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Congestive Heart Failure

Cause of the disease and its impact on body systems (acute and chronic)

The patient is suffering from congestive heart failure, left-sided heart failure to be specific owing to involvement of the pulmonary system that presents with coughing frothy sputum, shortness of breath, Exertional dyspnea as well as as tightness of the chest (Trevor et al., 2015). The causes of this condition are, primary diseases of the myocardium (This includes amyloidosis, myocarditis (inflammation of the myocardium), Valvular heart diseases (mitral valve disease), systemic hypertension, and ischemic heart diseases. The disease also has a familial predisposition as well as genetic predisposition. Patient’s age, lacks of physical exercise as well as too much fat consumption are aggravating factors (Hosenpud & Greenberg, 2007).

The patient’s age is an aggravating factor to atherosclerosis, ischemic heart disease, which would lead to obstruction of the vessel lumen with the atheroma. From the history, the patient is overweight which imply excessive fatty acid deposition in the body. This would lead to deposition in the lumen obstructing the normal blood flow to the heart muscles as well as output to the essential body organs. Ischemic injury led to the dyspnea experienced by the patient.

From the patient’s history, the condition has a family predisposition pointing to a possibility of a genetic defect those codes for the normal functioning of the heart as well as lipid accumulation (Hosenpud & Greenberg, 2007). The patent’s mother and father have been diagnosed with a similar condition.

The condition is chronic owing to the patient’s past medical history in which the patient has been on antihypertensive drugs, anti-angina drugs, treatment for dyslipidemias, and treatment for myocardial infarction (LeMone, 2014).

The conditions chronicity is also observed by the patient’s past surgical history in which the patient has been on a left anterior descending stent for 1 year.

Pathogenesis of the patients’ disease development

Primary Heart Disease (Amyloidosis and, or myocarditis): Deposition of the amyloid proteins (transthyretin, for example leads to restrictive cardiomyopathy) on the myocardium of the heart leads to its thickening and subsequently inhibits blood flow, ischemia and infarction due to lack of nutrients and appropriate blood supply (LeMone, 2014).

Valvular heart diseases (Mitral valve disease): This occurs when the valves either failure to open or when the valves fail to close. Pathologic failure of the valves to open leads to obstruction of the normal blood flow from the heart ventricles and the atria leading to increased blood volumes in the heart chambers thus failure of the heart (Peacock et al., 2016). Failure of the valve to close primarily leads to backflow of blood into the heart chambers and build up of intra cardiac pressures which then leads to extra exertion of pressure on the heart and in the long term effect leads to heart failure.

Systemic hypertension: This occurs as a compensatory measure to the reduced cardiac output by the etiologies listed above. The body has two mechanism of compensating for the reduced cardiac output (Neurohormonal system activation and the ventricular dilation). Systemic hypertension is as a result of neurohormonal activation. Reduced cardiac output to the renal system leads to stimulation of he juxtaglomerulus cells to secrete renin. Renin converts angiotensinogen into angiotensin I (Peacock et al., 2016). This would later on be converted to angiotensin II by angiotensin converting enzyme. Angiotensin II leads to retention of both water and sodium into the blood leading to increased peripheral pressure of the systemic blood. This is so because angiotensin II activates release of aldosterone that leads to increased sodium reabsorption after its ultrafiltration by the glomerulus. Angiotensin II also activates antidiuretic hormone (vasopressin) which acts at the renal tubules through insertion of the aquaporin through which water is reabsorbed into the body system. The two impacts leads to increased peripheral volume. This is evident in the patient as pitting edema is evident in both legs, a manifestation of systemic hypertension due to heart failure (Left-sided heart failure) (Champe, 2005).. The increased peripheral pressure in turn acts as an antagonizing force to the normal blood flow. The heart will therefore compensate for this increased force through vasodilation but in the long run without proper medical intervention, it will not be able to compensate for the increased peripheral pressure (Peacock et al., 2016).

The build up of systemic blood flow due to increased blood volume as a result of increased sodium and water reabsorption by the kidneys, the patient blood pressure would be elevated. This is the observation made at the examination of the vital signs of the patient, with his systolic pressure at 180 mmHg and diastolic pressure at 100mmHg.

