Conduct and report an RCA for the area of improvement you selected.

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Using the strengths, weaknesses, opportunities, and threats (SWOT) analysis you did in Week 3, select an area of improvement in the healthcare setting. You will do an RCA for this area this week.

Tasks:

  • Visit the following link:

Determine-root-cause-5-whys (https://www.isixsigma.com/tools-templates/cause-effect/determine-root-cause-5-whys/ )

    • Read the introduction to RCA.
    • Read the RCA process.
  • Conduct and report an RCA for the area of improvement you selected. Include in your analysis:
    • A diagram of the clinical or workflow process
    • A fishbone diagram of constraints
    • The steps for improvement, utilizing the five-whys tool
    • Suggested changes for making the improvement

Educational Flyer: Internal Factor Evaluation

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Educational Flyer: Internal Factor Evaluation & Internal–External Matrix

Discipline:
– Healthcare

Type of service:
Poster

Spacing:
Double spacing

Paper format:
APA

Number of pages:
1 page

Number of sources:
3 sources

Paper details:

Scenario: You are the Director of Strategic Planning for a large hospital. In three weeks, the senior leadership team will embark on its annual strategic planning cycle. The CEO has decided that the team needs a “refresher” on two important topics: Internal Factor Evaluation and Internal-External Matrix. She has asked you to develop a one-page “flyer” that compares them in a side-by-side format. The flyer should describe each tool and bullet the following items: How the tool is used, strengths of the tools, limitations of the tools, and challenges that organizations usually face in trying to use the tools.

The flyer should be well organized and written and meet the following requirements:

One page in length (excluding reference list, which is required)
Include at least three current references from the peer-reviewed articles.
Here are some resources for information about developing flyers:

https://business.tutsplus.com/articles/10-design-tips-to-make-a-professional-business-flyer–cms-26226 (Links to an external site.)Links to an external site.
https://designshack.net/articles/graphics/how-to-design-an-awesome-flyer-even-if-youre-not-a-designer/ (Links to an external site.)Links to an external site.
Make a Flyer using Word (Links to an external site.)

The importance of diversity in the workplace

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Discipline:
Management

Type of service:
Essay

Spacing:
Double spacing

Paper format:
Not applicable

Number of pages:
1 page

Number of sources:
0 source

Paper details:

Within one page, I need the following questions answered.

1) Diversity is among an organization’s values because a multiplicity of values and beliefs, interests and experiences, intellectual and cultural viewpoints enrich learning, inform scholarship, and enhance all aspects of the healthcare industry that we prepare our students to enter. The organization is committed to fostering an environment that contributes to the robust exchange of ideas within a diverse community. Why is inclusion and diversity important to an organization?

2) If hired at the organization above (see scenario), what contributions could someone make to the organization becoming more inclusive and diverse?

ONLY U.S. writers and someone with experience in human resources.

