Pectoralis (UAP). This umbrella
term was adapted to discuss the conditions as they all share a similar pathology.
ACS refers to an acute event caused by plaque rupture and thrombus formation
within the coronary arteries. This results from a complex series of events,
which result in the rupture of a vulnerable lesion.
Coronary arteries contain varied amounts of plaque deposits within individuals.
Unstable plaque, which as susceptible to rupture have certain defining
characteristics.
 A soft Lipid core: this allows the plaque to be more mobile and therefore
less stable
 The presence of Inflammation: macrophage activity denatures the plaque,
making it more susceptible to rupture
 Irregular borders which occur due to plaque fissuring and ulceration
 Stenosis of up to 70%: larger lesions have the ability to stretch and
adapt to pressures more so than their smaller counterparts. Increased
stenosis is more likely to be associated with collateral flow.
 Very thin fibrous cap: which has few muscle cells and little collagen. It is
these structures that would normally give the cap is strength. Also high
in macrophages.
 Tissue Fatigue on the fibrous cap: caused by intraluminal pressures. Like
a paperclip that you bend continually – eventually it snaps and breaks.
ACS occurs more frequently in the morning, in colder temperatures, during
times of emotional or physical stress, and after smoking or overeating. This is
due to the effects of changing circadian rhythms and the impact of associated
stressors on the body.
Patients who present with the symptoms of ACS are categorized into groups of
risk according to their symptoms and history. This ensures that patients
receive optimal treatment from the beginning for the possibility of an acute
event.
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STEMI:
STEMI patients must receive early revascularisation in order to preserve
myocardial function. With the presentation of a history of chest pain, a STEMI
is diagnosed by ECG. ECG findings would include ST segment elevation.
A STEMI indicates that there is prolonged coronary artery occlusion, initially
resulting in myocardial injury, progressing to infarction if left untreated. This
is the result of the formation of a red thrombus, rich in red blood cells.
STEMI’s are treated with a Primary angioplasty if the hospital has access to a
24hour cardiac catheter lab. In hospitals without such facilities STEMI’s
receive intravenous thrombolytic therapy, which breaks down the red blood cell
rich thrombus. Due to the nature of these drugs patients are at an increased
risk of bleeding. This is important to consider when patients are transferred
from other hospitals after having received thrombolytic therapy.
The success of revascularisation is measured by a decrease in ST segment
elevation on ECG, relief of chest pain, early peak in cardiac enzymes and
reperfusion arrhythmias.
NSTEMI:
NSTEMI indicates a transient occlusion of a coronary artery that is usually
short lived, up to 1 hour. These involve the formation of a white thrombus,
which is rich in platelets therefore not suitable for treatment with
thrombolytic drugs. Initial treatment of NSTEMI’s involves antiplatelet and
anticoagulation therapy, and optimization of antianginal therapies. A cardiac
catheterization would then be attended.
UAP:
UAP patients may have an Exercise Stress Test prior to discharge from
casualty. If they have a known history of Ischaemic Heart Disease or a positive
EST, admission may be required to optimize or introduce antianginal therapy. A
cardiac catheter may be attended as an inpatient or outpatient.
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Nursing Management of ACS Patients:
The focus of nursing care of the ACS patient is to decrease myocardial oxygen
demand, and to optimize medical treatments. This includes the prompt
assessment and treatment of chest pain, graduated activity, alleviation of
anxiety, and the monitoring of medication regimes.
Monitoring for complications is an essential part of nursing the ACS patient.
Any ongoing or unrelieved chest pain must be documented and medical staff
notified.
Arrhythmias may occur due to Ischaemia, electrolyte imbalance, or medications.
Monitoring as per the ACS protocols allows us to detect early and treat such
arrhythmias.
The effects of cardiac medications must be continually monitored.
The possibility of ventricular dysfunction must be noted and steps taken to
detect any problems.
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CHEST PAIN MANAGEMENT:
Patients admitted to CCU often present with, or have a history of chest pain.
