Recognition & Clinical Assessment of the Deteriorating Patient - The Nurses for Nurses Network & Education at Sea

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The Nurses for Nurses Network
                     &
           Education at Sea
                  Presents

Recognition & Clinical Assessment
   of the Deteriorating Patient
                    with
            Anne Evans-Murray

       23rd February to 6th March 2019
                   aboard
            Radiance of the Seas

Recognition & Clinical Assessment of the Deteriorating Patient                            1

                                          Disclaimer:
Health Ed Professionals Pty Ltd and Anne Evans-Murray makes all reasonable efforts to
ensure that the content of their course is correct at the time of presentation, and as much
as is allowed by law expressly disclaim all and any liability for the results of any actions taken
on the basis of information given at this educational event, and are not responsible for any
error or omission from such information.

The presenter/s reserve the right to make reasonable changes to their presentations when
in their judgment such changes are necessary to update latest information available to
them since the course was advertised, or the timing of the sessions require such changes.

                       Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient                              2

                                                      Workbook

Developing knowledge on how to recognise and perform advanced clinical assessment on a patient who is
deteriorating is an expectation of the evolving role of the clinical Nurse. In this conference we will explore the
assessment of a patient with a variety of clinical disorders and conditions that include cardiac, respiratory,
abdominal, and electrolyte imbalance. The teaching methodology will contain clinical scenarios that will assist
the Nurse to recognise clinical deterioration and apply a critical thinking approach.

The communication strategies to support patient assessment will also be investigated. Assertion training is
incorporated into the conference content in recognition of this skill as a vital component of ensuring effective
communication within the health care team.

Knowledge + Critical Thinking + Assertive Skills = Expert Nurse. All three of these components will be explored in
this conference framework.

Learning Outcomes:

In this conference you will:

       Explore the skills required to recognise and undertake clinical assessment of the deteriorating patient
       Review a variety of clinical conditions relating to cardiac and respiratory disease, abdominal disorders,
        and electrolyte imbalance
       Discover how to apply critical thinking via a scenario-based teaching approach
       Gain assertiveness skills to enhance effective communication, and timely intervention, within the health
        care team

You are encouraged to work your way through this workbook as you listen to the lecture presentations. The
main concepts of the conference are presented in this workbook, with sections for you to enlarge on.
Throughout the workbook you are invited to take part in the exercises and you will see the following image,

which encourages you to take part in the exercise:

Learning advanced ECGs is enhanced by you performing the exercises in the cardiac sessions. During the
‘Managing Difficult People’ and Assertion sessions learning will be enhanced by being interactive with the
exercises.

Presenter: Anne Evans-Murray

Health Ed Professionals

                                   Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient   3

 Day One
of Seminar

            Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient 4

Basic Electrophysiology and Atrial Arrhythmias
Demonstrating understanding of the heart’s conduction assists with learning abnormal arrhythmias.

The electrocardiograph (ECG) was developed by the Dutch scientist Willem Einthoven (1860–1927). He initially
measured the electrical activity found in frog’s hearts. This led to him developing leads which he placed on a
human. He was able to observe the particular deflections and waveforms, which were eventually placed on a
graph paper.

Even today the terminology that Einthoven developed is still being used and his original concepts remain the basis
for electrocardiography. Einthoven used the term ‘Leads’ to describe the three limb electrodes, Lead I, II and III.
Additional leads were added over the years and today the standard ECG examines the electrical activity of the
heart from 12 views. If we looked at the heart only from one area or position, we wouldn’t get an accurate picture.
(Text book: ECGs simply, 2016: Chapter 1)

In the following space draw an outline of the heart and its conduction.

ECG paper.

Sinus rhythm is recorded on special Electrocardiograph (ECG) paper. This paper has many lines and squares on it.

Review the following sample and note that every little square is 1 mm. or 0.04 seconds.

A large square consists of five small squares and is equal to 5 mm. or 0.2 seconds.

0.04 second (Picture enlarged - not actual size)

Recognition & Clinical Assessment of the Deteriorating Patient                       5

The value of a small square is 0.04 sec. The universal paper speed is 25 mm. per second and this is equal to each
small square being 0.04 second. It is this value that enables clinicians to analyse P-R intervals and QRS widths,
which are so important in monitoring patients.

