Answer :

INTRODUCTION

The document is a report based on the case of Deependra Sidhu, a 68-year-old male admitted with a complaint of breathlessness and pain in the chest (8/10 pain score). He has past medical history of Myocardial infarction, Stable Angina, Hypertension, Hypercholesteremia, and Type 2 Diabetes Mellitus. His Current Medications includes Aspirin 100mg mane, Atenolol 25mg mane, Furosemide 40 mg, Pravastatin 40mg oral. Deep works three days a week but would like to retire soon. He has treatment compliance issues with Lasix due to a complaint of frequent urination. His vitals on examination were HR 90, regular; BP 145/85; Skin – sweaty and pale, RR 26, regular; SpO2 94% RA; Temp. 36.7oC; Oedematous legs, moderate pitting oedema . ECG, troponin T and MKMB blood were advised. He was later diagnosed with heart failure.

The report demonstrates the understanding of the scenario's pathophysiology, pharmacology, and psychosocial aspects by answering the questions.

RATIONALE FOR ECG

As deep is presented with signs and symptoms including acute chest pain, skin pale and sweaty, edematous legs with pitting edema and altered significant findings (HR 110, BP 85/50), the ECG becomes a vital assessment in understanding the ischemic cause of pain in the chest. Deep is also having a history of conditions like hypertension, diabetes and angina with MI in 2017, these act as the risk factors for probable heart failure; hence it becomes necessary to conduct ECG for understanding the cardiovascular cause of his current complaints (Sawai et al., 2017). As per the management of acute coronary syndromes, the most critical consideration in the patients having a positive history for risk factors like Deep the first and foremost assessment should be to establish the ECG diagnosis (Sawai et al., 2017). The nurse has advised blood test preparation for analysing the biochemical markers for myocardial injury, including cardiac troponins (troponin I and T subtypes) for establishing the diagnosis for Myocardial infarction. They both are advised for diagnostic algorithm improving the efficacy of triaging substantially and so that patients with high-risk outcomes can be identified and immediate percutaneous coronary interventions can be recommended to them avoiding eth life-threatening situation (Sattar & Chhabra, 2021).

PATHOPHYSIOLOGY OF HEART FAILURE

Heart failure is a condition with diverse etiologies and mechanism; it is defined as the heart's inability to pump the blood maintained at a sufficient rate to meet the body's metabolic demands, including nutritional and oxygen (Inamdar & Inamdar, 2016). It is known that heart failure is prevalent among individuals with comorbidities, including hypertension, coronary artery disease, pulmonary hypertension and cardiovascular disease such as diabetes. With these causative factors, complex cardiac, vascular and systemic dysfunctions occur, resulting in heart failure. The heart must undergo relaxation for proper blood flow during diastole and contraction during systole, depending on the heart's functional myocardium (Malik et al., 2021). Heart failure affects the left or right ventricle and is referred to as left or right heart failure.

Cause:

The aetiology of heart failure is diverse and may vary as per race, ethnicity and gender. The understanding of the cause of heart dysfunction plays an essential role in determining the course of treatment (Inamdar & Inamdar, 2016). The cause of heart failure can be broadly divided into diseased myocardium, Abnormal loading and Arrhythmias. The diseased myocardium includes causes including coronary artery disease, alcoholic myopathies, infections, auto-immune mediated disease, and genetic abnormalities, including Muscular dystrophies and ventricular myopathies (Malik et al., 2021). The abnormal loading causes are hypertension, congenital valvular abnormalities, pericarditis, renal failure and high output, causing conditions like thyrotoxicosis and anaemia. These arrhythmias are also the known cause of heart failure, which includes sinus node and conduction disorders (Hajouli & Ludhwani, 2021). In Deeps case, the presence of the past medical history of Myocardial infarction, hypertension, hypercholesteremia, type 2 diabetes has predisposed the development of heart failure (Chahine & Alvey, 2021).

