Understanding Congestive Heart Failure And Its Impact On Patient And Family

Risk factors for Congestive Heart Failure

Congestive heart failure (CHF) is a diseased condition which is associated with reduced  pumping of blood due to narrowed arteries and high blood pressure. Risk factors responsible for the congestive heart failure (CHF) include age, augmented cholestrol, diabetes mellitus, hypertension and active smoking. In the present case study, older age of Sharon Mckenzie (77 yrs) might be responsible for CHF. Literature mentioned that, risk of CHF increases with the age. 2 % people of age 40 to 60 years and 5 % people of age 60 to 70 years are usually at risk of CHF. Moreover, other factors responsible for CHF include lack of physical activity, family history, obesity and alcohol consumption (Dhingra et al., 2014). Hypertension is also responsible for the occurrence of CHF. Moreover, her current assessment indicated hypertension in her. Females with hypertension are approximately four times more susceptible to CHF in comparison to the non-hypertensive females. 40 and 60 % male and female respectively are prone to CHF (Mahmood and Wang, 2013). Low-density lipoproteins (LDL) and high-density lipoproteins (HDL) with high and low levels respectively play significant role in CHF. Smoking (36 % people) and obesity (20 % people) are prone to CHF. Intake of saturated fats lead to development of CHF. Increased levels of β-type natriuretic peptides are responsible for the occurrence of CHF (Australian Institute of Health and Welfare, 2014; Díaz-Toro,Verdejo, and Castro, 2015; Mirkin, Enomoto, Caputo,  and Hollenbeak, 2017).

Save Time On Research and Writing
Hire a Pro to Write You a 100% Plagiarism-Free Paper.
Get My Paper

Cardiovascular conditions like coronary artery disease (CAD), myocarditis, congenital heart defects, heart attack, cardiomyopathy, heart arrhythmias, and faulty heart valves might lead to development of CHF. Mckenzie is associated with the MI, which further augment chances of CHF in her. Medications like medications for diabetes (rosiglitazone and pioglitazone), certain anaesthetics, nonsteroidal anti-inflammatory drugs (NSAIDs) and anticancer are also produce CHF (Gotto, Lenfant, Paoletti, Alberico and Catapano, 2012; Castillo, Edriss, Selvan,  and Nugent, 2017). Literature mentioned that people with CHF die within 5 years duration of its diagnosis. People with CHF would have about 10 % more death as compared to the normal people (Australian Institute of Health and Welfare, 2014).

Her overall health condition indicate that she would not be able to perform her activities of daily living. Hence, she should seek assistance from others or family members. Family members should monitor her activities of daily living. It might produce psychological impact on her. Since, family members need to take care of her which might lead to stressful condition to other family members and produce economic burden on the family members.  Family members and care providers should monitor her diet, medications and risk factors. Moreover, they should establish positive communication and positive approach with her (Cooper, DeVore,and Michael Felker, 2015; Raman, 2016). 

Causes of CHF

Q2. :

Symptom

Save Time On Research and Writing
Hire a Pro to Write You a 100% Plagiarism-Free Paper.
Get My Paper

Pathophysiology

Dyspnoea

Reduced cardiac output results in the decreased blood supply various organs and tissues along with skeletal muscle. It produces augmented left ventricular pressure to restore necessary cardiac output. Subsequently, it leads to lessened pulmonary diffusion and subsequently interstitial oedema. Breathlessness occur due to interstitial oedema. Increased expenditure of myocardial energy occurs due to augmented diastolic pressure which require increased amount of energy. Ventricular remodelling, increased myocardial oxygen demand and myocardial ischemia occur due to raised requirement of energy (Güde, Brenner, Störk, Hoes, and Rutten, 2014; Hosenpud and Greenberg, 2013). From the case study, it is evident that McKenzie is suffering through shortness of breath problem.