Caring for patient in acute heart failure

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Heart failure it the term used to describe state where the heart fails to maintain an adequate circulation for the needs of the body despite
an adequate venous return. Acute heart failure occurs as a result of a sudden decrease in ventricular function and may be associated with
an acute event such as a viral illness, valvular dysfunction or an acute myocardial infarction. Chronic heart failure develops over time and
is often the result of inability of auto regulatory mechanisms to compensate for decreased ventricular function. Acute heart failure
frequently occurs in patients with chronic, long standing impairment of ventricular function.
Learning Outcomes
Upon successful completion of this section, you should be able to:
describe the pathophysiology and classifications of heart failure
identify the risk factors and conditions that contribute towards heart failure
identify the neuro-hormonal compensatory mechanisms which occur in heart failure
relate the clinical manifestations of heart failure to the relevant pathophysiological processes
identify rationales for the investigations that aid in the diagnosis of heart failure
describe how the pathophysiology of heart failure impacts upon patient care, particularly in relation to pharmacological regimes
discuss the nursing care required for a patient in acute pulmonary oedema
discuss the psychosocial issues surrounding the patient with heart failure.
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
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Review
Heart failure is associated with a failure of the normal body mechanisms which regulate blood flow. It is important
that you understand the role of the following compensatory mechanisms in the pathophysiology of heart failure.
You may need to consult a pathophysiology text to review the following.
Note the definitions of stroke volume, preload, afterload and contractility.
Describe the Frank Starling mechanism and its effect on cardiac output.
Describe the role of the following compensatory mechanisms for decreased cardiac output.
Include both the short and long term effects of stimulation of these systems
the sympathetic and parasympathetic nervous systems
the rennin angiotensin system
myocardial hypertrophy or remodeling
the naturetic peptides.
Define the following terms:
positive and negative inotropes
positive and negative chronotropes
dromotrophy
adrenergic receptor.
Lecture Notes – Click Here
Acute Heart Failure physiology and CP…
4/9/2020 Study plan: Week 6 – Caring for a patient in acute heart failure
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Core text reading
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W., 2015, ACCCN’s critical care nursing, 3nd edn, Elsevier, Australia, Chapter 10, pp 285-304.
Optional Reading
Laurent, D 2010, chapter 24 ‘Heart failure and cardiogenic shock’, in Wood, S, Froelicher, M & Motzer, S (eds),
Bridges cardiac nursing, 6th edn, Lippincott,Williams and Wilkins, Philadelphia, pp. 555-578. (Also available on
Journals at Ovid (Books) database.)
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Heart and lung interaction
Understanding the interaction between the heart and lung in spontaneous breathing is important for understanding some of the clinical
signs and symptoms related to heart failure.
Blood flows through the right side of the heart to the lungs, and then back to the left side of the heart through the aortic valve and root to
the systemic circulation. This flow is mainly dependent on differences in pressure between circulation compartments with blood flowing
from high pressure to low pressure. These pressures are affected by gravity and movement of the chest wall for breathing and the
contraction of the heart muscle. The compartments are the venous bed (mainly the abdominal and splanchnic circulation) the right atrium,
the right ventricle, the pulmonary circulation, the left atrium, the left ventricle, the aortic root and the arterial bed. The pressures are higher
in the thicker walled elastic arterial and left ventricle compartments than the thin walled, easily collapsible venous compartments.
Blood returns to the heart during inspiration when the pleural pressure becomes more negative from chest wall moving out causing the
right atrium to dilate—lowering its pressure hence the gradient between the venous bed (in the abdomen and muscle) is increased to a
point that blood flows from a higher to a lower pressure into the right atrium. The right ventricle dilates to receive the incoming blood as
does the pulmonary bed from the release of atrial naturetic peptide that the dilating right atrium releases. The larger the breath volumes
during inspiration the greater the diaphragm and intercostals movement and hence the lower the pleural pressures. The pulmonary bed
dilates and constricts in response to the lung volumes and compliance and oxygen concentration which is varied throughout the lung. This
pulmonary blood once oxygenated flows into the left atrium and left ventricle during diastole from a high to a low pressure with some
assistance from gravity.
The term transmural pressure (PTM) or the difference in pressure across the walls of each of the compartments or vessel or organ
(Transmural pressure = internal surface pressure—external surface pressure) is referred to in literature you will read. There is a transmural
pressure of the heart, the aortic root and the lung—but the lung is explained in terms of transpulmonary pressure (pressure difference
between blood vessels and alveolar) and intrathoracic pressure as the large vessels in the thoracic as well as the pleural space have a
larger impact on pressure than just the lung and lung tissue.
As ventricular afterload is defined as the force opposing ejection, ventricular afterload is represented by the level of transmural pressure,
in the course of systole, within either the aortic root (LV afterload) or the pulmonary artery trunk (RV afterload). In terms of the LV; at the
onset of spontaneous inspiration, the intraluminal pressure in the aortic root decreases less than does intrathoracic pressure, due to the
connection of this vessel with extrathoracic arteries. As a result, aortic transmural pressure increases.
Spontaneous deep breathing places the acute failing heart under stress as it increases preload and afterload
With spontaneous breathing therefore, LV afterload is greater in inspiration than in expiration. Respiration has a profound effect on LV
afterload in pathologic conditions, such as when negative intrathoracic pressures (from large spontaneous breaths and increased work of
breathing) are exaggerated (e.g. in sleep apnoea, acute pulmonary oedema or respiratory failure) or when LV systolic function is impaired.
This concept is exampled in sleep apnoea where large breath volumes after periods of apnoea increase the aortic root pressure hence
increasing the LV afterload, causing the left ventricle to dilate to work harder to contract and over time leading to systolic heart failure
(large dilated LV) similar to those with chronic hypertension.
Heart Lung interactions in spont breath…
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Pathophysiology of heart failure
eReadings

