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1. Outline the disease, causes, incidence and risk factors. Discuss the impact of the selected disease on the patient and their family

2. Discuss three (3) common signs and symptoms of the selected disease and explain the underlying pathophysiology of each
a. This can be done in the form of a table – each point needs to be appropriately referenced
3. Discuss the pharmacodynamics & pharmacokinetics of one (1) common class of drug relevant to the chosen patient
a. This does not mean specific drugs but rather the class that these drugs belong to.
4. In order of priority, develop a nursing care plan for your chosen patient who has just arrived on the ward from ED. Nursing care plan goals, interventions and rationales must relate to the first 8 hours post ward admission

Causes of Congestive Cardiac Failure

Congestive Cardiac Failure (CCF), often referred to as Congestive Heart Failure (CHF), is a disorder in which the role of the heart as a pump is insufficient to cater for the body’s needs. Several disease progressions can damage the pumping effectiveness of the heart to cause congestive heart failure (Burg, 2018).

Heart failure is caused by various illnesses that impair the heart muscle, comprising:

Coronary artery disease (CAD), an illness of the arteries that stream blood and oxygen to the heart, leads to reduced blood current to the heart muscle. If the arteries are obstructed or sternly constricted, the heart becomes ravenous for oxygen and nutrients (Bartunek et al., 2018). 

A heart attack happens when a coronary artery is precipitously obstructed, preventing the stream of blood to the heart muscle. A heart attack impairs the heart muscle, causing a damaged region that fails to work well (Burg, 2018)

This is impairment to the heart muscle from sources other than artery or blood current complications, like from contaminations or liquor or substance abuse (Al Biltagi 2015).

Disorders comprising high blood pressure, thyroid illness, valve ailment, diabetes, kidney illness, or heart weaknesses existent innately may all occasion heart failure (Keith, 2017). Additionally, heart failure can ensue when numerous illnesses or disorders are existent on one occasion.

Unusual heart paces, they might cause the heart to beat excessively fast, producing extra work for the heart. Ultimately the heart could deteriorate, resulting in heart failure. If the heartbeat is extremely slow not adequate blood could get out from the heart to the body, resulting in heart failure (Dornelas and Sears, 2018).

It is an uneven, repeated rapid heartbeat. A study found that patients with atrial fibrillation have a higher risk of hospitalization owing to heart failure (Meystre, 2017) 

Individuals who are both overweight and have diabetes type 2 have a higher chance risk of suffering from CCF.

Individuals who regularly smoke run a considerably higher risk of developing heart failure.

Studies show that CCF is the primary cause of hospitalization in individuals of above 65 years (Healthcare Financial Management, 2018).

The prevalence of heart failure is considerably higher in males than females according to Burg (2018).

Numerous cardiac illnesses can be hereditary, comprising congenital heart illness, arrhythmias, high blood cholesterol, and cardiomyopathy. Coronary artery disease resulting in heart spasm, stroke, and heart failure may be progressive in families, signifying hereditary genetic possibility aspects (Patel, 2014).

Patients with heart failure have many readmissions to hospice, a poor projection and wavering eminence of life. An investigation indicated that living with heart failure can be terrifying, limiting and disturbing for both patients and their family careers (Keith, 2017). Patients found the most significant trouble dealing with practical constraint and adjusting to living with heart failure. Patients furthermore described specific complications owing to side effects of treatments, co-morbidities, and privation of psychosocial care and rehabilitation facilities.

Diseases That Can Impair the Heart Muscle

Caring for an individual with heart failure frequently has a substantial influence on the mental and physical well-being of family caregivers. Psychosocial care and rehabilitation facilities provided at identification and following a severe occurrence would support families to better cope living with this condition (Maramattom, 2018). 

A mutual outcome in patients with heart failure is an escalated heart pace, roused by augmented sympathetic action to retain a sufficient cardiac output. Primarily, this aids make up for heart failure by preserving blood pressure and perfusion, however puts extra pressure on the myocardium, snowballing coronary perfusion necessities, which may result in the waning of ischemic heart illness. Sympathetic activity can likewise cause possibly serious unusual heart paces. An escalation in the outward dimension of the heart's muscular sheet could ensue. This is occasioned by the fatally separated heart muscle filaments growing in proportion to progress contractility. This can add to the augmented rigidity and consequently lessen the capacity to relax through diastole. Expansion of the ventricles may likewise happen and adds to the increase and sphere-shaped form of the failing heart. The escalation in ventricular capacity also causes a drop in stroke capacity owing to the automatic and ineffective contraction of the heart (Hedau, Chakravarthi, and Reddy, 2018).

The heart of an individual with heart failure could have a lessened potency of contraction owing to overcapacity of the ventricle. In a healthy heart, augmented filling of the ventricle leads to augmented contraction potency (Frank-Starling law of the heart) and consequently an escalation in cardiac output. In heart failure, this mechanism flops, as the ventricle is laden with blood to the point where heart muscle contraction becomes less effective. This is as a result of abridged capacity to cross-link actin and myosin filaments in over-stretched heart muscle (Nebel, and Bjarnason-Wehrens, 2018). 

