This assessment is meant to assist students in:1.
In visual format (conceptmap), explain the causes, pathogenesis of clinical manifestations, diagnosis procedures, management, course and prognosis.2.
Describe the pathophysiology that causes the clinical manifestations associated with acute exacerbation chronic left-sided cardiac failure.3.
Discuss nursing strategies, evidence-based arguments and how to manage patients with acute exacerbations of chronic left-sided cardiac failure (acute pulmonary oedema).4.
Please describe the nursing role as well as responsibilities for the use of pharmacological intervention in an acute exacerbation or chronic left-sided cardiac failure.
Answer to Question: 401015 Health Variations 3
Mrs. Brown was a patient with several clinical manifestations.
High respiratory rates, breathing difficulties, breathing difficulties, etc.
24 breaths/minute, low oxygen saturation in the air. SpO2 85 %, high BP, 170/95 mmHg, high HR, i.e.
120 beats per hour, auscultation to the lungs identifies bilateral bases crackles.
Arial fibrillation was diagnosed when the ECG monitor was connected to her. This indicates that she has suffered from acute left-sided chronic heart failure.
In this context, left-sided cardiac failure can be explained by the decreased ability of the left chambers of the heart to pump oxygen rich blood throughout a person’s body.
Mrs. Brown describes fatigue as one of the symptoms of left-sided heart failure. This is because the left side of your heart has a reduced ability to work.
The other side of the coin is that as blood flows through the left-sided chambers of your heart, it decreases the pressure in your lungs, which leads to fluid accumulation and shortness.
Mrs. Brown had symptoms of shortness in her breathing since the morning. She was admitted to hospital’s emergency room (Allen, et al. (2012).
The heart fails occurs when the heart cannot produce sufficient cardiac output to satisfy the body’s needs.
It is caused when the structure or function of the heart fails to function properly.
It is caused by damage to heart tissue.
The left heart disease can lead to a reduction in blood flow from the heart to the brain, and elsewhere in the body.
Left ventricular disease is life-threatening.
The development of left heart disease can occur for many reasons, including alcohol abuse, fluid overload, systemic hypertension and hypothyroidism.
As left-sided cardiac failure progresses in severity, it will cause changes to the heart’s structure as well as function.
In one instance, fibrous tissue damage is increased due to changes in cellular function and cellular apoptosis.
Due to the overloading of ventricle, contractility (or ability to contract frequently) is decreased (Vachiery, et al. 2013, 2013).
The reduced ability of the heart muscle to contract efficiently due to over-stretching, the ventricle is filled with blood.
Stroke volume decreases due to failures of diastole, systole or both.
Reduced compliance leads to decreased diastolic volume at the end.
In contrast, decreased contractility results in an increase of the systolic size.
Hypertrophy, another manifestation of the disease, is also a physical manifestation. This refers to the condition in which myocardium grows larger due to an attempt of improving contractility.
It can be caused by an increase of terminally distinct heart muscle fibres.
These results may lead to increased stiffness or decreased ability to relax during diastole.
The common effects are decreased cardiac output and greater strain on the heart. This increases the risk of cardiac arrhythmia (Daubert et. al., 2012).
The symptoms include fatigue, shortness of breath, weakening, rapid pulse and fluid retention.
Mrs. Brown can confirm her condition with clinical evidence.
These are the two top priority nursing strategies Mrs. Brown has to manage and why they are so important.Strategy
ArgumentsControl cardiac outputEvaluate heart rate, apical pulse, note dysrhythmia
The risk of having further attacks is increased by the commonality of atrial fibrillation (tachycardia)Palpate peripheral pulse
Increased cardiac output may cause irregular palpitations or radial pulses (Gheorghiade.
Monitor blood pressure
A higher systematic vascular resistance increases blood pressure. The side effects of medication can also include hypotension
Proper ventilation and tissue oxygenationMonitor arterial blood gases
Hypoxemia in cases of severe pulmonary edema could result in hypoxemia. However, compensatory changes can be seen in HF (Schwartzenberg und al., 2012).
Auscultate breath sound, note wheezes & crackles
Congestion of the lungs can be caused by fluid buildup or accumulation.
Make sure you get a good night’s rest.
It will improve lung inflation by reducing oxygen demand.
Two medications were given to Ms. Brown:
Injectable furosemide, and sublingual glycocer trinitrate were given to Ms.
The IV furosemide is part of a diuretic class of medications that helps the body get rid excess water and salt through the urine.
The heart can perform its normal functions and maintain blood pressure easily.
It’s used to treat fluid buildup or high blood pressure in left-sided cardiac failure (Fitzgerald. et. al., 2011).
It is similar to other loop diuretics in that it inhibits N-K-Cl2 (Luminal N-K-Cl Cotransporter) located at the thick ascending end of Henle’s loop. However, this does not prevent the action on carbonic anhydrase and aldosterone.
It can block the negative or positive free water clearance and also abolishes the corticomedullary anosmotic slope.
McKelvie et. al., (2013).
Furosamide can inhibit GABA-evoked GABA a6b2g2 even when it is in very low amounts. This is due to Henle’s loop’s large NaCl absorption capability.
Glyceryl trinitrate can be used to reduce the ventricular pressure. In high doses, however, it decreases the systematic vascular resistance.
Its main action is relaxation of the vascular smooth muscle. This results in dilation and expansion of the post-capillary beds.
The dilation and return of blood to the heart via dilation in the post capillary beds results in a reduction in left ventricular or end diastolic pressures (Bui Horwich & Fonarow 2011).
GTN should not mixed with other drugs. This will eliminate the risk of drug reactions.
Administration should prefer central routes. This includes strict monitoring of BP CVP, HR and capillary refill, fluid intakes, and outputs (Felker et.al., 2011).
Mrs. Brown might experience side effects such tachycardia. hypotension, bradycardia.
Furosemide must be administered intramuscularly (or intravenously) if it is to be used in combination with corticosteroids.
Furosemide should not mixed with anesthesics. It can interact with other drugs (Heidenreich und al., 2013).
Mrs. Brown’s side effects should be monitored carefully, including electrolyte imbalance or dehydration.
As overdose could cause kidney damage, or even collapse, it is important to follow the recommended dosage.
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