Swollen ankle

In swollen ankle, there would be more swelling in the leg or ankle. Swelling predominantly befalls as result of accumulation fluid in the particular organ which results due to reduced cardiac output. Vasodilation and decreased ventricular filling pressure occur mainly due to augmented indigenous peptides like natriuretic peptide and β-type natriuretic peptide. It leads to decreased cardiac preload and afterload which lead to reduced back flow of blood to the heart through veins. This reduced back flow of blood occurs due to narrowing of the valve. It results in the insufficient pumping of the blood by the heart (Moe, 2016; Eisen, 2014). Swollen ankle in McKenzie occurs due to cardiovascular impairment and abnormality.

Dizziness

CHF lead to reduced blood flow to different organs including brain which lead to dizziness in the patient. Heart rate and rhythm abnormality predominantly accountable for reduced blood supply to the brain. Six primary neurotransmitters of the three-neuron arc drives the  vestibulo-ocular reflex (VOR). Glutamate remains in the resting discharge which modulate synaptic transmission of the three neuron arc of vestibulo-ocular reflex (VOR). Acetylcholine act as excitatory neurotransmitter in both peripheral and central synapses. Gamma-Aminobutyric acid (GABA) act as  inhibitory neurotransmitter in the medial  vestibular nucleus, lateral vestibular nucleus, and the vertical vestibulo-ocular reflex (VOR). Dopamine, norepinephrine and histamine act centrally. Dopamine accelerate vestibular compensation, norepinephrine control vestibular stimulation and facilitates compensation. However, central role of histamine is unclear. This cardiovascular abnormality and impairment produced dizziness in McKenzie (Kovács, Papp, and Nagy, 2014; Hosenpud and Greenberg, 2013’ Kemp and Conte, 2012).

 Q.3.  

Drug class like angiotensin-converting-enzyme inhibitor (ACE inhibitor) is useful in cardiovascular patients like McKenzie.

ACE inhibitor is the primary selection of medicine for patients with CHF. These drugs exhibit its action through inhibition of angiotensin-converting enzyme which is a vital portion of renin–angiotensin- aldosterone (RAAS) system. Impaired RAAS functioning is one of the prominent reasons for occurrence of hypertension. This class of drugs produce its action  through inhibition of Angiotensin I (ATI) conversion to Angiotensin II (ATII). Decreased arteriolar resistance, augmented venous capacity, decreased cardiac output and volume, decreased blood vessels resistance and increased sodium excretion in the urine are the physiological alterations occur due consumption of ACE inhibitors (Opie and Gersh, 2011; Muneer and Nair, 2017; Dinicolantonio, Lavie, and O’Keefe, 2013). ACE inhibitors exhibit its action through blood vessel relaxation and blood volume reduction which lead to reduced blood pressure and oxygen requirement by the heart (Sayer and Bhat, 2014; Scott and Winters, 2015). ACE inhibitors like Enalapril are also useful in the treatment of CHF associated cardiovascular conditions like hypertension, symptomatic heart failure, and asymptomatic left ventricular dysfunction. It is useful in protecting kidney functions and diabetes (Dinicolantonio, Lavie, and O’Keefe, 2013). Management of all these conditions is necessary in case of Mckenzie because all these cardiovascular related conditions are risk factors of CHF.

Mckenzie is consuming enalapril drug from the ACE inhibitors class of drugs. Onset of action of enalapril is 1 hour. Enalapril exhibit peak effect between 4 – 6 hours. Duration of action of enalapril is 12 – 24 hours. Oral bioavailability of enalapril is 60 %. Enalapril is a prodrug which get metabolised to Enalaprilat. Enalaprilat is an active metabolite of Enalapril which inhibits ACE (Opie and Gersh, 2011; Muneer and Nair, 2017).

Q.4. Nursing Intervention for Mckenzie within first 8 hours of her admission.

Intervention

Rationale

Cardiovascular intervention

Monitor parameters like heart rate and heart beat rhythm.

Record and note heart rate.

Auscultate apical pulse.

Record heart sound.

Record peripheral pulses.

Record and note blood pressure.

Record and note urine output and concentration of urine.

Ensure that McKenzie is adhering to her medicine consumption like furosemide and enalpril.