Acute coronary syndromes

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So far you have learned the essential elements of cardiac assessment, and rhythm and ECG analysis. In this section the focus is on
caring for the patient who is suffering acute coronary syndrome. This encompasses myocardial ischemia as well as acute myocardial
infarction (AMI). The nursing responsibilities in caring for a patient experiencing acute coronary syndrome includes community education
for early symptom recognition, prompt attention and prioritised management in the acute phase, discharge planning and cardiac
rehabilitation.
Learning outcomes for this section
Upon successful completion of this section, you should be able to:
identify assessment strategies for patients presenting with signs and symptoms of AMI
describe the differential diagnoses that may present with chest pain
relate the pathophysiology of heart disease to the anticipated plan of care for a patient experiencing an acute myocardial infarction
(AMI)
demonstrate an advanced physiological understanding of medication used in your practice setting
plan collaborative care that extends across the health care continuum for patients experiencing an uncomplicated AMI.
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Review
Acute coronary syndromes are most commonly associated with the rupture or erosion of an unstable atherosclerotic plaque and
subsequent formation of a platelet-fibrin thrombus. It is important to understand the pathophysiology of acute coronary syndromes
including the following:
Risk factors for the development of coronary artery disease.
Pathophysiology of the development of atherosclerosis.
The classifications of the different forms of angina.
The ECG characteristics of myocardial infarction from section 4.
Acute Coronary Syndrome (ACS) Patho…
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Readings (a choice)
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W., chapter 9 ‘Cardiovascular alterations and management’, in ACCCN’s critical care nursing, Else
eReadings
Thompson, P 2011, Coronary care manual, 2nd edn, Elsevier, Australia.
Chapter 8 ‘Pathophysiology of atherosclerosis’, pp. 54-61.
Chapter 9 ‘Pathophysiology of coronary thrombosis’, pp. 62-71. – Click Here
Chapter 10 ‘Pathophysiology of myocardial infarction’, pp. 72-78.
Chapter 16 ‘Biochemical markers of myocardial necrosis’, pp.125-129 – Click Here
Chapter 60 ‘Prehospital coronary care’, pp. 454-458.
Chapter 61 ‘ACS: emergency department care’, pp. 459-466.
Chapter 62 ‘ACS: coronary care unit admission and care’, pp. 467-473. – Click Here
Chapter 63 ‘Management of ST elevation myocardial infarction’, pp. 474-484.
Chapter 64 ‘Management of non ST elevation ACS’, pp. 485-493.
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ACS in Women and ANZCOR Updates
eReading
Mehta, L.S., Beckie, T.M., DeVon, H.A., Grines, C.L., Krumholz, H.M., Johnson, M.N., Lindley, K.J., Vaccarino, V., Wang, T.Y., Watson,
Infarction in Women A Scientific Statement From the American Heart Association. Circulation, pp.CIR-0000000000000351. – Click He
Website
There have been some updates from the Australian and New Zealand Committee on Resuscitation (ANZCOR) (Australian Resuscitati
Australian and New Zealand Committee on Resuscitation: Guidelines Section 14: Acute Coronary Syndromes – Click Here
ANZCOR Guidelines Update on Acute Coronary Syndromes – Click here
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Safety and Quality ACS Clincial Care Standard
Australian Commission on Safety and Quality in Health Care. Acute Coronary Syndromes Clinical Care Standard. Sydney: ACSQHC, 2
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Classification of acute coronary syndromes
In the previous module you learned the ECG characteristics of acute MI. It is important to distinguish between unstable angina, non ST
elevation myocardial infarct (NSTEMI) and ST elevation myocardial infarct (STEMI). Patients with symptoms of ischemic discomfort may
present with or without ST segment elevation on an ECG. Patients who present without ST segment elevation are experiencing either
unstable angina or NSTEMI. The distinction between these is made by assessment of the presence of elevated serum cardiac markers.
The majority of patients with NSTEMI do not develop Q waves (indicating irreparable necrosis) on their ECG and you may hear referred to
as having a Non Q wave MI (NQWMI) although this terminology is no longer commonly used. However some patients with NSTEMI do
develop Q waves on their ECG, (QWMI). Patients experiencing STEMI can also develop Q waves on their ECG with a smaller number
experiencing NQWMI. With a strong current focus on client early action and early clinical intervention in this cohort of patients the number
of people exhibiting Q waves is decreasing.
Figure 5.1: Classification of acute coronary syndromes (Adapted from Thompson, P 2008, Coronary care manual, 2nd edn, Churchill
Livingstone, Australia, and White, HD & Chew, DP 2008, ‘Acute myocardial infarction’, Lancet, vol. 372, pp. 570–584.)
The presence of Q waves is often associated with transmural infarction, or one which extends through the full thickness of the
myocardium. However, Q waves are not a consistent indicator of transmural infarction. Similarly the presence of ST segment depression
without elevation elsewhere on the ECG is usually but not always associated with subendocardial injury. The lack of consistency of ST and
Q wave changes as indicators of subendocardial or transmural zones of injury has lead to the classification of acute coronary syndrome by
their ECG characteristics alone.
4/9/2020 Study plan: Week 5 – Acute coronary syndromes
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Clinical assessment: the patient with chest pain
Activity
Some disorders mimic the chest pain of AMI. Construct a table that describes the pain location, pain
characteristics and common assessment findings such as any ECG changes for each disorder listed below.
Disorders that may mimic the chest pain of AMI
pulmonary embolism pneumonia
aortic dissection pneumothorax
angina gastric reflux
Pericarditis
Approach to Chest pain
An Approach to Chest Pain
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Diagnosis of acute myocardial infarction
Acute cardiac care is a dynamic discipline. Research in regard to management strategies including diagnostic tools, drug therapy, invasive
and non-invasive treatments are under constant review by clinicians and researchers. Evidence based practice at this stage supports early
clinical presentation, cardiac enzymes and ECG changes as the standard for diagnosis of AMI. However, there are circumstances when
further intervention such as catheter lab or CT is required to confirm suspected diagnosis.
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Clinical presentation
The diagnosis and determination of the severity of an AMI is on a clinical diagnosis which requires a thorough history and physical
examination.
Pain, shortness of breath, diaphoresis are usually the most significant symptoms for most patients experiencing a STEMI or NSTEMI and
normally follow a characteristic pattern. However, some patients with acute coronary syndromes may not experience pain, and the
intensity of pain varies with the pain threshold of different patients. The intensity of the pain experienced is neither indicative nor diagnostic
of the severity of the ACS the patient may be experiencing.
Chest pain may be caused by many different conditions; however, it is important to remember that the patient with chest pain should be
considered cardiac in origin until proven otherwise. The patient who presents with acute chest pain requires prompt efficient nursing care
to help alleviate their suffering and the potential damage to the myocardium.
Myocardial Infarction in the ICU setting –
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Diagnostic tools and procedures
Activity

  1. Research the clinical signs which are common on presentation with an acute MI. Are there any signs or
    symptoms which are common with particular types or zones of infarction?
  2. Using your text find the sections that discuss the variety of diagnostic procedures and tools available for the
    diagnosis and treatment of Acute Coronary Syndromes. The list of investigations below can be performed to
    assist with the diagnosis and ongoing management of myocardial infarction and heart failure.
    Chest x-ray
    ECG
    Arterial blood gases
    Echocardiograph (two types and why use different methods?)
    Stress exercise electrocardiography
    Cardiac catheterisation: angiography and angioplasty
    Complete blood count
    Serum electrolytes/liver function tests/complete cholesterol screen
    Radionuclide studies
    Magnetic Resonance Imaging
  3. Provide information on why each test/procedure may be performed. (That is, what do you think the team is
    looking for or treating?) There could be more than one reason.
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    Biomarkers
    Knowledge of the purpose and significance of laboratory values assisting in the diagnosis and prognosis of AMI can enhance the quality of
    nursing care available to patients. Laboratory studies include routine blood analysis and special studies such as cardiac enzymes.
    Enzymes are found in all living cells and act as catalysts in biochemical reactions. They are present in low amounts in the serum of
    healthy people. The loss of membrane integrity in myocardial cells undergoing necrosis allows intracellular molecules to diffuse out into
    the cardiac interstitium and subsequently the blood stream. Detection of the abnormal presence of biomarkers is the ultimate diagnostic
    criteria for distinguishing between unstable angina and NSTEMI. Some cardiac enzymes are present in other organs, so elevation of these
    enzymes is not always an indicator of cardiac damage.
    A biomarker, known as Troponin or, in correct terminology, ‘cardiac Troponin’ was discovered in the 1990’s and is used successfully today
    for assisting in the diagnosis of cardiac muscle damage. There are three different types of Troponin; Troponin I (TnI), Troponin C (TnC)
    and Troponin T (TnT), with Trop I and T used for detection of damage specifically to the cardiac muscle. Troponin is a protein consisting of
    three sub-units and plays a key role in muscle contraction alongside actin and myosin. These are known collectively as contractile
    proteins.
    Activity
    Consult the section on biomarkers in your prescribed text to find the answers to the following questions.
  4. Describe how Troponin (T/I) differs from existing cardiac enzymes, namely creatine kinase (CK), and the
    isoform of creatine kinase (CK-MB).
  5. Compose a table that lists all of the current biomarkers associated with AMI, the time they take to peak, and
    the duration of elevation.
  6. Consider how these and other investigations might be of some benefit in the diagnosis of myocardial
    infarction. Your list should include procedures such as laboratory assessments.
    It is important to note that the initial diagnosis of STEMI can be made by clinical and ECG criteria alone.
    It is not necessary to wait for results of biochemical markers to arrive before initiating therapy in patients
    at risk.

