Pathophysiologic Model

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

Mr. Steward’s priority problems include impaired cardiac tissue perfusion, impaired gas exchange, and pain. We are concerned about impaired cardiac tissue perfusion because the pt. is exhibiting signs of myocardial ischemia including chest pain and shortness of breath (Gillespie, 2012). Although we acknowledge that impaired cardiac tissue perfusion can decrease the function of the heart and will have the potential to affect the perfusion and delivery of oxygen to other end organs, our primary focus will be a focused cardiovascular assessment (House-Kokan, 2012). At 1800, Mr. Steward was SOB, had shallow and rapid breathing (RR = 44), and a SaO2 of 72% on RA. Due to the fluid buildup in his lungs, Mr. Steward has impaired gas exchange, and requires supplemental oxygen to maintain his SaO2; this warrants a focused respiratory assessment.

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

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

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.

Contractility is the pumping of the heart muscle. It is measured as the ejection fraction. Contractility directly influences stroke volume. Increased contractility will increase stroke volume with any amount of preload. Diseases that disrupt myocyte activity reduce contractility. Myocardial infarction is the most common. Others include, but are not limited to, cardiomyopathies, degenerative valve disease, and myocarditis (Francis & Tang, 2003). Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to neurohumoral , immune, and inflammatory changes and can cause ventricular remodeling. Ventricular remodeling occurs when the size, shape, and function of the affected chamber is distorted. Ventricular remodeling causes hypertrophy and dilation of the heart muscle and causes progressive myocyte contractile dysfunction over a period of time. When contractility is decreased, stroke

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

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

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

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

In today’s society nearly every individual experiences some sort of stress, whether it is chronic stress or acute. Acute stress is the immediate response to a demanding situation, for example, managing your home life, finances and the status of ones health. According Time Magazine, a recent survey reports that the incidence of stress has declined but is still lingering over the lives of young adults. The National Stress in America survey had two thousand participants ages eighteen to thirty –three, more than half of this population reported receiving minimal to no support in coping with the stress (Sifferlin, 2013). Most of the young adults reported that a single source

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

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

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.

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.