Define the PR interval

______________________________________________________________________________

State how the QRS complex is measured

______________________________________________________________________________

            Label the following diagram:

P wave / QRS / PR interval / QRS width / J point

Rates:

Sinus Rhythm: ________________________________________________________

Sinus Bradycardia:_______________________________________________________

Sinus Tachycardia:_______________________________________________________

Sinus rhythm is diagnosed according to the following criteria

 QRS complex is narrow -less than 0.12 sec (This is extremely important)
 P wave visible and preceding each QRS complex (Equally important)
 PR interval - has a QRS complex following each P wave and at constant intervals of normal duration (0.12 to
  0.2 sec) Text book: ECGs simply: Chapter 1, Pages 1- 48
                                    Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient                          6
QT interval

QT interval reflects the time of ventricular activity including both depolarization and repolarization. Is measured
from the beginning of the QRS complex to the end of the T wave. The QT interval will vary with patient gender,
age and heart rate.

Every 12 lead ECG should include the assessment of the QT interval to assess the risk of malignant arrhythmias
and sudden death associated with an abnormal QT interval. For difficult shaped T waves, use a tangent drawn to
the steepest last limb of the presumed T-wave to define the end of the T-wave. The acquired QT interval should
be corrected for heart rate, i.e. the QTc interval, to enable comparison with reference levels. Normal cardiac
repolarization adapts to heart rate. (Postema, & Wilde 2014)

QT interval

              Mark in the QT measurement in the diagram.

Essential knowledge.

              Exercise, draw on the following:

       Include all the parameters discussed: PR interval, QRS width, QT interval

                                   Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient 7
Extra content:

Steps of interpretation

When interpreting rhythms, the following systematic approach can be used.

Step One

Calculate the heart rate.

On the basis on heart rate determination alone, arrhythmias can be classified as

 slow rate: bradyarrhythmias -where they are less than 60 beats per minute
 normal rate: arrhythmias where the rate is between 60 to 100 bpm
 fast rate: tachycardia arrhythmias where there are more than 100 bpm.

Step Two

Determine the regularity (rhythm) of the R waves. The regularity of the heart beat can often be determined by
looking at the ECG.

Step Three

Identify and examine the P waves. P waves often provide more information about the type and mechanism of a
cardiac arrhythmia than any of the other wave forms.

Step Four

Measure the P-R interval

Normal P-R interval is between 0.12 sec and 0.2 sec.

Step Five

Measure the duration of the QRS complex. The width of the QRS complex represents the time required for a
stimulus to activate both ventricles. The normal duration of the QRS complex is not more than 0.12 seconds.

Note: The atria start to contract part way through the P wave, but you won’t see this on the ECG, remember
the ECG records electrical activity only, not mechanical activity or contraction (significance: PEA).

Atrial Fibrillation
Atrial Fibrillation Characteristics

 NO P waves
 Irregular
 QRS complexes usually narrow
Text book: ECGs simply: Chapter 2, Pages 49 –

Recognition & Clinical Assessment of the Deteriorating Patient 8

Exercise; draw in the following space the characteristics of Atrial Fibrillation, focusing on the three
identified characteristics above.

Its prevalence increases with age, from about 2% in the general population, 5% in people older than 65 years, 10
to 15% in people older than 75 years. During the past 20yrs, hospital admissions for AF have increased by 66%
(Kalman 2013, Thompson 2011).

Causes of AF

Atrial stretch is highly arrhythmogenic. Hypertension is the most prevalent risk factor for the development of
AF. Increased strain on the cardiac muscle. Cardiac remodeling due to increased afterload .

How does AF form

Many areas in the atria are potential sources of initiating triggers, the pulmonary veins (PV) are recognized as
the dominant source, causing up to 94% of AF symptoms.

Effects of Atrial Fibrillation

 Loses its atrial kick and mural thrombi form
 Thromboembolism can lead to CVA
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Classification

Recurrent AF - 2 or more episodes
Paroxysmal AF - self-terminating, spontaneously converts
Persistent AF - lasts longer than 7 days, is not self-terminating
Permanent AF – refractory to cardioversion and has persisted
Valvular and nonvalvular AF – occurs in a patient who has evidence or history of rheumatic mitral valve disease,
who has a prosthetic heart valve, or who has valve repair; all other forms of AF are classified as nonvalvular AF
(Australian Therapeutic Guidelines, 2018).
Lone AF

Occurs in the absence of known structural heart disease or hypertension, and accounts for about 10% of cases.
Lone AF is also called ‘Familial’ AF. Familial AF, runs in a family, is more common than previously recognized.
Have less episodes of thromboembolism. Alcohol and drug use (especially withdrawal) have also been linked to
lone AF.