Haemodynamic monitoring

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Hemodynamic monitoring is the active assessment of cardiopulmonary status by the use of biosensors that assess physiologic outputs.
The simplest form of monitoring is the individual health care professional, inspecting the patient for consciousness, agitation or distress,
breathing regular or labored, the presence or absence of central and peripheral cyanosis; touching of the skin of a patient to note if it is
cool and moist, and if capillary refill is rapid or not; palpation of the central and peripheral pulses to note rate and firmness.
Although well established and important as bedside diagnostic tools, these simple “human-instrument” measures can be greatly expanded
by the use of pulse oximetry to estimate arterial oxygen saturation (Spo2), and the sphygmomanometer and auscultation to note systolic
and diastolic blood pressure and identify pulsus paradoxus. These classic measures of hemodynamics, often referred to as routine vital
signs, are central to the assessment of cardiorespiratory sufficiency and much of diagnostic bedside medicine is rooted in these important
techniques.
However, with some exceptions, these simple and inexpensive measures do not have the discriminatory value in identifying patients as
being stable or unstable when compensatory processes mask instability or when changes in physiologic state occur rapidly. Furthermore,
they predict poorly who are at an early stage of an instability process, such as hypovolemia or heart failure, but compensating. Within the
context of circulatory shock, tachycardia may or may not develop early and even if it is present, it is nonspecific. However, these simple
measures can be markedly helped in their sensitivity to detect effective hypovolemia by making these same measures before and during
an orthostatic challenge.
For example, measuring blood pressure and pulse rate changes between lying supine, sitting, and standing markedly increase the
diagnostic capability of the measures to identify functional hypovolemia. If heart rate increases and/or blood pressure decreases with
sitting or standing, it is reasonable to presume that some degree of compatible hypovolemia exists. However, the other important concept
in making these observations is that the measures themselves do not change, but their measured values change in response to a defined
physiologic challenge: this is an example of functional hemodynamic monitoring. Functional hemodynamic monitoring is the use of a
defined physiologic stressor to access the physiologic reserve of the system.
Both invasive and non invasive hemodynamic monitoring is used extensively in critical care practice. Invasive monitoring is used to obtain
continuous pressure measurements in the central and systemic circulation. These parameters are used to estimate physiological variable
such as cardiac output and volume status.
Learning outcomes for this section
Upon successful completion of this section, you should be able to:
discuss the theoretical principles of haemodynamics
safely action haemodynamic monitoring procedures and protocols
interpret hemodynamic monitoring output
relate hemodynamic monitoring parameters to physiology of critically ill patients
realise the contribution hemodynamic monitoring makes as part of continuous patient assessment.
1
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Review
The material discussed in this section requires an appreciation of the factors which are related to cardiac output.
Revise the following and list the normal values for each:
cardiac output
cardiac index
stroke volume
stroke volume index
preload
afterload
systemic vascular resistance
pulmonary vascular resistance
contractility.
Cardiac Cycle animation
Blood Pressure Animation
4/9/2020 Study plan: Week 4 – Haemodynamic monitoring
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Suggested readings
Core text reading
Aitken, A, Marshall, A, & Chaboyer, W.,2015, ACCCN’s critical care nursing, 3nd edn, Elsevier, Australia, Chapter 9, pp. 248-260.
Other readings are highlighted through-out this module
4/9/2020 Study plan: Week 4 – Haemodynamic monitoring
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Concepts of haemodynamics
Heart Lung.org – great resource – Click Here
Pressure and flow
Pressure is the force applied per unit area. In haemodynamics we always think of pressure in terms of a pressure difference. The
pressure difference along the axis, or pressure gradient, is the pressure that causes the flow of blood. The pressure difference
between the inside and outside of a vessel or the heart, which is often called transmural pressure, and causes the wall distension.
It is important to remember that even though pressure is measured with various endpoints that are manipulated and responded to
clinically; we can lose the focus of blood flow or perfusion which is the only hemodynamic concept that is associated with improved patient
survival.
Blood flow is represented by cardiac output (Q).
Cardiac Output (Q) = Stroke Volume x Heart Rate
The stroke volumes for each ventricle are generally equal, both being approximately 70-85 ml. Stroke volume is the difference between
end diastolic volume and end systolic volume.
Interesting, Q has no pressure measurement in the above formula yet pressure is what we measure regularly as volume is far more
difficult to measure. However,
Stroke volume = Pulse pressure x 2
(Pulse pressure is the difference between systolic and diastolic pressure)
Hence we have difference in pressure as explained above and it is used to calculate stroke volume which is related to flow (Q) once we
add a driving force of heart rate. Invisible to this assumption is that heart contractility and elastance determine the filling, stroke volume
and driving force contraction of the heart and must not be forgotten.
The vascular beds are a dynamic and connected part of the circulatory system against which the heart must pump to transport the blood.
Q is influenced by the resistance of the vascular bed against which the heart is pumping. For the right heart this is the pulmonary vascular
bed, creating Pulmonary Vascular Resistance (PVR), while for the systemic circulation this is the systemic vascular bed, creating Systemic
Vascular Resistance in dynes-sec-cm (SVR).
Put simply, increasing resistance decreases Q; conversely, decreasing resistance increases Q.
By simplifying Darcy’s (and Ohm’s)Law, we get the equation that
Flow = Pressure/Resistance
When applied to the circulatory system, we get:
Q = Mean Arterial Pressure/Systemic Vascular Resistance
Much of the focus clinically on haemodynamics is the Mean Arterial Pressure (MAP) but as you can see it is related to Q or blood flow only
when Systemic Vascular Resistance (SVR) is added to the equation. Hence a patient may have MAP that is matching a prescribed
endpoint of 75 mmHg, but if the SVR is high the Q will be reduced to below the cell’s metabolic need for oxygen and nutrients and the
patient will struggle to survive.
So it is worthwhile to assess SVR in conjunction with MAP.
SVR can be measured through various haemodynamic devices and can be assessed clinically as peripheral coolness and capillary return.
However as you can see in the equation below, the SVR can be calculated with simple monitoring.
Q = (HR × SV) = MAP / SVR
Calculate the HR and the SV; then you can calculate the Q or cardiac output. As you are measuring the MAP with monitoring and it is
easily accessed, you can divide the MAP by Q to get an approximation of the SVR in dynes-sec-cm by multiplying MAP in mmHg by 80.
SVR = 80 x MAP/Q
Ohm’s Law and Hemodynamics (Fluid …
5
5