The heart in turn will tend to pump blood faster and more rapidly into the systemic blood flow to meet the specific organ oxygen requirement. This would then lead to the increased pulse rate observed in the patient.

Ischemic heart diseases: This leads to obstruction of the normal coronary blood flow to the heart myocytes. This would then lead to reduced oxidation of the tissues leading to their ultimate death. The myocytes will no longer be able to pump adequate blood to the rest of the body organs. This resulted into paleness and cold body witnessed in the patient during observation.

Ischemic heart diseases primarily manifest due to atherosclerosis which leads to deposition of atheroma on the cardiac vessels leading to reduced vessel lumen and in severe cases complete obstruction of the vessels. From the history, the patient is overweight which indicates excessive fatty deposits in the body. This when oxidized would lead to atheroma formation within the vessel lumen. Obstruction of the blood flow leads to lack of oxygen among other nutrients carried by blood to the myocytes and they would ultimately die. Myocytes depend on the oxygen for ATP generation for the additional heart functioning apart form the SAN and the AVN automatic impulse generators. Lack of oxygen would not permit this function making the left-side of the heart unable to pump adequate blood to the other organs (Jefferies et al, 2017). This is among others the causes of the compensatory systemic hypertension which is an aggravating factor in the pathogenesis of the congestive heart failure.

This then leads to build up of blood in the atrium of the left heart chamber. This build up of pressure in the atria of the left chamber leads to its dilation and then atrial fibrillation. This is the cause of irregular heartbeats and abnormal rhythms experienced by the patient. The build up pressure is then transferred to the lungs through the pulmonary veins whose hydrostatic pressures are increased compared to their counter part visceral hydrostatic pressures. This would then lead to accumulation of fluids into the lungs and consequently leads to reduced surface area for gaseous exchange by the alveoli (Jefferies et al, 2017). Shortness of breath occurs subsequently in the patient. This would then lead to rapid breathing experienced by the patient as a compensatory measure to meet increased oxygen demands on a small surface area. It is the reason the patient is trying to lean forward, in order to increase surface area for gaseous exchange. This would, as a compensatory measure, exertion of more force during breathing, an element that has led to involvement of the accessory muscles and generally increased force of breathing. This was observed with the breathing rate at28.

The presence of fluid in the lungs due to the imbalance between the hydrostatic of the pulmonary vein pressure and that of the lung viscera leads to the basal and the mid crackles (Jefferies et al, 2017).

The decreased partial pressure of oxygen, recorded at 92% is as a result of reduced gaseous exchange surface area due to the fluid accumulation in the lungs (Hosenpud & Greenberg, 2007). The fluid accumulation also leads to the dull observation non at the base of the lungs during percussion. Morphological changes taking place (injury and adaption)

  1. The Heart

  1. Gross manifestation

Valvular heart diseases as mentioned above due to infections or other primary or secondary reasons would lead to reduced blood outflow. Mitral valve abnormalities lead to regurgitation of blood into the heart chambers. This leads to dilation of the left ventricle and left atrium of the heart (Hosenpud & Greenberg, 2007).

Left sided dilation in the long term effect lead to hypertrophy of the myocytes to accommodate the increased demand of systemic blood flow against increased peripheral pressure from systemic hypertension.

  1. Microscopic manifestation of the heart

Microscopic manifestation of the heart is evident in this pathological condition as the myocytes are hypertrophied with variable fibrosis. Fibrosis is experienced on the lesions of the healing lesion of the myocytes as element of healing takes place as the injured myocytes try to heal (Hosenpud & Greenberg, 2007).

  1. The Lungs

  1. Gross Manifestation of the Lungs

Increasing pressure at the left atrium, of the heart is carried by the pulmonary vein which thenceforth has more hydrostatic pressure than that of the viscera. The increased pressure leads to increased fluid accumulation in the lung. This is witnessed morphologically as congestion and edema. Pleural effusion is experienced in the pleura.

The lungs are therefore increased in size and weigh (Champe, 2005). The lungs presents as boggy and heavy.

  1. Microscopic appearance of the lungs

Edema in the perivascular spaces and the interstitial spaces showing exudates is observed. The septum of the alveolar also has accumulated fluid. The capillaries permit entrance of red blood cells which are subsequently lysed by macrophages into hemosiderin-laden macrophages aka heart failure cells (Champe, 2005).