Pulmonary vein ablation

Terminates AF in 75% to 85 % of cases, May need a repeat session in the catheter lab. It is also referred to as
'pulmonary vein isolation‘ (as it isolates the impulse). Other names: Circular Radiofrequency (RF) Ablation,
"Circumferential" or "Empirical Ablation".

Recognition & Clinical Assessment of the Deteriorating Patient                              9

Atrial appendage occlusion devices

Inserted percutaneously to isolate the left atrial appendage. Studies showing effectiveness of reducing the risk
of stroke (Thompson, 2011).

It is the nurse’s responsibility to have knowledge of the hospitals policy relating to a patient presenting with
new onset AF. Accurate assessment and early intervention are aimed at preventing the complications of
tachycardiomyopathy and development of mural thrombi

Main concepts:

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                                   Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient 10

Metabolic syndrome – examining the fat/sugar debate.
Disclaimer:

The following information regarding the fat / sugar debate is offered only as education. This session is aimed at
increasing knowledge of the controversy regarding saturated fats and discussions relating to the controversy of
cholesterol and heart disease. It is not intended, that any Health Professional advise patients / clients to go
against national and nutritional guidelines. Nurses are required to work within their scope of practice. Nor
should you advise any patient / client to come off any medications. It is not intended to criticise any
establishment or food industry.

Saturated fats

Saturated fatty acids - their carbon atoms fully "saturated" with hydrogen atoms. The different types of fats
contain a combination of different fatty acids. Fats that are mostly saturated (butter) tend to be solid at room
temperature. While fats that are mostly unsaturated are liquid at room temperature. Artificial trans fats, have
been considered to be harmful. Trans fats are made by exposing polyunsaturated vegetable oils to a chemical
process that involves high heat, hydrogen gas and a metal catalyst. Studies show that trans fats lead to insulin
resistance, inflammation, belly fat accumulation and drastically raise the risk of heart disease
(https://www.healthline.com/nutrition/saturated-fat-good-or-bad )

During the 1960’s the American Heart Association published the world's first recommendations to avoid
saturated fats, along with dietary cholesterol, in order to prevent a heart attack. This theory had never been
tested in a clinical trial despite being adopted by most leading experts. It lacked a firm scientific foundation. It
became accepted that low cholesterol reduces heart disease and strokes and high cholesterol increases the risk.

However, many studies have found there was no statistically significant difference in deaths from Coronary
Heart Disease if a person had high cholesterol. Review papers, on upwards of 550,000 people, have uniformly
found no association between the consumption of saturated fats and coronary heart disease. (Teicholz, Thorn
2017)

Research: American Journal of Clinical Nutrition. 350,000 people in a follow-up period of five to 23 years. No
relationship between saturated fat intake and heart disease. Large Japanese study of about 58,000 people
actually found an inverse association between saturated fat intake and strokes. Adults who were eating the
most saturated fat actually had the lowest levels of stroke (Siri-Tarino et al. 2010).

Diabetes

Around 1.7 million Australians have diabetes. More than 100,000 Australians have developed diabetes in the
past year. Total annual cost impact of diabetes in Australia estimated at $14.6 billion.

(https://www.diabetesaustralia.com.au/diabetes-in-australia)

Hormones

Ghrelin is an appetite-stimulating peptide, whereas Leptin is an appetite-suppressing hormone.

The world leptin means “full” in Greek. The hormone Leptin gives a feeling of satisfaction. High saturated fat –
stomach stretches and leptin is secreted which then tells the brain that the person is ‘full’ – no more desire to
eat. Desire to stop eating. High levels of saturated fat decreases appetite.

Recognition & Clinical Assessment of the Deteriorating Patient 11

While ghrelin enhances appetite, leptin acts as a signal to diminish it.
(http://www.montereydiet.com/ghrelin_and_leptin.html)

Metabolic syndrome

Refers to a cluster of metabolic risk factors. Pooled data from 37 studies involving more than 170,000 patients
have shown that metabolic syndrome doubles the risk of coronary artery disease. It also increases risk of
stroke, fatty liver disease, and cancer (Wang, 2012).

Over many years a person consumes abnormally high levels of processed foods, refined carbohydrates. Insulin
resistance starts small and develops slowly. As a result large amounts of insulin are required to metabolize the
glucose. Cells eventually become resistant to insulin. As a result, some of the glucose is locked out of the cells
and builds up in the blood. However cells require more energy, so the pancreas pumps out more insulin to try
and move the glucose into the cells.