During their admission, chest pain management can be an ongoing issue. It is
essential that nursing staff are able to quickly assess and treat chest pain
appropriately. Chest pain should always be assumed to be of cardiac origin, until
proven otherwise.
Indicators of Cardiac Chest Pain:

Location:
Central anterior/lateral upper chest (sub-sternal)
Area = approx size of clenched fist

Radiation:
Left arm, possibly extending to fingers
Neck, jaw, tongue, teeth (sometimes experienced as primary site)
“chocking sensation”
Upper abdomen

Quality:
Squeezing, tightness, dull, weight on chest
May deny “pain”, instead describing pain as a “discomfort”

Intensity:
Score pain on scale of 1 – 10

Duration:
Varies, if >30 minutes, consider AMI

Onset:
Can be gradual or sudden, with activity or at rest

Precipitating Factors:
Exercise, emotional stress, smoking, cold, eating

Relieving factors:
Rest, Nitrates

Associated Symptoms:
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Dyspnoea, diaphoresis, nausea & vomiting, abdominal
discomfort/gas (due to decreased gastric motility), weakness,
palpitations/syncope, anxiety
Differential Diagnosis:
Pericardial Pain:
Described as a sharp intermittent pain, relieved by leaning forward
Pleural pain:
 sharp stabbing pain
 worse on inspiration
Oesophageal Pain
 burning
 precipitated by eating, leaning forward, lying down
Treatment of Chest Pain:
REST – primary action to take
Oxygen supplementation: to optimize blood oxygen saturation and therefore
delivery to myocardium
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Pharmacological treatment:
Anginine/GTN:
Anginine may be administered sublingually, via skin patches and creams, and
intravenously. In the treatment of chest pain the sublingual and intravenous
routes are utilized due to their speed of effect.
Anginine has a variety of effects that are of benefit to the patient
experiencing cardiac chest pain.
 Improve coronary blood flow through vasodilatation ( preload),
interrupt spasm, augment collateral flow (arterial dilatation), reduce O2
demand with peripheral vasodilatation
It is essential when administering Anginine that the practitioner be aware of its
effects and possible side effects.
Of greatest concern is its ability to lower blood pressure. This is of benefit to
many patients, others however are extremely sensitive to the drug and it may
lower their blood pressure adversely.
Never let systolic BP drop below 90mmHg. Below this point coronary artery
perfusion becomes compromised.
Prior to administrating of Anginine a blood pressure recording must always be
attended.
The development of a sever headache is a common side effect of Anginine. This
is due to vasodilatation of cerebral vasculature and the associated pressure
created by the increased blood flow.
When treated early, Paracetamol is often the only treatment required.
Patients can build a tolerance to Anginine, which reduces the drugs efficiency.
Patients who wear a GN patch must have a nitrate free period daily to help to
avoid tolerance.
Morphine:
The experience of pain causes sympathetic nervous system stimulation resulting
in vasoconstriction ( afterload),  HR, contractility, and therefore 
oxygen demand.
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In the setting of a patient with Ischaemic chest pain this is undesirable as it
causes further demands on a heart that is already struggling to meet its
metabolic demands.
By decreasing the perceived level of pain, Morphine can reduce this demand and
also has the effect of reducing anxiety as pain is relieved.
Morphine also produces venous and arterial dilatation, resulting in a greater
amount of blood flow to occur throughout the body. Caution is required when
administering Morphine due to its ability to lower blood pressure, perhaps
adversely.
Users of Morphine must also be aware of its potential to cause respiratory
depression. Respiratory depression correlates highly with dosage.
Serious respiratory depression is less likely when Morphine is given in small
increments, frequently. In the practice of administration for chest pain, this is
how Morphine is given. It remains essential however to monitor closely for any
adverse effects.
Please read Appendix 3: What’s at the heart of your patient’s chest pain
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DIAGNOSTIC TESTING IN ACS:
Angiogram: (Cardiac Catheter)
This



procedure is performed to:
define the extent of coronary artery disease
assess heart valve function
assess ventricular function
By injecting contrast medium into the heart and coronary arteries the physician
can visualize the heart chambers, valves, great vessels, and coronary arteries.
