Congestive cardiac failure case study

Congestive heart failure is a syndrome that can result from both functional or structural disorder of the ventricles which affect their ability to either fill or eject blood (Udelson & Stevenson, 2016). The major causes of congestive heart diseases include; hypertension, degenerative valve disease among others. In Sharon’s case, poorly managed hypertension which is identified with a blood pressure measurement of 170/110mmHg is the key cause of her condition. Hypertension is characterized by increased peripheral resistance (Messerli, Rimoldi & Bangalore, 2017). The increased pressure, consequently causes the heart to compensate by ventricular hypertrophy. The financial cost of heart failure is high more so due to increased risks of readmissions and prolonged hospitalization and demands such as lifestyle modifications (Sahle, Owen, Mutowo, Krum & Reid, 2016). Discuss three (3) common signs and symptoms of the selected disease and explain the underlying pathophysiology of each (350 words) Shortness of breath: Shortness of breath in congestive heart disease occurs as a result of pulmonary edema.

The left ventricular hypertrophy as a response to increased blood pressure, with time, causes the ventricles to weaken with a reduction in contractility. The ventricles are unable to pump blood from the lungs to the body causing the pressure in the heart to build up pushing the fluid into the air sacs in the lungs (Mangini, Pires, Braga & Bacal, 2013). The accumulation of fluid in the lung limits the expansion of the lungs causing inability to breathe effectively hence a reduction in intake of oxygen through the lungs (Mangini, Pires, Braga & Bacal, 2013). Discuss the pharmacodynamics & pharmacokinetics of one (1) common class of drug relevant to the chosen patient (300 words) Pharmacodynamics ACE inhibitors are ingested as prodrugs which are then converted into the active form of the drug.

The prodrug usually has a low efficacy compared to the active form. ACE inhibitors act through antagonization of the Renin-Angiotensin-Aldosterone System (RAAS) to affect their blood pressure lowering mechanisms (Dézsi, 2014). The RAAS system is activated by a sympathetic response to a reduction in blood pressure. Its activation leads to the production of renin hormone by the juxtaglomerular apparatus kidneys which convert the circulating Angiotensinogen to Angiotensin 1 which is later converted to active form Angiotensin II (Dézsi, 2014). The active drug forms have an increased half-life of up to 35 hours ("Enalapril - DrugBank", n. d. The half-life of the drug is increased in patients with congestive heart failure due to slowed renal excretion (Li et al. Increased half-life in congestive heart disease poses a risk for overdose of the medication which may result in hypotension.

Nursing Diagnosis goal Intervention Rationale implementation evaluation Impaired gaseous exchange related to an accumulation of fluid in the alveoli as evidenced by fast breathing and verbalization of shortness of breath. Increased pumping will reduce the underlying pressure in the heart and reduce pulmonary edema and increase perfusion to central and peripheral areas reducing signs of inadequate perfusion such as dizziness and coldness of the extremities. -Enalapril acts to inhibit the angiotensin system hence reducing the blood pressure by preventing the action of angiotensin on the RAAS(Dézsi, 2014). Reduction of the blood pressure will consequently reduce the workload on the heart enhancing the ability of the heart to pump effectively to increase perfusion and increasing venous return reducing pooling of fluid in tissues.

-Digoxin administered 250mg at 12 by nurse Dingol Enalapril 5Mg adminnsitred by nurse Dongol at …. Increased fluid volume related to reduced glomerular filtration and increased isotonic fluid retention evidenced by oedema of the ankles and respiratory distress. ca/drugs/DB00584 Fry, M. , McLachlan, S. , Purdy, S. , Sanders, T. , Kadam, U. 000285 Inamdar, A. , & Inamdar, A. Heart Failure: Diagnosis, Management and Utilization.  Journal of Clinical Medicine, 5(7), 62. doi: 10. , Pan, J. , & Xu, P. Pharmacokinetics and drug-drug interaction between enalapril, enalaprilat and felodipine extended release (ER) in healthy subjects.  Oncotarget, 8(41). doi: 10. , & Bangalore, S. The Transition from Hypertension to Heart Failure.  JACC: Heart Failure, 5(8), 543-551. doi: 10. 1016/j. 12130 Jhund, P. , Campbell, R. , & McMurray, J. Assessment and prevalence of pulmonary oedema in contemporary acute heart failure trials: a systematic review.