McKenzie is experiencing bradycardia. Moreover, she is associated with CHF; hence, she would be experiencing different kinds of dysrhythmias like premature atrial contractions (PACs), paroxysmal atrial tachycardia (PAT), PVCs, multifocal atrial tachycardia (MAT), and atrial fibrillation (AF) (Paul and Hice, 2014).

CHF patients like McKenzie are associated with impaired pumping action. Henceforth, S1 and S2 heart sounds would be weak. Murmurs occur due to valvular incompetence (Hupcey, Kitko, and Alonso, et al., 2015).   

It is necessary to record peripheral pulses in CHF patients like McKenzie because these patients produce abnormal pulses like radial, popliteal, dorsalis pedis, and post tibial pulses (Paul and Hice, 2014).

In the patients with CHF, in the initial phase there might be hypertension due to increased systemic vascular resistance (SVR) (Hupcey, Kitko, and Alonso, et al., 2015).

Reduced cardiac output results in reduced urine output.  It largely occur due to retention of sodium and water (Paul and Hice, 2014).

Furosemide is a diuretic which produce effect through reducing preload, maintaining normal cardiac output and reducing congestive symptoms (Hupcey, Kitko, and Alonso, et al., 2015).

Enalpril is a ACE inhibitor.  It exhibits its action through ventricular filling pressure and by increasing cardiac output (Paul and Hice, 2014; Hupcey, Kitko, and Alonso, et al., 2015).

Respiratory intervention

Record and note respiratory rate every four hour.

Assess ABG levels.  

Observe and note breathing pattern.

Encourage and demonstrate deep breathing technique to McKenzie.

Encourage McKenzie for diaphragmatic breathing.

Educate and demonstrate McKenzie about lip breathing, abdominal breathing, and relaxation technique.

Administer McKenzie with bronchodilator medications and initiate supplemental oxygen to her after physician’s consultation.

Normal range respiratory rate is 10 – 20 bpm. Deviation of respiratory rate from this normal range indicate abnormal breathing pattern and abnormal functioning of respiratory system (Rogers  and Bush, 2015).

ABG levels assessment is useful in the assessment of oxygen saturation level and ventilation pattern. Shortness of breath lead to alteration in the ventilation pattern. ABG assessment include measurement of pH, PaCO2, HCO3 and PaO2. Hence, it is useful in determining hypoxia and acidosis (Suter, Gorski, Hennessey, and Suter, 2012).  

Breathing pattern observation would be helpful in assessing potential disease condition and abnormal respiratory function (Rogers  and Bush, 2015).

Deep breathing is helpful in deep respiration and improving oxygen saturation level. Air trapping can be prevented by extended expiration. Deep breathing technique include slow inhalation, end respiration holds, passive exhalation and use of spirometer (Suter, Gorski, Hennessey, and Suter, 2012).

Diaphragmatic breathing is helpful in muscles relaxation and oxygen saturation (Rogers  and Bush, 2015).

It is helpful in improving ventilation (Suter, Gorski, Hennessey, and Suter, 2012).

Bronchodilator medicines exhibit its effect through improvement in bronchodilation and opening the airway passage (Rogers  and Bush, 2015).

References:

Australian Institute of Health and Welfare (2014). Cardiovascular disease, diabetes and

chronic kidney disease— Australian facts: Prevalence and incidence. In:

Cardiovascular, diabetes and chronic kidney disease series no. 2. Cat. no. CDK 2.

Canberra. Retrieved from https://www.aihw.gov.au/reports/heart-stroke-vascular-disease/cardiovascular-diabetes-chronic-kidney-prevalence/contents/table-of-contents on 14.03.2019.

Castillo, A., Edriss, H., Selvan, K., and Nugent K. (2017). Characteristics of Patients With Congestive Heart Failure or Chronic Obstructive Pulmonary Disease Readmissions Within 30 Days Following an Acute Exacerbation. Quality Management in Healthcare, 26(3), 152-159.

Cooper, L.B., DeVore, A.D., and Michael Felker, G. (2015). The Impact of Worsening Heart

Failure in the United States. Heart Failure Clinics, 11(4), 603-14.