Process

In response to etiological events, the left ventricle load is increased, and the myocardium becomes hypertrophied. This increased size and number of myocytes raise the demand for oxygen resulting in increase oxygen diffusion (Hajouli & Ludhwani, 2021). In this process, few muscle fibres become ischemic, causing fibrosis and stiffness, hence reducing contractility (Chahine & Alvey, 2021). The increased workload causes the ventricle to dilate and stretch, exerting additional load on the ventricle to maintain the cardiac output. The reduced contractibility of heart and end-diastole pressure increases the pressure in the pulmonary veins causing pulmonary oedema (Hajouli & Ludhwani, 2021). The increased pulmonary pressure raises the pressure on the right ventricle, and the hypertrophy, ischemia and fibrosis of the right ventricle also appear, affecting the contractibility, and heart failure develops (Malik et al., 2021).

Outcome

Inpatient with heart failure, the cardiac output is reduced, resulting in activation of the compensatory mechanism, namely the sympathetic compensatory mechanism, Renin-angiotensin-aldosterone (RAA) compensatory mechanism and Frank-Starling mechanism (Chahine & Alvey, 2021). As deep is having reduced blood pressure indicated through his vitals, the baroreceptor sense the decrease in the blood pressure leading to activation of the sympathetic compensatory mechanism and release of catecholamine, ultimately stimulating the beta-adrenoreceptor cells responsible for increasing the heart rate, contraction and stroke volume increasing the cardiac output (Hajouli & Ludhwani, 2021). In response to heart failure, the stretch of cardiac muscle increases contraction force, increasing the myocardial oxygen demand (Frank-starling mechanism).

As the reduced blood pressure is established, the under perfusion is detected by the kidneys releasing the RAA pathway responsible for controlling electrolyte balance (Hajouli & Ludhwani, 2021). This results in peripheral vasoconstriction and salt and fluid retention, evidenced in the Deep case in the form of peripheral pitting oedema. Adequate renal vasoconstriction causes the decreased renal perfusion and eventually renal failure. Fluid retention also increases the preload and afterload, further exerting pressure on the left ventricle.

Left ventricular failure

In heart failure involving the left ventricle dysfunction, the cardiac output decreases and the pulmonary venous pressure increase when this pressure exceeds the oncotic pressure of 

plasm protein, the fluid moves out from the capillaries into the interstitial space reducing pulmonary compliance resulting in laboured breathing (Chahine & Alvey, 2021).

Right ventricle failure

This appears secondary to pulmonary hypertension, pulmonary embolism and congenital heart disease. The stated conditions caused the enlargement of the right ventricle, called Cor pulmonale, caused by hypoxic vasoconstriction and pulmonary hypertension (Hajouli & Ludhwani, 2021).

INTERPRETATION OF ECG

Heart rate can be calculated by multiplying the number of boxes between the QRS complex and dividing it to 300. That is, in the given EKG, the number of boxes between two QRS complexes is four; hence the rate is 300/4 = 75bmp

As the number of boxes through the EKG strip between the QRS complex is the same, the rhythm is regular.

The p wave is present, regular and followed by QRS complex

ST wave is elevated

In lead v6 and v5, there is marked ST- elevation; hence it is st wave elevation myocardial infarction.

PHYSIOLOGY OF HEART FAILURE

Deep's shortness of breath results from impaired lung and systemic organ perfusion and reduced cardiac output in heart failure. In response to decreased contractibility of heart muscles, the pressure within the blood vessels is increased. The increase in the pulmonary venous pressure moves out the fluid from interstitial spaces reducing pulmonary compliance and causing pulmonary oedema (Chahine & Alvey, 2021).. The raised left ventricular filling pressure increases to maintain the cardiac output resulting in increased pulmonary diffusion. Decreased pulmonary function with increased pulmonary pressure impairs the gaseous exchange between the alveoli and capillaries, causing difficulty and shortness of breath (Malik et al., 2021).