Measures of pressures and blood volumes can also be made to assess cardiac
function.
Cardiac Catheterisation is performed in the Cardiac Catheter Lab under local
anaesthetic. Access is usually gained via the right femoral artery and / or vein.
Fluoroscopy is used to guide the catheter to the desired location within the
vascular system.
A Left Heart Study is the most common procedure and includes coronary
angiography to assess the coronary arteries, and ventriculogram to assess
ventricular function. A catheter is inserted via a peripheral artery and fed into
the aorta and then into the right and left coronary arteries.
A Right Heart Study measures right-sided heart pressures including the right
atrium, ventricle and pulmonary artery pressures. The pulmonary and tricuspid
valves are also assessed.
EXERCISE STRESS TEST: (EST or ETT)
Exercise stress testing is a relatively inexpensive and simple means of assessing
for Myocardial Ischaemia. The objective is to assess the coronary arteries
ability to deliver sufficient blood supply during a period of an increased,
exercise induced demand.
During the test demand on the heart is increased within controlled conditions
using either exercise or drugs (pharmacological stress testing). Most commonly
the patient exercises on a treadmill with ECG monitoring insitu. During this
time patients are assessed for chest pain and, or ischaemic ECG changes.
This test is performed in the cardiology department.
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THALLIUM / SESTAMIBI: (MIBI)
These tests assess myocardial perfusion. The patient is injected with
radioisotopes at rest and again during stress (exercise) to produce images of
myocardial regional uptake, proportional to regional blood flow. With maximum
exercise, myocardial blood flow should increase dramatically above the resting
state.
In the presence of a fixed coronary Stenosis, there is an inability to increase
myocardial perfusion within the territory fed by the stenosed vessel. This
results in a flow differential and decreased uptake of the isotope.
If a patient is unable to exercise, pharmacological agents can be used to induce
a state of maximum exercise capacity.
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INTERVENTIONAL PROCEDURES IN ACS:
PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY: (PTCA)
Angioplasty is a non-surgical procedure used to dilate diseased and narrowed
coronary arteries. The procedure is relatively simple and has high initial
success rates.
The main indicator for revascularisation therapy, including both PTCA and
surgery is symptomatic coronary artery disease. Patients who have single
lesions are most suitable for angioplasty, while those with multiple lesions are
most suited for surgery.
Angioplasty is similar to cardiac catherterisation, proceeding to the
intervention stage. A balloon catheter is placed over the target lesion with the
assistance of fluoroscopy. The balloon is then inflated a number of times to
stretch the lumen, reopening the artery and causing the plaque to crack and
flatten against the arterial wall. Patients may experience significant chest pain
at this point of the procedure.
Coronary Artery Stenting is used in combination with most angioplasty
procedures. Coronary artery stents are metallic mesh or coil splints which prop
open the artery. Stents are positioned with the use of the balloon catheter.
At POWP Acute Myocardial Infarctions are treated with angioplasty. In this
circumstance it is called a Primary Angioplasty.
As soon as a patient in casualty is diagnosed with an AMI, processes begin to
get them to the cath lab for a PTCA as soon as possible. Therefore, the initial
treatment for an AMI is angioplasty.
Angioplasty in the AMI setting has been shown to have higher success rates and
fewer side effects than thrombolytic medications, which were previously used.
Hospitals without a 24hour cath. lab however continue to use thrombolytics in
AMI patients. Occasionally this treatment is unsuccessful and the patient
requires further emergency intervention. These patients are transferred to a
hospital with a 24-hour cath. lab urgently and have a Rescue Angioplasty in an
effort to reopen the occluded vessel.
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Heart Failure
HEART FAILURE BASICS
Patients in the Coronary Care Unit may be admitted with complications of heart
failure, or it may arise as a complication of their current condition. Post AMI,
all patients must be monitored for the development of heart failure.