Symptoms of CHF

Dhingra, A., Garg, A., Kaur, S., Chopra, S., Batra, J.S., Pandey, A., Chaanine, A.H., and  Agarwal SK. (2014).  Epidemiology of heart failure with preserved ejection fraction. Current Heart Failure Reports, 11(4), 354-65.

Dinicolantonio, J.J., Lavie, C.J., and O’Keefe, J.H. (2013). Not all angiotensin-converting enzyme inhibitors are equal: focus on ramipril and perindopril. Postgraduate Medicine, 125(4), 154-68.

Eisen, H. J. (2014). Heart Failure, An Issue of Cardiology Clinics, E-Book. Elsevier Health Sciences. New York. United States.

Gotto Jr, A. M., Lenfant, C., Paoletti, R., Alberico L. Catapano, A. S.  (2012). Multiple Risk Factors in Cardiovascular Disease: Strategies of Prevention of Coronary Heart Disease, Cardiac Failure. Springer.  Science & Business Media. Berlin, Germany,

Güde, G., Brenner, S., Störk, S., Hoes, A., and Rutten, H. (2014). Chronic obstructive pulmonary disease in heart failure: accurate diagnosis and treatment. European Journal of Heart

Failure, 16(12), 1273-82.

Hosenpud, J. D., and Greenberg, B. H. (2013). Congestive Heart Failure: Pathophysiology, Diagnosis, and Comprehensive Approach to Management. Springer Science & Business Media. Berlin, Germany.

Hupcey, J.E., Kitko, L., and Alonso, W. (2015). Palliative Care in Heart Failure. Critical Care Nursing Clinics of North America, 27(4), 577-87.

Kemp, C.D., and Conte, J.V. (2012). The pathophysiology of heart failure. Cardiovascular Pathology, 21(5), 365-71.

Kovács, Á., Papp, Z., and Nagy, L. (2014). Causes and pathophysiology of heart failure preserved ejection fraction. Heart Failure Clinics, 10(3), 389-98.

Mahmood, S. S., and Wang, T. J. (2013). The epidemiology of congestive heart failure: the Framingham Heart Study perspective. Global Heart, 8(1), 77–82.

Mirkin, K.A., Enomoto, L.M., Caputo, G.M., and Hollenbeak, C.S. (2017). Risk factors for 30-day readmission in patients with congestive heart failure. Heart Lung, 46(5), 357-362.

Moe, G. (2016). Heart failure with multiple comorbidities. Current Opinion in Cardiology, 31(2), 209-16.

Muneer, K., and Nair, A. (2017). Angiotensin-converting enzyme inhibitors and receptor blockers in heart failure and chronic kidney disease – Demystifying controversies. Indian Heart Journal, 69(3), 371-374.

Opie, L. H., and Gersh, B. J. (2011). Drugs for the Heart E-Book. Elsevier Health Sciences. New York. United States.

Paul, S., and Hice, A. (2014). Role of the acute care nurse in managing patients with heart

failure using evidence-based care. Critical Care Nursing Q, 37(4), 357-76.

Raman, J. (2016). Management of Heart Failure (2nd ed.). Springer. Berlin, Germany.

Rogers, C., and Bush, N. (2015). Heart Failure: Pathophysiology, Diagnosis, Medical Treatment Guidelines, and Nursing Management. Nursing Clinics of North America, 50(4), 787-99.

Sayer, G., and Bhat, G. (2014). The renin-angiotensin-aldosterone system and heart failure. Cardiology Clinics, 32(1), 21-32.

Scott, M.C., and Winters, M.E. (2015). Congestive Heart Failure. Emergency Medicine  Clinics of North America,  33(3), 553-62.

Díaz-Toro, F., Verdejo, H.E., and Castro, P.F. (2015). Socioeconomic Inequalities in Heart Failure. Heart Failure Clinics, 11(4), 507-13

Suter, P.M., Gorski, L.A., Hennessey, B., and Suter, W.N. (2012). Best practices for heart failure: a focused review. Home Healthcare Nurse, 30(7), 394-405.