More and more insulin is needed to open the gate into the cell. As a result of the poor response to insulin the
pancreas begins secreting more insulin to counteract the lack of response to normal levels. Then over time, the
pancreas becomes exhausted and produces less insulin. Beta-cells in the pancreas become "exhausted," but it
may be that the high insulin or higher blood glucose damages the beta cells. Glucose now builds up in the
blood, initially called prediabetes, then Type 2 diabetes develops. More evidence in recent years highlights that
sugar, not saturated fats cause heart disease.

Extra notes of cholesterol and statins

Main concepts:

Recognition & Clinical Assessment of the Deteriorating Patient 12

Cardiac Auscultation
Cardiovascular diseases continue to be one of the leading causes of morbidity and mortality worldwide. The
nurses role in clinical assessment is essential in recognition of deterioration of a patient. Cardiac disease is
often present with many other disorders.

Auscultation of the heart forms the core of cardiac physical examination.

 Systole: Heart contracting
 Diastole: Heart resting and filling up with blood

Clinical hints

First, identify the sound of S1, if you have difficulty trying to work out which sound is the S1, then feel the
patient’s carotid pulse, and listen at the same time.

It is vital for you to identify which sound is S1 and which one is S2, otherwise you will be unable to identify an
S3. If you are a cardiac nurse you might use the cardiac monitor to view the R wave on ECG monitor, this will
also assist you to identify S1.

Listen with the diaphragm of your stethoscope.

• The pause between S1 and S2 is shorter than between S2 and S1 (diastole is longer). This is usually the
best way to identify the S1.

• S1 is best heard over Apex - but can be heard over entire precordium

• Diastole is generally longer than systole and is generally described as the “dub”.

Landmarks

• Aortic – 2nd intercostal – right.

• Pulmonic – 2nd intercostal – left.

• Erbs – 3rd intercostal – left.

• Tricuspid – 5th intercostal – left sternal border.

• Mitral – 5th intercostal left midclavicular, it is also called the Apex

Recognition & Clinical Assessment of the Deteriorating Patient 13

S3 (Abnormal heart sound)

The first clinical sign of congestive cardiac failure. It occurs early in diastole and due to a dilated ventricle and
results from the rapid flow of blood into non pliable ventricles. Filling of ventricles with limited distensibility.
The ventricles are resisting the filling because they are already congested because of the failure. S3 occurs
when rapidly rushing blood flow from the atria is suddenly decelerated by the ventricle when it reaches its
elastic limit. The non compliant ventricle just can’t distend anymore to accept this rapid flow of blood.

S3 can also occur in a normal ventricle, with excessive intravenous volume. It is also found in chronic
hypertension, mitral, aortic or tricuspid insufficiency.

Please note it may be normal in children and young adults.

S4 is known as atrial gallop, sound occurs immediately before S1. The exact mechanism of S4 generation is
debatable. It is associated with the atrial kick - late diastole where the atria of the heart are vigorously
contracting. S4 is caused by the atria contracting forcefully in an effort to overcome an abnormally stiff or
hypertrophic ventricle. The atria is contracting to force blood into the ventricle.

Pericardial friction rub

May mask the other heart sounds. Sounds like squeaky leather, grating scratching.

It is best heard at the apex (use the diaphragm) (in both systole and diastole). Ensure the patient is not taking
breaths when you listen for a pericardial friction rub.

Pericarditis is when there is inflammation of the pericardial sac causes the parietal and visceral surfaces of the
roughened pericardium to rub together against each other.

Murmur

Any reason that causes a turbulence in blood flow, or any alteration in movement of blood.

The movement of blood is significantly altered when there is leakage through insufficient valves or turbulence
across a narrowed outlet as with stenosis

A new murmur is a clinical alert, or a red flag, especially relevant when the patient develops one after a
myocardial infarction.

Two main reasons for a new murmur after a myocardial infarcton:

 Ruptured interventricular septum resulting in a ventricular septal defect (VSD).
 Ruptured papillary muscle.

Recognition & Clinical Assessment of the Deteriorating Patient 14
Mitral valve regurgitation (MR)

This is a common heart valve disorder. The mitral valve does not close tightly and blood leaks backwards
through the mitral valve when the heart contracts. This reduces the amount of blood that is pumped out to the
body. Mitral regurgitation in the elderly population is expected to become a relevant health problem in the
future. According to data, moderate or severe MR is present in 10% (to 20%) middle age and older adults
(Ottavio Alfieri, et al 2011).