ECG analysis and application

/in /by

Previously you have examined cardiac assessment and the analysis and treatment ofarrhythmias. Analysis of the 12 lead ECG is a vital
component of cardiovascular assessment needed for many cardiac conditions. A systematic approach to the assessment of the ECG is
vital and ensures success. This is a large module and will continue to be work in progress throughout the year. Most of this is assumed
knowledge, so use it for revision and choose what is important in regard to your personal learning.
Learning outcomes for this section
Upon successful completion of this section, you should be able to:
describe how the 6 limb leads of an ECG are obtained
identify the sites of attachment of the six precordial leads and indicate over which region of the heart each electrode lies
list the leads which view the major surfaces of the heart
demonstrate a systematic approach to analysis of the 12 lead ECG
demonstrate a basic understanding of the physiology and characteristics of bundle branch blocks
demonstrate a basic understanding of the ECG characteristics of ischemia and infarction
describe the ECG changes associated with pericarditis and myocardial trauma
identify the changes associated with hyper and hypokalemia on an ECG
identify the major characteristics of chamber enlargement.
3/24/2020 Study plan: Week 3 – ECG analysis and application
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Suggested readings
Text reading
Thompson, P 2011, chapter 26 ‘Electrocardiographic monitoring’, in Coronary care manual, 2nd edn, Elsevier
Australia. – Click Here
.
Optional reading
Woods, S, Froelicher, E, Motzer, S & Bridges, E 2010, Cardiac nursing, 6th edn, Lippincott Williams and Wilkins.
Available online Flinders University Library www.flinders.edu.au/library through Ovid.
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The 12 Lead ECG
A 12 Lead electrocardiogram consist of the following:

  1. Six limb or extremity leads
    Three standard (bipolar) leads, I, II &III
    Three augmented (unipolar) limb leads aVR, aVL & aVF.
  2. Six precordial (unipolar) leads V1-V6.
    So far this Study plan has concentrated on the bipolar and unipolar limb leads. The six precordial unipolar leads are a vital part of ECG
    analysis as they give a view of the heart on its horizontal plane.
    The electrical activity of the heart consists of multiple individual currents with the ECG representing the sum result of these electrical
    impulses from a point on the body surface. If the sum result of the electrical impulse or mean vector is towards the positive ECG pole a
    positive deflection is recorded. A current flowing towards the negative pole records a negative deflection.
    The following diagram illustrates the normal sequence of depolarisation through the heart as recorded by the limb and the precordial
    leads. These give a view of the heart on its frontal and horizontal plane.
    Figure 4.1: (A) Normal sequence of depolarisation through the heart as recorded by the frontal plane leads. This diagram also includes
    the hexaxial reference system or axis wheel. (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010,
    Cardiac nursing, Lippincott.)
    Figure 4.2: (B) Cross section of the thorax illustrating how the six precordial leads record normal electrical activity in the ventricles. In both
    examples the small arrow (1) shows the initial depolarisation through the septum, followed by the mean direction of
    ventricular free wall depolarisation, larger arrow (2). (Adapted from Woods, S Froelicher, E, Motzer, S & Bridges, E (eds)
    2010, Cardiac nursing, Lippincott.)
    3/24/2020 Study plan: Week 3 – ECG analysis and application
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    Activity—Review the following
  3. The correct sequence of R wave progression through the precordial leads. Relate this to the normal
    sequence of depolarisation of the heart.
  4. The sequence of ventricular depolarisation through the right and left bundle branches and relate this to the
    ECG characteristics in the precordial leads.
  5. The configuration of lead AVR? Why does this lead normally record a negative deflection?
    12 Lead Interpretation Part 1: Introduct…
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    Examining the ECG: the process
    Examination of the ECG should follow a defined process. You may find that this process differs from many different processes in your text.
    Find one which suits you and use it with all of you ECG analysis exercises and in clinical practice. Your process should include
    examination of the each of the following:
    Patient identification and calibration (as in week 2)
    Rate and rhythm (as in week 2)
    Intervals: Is the PR and QT intervals normal? Use your ECG text to determine the normal characteristics.
    Waveforms: Are the P QRS and T waves within normal range?
    Cardiac axis. Determine if the axis is normal, left axis deviation, right axis deviation or indeterminate.
    ST segments: Is there any indication of myocardial injury or infarction.
    Other abnormalities: Signs of electrolyte abnormalities hypertrophy.
    12 Lead Interpretation Part 2: The 6 St…
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    Determining the electrical axis
    The axis represents a measurement of the sum of the electrical vectors during depolarisation of the heart. Determination of the electrical
    axis shows the mean vector generated by depolarisation of the ventricles as determined by examining the ECG leads of the frontal plane.
    Deviations in the electrical axis from normal or a change in axis may reflect anatomical alterations or significant pathology associated with
    myocardial damage.
    Axis is most commonly represented using the hexaxial reference system on the frontal plane leads represented in diagram (A) above. This
    labels each of the 6 frontal plane leads within a 360° circle beginning with lead I at 0°. The mean QRS vector or normal axis lies between 0
    and +90°.
    There are several methods of determining the mean frontal plane QRS axis each of which require examination of leads I and AVF. The
    exact axis as a percentage value can be plotted on the hexaxial wheel, or a simpler method classifies the axis as normal, left axis
    deviation, right axis deviation or indeterminate as demonstrated in the following diagram.
    Figure 4.3: The four quadrants of the axis wheel. (A) If the QRS in lead I is positive and the QRS in aVF is negative, the axis is in the left
    quadrant. (B) If the QRS is positive in both leads I and aVF, the axis is normal. (C) If the QRS in lead I is negative and the QRS in aVF is
    positive, the axis is in the right quadrant. (D) If the QRS is negative in both leads I and aVF, the axis is indeterminate. (Adapted from
    Woods, S Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    It is important that you can determine the axis within the four categories described above. Consult your ECG text to practice a method axis
    determination to achieve this. Consult your mentor or clinical facilitator if you have difficulty with this process.
    Activity
  6. What is meant by electrical axis? Use your diagram of Einthoven’s triangle from the previous section to
    determine the direction of the electrical axis in the limb leads.
  7. Read the section in your texts regarding determining the electrical axis. What are the characteristics and
    clinical significance of a left or right axis deviation? Relate this to the patients that you are caring for in the
    clinical area.
    12 Lead Interpretation Part 3: R-wave P…
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    The normal ECG
    Examine this ECG and follow the examining process.
    Normal sinus rhythm is present at a rate of 110 beats per minute.
    PR and QRS intervals are normal
    The QRS complexes and R wave progression is normal
    The T waves are normal
    There are no abnormal Q waves
    The Cardiac Axis is normal
    The ST segment is at baseline in all leads.
    There are no other abnormalities.
    This ECG can be used for comparison as abnormalities are discussed throughout this module.
    Figure 4.4: The normal ECG
    (Adapted from Hampton, J 2014, The ECG made easy, Churchill Livingstone.)
    3/24/2020 Study plan: Week 3 – ECG analysis and application
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    Q wave and ST segment abnormalities
    ECG analysis involves careful analysis of the Q wave and ST segment for indicators of myocardial pathology.
    The Q wave represents depolarisation of the interventricular septum. The Q wave is always a negative deflection, and may be present in
    some leads of the 12 lead ECG. In all leads accept leads III and AVR a Q wave is considered abnormal or pathological if it is greater than
    0.04 second in duration and more than one third the height of the following R wave.
    Pathological Q waves are highly suggestive of myocardial damage. Dead tissue is electrically inactive, therefore an electrode placed over
    such an area will see through it (like a window) to detect the electrical force generated by the opposite wall, i.e. current flow moving away
    from it as the cells are depolarised from the endocardium to epicardium. It is important to be aware of the characteristics of and be able to
    distinguish between normal and pathological Q waves.
    Figure 4.5: (A) Lead III in a healthy patient. (B) The same lead in the same patient 2 weeks after undergoing an inferior myocardial
    infarction. Note the deep Q wave.
    (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    The ST segment of the ECG is the line following the QRS complex connecting the QRS to the T wave. This represents the repolarisation
    segment of the ECG and is highly indicative of myocardial injury ischemia and infarction which can delay the repolarisation process.
    Analysis of the ST segment necessitates identification of the J point, or the connection between the end of the QRS and the beginning of
    the ST segment. A normal ST segment is flat with a variation of a minimum of 0.5-1.0 mm from the isoelectric line.
    Figure 4.6: ST segment elevation associated with myocardial infarction
    (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    Figure 4.7: Different types of ST segment depression highly indicative of myocardial ischemia. This example shows (A) down-sloping (B)
    up-sloping (C) horizontal ST depression
    (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    Activity
  8. Read your ECG text to become familiar with the characteristics of normal and abnormal Q waves and ST
    segments.
  9. Distinguish between the characteristics of normal and pathological Q wave.
  10. Describe the characteristics for ST elevation and depression in the both the precoridial and limb leads.
    3/24/2020 Study plan: Week 3 – ECG analysis and application
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    The indicative leads in altered state ECGs
    Figure 4.8: Localising myocardial ischemia, injury, or infarction using the 12-lead ECG. The different areas of the heart are pattern-coded.
    Standard 12-lead ECG format is illustrated at upper right with leads pattern-coded to correspond to the area of the heart that each lead
    faces.
    (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    Now you have examined the characteristics of all the leads in the ECG you can begin to determine their relationship to the relevant parts
    of the heart. This is particularly useful when identifying an area of the myocardium which is affected by an alteration in blood supply. The
    following diagram identifies the anatomical lead groupings of the heart.
    ECG activity 1
  11. Check your answers when you reach the end of this section.
  12. Take a look at the ECG below.
  13. Can you identify the leads which show ST segment elevation?
  14. Which surface of the heart are these leads viewing?
  15. What coronary artery supplies the area of the ECG that is altered?
  16. Use your ECG text to determine what coronary arteries supply each of the patterned areas in Figure 4.8.
    3/24/2020 Study plan: Week 3 – ECG analysis and application
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    ECG—ischemia patterns
    Myocardial ischemia results from an imbalance between oxygen supply and demand. The ECG changes associated with myocardial
    ischemia are associated with changes in the depolarisation process, and therefore are often reflected by an inverted T or depressed ST
    segment. However T wave inversion may also associated with other conditions such as bundle branch block, and it can be normal in some
    people. A diagnosis of myocardial ischaemia is often made based on the presence of chest pain and ECG changes. These changes may
    be transient, and may occur during chest pain or exercise testing.
    Figure 4.10: ECG patterns and myocardial ischaemia. Refer to the grey area for the identified change.
    (Adapted from Huszar 2002, Basic dysrhythmias: interpretation & management, 3rd edn.)
    Figure 4.11: ECG patterns associated with myocardial ischemia.
    (Adapted from Woods, S, Froelicher, E, Motzer, S & Bridges, E (eds) 2010, Cardiac nursing, Lippincott.)
    ECG activity 2
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    ECG—injury and infarction
    Myocardial injury is the next stage beyond ischaemia. Injured myocardial cells are still alive, but are vulnerable to progress to infarction
    (cell death). Diagnosis is made in by analysis of the ECG as well as specific and sensitive cardiac biochemical markers, such as troponin
    which detect myocardial damage.
    The underlying pathophysiology of myocardial infarction is associated with that of a ruptured plaque and subsequent thrombus formation
    which may partially or completely occlude a coronary vessel. The injury pattern that is recorded on the ECG as a result are classified as
    ST elevation myocardial infarction, (STEMI) non ST elevation myocardial infarction NSTEMI depending on the ECG pattern and
    measurement of cardiac enzymes.
    The term myocardial infarction (MI) is used loosely to encompass both myocardial injury and necrosis. Not all patients who have a MI
    actually develop tissue necrosis. Early reperfusion intervention can reverse the injury and prevent muscle death.
    The ST segment changes are caused by changes produced by injured myocardial cells. Hence the leads which are facing the injured area
    will reflect a raised or depressed ST segment. The degree of ST segment elevation or depression is variable, an increased or decreased
    of more than one millimetre above the isoelectric line in two or more leads is considered as abnormal. ST changes usually occurs within
    minutes of the onset of infarction.
    Certain characteristics of the Q, ST segment and T wave can provide some clues to the age of the infarction:
    Prominent Q wave (normal ST segment)—old MI
    Q wave + ST elevation (with or without T wave inversion)—acute MI
    Q wave + inverted T wave—indeterminate age
    Reciprocal changes
    This is reflected as ST depression in the reciprocal leads, or those opposite the zone of injury. This is a common phenomenon seen in
    ECG leads facing the opposite side of the area of injury, e.g. ST depression will be seen in the anterior lateral leads in the presence of an
    acute inferior MI.