In severe cardiomyopathy, the results of lessened cardiac output and reduced perfusion turn out to be extra ostensible. The consequential low blood oxygen triggered by pulmonary edema causes vasoconstriction in the pulmonary circulation, which leads to pulmonary hypertension. Because the right ventricle produces way lesser pressures than the left ventricle but produces cardiac output precisely equivalent to the left ventricle, a slight upsurge in pulmonary vascular resistance leads to massive upturn in quantity of task the right ventricle has to perform (Hedau, Chakravarthi, and Reddy, 2018). Conversely, the central mechanism by which left-sided heart failure leads to right-sided heart failure is in fact not precisely comprehended. Some concepts beseech mechanisms that are facilitated by neurohormonal stimulation. Automatic influences might similarly add to it. As the left ventricle enlarges, the intraventricular septum bends into the right ventricle, lessening the volume of the right ventricle.

Symptoms of Congestive Cardiac Failure

Pharmacodynamics and Pharmacokinetics of one common class of drugs used for patients with CCF

Digoxin

Pharmacology

Indication

For the treatment and management of congestive cardiac deficiency, arrhythmias, and heart failure.

Related Disorders

Chronic Atrial Fibrillation, NYHA Class I or II heart failure, protracted heart failure with abridged expulsion fraction (NYHA Class III)

Digoxin, a cardiac glycoside comparable to digitoxin, is used in the treatment of congestive heart failure and supraventricular arrhythmias due to re-entry mechanisms, and to regulate ventricular degree in the management of protracted atrial fibrillation (Bartunek et al., 2018).

Digoxin impedes the Na-K-ATPase sheath thrust, leading to an escalation in intracellular sodium. The sodium-calcium exchanger (NCX) in turn attempts to extrude the sodium and in so doing, pushes in additional calcium. Higher intracellular concentrations of calcium could rouse stimulation of contractile proteins (e.g., actin, myosin) (Maramatton et al., 2018). Digoxin similarly acts on the electrical activity of the heart, snowballing the gradient of phase 4 depolarization, lessening the stroke latent period, and reducing the leading diastolic potential.

Uptake

Uptake of digoxin from the pediatric elixir devising has been verified to be 0.7 to 0.85 complete (0.9 to 1 from the capsules, and 0.6 to 0.8 for tablets) (Meystre et al., 2017).

Protein binding

The protein binding is confirmed to be 25%.

Breakdown

Hepatic (not reliant on the cytochrome P-450 scheme). The end metabolites, which comprise 3 b-digoxigenin, 3-keto-digoxigenin, and their glucuronide and sulfate conjugates, are polar and are proposed to be formed via hydrolysis, oxidation, and conjugation (Hedau, Chakravarthi, and Reddy, 2018).

Digoxin > 3 b-digoxigenin

Digoxin >3-keto-digoxigenin

Path of removal

After intravenous administration to fit undertakes, it was confirmed that 0.5-0.7 of a digoxin dose is emitted unaffected in the urine (Burg, 2018).

Half-life

The expected half-life of the drug is between 31/2 to 5 days.

Harmfulness

Poisonousness comprises ventricular fibrillation or ventricular tachycardia, or progressive brad arrhythmias, or heart block. LD50 = 7.8 mg/kg (orally in mice).

Impacted entities; Human beings and other animals

Nursing care plan goals, interventions, and rationales for the management of patients with Congestive Cardiac Failure within the first 8 hours post ward admission

Desired outcome

Maximized cardiac functionality plus reduced pressure on the cardiovascular scheme. 

Congestive Cardiac Failure Nursing Care Plan

Subjective Data Objective Data

-Breathing difficulties  -Limb edema

-Coughing (yields a pink or white colored phlegm)  -Scrunches in the lung bottoms

-Heart tremors.  -Breath shortness

 -Misperception

  -Possible Atrial Fibrillation on ECG

  -SpO2

  -Cues of reduced perfusion

Pharmacodynamics and Pharmacokinetics of Digoxin

Observe heart pace Get a 12 lead ECG

Patients with CCF often have a small voltage ECG once exterior edema is fixed the ECG increases voltage once more and turns out to be of a normal appearing ECG.
Patients could likewise have Atrial Fibrillation - a disorder where the atria tremor rather than constricting - this may result in the advancement of heart failure (Al-Biltagi et al., 2015).
Could correspondingly observe cues of existing or preceding infarction or ischemia.

  1. Limit sodium consumption

Water trails salinity! The patient has excess liquid in the body and prerequisites to do away with it, limiting the sodium assist with this (Bartunek, 2018).
This implies enlightening the patient on dietetic alterations that should occur and be observed. This may include; 300-600 mg of salt each plateful, shun refined diets, do not put more salt in food. Restraint with saline supernumerary in renal deficiency - it is produced with potassium chloride and could increase sodium levels of the patient.

  1. Observe Brain Natriuretic Peptide (BNP) Average range: <100 pg/mL

Brain natriuretic peptide (BNP): is a hormone produced by the heart. When the heart is strained, it discharges Brain Natriuretic Peptide (Dornelas and Sears, 2018).

