Pathogenesis And Pathophysiology Of Congestive Heart Failure
The notable symptoms, history and nursing assessments of Mr Aloha Das can infer him to be affected with congestive heart failure.
An adult mammalian’s heart has negligible regenerative capability, which would lead to the formation of scars despite gradual healing of the heart with time (Rickenbacher et al., 2017). The cascades of inflammation can determine the level of “infarct healing’ standard while released alarmins from numerous dying cells trigger the reaction. As matrix debris and dead cells is cleared by phagocytic infiltration through activation of anti-inflammation pathways, it leads to suppression of the signalling of chemokines and cytokines. “Renin-angiotensin-aldosterone systems” are further activated to release transformation proteins like the ‘growth β factor’ to consequently lead to the conversion of fibroblasts to different myofibroblasts (Gawrys et al., 2018)Pathogenesis And Pathophysiology Of Congestive Heart Failure. The process of depositing proteins of the extracellular matrix is promoted. “Infarct healing” causes hypertrophy of various viable factors, progressive dysfunction and dilation.
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Congestive failure of the heart happens for different abnormalities like pressure overload and excessive volume build up, inducing the contractility of the heart muscles. It causes lowered cardiac output wherein there is an intrinsic decrease if the muscle contractility, along with an increase in pulmonary congestion or dyspnea. The reduced “systemic blood pressure” results in an enhancement of systemic resistance, thereby aiding a decrease of cardiac output. Consequently, heart rate starts to increase as it is linked to circulating catecholamines.
There is an involvement of a cascade of various mechanisms for the early events in congestive heart failures through maintenance of cardiac outcomes and meeting the systemic demands. It includes, for instance, myocardial hypertrophy, Frank Starling mechanism, hyper contractility, and myocyte regeneration (Malik et al.,2021). The reduced cardiac outputs cause a stimulation for the neuroendocrine system to be releasing epinephrine, norepinephrine, endothelin-1, and vasopressin. This increases afterload through vasoconstriction. The increase of “cAMP (cyclic adenosine monophosphate)” causes an increase in the myocytic cytosolic calcium. Thereby, it stops myocardial relaxation. The enhancement of afterload and myocardial contractility leads to a myocardial oxygen demand. The requirement for the risen cardiac output will lead to cell death and myocardial apoptosis. The reduction of cardiac output would stimulate the RAAS system as discussed above. The secreted Angiotension-II from the system causes an increase in the myocardial cellular hypertrophy along with interstitial fibrosis (Malik et al., 2021)Pathogenesis And Pathophysiology Of Congestive Heart Failure.
Kidneys respond through the retention of excessive sodium and fluid. This fluid can build up in legs, ankles, feet, and lungs as well amongst various body organs, inducing congestive heart failure. Mr. Aloha Das’s ECG also suggests hypertrophy occurring in the left ventricle, poorly progressing R wave, pathological Q wave influencing ST and T segments.
Congestive Heart Failure And Pathology
Nursing investigations, managerial options, and practice implications, assist nurses to play a big role in supporting, informing and advising patients like Aloha Das. In this case, the high-quality intervention of nursing chosen for Mr Aloha Das will be Oxygen Therapy. The nurse would require to administer oxygen for relieving signs and symptoms in the patient. Healthy oxygen levels are indicated to be in between 95-100%. Normally patients are able to receive oxygen flow up to 15 liters, however critical states like that of Aloha Das 40-60 liters of oxygen can be administered for him. Supplemental oxygen has been routinely used for the treatment of patients inflicted by congestive heart failures, and myocardial infarctions, as per clinical recommendations (Masip et al., 2018). Oxygen can be inhaled by the patient as per delivery through mask or nasal cannula, at every concentration. It is essential that oxygen is delivered immediately as the flow of the oxygenated blood flow in the heart gets interrupted for large intervals of time.
Oxygen provision can make Mr. Aloha Das, the concerned patient, portray an improvement of ‘ischemic myocardial tissue” oxygenation and reduction of symptoms such as pain, infarct size, issues of morbidity and mortality (Harjola et al., 2017)Pathogenesis And Pathophysiology Of Congestive Heart Failure. Without oxygen administration, the insufficient level of oxygen reaching up to the heart will lead to the complete failure of the heart or fatal strokes.
Furosemide 40mg IV Stat
Furosemide is found to be a diuretic potently working for the enhancement of water and Na+ excretion from the kidneys for the inhibited reabsorption from proximal and distant tubules, along with the Loop of Henle. It acts on nephron cells directly while altering the renal filtrate content (Dillon 2020).
Furosemide is administered on the need of prompt diuresis, as observed in Aloha Das’s case. This emergency case displays pertinent symptoms of cardiac disease led oedema, and pulmonary oedema for acute failures of the heart. It is used in hypertensive crises observed in patients as well.
Nursing consideration involves the maximum administration dose to 1500 mg (Sica et al., 2018)Pathogenesis And Pathophysiology Of Congestive Heart Failure. It is administered through infusions, where undiluted administration can be utilized as constant pumps of rate infusion, or the dilution can be increased by compatible carrier fluids such as Ringer solutions or NaCl injections. The rate of infusion cannot be over 4 mg/min. Dosages should be adapting to body weight correctly.
Expected response for this medicine entails induction of an increased urine output. Treatment will assist in fluid retention and swelling, that results out of congestive heart failure. It leads to the clinical observation wherein inhibition of electrolyte reabsorption occurs and enhances excretion of water from body (Emmens et al., 2022). The blood pressure will be under check for Aloha Das.
Nursing Interventions For Mr. Aloha Das
“Glyceryl Trinitrate IV Infusion 10 mcg/min”
Glyceryl trinitrate helps in reducing tones of vascular smooth muscles. It occurs in the vessels of venous capacitance rather than the arterial vessels. Consequently, there is decreased venous return in the heart and lowering of elevated filling pressures. Glyceryl trinitrate works as a vasodilating agent enhancing the dilation of arterial and venous beds (Lewis et al., 2017)Pathogenesis And Pathophysiology Of Congestive Heart Failure. Blood vessel relaxation leads to promotion of the heart’s oxygen supply.
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As for the case patient Aloha Das, the administered dosage of the Glyceryl Trinitrate can treat unresponsive and congestive heart failures, left-sided heart failures, myocardial infarctions, including control of hypertensive states.
Nursing considerations should entail evaluating therapeutic effects as patients on long-acting or transdermal preparation commonly develop lowered therapeutic impact or tolerance induction. Transdermal systems containing metals needs to be removed effectively before cardioversion or diathermy. The blood pressure should be checked in regular intervals.
It is given to patients in slow undiluted intravenous infusions. GTN infusions helps in treatment of acute failure of the left ventricle. Clinical responses trace the lowering of cardiac output and preload for reducing spasms in coronary artery, reducing vascular resistance systemically, along with associated systolic and diastolic blood pressure (Divakaran & Loscalzo, 2017). Notable observations include rising heartbeat in patients Pathogenesis And Pathophysiology Of Congestive Heart Failure