Recognising physiological deterioration

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Recognising physiological deterioration
The onset of clinical deterioration refers to the stage when the person’s clinical state becomes physiologically unpredictable and unstable. It can result in incapacity or
death within minutes or hours. Several conditions can lead to sudden and/or unexpected deterioration of patients, and clinicians must possess knowledge and clinical
experience of specific critical illness states to be able to identify key early warning signs and symptoms indicating physiological deterioration.
The clinical signs of critical illness and deterioration are usually similar regardless of the underlying cause, because they reflect compromise of major body systems. The
identification of abnormal clinical signs [together with the patient’s history, examination and appropriate investigations] is central to objectively identifying patients who are
at risk of deterioration. These signs and symptoms are often subtle and can go unnoticed. Therefore developing assessment skills that are alert to the signs and risk of
deterioration in a patient is essential in specialist clinical practice.
Learning Outcomes
Upon successful completion of this section, you should be able to:
explain the importance for the assessment of critically ill patients
describe the key elements of advanced clinical assessment
describe the principles and practice of clinical assessment
understand the importance of recognising and preventing further deterioration in patient care
Early recognition of clinical deterioration, followed by prompt and effective action, can minimise the occurrence of adverse events s
uch as cardiac arrest, and may mean that a lower level of intervention is required to stabilise a patient.
Prevention of deterioration that results in respiratory and cardiac arrest represents the most important and most effective step in the chain of survival. It is widely
recognised that cardiac arrest in patients in unmonitored ward areas most commonly occur following a period of progressive physiological deterioration rather than a
sudden unpredictable event.
The consensus statement of the Australian Quality and Safety Health Care Commission (2010) recommends that all facilities have systems in place for measurement and
documentation of vital signs and escalation of care including rapid response systems with organisational support.
Nature of the deficiencies in the recognition and response to patient deterioration often include: infrequent, late or incomplete vital signs assessments; lack of knowledge
of normal vital signs values; poor design of vital signs charts; poor sensitivity and specificity of ‘track and trigger’ systems; failure of staff to increase monitoring or
escalate care, and staff workload. There is also often a failure to treat abnormalities of the patient’s airway, breathing and circulation, incorrect use of oxygen therapy,
poor communication, lack of teamwork and insufficient use of treatment limitation plans.
One of the most important directives of the ARC Guidelines include increased emphasis on the use of ‘track-and-trigger systems’ to detect the deteriorating patient and
enable treatment to prevent in-hospital cardiac arrest in order to improve survival.
Figure 1: Early recognition and access are essential components of effective resuscitation
The Chain of Survival represents the link between the essential elements in resuscitation which, if performed effectively, can lead to an increase in the number of persons
who survive a cardiac or respiratory arrest.