Heart failure is a diagnosis secondary to any disorder resulting in damage to the
myocardium causing a disruption to its normal functioning and ability to pump
blood throughout the vascular system. Heart failure can be associated with
either the left or right systems of the heart, or both.
Causes:
Coronary Artery Disease: due to potential ischaemic events and long-term
increased demands on the heart
Aging: with increasing age the heart muscle naturally weakens
Hypertension: increased systemic vascular resistance places greater workload
on the heart as it is required to pump against increased pressure, thus
increasing the workload on the myocardium.
Dilated Cardiomyopathy: large thin ventricle walls result in decreased
contractility
Hypertrophied Cardiomyopathy: thickened ventricle wall with poorly
functioning muscle fibers
Restrictive Cardiomyopathy: stiff ventricle wall results in decreased
contractility
Mitral & Aortic Valve Disease: Interfere with the forward flow of blood and
disrupt ventricular filling. The path of blood through the heart is disrupted
making it more difficult for it to move through the system
Pulmonary Disease: can cause right ventricular hypertrophy and failure due to
the backlog of blood.
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Behavioral: obesity, smoking, high fat & sodium diet, high alcohol consumption,
sedentary lifestyles have all been found to contribute to the risk of developing
heart failure.
Pathophysiology of Heart failure:
As the heart fails its ability to continue pumping effectively diminishes,
resulting in decreased cardiac output (C.O). Cardiac output is indicative of
myocardial functioning capacity.
CO = SV x HR
Stroke Volume:
 preload – amount of blood within the ventricles immediately prior to
contraction
 afterload – the pressure against which the heart must contract
 contractility – ability fo muscle fibres to strech and contract
Heart Rate:
 heart rate & rhythm
Dilatation of Heart:
As the myocardial muscle of the left ventricle fails, it dilates in response to
increased preload. This is an attempt to increase Co by means of having a
greater muscle mass.
However, as muscle size increases, so does the myocardial oxygen demand. This
results in an increased demand being placed on an already failing heart.
Neuroendocrine Response:
Baroreceptors are activated in response to the falling blood pressure associated
with heart failure. Activation results in an increased heart rate, contractility ,
and vasoconstriction. This increase in blood pressure however increases the
workload of the heart, resulting in greater oxygen demands.
RAA System:
When CO decreases, so does the kidney perfusion. This decrease in perfusion
results in an increase in Renin secretion, and therefore angiotension I.
Angiotension I is then converted to Angiotension II in the presence of
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Angiotension Converting Enzyme. Angiotension II is a potent vasoconstrictor,
resulting in increased blood pressure, retention of sodium and water, leading to
increased congestion and preload. Vasopressin and Aldosterone levels are also
increased, causing further water retention.
INTRA AORTIC BALLOON PUMP:
The Intra Aortic Balloon Pump (IABP) is a cardiac assist device designed to
increase coronary artery perfusion and decrease myocardial oxygen demand.
This is achieved with the insertion of a balloon into the descending thoracic
aorta which is timed to inflate and deflate at set times throughout the cardiac
cycle.
IABP insertion is indicated in variety of clinical settings. Predominantly we see
their insertion with Cardiogenic shock, mechanical complications post AMI,
severe ventricular failure, and as a means of support for high-risk patient to
enable coronary interventions or surgery to occur.
There are relatively few contraindications to IABP insertion, and in most
instances it is a matter of weighing benefit against risks to the patient.
Absolute contraindications to IABP insertion are chronic and end stage heart
disease, and brain death.
Primary Effects of IABP:
Supply Increases
 Increases aortic pressure during
diastole to augment coronary artery
perfusion.
Demand Decreases
 Decreases aortic pressure during
systole to lessen workload of the left
ventricle.
Secondary Effects of IABP:
A number of secondary, beneficial effects, in addition to those exhibited by
the myocardium. An improvement in the functioning of the heart results in
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better perfusion of other organs. Improvements in neurological state,
respiratory functioning, renal functioning and vascular perfusion are seen.