Clinical manifestation of the disease (signs and symptoms)

The clinical manifestations of congestive heart failure are among others, dyspnea (shortness of breath). This occurs due to fluid accumulation in the lungs at the alveoli gaseous exchange surfaces. It is more severe on exertion (Champe, 2005). Orthopnea also occurs in the patient when in recumbent position as venous return occurs in supine position from the legs.

When the patient is sleeping (recumbent position), paroxysmal nocturnal dyspnea occurs awakening the patient from sleep to resume the alleviating standing position.

The patient also presents with increased heart, cardiomegaly, which is mostly due to the primary heart diseases such as amyloidosis and myocarditis.

Tachycardia also occurs as the patient as the peripheral resistance increases due to systemic hypertension thus the heart need to pump rapidly to meet the increasing oxygen demand by the other body systems (Carton, 2017). With atrial fibrillation and the stagnation of blood flow, stasis, there is an increased propensity to thrombi formation within the vascular system. As the blood flows to the essential organs, these would be carried through the blood as emboli and deposited into the end arterial blood flow leading to obstruction no blood flow thus, infarction occurs.

Fluid accumulation leads to the observed crackles at the base of the lungs. This is so due to elevated pulmonary vein hydrostatic pressure above the visceral hydrostatic pressure. Fluid accumulation also leads to decreased oxygen uptake into the blood thus the body increases the breathing rate.

Other manifestations due to the pulmonary involvement are decreased oxygen saturation as a result of small surface area exposed for gaseous exchange due to increased fluid accumulation in the lungs. Coughing would be a common phenomenon (Anatomy, pharmacology, physiology, 2010). This is so due to increased fluid accumulation. Fluid accumulation in the lungs would be a fertile ground for bacterial culturing leading to pulmonary infections such as pneumonia and, or pneumonitis. As a result, the cough receptors are triggered to expel the bacteria and clear the pulmonary system. Due to the infection, the cough is productive with sputum as well as blood are produced.

The elevated pressure within the left ventricle due to obstruction of cardiac outflow of blood is translated to the left atrium which is subsequently dilated. The dilated left atrium leads to atrial fibrillation which is observed as irregular heartbeats.

Elevated systemic blood flow due to increased reabsorption of sodium and water leads to elevated peripheral resistance and subsequent elevated body pressures. Therefore both systolic and systolic pressures are elevated. The increased vascular pressure would result into increased pulse rate (Anatomy, pharmacology, physiology, 2010).

With decreased cardiac output, the essential organs are inadequately supplied with oxygen. For the renal system, pre-renal azotemia would occur as a result of improper exertion of nitrogenous waste. The systemic blood flow to the brain and the entire central nervous system would also be compromised leading to hypoxic encephalopathy as well as irritability, improper cognitive function as well as increased restlessness which could progress to coma and stupor (Anatomy, pharmacology, physiology, 2010).


Anatomy, pharmacology, physiology. (2010). Cardiac Anaesthesia. doi:10.1093/med/9780199209101.010.0002

Carton, J. (2017). Cardiac pathology. Oxford Medicine Online. doi:10.1093/med/9780198759584.003.0004

Champe. (2005). Lippincott’s Illustrated Reviews :Pharmacology. Lippincott Williams & Wilkins.

Hosenpud, J. D., & Greenberg, B. H. (2007). Congestive heart failure. Philadelphia: Lippincott Williams & Wilkins.

In Jefferies, J. L., In Blaxall, B. C., In Robbins, J., & In Towbin, J. A. (2017). Cardioskeletal myopathies in children and young adults.

In Peacock, A. J., In Naeije, R., & In Rubin, L. J. (2016). Pulmonary circulation: Diseases and their treatment.

LeMone, P. (Ed.). (2014). Medical-surgical nursing: Critical thinking for person-centred care (2nd Australian ed.). Frenchs Forest, Australia: Pearson Australia.

Trevor, A. J., Katzung, B. G., & Kruidering-Hall, M. (2015). Katzung & Trevor’s Pharmacology: Examination & Board Review.