role in the management of a modern crisis

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QUESTION 1
CASE
The highly contagious novel coronavirus SARS-CoV-2 also called coronavirus disease of 2019 (COVID-19) is
a global health emergency of unprecedented proportions. The ongoing loss of life globally as well as the virus’
ability to spread rapidly through communities, has generated a need for significant changes to the foundations
of the well and least developed countries. In the last few months, political leaders globally have been making
new announcements to respond to COVID-19 impacts, on both people and the economy. These have been crucial
steps to ensure public safety and financial stabilization. As it stands now, nobody knows how long this crisis
will last, but we do know that when it finally recedes our world will look very different. This crisis has not just
created new disasters, it has exposed the flaws of our existing system. Several leaders have done well including
few female leaders like Taiwan’s president, Tsai Ing-wen; New Zealand’s prime minister, Jacinda Ardern; the
German chancellor, Angela Merkel; and Denmark’s prime minister Mette Frederiksen.
In the case of Ghana, the Ghanaian government has so far followed a step-by-step model, including initiating
travel restrictions outside the country, restrictions on events and on places of social gathering including
churches, schools, restaurants, theatres and gyms and now currently just lifted a 21-day partial locked down in
two of the most affected regions in Ghana. Inequality in Ghana meant that now, in this time of deep need, we
risk sacrificing the health and safety of vulnerable people for whom the social safety net has been weakened.
Several proposals, both economic and health related are suggested to assist the entire nation. Health care
workers and security personnel have become heroes. Government has been asked to show leadership in
transforming or restoring the economy to one that works toward well-being for all as it takes steps to gradually
relax the restrictions. It is believed that the brighter side to the crisis is the momentum and opportunity to shift
our systems to prioritize our care and wellbeing in the long run.
a. Explain how decisional and informational roles of leaders can influence the effective management of
the COVID-19 crisis in Ghana. (4 marks)
b. In the management of the health crisis, how can technical, human, and conceptual skills be relevant for
the Minister of health to enable him rally around health workers? (4 marks)
c. The internal and external environment will cause changes for companies in Ghana (Large, Medium, and
small-Scale Enterprises) during this crisis. Explain (4 marks)
d. Discuss two (2) ways by which transformational leadership style can be relevant to the management of
the crisis at all levels of management. (4 marks)
e. Explain four (4) ways by which scientific management play a role in the management of a modern crisis

Topic 6 Diversity management

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You are working in a large accounting firm that has recently received bad press regarding diversity. The majority of senior staff are longstanding male staff, and over 80% of the new recruits in the last 3 years are under the age of 35. No one in the organisation seems to mind as the culture is generally good and the teams are productive. The organisation is profitable and growing quite well.

Do you think any action should be taken to manage the bad press received? If so, what approach/es do you think will be best? If not, justify your position.

Topic 7 Performance management

You are working for a medium sized engineering firm. The firm has regularly ‘checked in’ with its employees annually, sometime twice a year. Your HR manager also deals with any issues regarding performance as they arise. As the firm is growing quite quickly the executive team has decided a more formal performance management system is needed. A meeting will be held to brainstorm what this process should look like. As your character, address what you think the best approach to performance management will be. What will this approach achieve in your individual performance measurement system? What will some of the potential challenges be?

Topic 8 Rewarding people

As a higher level executive in your organisation (director or manager depending on the character you choose), it has been brought to your attention that there is some inequity in pay and bonuses between you and people at the same level. Do you believe this is an issue? Given fair work and other legislation should everyone be getting paid the same? What process do you believe should be followed when setting pay and bonuses for executive staff?

Topic 9 Employee learning and development

In your role you manage a total of 20 people: 3 direct reports who are team leaders in your division, each of whom have 5-6 people in their teams. You have noticed recently performance is lower and you suspect it is time to update a few processes to increase efficiency. You have implemented a few changes but people do not seem to be following them and there is a sense of demotivation in the teams. What do you think is the best way to go about this process? What key steps do you ensure are carried out?

(Hint: you will need to consider the training process and career management aspects).

Topic 10 WHS

Along with the well-known physical WHS issues, mental health of staff is becoming more and more of an issue in workplaces. Bullying, stress, work-life balance pressures, flexible working arrangements and a rise in drug and alcohol use all provide new complexities for managers. This is on top of safety things such as safety training, operation of machinery, personal protective equipment and other physical hazards. Within your role you manage of team of 15-20 people.

(for initial post) What do you identify as the 3 main WHS hazards to your team and why? What steps can be taken to address these problems?

(for response post) Offer feedback on your colleagues’ concerns. What would be the best WHS management system for them given the issues they have identified? Is there an additional issue you think they should also consider?

Topic 11 Ethics

You are part of a large organisation in which a couple of job openings have emerged in one of your colleague’s teams (Jennifer Bodel is the Director of the Public Relations department). Like you and most others at your level in the organisation, Jennifer has a team of about 15-20 staff. The recruitment process has started and you overhear Jennifer asking someone else to be on the interview panel with her. She states,

“It’s just the formal part of the process. I already know the two I’m hiring – they’re my friends and I worked with them at my previous job.”

You trust Jennifer and her team is highly productive so you know she wouldn’t hire anyone who was incapable, however, you can’t help but feel this is the wrong way to go about it. What action (if any) do you take?