Aortic Stenosis (AS)

AS is the most common valvular heart disease in the developed world. Incidence: 9% in a study in which the
mean age was 54 years to 42% in which the mean age was 81 years. (Coffey, 2014)

It refers to narrowing of the aortic valve opening. It restricts the blood flow from the left ventricle to the aorta
and may also affect the pressure in the left atrium. Aortic stenosis is associated with increased risk of Sudden
Cardiac Death (SCD).

Prior to the advent of surgical therapy, SCD was common in patients with progressive aortic stenosis. The
incidence of SCD after aortic valve surgery is highest in the first 3 weeks after the procedure. The risk of SCD is
much lower in other valvular diseases compared with aortic stenosis. (Sovari, 2014)

The classic triad of symptoms in a patient with aortic stenosis, who is deteriorating and at risk of sudden cardiac
death:

 Chest pain: precipitated by exertion and relieved by rest
 Heart failure: Symptoms include paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, and
shortness of breath
 Syncope: Often occurs upon exertion

Murmurs are graded from 1 to 6.

A grade of 1 out of 6 (1/6) is very faint.

A grade 6 out of 6 (6/6) is extremely loud, and can be heard with a stethoscope even when slightly removed
from the chest. Short, quiet murmurs may be more likely to be benign

Thrill

It is a vibration accompanying a cardiac or vascular murmur that can be palpated. It is a palpable heart murmur.
A grade 4 or greater intensity can be felt by examiners hand. Can be felt over the carotids if a bruit is present
and over an arteriovenous fistula in haemodialysis. It results from turmoil in the flow of blood.

Examination of heart sounds

 Place patient 45 o
 Commence in the aortic area, with the diaphragm, listen where S2 is the loudest. Spend time listening
to differentiate between the two sounds.
 Don’t listen all at once, just isolate each sound
 If able – ask patient to hold their breath
 Now use the bell, listening for low frequency sounds, especially S3 and murmurs.
 Move the stethoscope slowly down the chest, you can use the zigzag method.
 Turn patient on left lateral side if you are having difficulty hearing the sounds.
___________________________________________________________________________________________
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Recognition & Clinical Assessment of the Deteriorating Patient 15

Measuring for an elevated JVP

Assessing your patient for venous hypertension (right sided heart failure) or overload

Procedure

Internal jugular veins are not normally visible, the goal is too find the highest point of visible pulsation above the
sternal angle (Angle of Louis). Find the sternal notch - distinct bony ridge on the sternum. You are checking to
see if there are pulsations 4 cms above this point. This is abnormal and indicates a high JVP.

You must differentiate the JVP from the carotid pulse. Non-palpable - the JVP cannot be palpated. If one feels a
pulse in the neck, it is generally the carotid artery. Usually the right internal jugular vein is superior. When the
neck muscles are relaxed, shining a beam of light across the skin overlying the internal jugular vein exposes its
pulsations. Best if the patient is reclining with head elevated 45°. Turn the patient’s head slightly to the left.
Normally the highest pulsation occurs no more than 4cm above the sternal notch. Pulsations above that level
indicate jugular venous distension.

There will be a more in-depth discussion on pericardial effusion and cardiac tamponade in the future session.

Main concepts:

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Recognition & Clinical Assessment of the Deteriorating Patient   16

 Day Two
of Seminar

            Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient 17

Interpretation of Myocardial Infarction on a 12 ECG

Acute Coronary Syndrome ACS
It is important to interpret a 12 lead ECG in order to communicate to the medical officer and instigate treatment
immediately. The time-frame to treatment is extremely important and this is an essential skill of nurses who
perform ECGs on a patient with chest pain or symptoms of MI.

A myocardial infarction is a result of inadequate oxygenation which causes ischaemia injury and necrosis. The left
ventricle is more commonly affected. It is caused by death of myocardial tissue resulting from an acute decrease
in coronary blood flow or an abrupt rise in myocardial oxygen demand without sufficient coronary artery
perfusion. Blood is supplied to the heart by the right and left coronary arteries. (Text book: ECGs simply: Chapter
5, Pages 149

The left ventricle is the ventricle more likely to be affected by an infarction because it is the thickest chamber
and does most of the work. The right ventricle can also suffer infarction but it is not as common as a left
ventricular myocardial infarction.

The heart is supplied with arterial blood by the right and left coronary arteries. These are the first branches that
arise from the aorta as it leaves the heart.

Gender differences in presentation of a myocardial infarction:

12 lead ECG comprised of the following:

The standard ECG consists of 12 leads.

