Health Variation Question 2022

Running head: HEALTH VARIATION 3
Health variation 3
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HEALTH VARIATION 3 2
Table of Contents
Concept map....................................................................................................................................3
Guided Questions.............................................................................................................................4
Question 1....................................................................................................................................4
Question 2....................................................................................................................................6
Question 3....................................................................................................................................7
Reference list...................................................................................................................................9

HEALTH VARIATION 3 3
Concept map
Definition
Aetiology
Heart diseases can cause heart
failure.
Common causes of heart
failure can be coronary disease
or even the amount of blood
flowing is blocked
Cardiomyopathy
Damaged cardiac muscles
Breathlessness
Pathogenesis
The condition
where the left
ventricle loses its
normal ability to
contract and fails
to provide blood to
the body
Course of disease
Poor cardiac muscles
Narrow arteries
Faulty left ventricle
Blood clots
High blood pressure
Left ventricle loses its
ability to contract normally
Prevention
Limit sodium
consumption
Keep check on
blood pressure
Do not take stress
Keep check on diet
Diagnosis
Increase in blood
pressure
Low oxygen saturation
level in body
Breathlessness
Increase in pulse rate
The pathogenesis
can be clearly
determined by the
failure of the body
to deliver oxygen
enough for the
metabolic process
due to failure of the
circulatory system.
This can be termed
as an intrinsic
abnormality in the
cardiac function
Treatment
Use of medicinal
drugs such as
 Glyceryl
trinitrate
 furosemide
Non-invasive ventilation
Understanding the vital signs
Providing comfort and even
reassurance

HEALTH VARIATION 3 4
Guided Questions
Question 1
Clinical manifestation of atrial fibrillation
Atrial fibrillation can be termed as an irregular mode of heartbeat that increases the
chances of stroke and cardiac related problems (Køber et al. 2016). During the mentioned
scenario there is irregular beating of upper heart chambers and is often marked by shortness of
breath. Episode related to atrial fibrillation may not be life threatening; however, if the
conditions prevail, then emergency medical treatment is required. Shier, Butler and Lewis
(2015), pointed out the fact that a major problem with atrial fibrillation can be termed as
formation of blood clots in the upper chambers. The blood clot may circulate to other body parts
leading to ischemia. The symptoms of atrial fibrillation include palpitations and even weakness
coupled with chest pain and shortness of breath. The shortness of breath can worsen the scenario
The clinical manifestation of atrial fibrillation in Mrs. Brown can be termed as a
withstanding history of heart failure. It is for the same reason Mrs. Brown is subjected to acute
case of breathlessness. The breathless can be attributed to paroxysmal nocturnal dyspnea.
Paroxysmal nocturnal dyspnea can be caused due to either COPD or congestive heart failure
(Tang et al. 2015). However, after analysing the previous medical history, COPD can be ruled
out in the mentioned case study.
Pathophysiology and mechanisms
Hypersensitive, ischaemic or valvar defects in the heart can be termed as permanent
cause of AF (Atrial fibrillation). Familial atrial fibrillation is described well, although rare in
present condition. A region of 10th chromosome is responsible for presenting AF as an autosomal

HEALTH VARIATION 3 5
dominant trait (Leach et al. 2017). However, as argued by Jankowska et al. (2016), familial AF is
often considered to be a heterogeneous disease. The pathogenesis of AF is thought to initiate
through ectopic foci within the pulmonary veins and abnormal atrial tissue substrate is seen to be
responsible for maintaining arrhythmia. In similar regards, structural heart disease can underline
several cases of AF, the pathogenesis of AF is seen to result from trigger agents and is usually
less understood.
Clinical manifestation in regards to vital signs of Mrs. Brown can be made as follows:
 Increase in pulse rate of the patient
 Abnormal respiratory rate, an increase was observed coupled with breathlessness
 Low SpO2 85%, in room air, suggesting that level of oxygen within the blood is low
 High BP 170/95mmHg, high BP can lead to further cardiac problems
The above mentioned vital signs provide a clear idea that Mrs Brown is subjected to
increase in respiratory rates due to low level of saturated oxygen in the body. Based on the above
data it can be clearly stated that there is a clear lack of blood circulation within the body. In
similar regards, it can be seen that the pulse rate is extremely high. In case of high pulse rate, the
body fails to pump the blood effectively to the rest of the body parts. The lack of proper
circulation can deprive the organs of oxygen leading to shortness of breath (Münzel et al. 2015)
In regards, to increase in blood pressure in Mrs. Brown, it becomes important to note the
fact that if blood pressure is left untreated, can lead to problems such as cardia issues. After
analysing the condition of Mrs. Brown, it becomes easier to understand the fact that she
definitely suffers from serious cardiac ailments. However, based on further analysis through
ECG monitor, it was found that Mrs. Brown was suffering from chronic systolic heart failure. On