  1. Evaluate respiratory function: Pay attention to breathe resonances, Monitor Oxygen capacity, Apply oxygen as required

The liquid may flow back into the lungs and lead to breath shortness, particularly when physical exertion ensues. Be cautious on positioning such patients horizontal as you could position them in respiratory agony (Keith, 2017).
Put the patient on oxygen as required to assist them in maintaining their oxygen capacities sufficient - regularly higher than 92% or as recommended by the physician.

Edema is occurs as a result of capacity surplus owing to blockage inside the scheme. Deteriorating edema could designate waning heart failure.

Edema is evaluated by pressing over a lean distinction, typically the tibia or the uppermost foot  and is recorded by a numeral and if the membrane springs back or remains pitted (termed pitting edema) (Patel et al., 2014).

Non-pitting – does not remain pitted

+1: minor pit, 2mm

+2: Temperate pit, 4mm

+3: Profound indent, 6mm

+4: Very profound pit, 8mm

Such patients are supposed to take approximately 8 glasses of liquid only or faintly below two liters of liquid daily (Nebel, and Bjarnason-Wehrens, 2018). This can vary per patient and physician commendation, so ensure to get an objective from the doctor.

Stringent I&O means quantifying each droplet that is taken in and discharged by the patient.

Advise the patient to take a glass at a go and to give info on the number taken.

Place a cap in the lavatory if the patient has restroom freedoms.

Be conversant with popular drink alternatives and respective capacities (squash, coffee, milk, etc.) 

References 

Al-Biltagi, M. S. (2015). Echocardiographic assessment of left ventricular dyssynchrony in Egyptian children with congestive heart failure due to dilated cardiomyopathy. Cardiology in the Young, 25(6), 1173–1181. https://doi.org/10.1017/S1047951114001863

Bartunek, J. (2018). Clinical Experience With Regenerative Therapy in Heart Failure. Canadian Modern Language Review, 1344–1346. https://doi.org/10.1161/CIRCRESAHA.118.312753

Burg, M. M. (2018). Addressing end-of-life cardiac care. In Psychological treatment of cardiac patients. (pp. 137–146). Washington, DC: American Psychological Association. https://doi.org/10.1037/0000070-010

Burg, M. M. (2018). Social support and the impact of coronary heart disease on the family. In Psychological treatment of cardiac patients. (pp. 121–136). Washington, DC: American Psychological Association. https://doi.org/10.1037/0000070-009

Dornelas, E. A., & Sears, S. F. (2018). Living with heart despite recurrent challenges: Psychological care for adults with advanced cardiac disease. American Psychologist, 73(8), 1007–1018. https://doi.org/10.1037/amp0000318

Hedau, S., Chakravarthi, R., & Reddy, V. (2018). Ultrafiltration by Peritoneal Route in Refractory Chronic Congestive Cardiac Failure. Indian Journal of Nephrology, 28(4), 298–302. https://doi.org/10.4103/ijn.IJN_12_17

Keith, F. (2017). Anger, hostility, and hospitalizations in patients with heart failure. Health Psychology, 36(9), 829–838. https://doi.org/10.1037/hea0000519

Maramattom, B. V., Joseph, S., Bhattacharjee, S., Kumar, A., & Sreekumar, P. (2018). A Hot Body in a Cold Room Hyperthermia Secondary to Rapid Diuresis in Cardiac Failure; the Perils of Rapid Fluid Shifts. Indian Journal of Critical Care Medicine, 22(8), 608–610. https://doi.org/10.4103/ijccm.IJCCM_179_18

Meystre, S. M., Youngjun Kim, Gobbel, G. T., Matheny, M. E., Redd, A., Bray, B. E., … Kim, Y. (2017). Congestive heart failure information extraction framework for automated treatment performance measures assessment. Journal of the American Medical Informatics Association, 24(e1), e40–e46. https://doi.org/10.1093/jamia/ocw097

Nebel, R., & Bjarnason-Wehrens, B. (2018). High Intensity Interval Training in CHD-Patients with Chronic Heart Failure (CHF-HFrEF). / Hochintensives Intervalltraining bei Patienten mit koronarer Herzerkrankung (KHK) mit Herzinsuffizienz (CHF-HFrEF). German Journal of Sports Medicine / Deutsche Zeitschrift Fur Sportmedizin, 69(6), 216–223. Retrieved from https://search.ebscohost.com/login.aspx?direct=true&db=s3h&AN=130554653&site=ehostlive

Patel, J., Cotorruelo-Martinez, A., Gill-Duncan, N., Leveille, P., Pearson, J. M., Julliard, K., & Saxena, A. (2014). Resident Physicians Using Modern Practices for Excellent Documentation and Care in Heart Failure (PUMPED CHF). Hospital Topics, 92(4), 81–87. https://doi.org/10.1080/00185868.2014.968486

Preventing Readmissions with a Personal Touch. (2018). Hfm (Healthcare Financial Management), 1–3. Retrieved from https://search.ebscohost.com/login.aspx?direct=true&db=buh&AN=132859166&site=ehost-live

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