6 Limb leads: 1,11,111, AVR, AVL, AVF

Bipolar leads (1, 11, 111) a pair of electrodes, one positive and one negative.

Unipolar leads (AVR, AVL, AVF) one will be the positive electrode.

6 Chest leads: V1 to V6, chest leads also called precordial leads.

The classic electrocardiographic changes encountered in acute myocardial infarction are:

1. A Q wave

2. ST segment elevation

A definition of a Q wave is:

___________________________________________________________________________________________
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A significant Q wave should be:

 one third height (or 1/4) of QRS complex
 0.04 second in duration

Which lead has a Q wave and it is not considered to be pathological?

_______________________________________________________________________________
Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient                           18

The term myocardial infarction means physiological death, or necrosis of myocardial muscle tissue. The electrical
manifestation of necrosis - the abnormal Q wave indicates that the cells are electrically dead. These electrical
forces are directed away from an area of infarcted myocardium become negative (Q wave). Q waves will usually
appear within several hours of the onset of an infarction.

ST elevation seen in acute myocardial infarction is known as the current of injury.

             Three exercises. Examine the first diagram and note the differences.

In the following examples an interrupted line has been added to show you where the baseline should have
been. It will help you visualise the abnormality. Look at the J point. This is a very important exercise, you must
be able to recognise any abnormality of the J point.

Now identify below which diagrams are examples of the following. Place the correct letter beside each
description.

       ST elevation _______________
       T wave inversion_____________
       ST depression _______________

        A                                 B                            C

                                   Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient 19

Next exercise. Now it’s your turn to draw. In the following space draw an example of an accurate
PQRST. Label the diagram and indicate the Q wave as well as identifying the J point.

Inverted T waves are often seen in myocardial infarction, they signify ischaemia (diminished blood supply).

 Q waves reflects a zone of infarction - death of tissue
 ST elevation reflects current of injury
 T wave inversion reflects ischaemia

The ST segment is a sensitive indicator of myocardial damage. Thus by closely monitoring it you can detect
ischaemia or injury before an infarct develops.

Important clinical point:

ST elevation must return to the base line within days to weeks. If not, then further investigation to find the cause
is required.

Groups (vital knowledge)

Myocardial infarction occurs in groups of leads indicating an area has infarcted.

Inferior Infarction

Q waves and ST elevation are found in leads:

_______________________________________________________________________________

The artery involved in an inferior MI is usually the right coronary artery.

Anterior infarction

It is customary to classify anterior infarction into three sub groups according to the particular ECG findings. (Many
books give different leads for diagnosing anterior infarctions, listed below is just one way).

Recognition & Clinical Assessment of the Deteriorating Patient 20

Extensive Anterior infarction

Is manifested by an infarction pattern in all of the precordial leads well as in lead 1 and aVL

The artery involved is the left coronary artery.

Anteroseptal infarction

Leads V2 and V3 lie directly over the septum.

Changes that occur in Anteroseptal infarction are V1 to V3 or (V4)

Anterior Infarction

Myocardial Infarction

Elevation of the origin of the ST segment at its junction with the QRS (J-point) of:

 greater than or equal to 1.0 mm in two or more limb leads
 OR 2.0 mm in two or more precordial leads.

Cardiac marker assists with diagnosis of MI – to differentiate it from unstable angina.

Troponins:

Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial
necrosis occurs.

When a patient is admitted into the emergency department with chest pain, an ECG is performed immediately
and a blood sample is taken to check for a rise in cardiac biomarkers. Cardiac troponins (cTn) I and T are the
most commonly tested markers.

Troponin is not found in the blood of healthy people. Troponin blood levels can, however, take three or more
hours to rise after damage has occurred to the myocardial cells (although recent Troponin assay tests are more
rapid). They can also rise with other cardiac disorders such as myocarditis or cardiac trauma. Examination of
the 12 lead ECG is therefore vital.

T inversion, ST depression refers to:

Angina (ischemia) or myocardial infarction (NSTEMI)

Recognition & Clinical Assessment of the Deteriorating Patient                      21

                                                Acute Coronary Syndrome

 STEMI / STEACS                                           NSTEMI / NSTEACS

      ST elevation with chest pain                        T wave inversion, ST depression with chest pain

 The cause of ST elevation:                               The cause of T wave inversion or ST depression:

      •   Prinzmetal angina                                    •    Angina or ischemia:
      •   No troponin rise                                     •    ST depression / T wave inversion
 or                                                            •    Troponin levels will not rise
                                                          or
 STEMI
                                                          NSTEMI
      •   ST elevation
      •   Troponin levels will rise                            •    ST depression / T wave inversion
                                                               •    Troponin levels will rise

Prinzmetal angina

Unusual form of angina, also known as variant angina, associated with coronary artery spasm.