Complications from IABP pumping can range from minor discomforts to life
threatening problems. Close observation and care, with individual specialized
nursing is required.
Patients are gradually weaned from the IABP as their condition improves.
Sudden withdrawal could result in extreme cardiac compromise.
When an IABP is in place patients are required to lie flat in bed. This is
extremely debilitating. Factors such as pressure area care, nutritional
assistance and assistance with all activities of daily living are needed.
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CONTINUOUS POSITIVE AIRWAY PRESSURE:
Continuous Positive Airway Pressure (CPAP) is a form of ventilatory assist in
the conscious self-ventilating patients who are able to maintain their own
airway. Positive airway pressure is applied throughout the entire respiratory
cycle. The addition of Positive End Expiratory Pressure (PEEP) complements
this by applying a preset amount of airway pressure at end expiration.
PEEP is achieved by the actions of the valve. The patient breathes out until
the preset level of pressure is reached. Once this is achieved the valve
closes, preventing further exhalation, ensuring the preset pressure is
maintained. This prevents the full closure of alveoli at the end of the
respiratory cycle.
In the CCU CPAP is delivered via a facemask, with the PEEP set by attaching
a valve to the facemask. Various valves can be attached to achieve different
PEEP settings.
Humidification can be used with CPAP to prevent the drying effects of high
flow oxygen delivery.
In the CCU CPAP is used predominantly for the treatment of cardiogenic
pulmonary oedema. It other uses include acute respiratory failure, asthma,
chronic airway limitations, pulmonary contusion and flail chest, post operative
atelectasis and obstructive sleep apnea.
Advantages of CPAP:
CPAP has a number of advantages that can be difficult to separate out as they
are interrelated to one another.
Minimize alveolar collapse:
 By resolving atelectasis CPAP restores the surface area available within
the alveolar for gas exchange, and for the diffusion of fluid.
 CPAP reopens collapsed alveolar, and prevents the collapse of others
Improved Lung Compliance:
 By the application of positive pressure throughout the respiratory cycle,
alveolar collapse is prevented, therefore compliance is improved.
 A reduced amount of effort is required to reinflate the alveoli.
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Decreased Work of Breathing:
 The application of continuous flow creates positive pressure, making it
easier to breath in (for the same amount of effort the patient gets a
greater effect with inspiration)
 By decreasing the work of breathing we also reduce the oxygen
consumption, improving tissue oxygenation
Improved ventilation & perfusion matching:
 When blood flows past poorly ventilated alveoli, little gas exchange
occurs
 Blood returning to the heart is therefore poorly perfused
 Reinflation of alveoli results in improved gas exchange and tissue
oxygenation
Decreased Preload:
 Application of positive pressure reduces venous return and therefore
preload
 This is beneficial for pulmonary oedema as it can help to reduce
pulmonary congestion
 If hypovolemic , blood pressure and cardiac output can be negatively
effected.

The absolute contraindication to CPAP is the patients who is unable to maintain
their own airway. These patients require more invasive ventilatory support.
Other contraindications include facial injuries, any trauma or recent surgery to
oespohagus and trachea, base of skull fracture, significant pneumothorax, and
increased risk of vomiting.
CPAP has many minor complications associated with it such as skin pain and
breakdown related to the facemask, discomfort and nutritional declines. More
serious complications are rare, but with careful monitoring this can be
prevented or the impact minimised. Nursing of a patient on continuous CPAP is
on a one to one basis.
Patients are weaned from CPAP as their condition improves. When weaning
continuous monitoring of the patients condition allows us observe the ability of
the patient to cope without support. Throughout treatment continuous
monitoring of patients body systems is necessary to assess the effectiveness of
treatment and observe for any complications.
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Arrhythmias
ARRHYTHMIA RECOGNITION
What is an arrhythmia?
A cardiac arrhythmia is any heart rhythm other than sinus rhythm. It may be
too fast, too slow or start somewhere in the heart other than the SA node.