Deep has been skipping his medication Lasix that must have been prescribed to him for his condition, including hypertension. Lasix is a diuretic containing furosemide as the active ingredient prescribed to reduce fluid retention symptoms by reducing the pressure on the heart through its diuretic effect (Khan et al., 2021). The second mistake is not sharing the detailed information of OT medications he has taken. As he has taken Viagra with active ingredient sildenafil, it could have affected cardiac contractility, blood pressure and heart rate. If the patient has taken sildenafil recently, then nitrates should not be administered within 24 hours period to prevent the risk of hypotension (Smith & Babos, 2021)..

PHARMACODYNAMICS OF VIAGRA AND NITRATES

Response: I understand that you need your time in sharing information; however, if taking any over the counter medication, including Viagra, it is always necessary to disclose it when asked by healthcare professionals.

Rationale: Disclosing about Viagra could be challenging for the patient due to cultural and social viewpoints; however, Viagra has been found to accelerate heart failure and is known for its life-threatening hypotensive effect when taken with nitrates.

Viagra (sildenafil citrate) is a class V phosphodiesterase inhibitor drug used for penile erections and endothelium mediated vasodilatation (Smith & Babos, 2021). Phosphodiesterase inhibitor group of medicines is known to prevent cGMP breakdown (cyclic guanosine monophosphate), whereas Glyceryl Trinitrate also releases Nitric oxide increases the production of cGMP. When both these are co-administered, it generates an excessive accumulation of CGMP, causing vascular smooth muscle relaxation resulting in severe hypertension (Skeith et al., 2013). Therefore, PDE5I drug, including Viagra, should not be used along with nitrates, including nitroglycerin, glyceryl trinitrate and isosorbide mononitrate. The duration of contradiction of nitrate administration should be 24 hours, six half-lives after sildenafil intake, allowing full clearance of the drug from the body (Smith & Babos, 2021)..

Two factors that might have potentially led Deep with-holding the information, such as taking Viagra, could be due to cultural sensitivity towards taking sexual dysfunction medications, and the second factor may be related to incomplete information regarding significance or precaution while taking Viagra along with other medication that has been prescribed to him (Potki et al., 2017).

ATENOLOL AND FUROSEMIDE ORAL  

NON-COMPLIANCE TO TREATMENT

Meraz, 2019, observed that in some cases, the non-adherence was the result of forgetfulness, especially in older adults; however, in most cases, the result was primarily due to intentional avoiding the medicine deliberately taking medicine in different dose or regime as prescribed. The author suggested that medication adherence have several challenges for patients requiring long term medicine support cost and side effect have the significant role. Gilstrap et al., 2018 analysed chronic oedema and renal insufficiency as the cause of non-adherence of diuretics like frusemide. Kefala et al., 2018 emphasised that the patient's socio-economic status is a significant determinant factor in non-adherence of medication when given in combination with other drugs in hypertension. 

Yes, in Deep's case, most of the reasons for non-adherence are applicable. He has faced side effects of drugs forcing him to frequent urination; hence he stopped taking medications to avoid disturbance at her workplace. Also, he has family responsibilities that might restrict medication adherence. 

As a nurse, explain that furosemide can control hypertension but cannot cure it; hence, medication continuity is essential. Assist him in the suitable time for taking medication. Educate him on taking medication four hours before bedtime and his office time to avoid disrupting sleep and any activity (Kefale et al., 2018). With blood pressure is controlled, lower doses of Lasix can be used if recommended by the physician. Instruct to take medication as recommended and do not self medicate or double dose in case a dose is missed. Change the position slowly to reduce the risk of orthostatic hypotension (Gilstrap et al., 2018).

Conclusion

Through Deep's case presenting the heart failure and history hypertension, there are several aspects of Pathophysiology and Pharmacology that can be identified, analysed and evaluated for best patient outcomes. When administering to the patient, each medication has a particular course of action and interaction, which should be paid keen attention to avoid complications. In case of minor complications, as Deep was facing in the form of frequent urination appropriate counselling should be provided to encourage therapeutic adherence