Has ST elevation with the chest pain and resolves when the chest pain stops (most angina has T wave inversion
or ST depression).

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                                      Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient                      22

            Exercise. In the following squares:

1. Label each lead.
2. Identify and circle the one lead you would expect to be ‘upside down’. Draw in the ‘upside down lead’ – what
   does it look like?
3. Now draw in the expected changes in the PQRST complex that you would see in an Inferior STEMI.

Exercise: Interpretation of 12 lead ECG

Which coronary artery is usually affected in this myocardial infarction?

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What complication might you observe for with this type of infarction?

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                                   Copyright© 2019 Health Ed Professionals Pty Ltd

Recognition & Clinical Assessment of the Deteriorating Patient               23

            Exercise. In the following squares:

1. Label each lead.
2. Now draw in the expected changes in the PQRST complex that you would see in an Anterior STEMI.

Exercise: Interpretation of 12 lead ECG

Which coronary artery is usually affected in this myocardial infarction?

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What complication might you observe for with this type of infarction?

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Definition of SCAD
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Cocaine and the effects on the heart.

       Linked to the development of a myocardial infarction
       Vasoconstriction and vasospasm of the coronary arteries.
       Increase in rate of development of atherosclerosis
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Recognition & Clinical Assessment of the Deteriorating Patient                        24
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Other causes of T wave changes

Differentiate from Acute Coronary Syndrome:

Hyperkalemia (Text book: ECGs simply: Chapter 1, Pages 25-26)

          Tall peaked T waves
          No ST elevation

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Main concepts:

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Takotsubo Syndrome
Takotsubo Cardiomyopathy or Syndrome is also known as:

     neurogenic myocardial stunning /stress cardiomyopathy / stress-induced cardiomyopathy,
     transient left ventricular apical ballooning,
     "ampulla" cardiomyopathy /"broken heart syndrome".
It is a reversible disease also called "takotsubo" cardiomyopathy for the characteristic shape of left ventricle. The
Japanese word "takotsubo" means an octopus fishing pot with a round bottom and a narrow neck.

Etiology:

Although the etiology of Takotsubo cardiomyopathy is unclear, the transient left ventricular apical ballooning
observed is generally considered to be a form of myocardial stunning of the left ventricle with hyperkinesis of
the basal wall.

         Most cases are reported in postmenopausal women aged 60–75 years.
         Acute emotional or physiological stressors generally precede symptoms,
         The death of a close relative is the stressor reported most frequently

Presents

Presenting with overlapping symptoms and initial findings, it is difficult to distinguish Takotsubo
cardiomyopathy from an acute coronary syndrome.

Progression of electrocardiographic changes can also be similar, with anterior Q-wave formation and T-wave
inversions occurring in the precordial leads.

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Recognition & Clinical Assessment of the Deteriorating Patient 25

 Mimics an ST-elevation myocardial infarction (STEMI).
 A prolonged QT interval is sometimes also observed
 The typical presentation is a sudden onset of congestive cardiac failure or chest pain associated with ECG
changes suggestive of an anterior MI.
 Elevations in the levels of troponin are typically less than those observed in acute anterior STEMI, but this
difference cannot be used to exclude an acute coronary syndrome.
 Troponin, creatine kinase are only very slightly elevated, confirming that there is not much heart muscle
damage, but severe stunning instead.
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Prognosis can be good without any form of treatment, provided that the patients survived the heart failure
state.

The left ventricular function usually improves within 2 months. Repeat echocardiography is recommended
within a few months, and ejection fraction repeated. Likelihood of recurrence with similar events in the future.

Some studies have indicated chronic heart failure following an episode. Recent studies show variety of
presentation: even happy events may result in Takotsubo syndrome.

Main concepts:

Recognition & Clinical Assessment of the Deteriorating Patient                          26

Endocarditis
Endocarditis is an infection of the endocardium, the inner lining of the heart. It affects mainly the heart valves,
especially the mitral valve. Endocarditis generally occurs when bacteria, fungi or others attach to damaged
areas in the heart. There are risk factors that can predispose to the development of endocarditis but it can also
occur without risk factors. Bacteria may spread from an infected area, especially a tooth abscess or any
situation that allows the bacteria the opportunity to enter the bloodstream. Invasive procedures such as
catheters, intravenous drugs, needles used for tattoos and body piercing as well as intravenous illegal drug use
with contaminated needles. Patients with pre-existing heart disorders such as artificial heart valves, pacemakers
or congenital heart defects are also at risk.