What causes arrhythmias?
Underlying organic heart disease is the most common cause of abnormal heart
rhythms. This includes coronary artery disease leading to ischaemia and
myocardial infarction, diseases effecting the heart muscle such as heart failure
and some congenital conditions.
What are the signs and symptoms of arrhythmia?
Signs and symptoms of or arrhythmias are mostly due to decreased or absent
cardiac output. The severity depends on the heart rate, the type arrhythmia,
and the underlying ventricular function. Symptoms include:
 palpitations (tachycardia)
 hypotension (BP)
 diaphoresis (sweating)
 dysponea (difficulty breathing)
 confusion, presyncope (dizziness), syncope (blackout) – due to  cerebral
perfusion
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TYPES OF ARRHYTHMIA
Bradycardia
A bradycardia occurs when the heart beats too slowly (less than 60 beats
/minute.) In some people a slow heart rate may be normal. Elite athletes often
have a slow resting pulse due to their high level of physical fitness. In cardiac
patients, a slow pulse is usually due to damage to the SA or AV nodes resulting
in slow or blocked conduction to the ventricles. Patients with very slow heart
rates (< 30bpm) may be compromised.
Tachycardia
A tachycardia occurs when the heart beats too fast (more than 100 beats
/minute). This occurs in normal people when they exercise or get excited. In
cardiac patients, tachyarrhythmias usually occur because the heart is ischaemic,
scarred or as a result of various congenital defects. Tachycardias may be
classified as wide or narrow complex.
The most common wide complex tachycardia (more than 0.12 seconds wide) is
ventricular tachycardia (VT) which can be life threatening. During VT, the
heart beats so fast that the ventricles cannot adequately fill between beats.
This results in decreased blood and oxygen reaching the vital organs causing
dizziness, fainting or even cardiac arrest
Narrow complex tachycardias (less than 0.12 seconds wide) include atrial
arrhythmias and some types of congenital supraventricular tachycardias.
Narrow complex tachycardias may cause uncomfortable symptoms but are not
usually life threatening.
The most common narrow complex tachycardia is atrial fibrillation(AF) which is
an irregular rhythm.
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NURSING MANAGEMENT OF A CARDIAC
ARRHYTHMIA
The most important question to ask when confronted with an arrhythmia is “how
compromised is the patient”? This is far more important initially than trying to
work out what the arrhythmia is.
ALWAYS CHECK THE PATIENT FIRST!
1.
If the patient is unresponsive and has no palpable pulse, commence
resuscitation and call for help
2.
If the patient is conscious but obviously compromised (see symptoms
previous page) take the following steps:
a) Give oxygen at high flow via a Hudson mask
b) Arrange urgent medical review
c) Monitor vital signs (BP, pulse) and level of consciousness closely
d) If BP is very low, lay patient flat (if they will tolerate it)
e) Obtain a 12 lead ECG
f) Carefully document the event;
i)
ii)
iii)
how you found the patient
patient’s symptoms (in their own words) eg dizzy
ECG/rhythm strip
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DIAGNOSING AND TREATING PATIENTS WITH CARDIAC
ARRHYTHMIAS
Electrophysiology Study (EPS)
Cardiac electrophysiology is the study of the electrical system of the heart.
The purpose of the study is to establish the origin and mechanism of the
patient’s arrhythmia. The most common reason for a patient to undergo an
electrophysiology study is to investigate a known or suspected tachycardia.
Patients may present with a history supraventricular tachycardia, ventricular
tachycardia or cardiac arrest.
The post procedure care is similar to a cardiac catheterization. The focus is on
monitoring the vascular puncture site and vital signs, including oxygen
saturations.