HEALTH VARIATION 3 6
the basis of condition understood and evaluated through the use of electrocardiography, it can be
easily stated that chronic systolic heart failure can be termed as a condition that is marked by a
weak left ventricle. As stated by Keteyian et al. (2015), the chances of a weak left ventricle are
prominent as it is the left ventricle that pumps out maximum amount of blood. The reason for
such weak left ventricle can be attributed to the fact of increase in size. Thus, as opined by
Niewinski et al. (2017), due to increase in size, the ventricle fails to contract properly, and push
enough blood to the body
Some of the prominent causes of systolic heart failure are as follows. Firstly, high blood
pressure can be termed as common cause of systolic heart failure coupled with cardiomyopathy.
Thus, it can be seen that Mrs. Brown had both the condition and systolic heart failure is a
confirmed ailment in the mentioned case scenario. It is for the same recommended it is important
to ensure proper medical care as per the medical condition and history of the patient
Question 2
Given the high frequency of systolic heart failures, the nurses from specialities and even
settings are likely to be involved in managing patients suffering from heart failure. The first
intervention that can be undertaken for initiating a proper care is understanding the vital signs.
As influenced by Tayal, Prasad, and Cook (2017), vital signs must be understood properly, in
order to make sure what are the potential requirements of the patients. In the mentioned case
study, on recognising the vital signs the medication or even the basic treatment can be provided.
Thus, it can be stated the condition of Mrs. Brown is acute and thus, the treatment for treating the
condition must be appropriate (Heartfoundation.org.au, 2018)
The main stream of the treatment is to offload the fluid through the use of intravenous
injections, often making use of diuretics combined with nitroglycerin. However, the selection of

HEALTH VARIATION 3 7
drugs is based on the condition of Mrs. Brown. As mentioned by nitroglycerin is often used by
individuals suffering from cardiac ailments. Furthermore, it can be seen that drug selection is
based on patient’s heart condition and even weight. In long term nursing intervention, the patient
needs to be weighed on regular basis and input output of fluid must be charted to check whether
the medication is likely to cause any adverse effect on the renal system (Van Tassell et al. 2017)
In case of Mrs. Brown she reported breathlessness, this can be a matter of concern. The
use of nasal cannula can be used for increasing the level oxygen saturation within the body.
However, Zipes et al. (2016), presented the fact that nasal cannula can have low level of effect
usually slow on the patient. Hence, for faster results, non-invasive ventilation is required with
the use of tight face mask. In addition to that, nurses need to be sure, about the psychological
impact of heart failure (Hill, Hall & Glew. 2016). Providing comfort and even reassurance is
important as Mrs. Brown may suffer from anxiety due to breathlessness
Question 3
Mechanism of action of furosemide
As per Galbraith et al. (2015), furosemide can be termed as a loop loop that controls the
reabsorption of water within the nephron by causing a hindrance for sodium-potassium-chloride
cotransporter, within the loop of Henle (thick limb). The mentioned phenomenon is achieved
through the use of competitive inhibition at chloride binding site, preventing the transfer of
sodium. The lumen becomes hypertonic and the interstitium, hypotonic diminishing osmotic
gradation, facilitating reabsorption of water through nephron. Furosemide acts as a very potent
diuretic (Memon et al. 2017).
Mechanism of action of glyceryl trinitrate.

HEALTH VARIATION 3 8
Nitroglycerin is transformed by “mitochondrial aldehyde dehydrogenase” or mtALDH
into NO (nitric oxide). NO can be termed as an active substance that activates guanylate cyclase.
Activation of guanylate cyclase leads to synthesis of cGMP, triggering a synthesis of
phosphorylation dependent on protein kinase. The process results in phosphorylation, within the
smooth cardiac muscles causing relaxation even increase blood flow. The above process results
in decreased work of heart, coupled with decrease in blood pressure and equal blood distribution
to myocardium.
In worst case scenario, these drugs can lead to nausea, dizziness and even flushing.
However, these symptoms can indicate the body adjusting to the medication and need not be a
cause of worry (Zipes et al 2016). However, the interaction between the drugs provide a clear
idea that furosemide can lead to severe venodilator effect, preceding the diuretic effect. These
things must be taken into consideration while providing medicinal drugs