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Endocarditis have very interesting clinical presentations: Janeway lesions, Osler's nodes, Petechiae and Splinter
haemorrhages.
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Other signs and symptoms include, fever and murmur, fatigue and generalised aches. Two serious
complications can occur such as stroke; from movement of emboli to cerebral vessels and heart failure from
damaged valves.

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Diagnosis and treatment of endocarditis

Physical examination and history, blood cultures and diagnostic imaging such as ultrasound. Treatments for
endocarditis include antibiotics and, in certain cases, surgery.

Main concepts:

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Recognition & Clinical Assessment of the Deteriorating Patient   27

Day Three
of Seminar

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Recognition & Clinical Assessment of the Deteriorating Patient 28

Recognition of workplace bullying and managing difficult situations

Assertion skills of the Health Professional
Bullying can be covert or overt. Can be ignored or missed by managers or known by many throughout the
organization. Negative effects are not limited to the targeted individuals, and lead to a decline in employee
morale and culture of the institute. Bullying is associated with higher turnover, higher absenteeism, decreased
commitment and productivity, health care: affects care of patients, lower levels of job satisfaction,
psychosomatic symptoms and physical illness, possible loss of job, unable to find another position.

Bullying behaviour has certain features:

 Narcissistic traits or:
 Narcissistic personality disorder:

Sense of importance, untruths, expecting admiration, exploiting others, no empathy, arrogance, envying others,
rage if contradicted or confronted.

Bullying is often misunderstood. A once-of display of aggression is not bullying, the aggression and behaviours
must show a pattern of repetition towards a victim.

Summarised into the three components of bullying. Known as the Three B’s of bullying. The aim is to get the
victims to doubt their reality and thus become easy to be controlled.

Bully

abuse charm poor me

Usually the incidents of bullying seem too trivial to complain. Nevertheless, it is these small incidents that the
bully will use to undermine the target and eventually destroy their self confidence. Nurses are often very
reluctant to document the trivial incidents or even take the matter further which makes it difficult for management
to address.

If the bully is challenged about their behaviour they may take the position of ‘poor me’ or ‘victim’. They then
claim they are the one who is being bullied. Feigning distress and indignation changes the focus from their abuse
to their distress, so they are not called to account for their bullying behaviours. They can be callous and cold and
are also masters at manipulation. They know their rights and how to use the system for their own needs. They
take pleasure in destroying the target by causing distress which often leads to illness.

Convincing, and charming, the motive of the charm is deception. In many situations due to lack of
understanding of the culture of bullying techniques the person who is doing the bullying is protected.

Bullying is about power and control
Targets have admirable qualities which leads the bully to become envious
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Recognition & Clinical Assessment of the Deteriorating Patient                         29
Mismanagement of bullying is the norm rather than exception
It’s easier to remove the target than the bully!
(The above content taken from: Evans-Murray, A (2012) Uncomplicating Life Simply, How to recognise and avoid
destructive patterns in your life. Health Ed Professionals. Gold Coast.).

Communication and Assertion

SBAR

SBAR communication encourages nurses to use more critical thinking and to speak assertively. Using the SBAR
technique, nurses are encouraged to make suggestions. Encouraging nurses to not to hesitant to give their
opinion based on the assessment. Many authors claim that SBAR improves patient safety.

S - Situation

B – Background

A – Assessment

R – Recommendation

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Recognition & Clinical Assessment of the Deteriorating Patient                       30
                                          Assertiveness Skills List Training

                                     Building Resilience to Difficult Situations

              Exercise and interactive session.

Step one:

High emotional IQ

Identify your patterns (without self-blame)

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Problem

5 second pause

How you do you generally react?

               Passive                            Assertive                           Aggressive

    General percentage              Assertion means respect

Exercise

1.        Write down as many situations in your life as you can in which you feel that you are not being
          assertive enough

2.        Identify any recurring themes regarding:

  the kinds of situations in which you find assertion difficult
  the kinds of people with whom you find assertion difficult
  your feelings physical reactions thoughts and behaviours in situations and or with people where assertions
   is difficult for you
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3.        Rank them in the expected difficulty order

Start with number I and write a short task next to the situation you think would be least difficult, moving up to
10 etc. Always start your practice with safe people. Start small, success encourages you to keep trying, reward
after each attempt at each task. Ignore feelings of guilt.

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