Pathophysiologic Model

Heart failure can be attributed to either right sided, left or both. Left-sided heart failure is of two types, systolic failure and diastolic failure. Systolic failure is the when the left ventricle loses its ability to contract normally. The heart cannot pump with enough force to push enough blood into circulation. Diastolic failure is when the left ventricle loses its ability to relax normally. Which results in the heart not being able to fill with blood during the resting period. Both result in a decrease in cardiac output. (AHA, 2012). A decrease in the cardiac output into the systemic circulation causes blood to accumulate in the left ventricle, left atrium, and pulmonary circulation. This increase

Heart failure (HF) is defined as a multifaceted clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. In HF, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion1. In the United States, HF is increasing in incidence with about 5.1 million people suffering from HF and half of people who develop HF die within 5years 2. Over 75% of existing and new cases occurred in individuals over 65 years of age, < 1% in individuals below 60 years, nearly 10% in those over 80 years of age. HF costs the

Left sided heart failure occurs as a result of ineffective left ventricular contractile function. As the pumping ability of the left ventricle fails, cardiac output falls. Blood is no longer effectively pumped out into the body; it backs up into the left atrium and the into the lungs, causing pulmonary congestion, dyspnea, and activity intolerance. If the condition persists, pulmonary edema and right

In the valvular disease the regurgitation of blood back to the ventricles occurs when the valves fail to close tightly and this will result in ventricular overload and increased muscle stretching. This increases the heart muscles need for oxygen and energy resulting in the cardiac muscles to contract harder (Karch, 2013). The failure of the left ventricle to pump efficiently will lead to pulmonary vessel congestion and in severe cases, pulmonary edema whereas the inefficient pumping of right ventricle will lead to liver congestion and peripheral edema (edema of the legs and feet). The cardiovascular system works as a closed system and therefore, if one-sided failure left untreated, will eventually lead to failure of both sides (Karch, 2013). The American College of Cardiology (ACC)/ American Heart Association (AHA) has incorporated a classification system of heart failure that include four stages. This staging system (stage A to stage D) recognizes that there are established risk factors and structural abnormalities that are characteristics of the four stages of heart failure.

Mechanical inadequacy of left ventricle; causing fluid in lungs. (Hart, RHIA, CCS, CCS-P, Stegman, MBA, CCS, and Ford, RHIT, CCS)

Congestive heart failure (CHF) is a weakness of the heart that has an insufficient circulation of blood throughout the body, which leads to the build-up of fluid in the lungs and edema in the surrounding tissues of the body. “As the intravascular pressure increases along with the amount of extravascular liquid, the lungs become less compliant and less permeable to oxygen, leading to respiratory discomfort (dyspnea), hypoxemia and tachypnea” (Garcia and Wright, 2010). As the condition deteriorates, the capacity of the interstitial space is exceeded, the fluid floods the alveoli and airways resulting in full blown CPE, an acute respiratory distress and a major medical emergency in heart failure patients” (Guyton 1991). There are two types of

Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further

The pathophysiology of hypertension (HTN) is best explained clearly if you have an understanding of how blood pressure (BP) works in the body. BP is seen as the function of both cardiac output (CO) in the human system and systemic vascular resistance (SVR). Cardiac output (CO) is made up of both heart rate (HR) and stroke volume (SV). SV in turn depends on contractility and preload of the system. SVR relies on contractility and afterload. There is literature that supports molecular and cellular levels relating to effects on blood pressure in terms of genetic make-up. Changes in any of these processes have the ability to alter CO or SVR, causing BP alteration and HTN.

Preload is the amount of stretch of cardiac muscle cells prior to contraction. It is controlled by the amount of venous return to the heart. The more venous return, the more the cardiac muscle cells are stretched, which causes a stronger contraction during systole, and this increases the stroke volume. Contractility is the strength of a ventricular muscle contraction. An increase in contractility results in an increase in stroke volume because more blood is ejected from the heart. Afterload is the resistance that the left ventricle must overcome before it can eject blood. An increase in afterload causes a decrease in stroke volume because less of the blood in the ventricle would be ejected.

Isolated diastolic heart failure is defined as pulmonary congestion despite a normal stroke volume and cardiac output. Two areas of pathophysiologic changes in the ventricle have been identified in diastolic dysfunction: decreased compliance of the left ventricle and abnormal diastolic relaxation

There are three systems that play an essential part in homeostatic response to intravascular volume reduction, these include; sympathetic nervous system, cardiovascular system, and neuroendocrine system. Adrenaline, noradrenaline, angiotensin II, and antidiuretics hormones assist to sustain cardiac output (CO) and sufficient tissue perfusion to the brain and the heart. Compensated, decompensated and irreversible are the 3 phases of hypovolaemic shock. Compensated shock phase is when there is a decrease in blood pressure identified by baroreceptors located in the aortic arch and carotid sinus that stimulate sympathetic output. Increased levels of catecholamines create an effect of increased heart rate, myocardial contractility, and vasoconstriction

The left ventricle (left sided heart failure) does not empty properly because the heart cannot efficiently pump the blood out of the heart into the body. This leads to increased pressure in the atria (upper chambers) and as a result the blood in the heart gets backed up. This backlog of blood affects the kidneys – interfering with their function and leading to fluid retention (oedema) in the lungs, abdominal

A great determinant of the afterload on the RV is the pulmonary vascular resistance. The RV can be exposed to high pressure overload states either acutely or chronically. Under acute pressure overload states, the RV responds initially by increased contractility in order to maintain the stroke volume. Initially, the increase in ESP is accompanied by increase in ESV and EDV which in turn stretches the ventricular wall augmenting the contractility (Frank-Starling-Law). However, the RV has limited capacity to generate higher pressure. It has been found from studies as well clinical practise that increase in RV systolic pressure by 60% is the maximum extent by which RV can respond. Later, the EF and SV will decrease as the mean ejection pressure increases, and this is reflected by a decrease in COP. In addition, the RV has thin wall and the high pressure load increase the wall tension and stress. Which leads to increase the oxygen demands causing RV ischemia. In addition, acute pressure load leads to RV dilation which cause a decrease in LV filling and eventually a decrease in COP. Acute RV pressure overload in adults often leads to RV dilation and failure. For example, in adults with acute pulmonary embolism, the RV is unable to generate pressure > 40 and the condition develops to RV failure early in the presentation of acute significant pulmonary. Another example is: idiopathic

Acute cardiogenic pulmonary oedema (ACPO) is a life threatening condition requiring rapid emergency care. ACPO occurs as a result of rapid fluid collection in the lungs interstitial and alveolar spaces (Pinto & Kociol, 2018). Consequently, gas exchange and lung compliance diminishes as the lungs are unable to cope with the rapid fluid accumulation (Purvey & Allen, 2017). ACPO is most commonly seen on a background of left ventricular failure which causes reduced cardiac contractility. This results in a lack of forward pressure leading to pooling of blood in the pulmonary vasculature. Left ventricular dysfunction is triggered by a variety of cardiac diseases such as myocardial infarction, chronic heart failure, cardiomyopathy, new onset arrhythmias

Define Pathophysiology: Pathophysiology may be defined as the study of function of diseased organs with application to diagnostic procedures and patient care. Pathophysiology involves the study of functional changes in the body that result from disease processes. Pathophysiology includes some aspects of pathology which refers to the laboratory study of cell and tissue changes associated with disease.