HEALTH VARIATION 3 9
Reference list
Cowie, M. R., Woehrle, H., Wegscheider, K., Angermann, C., d’Ortho, M. P., Erdmann, E., ... &
Teschler, H. (2015). Adaptive servo-ventilation for central sleep apnea in systolic heart
failure. New England Journal of Medicine, 373(12), 1095-1105.
Galbraith, A., Bullock, S., Manias, E., Hunt, B., & Richards, A. (2015). Fundamentals of
Pharmacology: An applied approach for nursing and health. Routledge.
Heartfoundation.org.au (2018) Improving diagnosis and care for heart failure patients Retrieved
from: https://www.heartfoundation.org.au/for-professionals/clinical-information/heart-
failure [Retrieved on: 1 Aug. 2019]
Hill, R., Hall, H., & Glew, P. (2016). Fundamentals of Nursing and Midwifery: A person-
centred approach to care. Wolters Kulwer.
Jankowska, E. A., Tkaczyszyn, M., Suchocki, T., Drozd, M., von Haehling, S., Doehner, W., ...
& Ponikowski, P. (2016). Effects of intravenous iron therapy in iron‐deficient patients
with systolic heart failure: a meta‐analysis of randomized controlled trials. European
journal of heart failure, 18(7), 786-795.
Keteyian, S. J., Patel, M., Kraus, W. E., Brawner, C. A., McConnell, T. R., Piña, I. L., ... &
Chase, P. J. (2016). Variables measured during cardiopulmonary exercise testing as
predictors of mortality in chronic systolic heart failure. Journal of the American College
of Cardiology, 67(7), 780-789.

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Køber, L., Thune, J. J., Nielsen, J. C., Haarbo, J., Videbæk, L., Korup, E., ... & Eiskjær, H.
(2016). Defibrillator implantation in patients with nonischemic systolic heart failure. New
England Journal of Medicine, 375(13), 1221-1230.
Leach, J. P., Heallen, T., Zhang, M., Rahmani, M., Morikawa, Y., Hill, M. C., ... & Martin, J. F.
(2017). Hippo pathway deficiency reverses systolic heart failure after
infarction. Nature, 550(7675), 260.
Memon, A., Sharma, P., Gilbert, J., Pettyjohn, E., Whelan, M., Nyamndi, B., ... & Carter, W.
(2018). Evaluation of Clinical and Social Factors for Patients Taking Very Low Dose of
Beta Blockers for Systolic Heart Failure. Circulation: Cardiovascular Quality and
Outcomes, 11(suppl_1), A164-A164.
Münzel, T., Gori, T., Keaney Jr, J. F., Maack, C., & Daiber, A. (2015). Pathophysiological role
of oxidative stress in systolic and diastolic heart failure and its therapeutic
implications. European heart journal, 36(38), 2555-2564.
Niewinski, P., Janczak, D., Rucinski, A., Tubek, S., Engelman, Z. J., Piesiak, P., ... & Javaheri,
S. (2017). Carotid body resection for sympathetic modulation in systolic heart failure:
results from first‐in‐man study. European journal of heart failure, 19(3), 391-400.
Shier, D., Butler, J., & Lewis, R. (2015). Hole's essentials of human anatomy & physiology. New
York: McGraw-Hill Education.
Tang, W. W., Wang, Z., Shrestha, K., Borowski, A. G., Wu, Y., Troughton, R. W., ... & Hazen,
S. L. (2015). Intestinal microbiota-dependent phosphatidylcholine metabolites, diastolic
dysfunction, and adverse clinical outcomes in chronic systolic heart failure. Journal of
cardiac failure, 21(2), 91-96.

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Tayal, U., Prasad, S., & Cook, S. A. (2017). Genetics and genomics of dilated cardiomyopathy
and systolic heart failure. Genome medicine, 9(1), 20.
Van Tassell, B. W., Canada, J., Carbone, S., Trankle, C., Buckley, L., Oddi Erdle, C., ... &
Schatz, A. (2017). Interleukin-1 blockade in recently decompensated systolic heart
failure: results from REDHART (Recently Decompensated Heart Failure Anakinra
Response Trial). Circulation: Heart Failure, 10(11), e004373.
Zipes, D. P., Neuzil, P., Theres, H., Caraway, D., Mann, D. L., Mannheimer, C., ... & Sarazin, S.
A. (2016). Determining the feasibility of spinal cord neuromodulation for the treatment of
chronic systolic heart failure: the DEFEAT-HF study. JACC: Heart Failure, 4(2), 129-
136.