Create Realistic And Relevant Learning Opportunities Docx.

Online Scenario 2 ─ Due date: 16/02/20
This assessment task will draw on content discussed in Topics 1, 6 and 7.
Some of the content was adapted from 2 NCCSTS case studies.
Your answers should be no longer than 200 words.
Whilst your lecturers aim to create realistic and relevant learning
opportunities within in a safe environment, you may find that when
working through a case study or scenario it may impact on you in
unexpected ways. This could include raising cultural, spiritual,
psychological or personal issues for you that you were not expecting. If
this occurs, it is important that you discuss these issues with a trusted
friend, family member, staff member, or counsellor.
Remember: CSU offers a free counselling service to internal and distance
education student’s in-person and via phone, Skype (webcam) and e-mail.
To access the CSU Counselling Service, please visit
https://student.csu.edu.au/services-support/health-wellbeing/counselling
The Heart of the Problem: from heart attack to respiratory failure
Part I — The wake-up call
It was 4:36 a.m. She was in a cold sweat and having difficulty breathing.
She felt as though she had run a marathon.
Fear swept through her—something terrible was going to happen. Panic-
stricken, she woke her husband, Jeremy.

"Denise, what is it? Is it a nightmare?" "No, it's like I'm having an asthma
attack. I feel lightheaded and I can't catch my breath. My heart feels like
it's beating a thousand times a minute."
Afraid to upset her husband further, Denise didn't tell him that an
immense feeling of apprehension suddenly overcame her. She got up to
drink some water and waited for the anxiety to subside.
Her mind was racing. Jeremy had a family history of heart disease. This
couldn't be happening to her. It was his problem. A few months earlier
Jeremy was diagnosed with coronary artery disease. He was only 48 years
old, the same age as Denise. The scare had encouraged him to gradually
end years of chain smoking and adopt a healthier lifestyle. He was
currently working on giving up the occasional cigarette for good.
"No," Denise thought to herself.
"There's no way this was a sign of heart
troubles. I didn't have a pain in my chest, I'm physically fit, and I have no
family history. There's just no way."
After assuring herself of this, Denise was somehow able to fall back
asleep.
The next day at work, Denise was having a hard time focusing. Maybe the
stress of her job was finally catching up with her. Managing a catering
business was no easy task. On top of that, her only daughter, Emily, had
left for college this year and, being the overprotective parent that she
was, Denise found herself constantly worrying about how her daughter
was faring in a different city, away from the comforts of home. Also,

Denise was perimenopause. The hormonal changes, combined with
fatigue, stress, and her general worrisome nature, were catching up to
her. Not only that, she couldn't get last night's scary episode out of her
thoughts. Was it just part of the whole perimenopause thing or was it
more? Her body was trying to tell her something, but Denise wasn't sure
she was ready to hear.
Conversation by the heart...
"I wonder if Denise realises how all those years of second-hand smoke
have taken a toll on her lungs and on ME, her heart! All that tobacco
inhalation has constricted her coronary arteries. Sure, Denise tries to stay
physically active but genetics and her food choices have brought her
blood cholesterol up pretty high to 6 mmol/L. She could be headed for
heart disease. A person's total cholesterol level shouldn't get above 5.5
mmol/L. That's right. I ought to know! Denise has hypercholesterolemia, a
major contributor to heart disease. Geesh. Get with it, Denise. That was a
major warning last night. I'm oxygen-starved! Luckily, only a small area of
my left ventricle had a big decrease in blood flow and oxygen supply
(cardiac ischemia). Thank goodness. If nothing else happens, my body will
start growing some new collateral vessels (bypass channels) and I can get
some repair work done. Denise didn't experience chest pain (angina
pectoris). But her rapid heartbeat and shortness of breath sure got her
attention. She had better shape up because I don't know if I can handle
much more oxygen deprivation. And, hey, all this unstable plaque lurking