Treatment for Cardiac Arrhythmias
Once the arrhythmia has been diagnosed, decisions can be made about
treatment. The treatment options depend on the type of arrhythmia and
include:
 Drugs – most suitable for supraventricular arrhythmias eg. Atrial fibrillation
 Elective Cardioversion – used for supraventricular arrhythmias unresponsive
to drug therapy
 Pacemaker – bradycardias
 Radiofrequency Ablation (RFA) – for some types of supraventricular
arrhythmias
 Implantable Cardiovertor Defibrillator (ICD) - for life-threatening
ventricular arrhythmias
Please read Appendix 4: Common cardiac arrhythmias
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DIRECT CURRENT CARDIOVERSION:
Cardioversion is the application of a direct current shock to a patient’s chest
wall, which results in the simultaneous depolarization of myocardial cells. This
allows for the SA Node or other intrinsic pacemaker to regain control. The aim
is the safe and effective conversion to sinus rhythm of patients currently
experiencing atrial fibrillation or flutter in the elective situation, or ventricular
tachycardia or fibrillation in the emergency situation.
As opposed to the use of defibrillation in an emergency situation where a
patient is unconscious, a patient requiring elective cardioversion is fully awake.
The patient must be anaesthetized to prevent the physical and psychological
pain associated with defibrillation in the awake patient. An anesthetist is
present during the procedure to achieve this.
Due to the risks associated with atrial arrhythmias, such as thrombus formation
and decreased cardiac output due to loss of atrial kick, the early return to sinus
rhythm is desirable. The patient must be adequately coagulated prior to the
procedure and have an INR and Electrolytes taken.
During atrial arrhythmias, normal ventricular activity is present. If a electrical
stimuli is delivered during the relative refractory period of myocardial cells, we
may potentialte life threatening arrhythmias. To prevent this, during elective
cardioversion the shock delivery is synchronized to the R wave of the QRS
complex. This is achieved by the use of the synchronization button on the
defibrillator.
There are relatively few complications associated with the procedure, which can
be avoided with good management. Complications include skin burns, nonlethal/lethal arrhythmias, pulmonary emboli, strokes, pulmonary oedema.
Good management includes the careful assessment of patient’s suitability for
the procedure. Relative contraindications include AV block, overuse of beta
blocking mediations, abnormal biochemistry, digitalis toxicity, poorly controlled
anticoagulation, atrial fibrillation with a slow ventricular rate.
Many patients undergo a Trans-oesophageal Echo prior to cardioversion to
assess for the presence of clot in the atria. This must be taken into account
when allowing patients to eat and drink post procedure.
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During an elective Cardioversion defibrillator placement is slightly different to
that of the emergency situation. One pad is placed over the Apex of the heart,
whilst the other pad is placed under the patients back in the infrascapular area.
This results in a much more effective delivery of current to a greater mass of
myocardium.
TEMPORARY PACEMAKERS:
Transvenous pacemakers (TVPM’s) are inserted in patients who require the
support of a pacemaker to generate electrical activity within the myocardium, in
the absence of intrinsic electrical activity. Indications include
Bradyarrythmias, atrioventricular blocks and sinus arrest. Predominantly these
arrhythmias occur due to drug overdose and age related degenerative changes
to the electrical conduction systems of the heart.
A Transvenous pacemaker is a temporary device, which is used to deliver an
electrical stimulus to the myocardium to cause depolarization of cells, resulting
in contraction. TVPM’s can be inserted in the subclavian, femoral or internal
jugular veins.
The pacing tip of the TVPM rests within the right ventricle of the heart. With
pacing this produces ventricular activity, which conducts and causes contraction
through both the right and left ventricles. Post insertion patients require close
observation to ensure the correct functioning of and early detection of any
complications from the insertion of a TVPM.
Pacemaker Terminology:
Threshold:
the lowest amount of energy (mV) which will cause
myocardial depolarization and contraction
Output:
the electrical energy delivered by the pacemaker box
Sensitivity:
the degree to which the pacemaker is sensitive to the hearts
intrinsic rhythm
The action of the pacemaker is determined by the settings it has.
Asynchronous pacing is desirable as it allows the heart to initiate its own
rhythm when it is present, but when this is absent or insufficient the
pacemaker will initiate activity.
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