around is not a good sign either. No indeed. Who knows when it may
rupture? I don't like the looks of this at all." (NCCTSTS case studies)
For your own revision and understanding (NOT FOR SUBMISSION),
do these tasks first:
1. Draw a sketch of the heart and show where the coronary blood vessels
lie.
2. List in order the blood vessels that a drop of blood would follow as it
makes a complete journey around the body starting as it enters the right
atrium until it returns to the right atrium.
Part II—"Heart Attack Basics"
It appears that Denise has suffered mild heart trauma, which may lead to
a more severe heart attack if not treated. But wait ... isn't a heart attack
when the heart stops beating? Not exactly. Cardiac arrest is the term
used when the heart muscle literally stops pumping blood. A heart
attack, also known as a myocardial infarction, may lead to cardiac
arrest, but it's defined as a sudden event where at least one of the three
major coronary arteries (right coronary artery, left anterior descending
coronary artery, and left circumflex artery) becomes partially or totally
blocked, usually by a blood clot (thrombus). A more rare cause of
coronary occlusion is an artery spasm that shuts down blood flow to the
heart. This can occur with cocaine use and severe emotional stress. Other
rare causes of heart attack include sickle cell crisis, allergic reactions,

carbon monoxide poisoning, extreme hypoxia, and an unmet increased
need for blood flow to the heart such as may occur during extreme
physical exertion, shock, or haemorrhage.
Heart cells can live for about 20 minutes without oxygen. The loss of
oxygen-rich blood to the heart cells during a heart attack leads to cell
damage, which may be permanent and lead to cell necrosis (death),
depending on the severity of the attack and the amount of heart tissue
that the blocked artery supplies. The area of infarction is where cell
necrosis occurs, if it does. Surrounding it is the area of injury, which may
or may not suffer permanent damage. The outermost affected area is the
zone of ischemia, which is weakened but regains function within two to
three weeks. Besides the possibility of cardiac arrest, other possible
complications include the following: cardiogenic shock (where the heart
is too weak to adequately pump blood), pulmonary edema (where a
weakened heart causes blood backup and leakage of plasma into the
lungs), irregular heart rhythm (arrhythmia), rupture of a heart wall or
valve, or death. It is a misconception that having a heart attack leads to
chronic coronary artery disease (CAD). In reality, CAD and
accompanying atherosclerosis (hardened, narrowed arteries) is the
number one cause of heart attacks. What causes CAD? The main culprit is
arteriosclerosis, or plaque buildup in the coronary arteries. Plaque is a
material composed mainly of lipids, cholesterol (lipoproteins), and
calcium. Cholesterol is carried through the bloodstream by two main types
of lipoproteins: high-density lipoproteins (HDLs) or "good" cholesterol, and
low-density lipoproteins (LDLs) or "bad" cholesterol. HDLs help prevent

heart disease by transporting lipids and cholesterol from the arteries to
the liver. LDLs, which contain more fat and less protein, are unstable and
stick to artery walls to help contribute to plaque formation. LDLs
(cholesterol-handling system) produce toxins that form tiny lesions on the
inner walls of arteries. These lesions attract triglycerides and other
substances in the bloodstream. White blood cells (inflammatory system)
rush to the injury site, but cause the inner wall to become stickier and
thus attract more LDLs. Platelets (blood-clotting system) collect at the
lesion site, only to trap more lipids and white blood cells. Plaque build-up
slowly occurs. (Note that cholesterol is not the sole cause of plaque
formation.) Over time, some of the plaque can develop a thick, hard,
calcified fibrous cap and is called stable plaque, yet causes the arteries to
become narrower and harder (atherosclerosis). Other plaque can develop
a large lipid and macrophage core, decreased smooth muscle cell content,
and a thinner, softer, more unpredictable fibrous cap (due to increased
metalloproteinase enzyme activity). This can rupture, producing a
thrombosis (artery blockage), cardiac ischemia, and a heart attack can
ensue.
(NCCTSTS case studies)
Part IV—"Call 000!"
It was April. Emily was home for Easter public holiday and Denise was
enjoying having her 19-year-old daughter around. Unfortunately, it was
going to be hard to spend much time with her because it was that time of
the year when weddings and other catered events were picking up again