Cardiogenic Pulmonary Edema caused by Left Heart Failure

Cardiogenic pulmonary edema (CPE) is the accumulation of fluid in the lung tissues and alveoli most commonly as a result of heart failure (HF).

           Heart failure is the condition in which the heart is weakened by several different causes and, because of which, unable to efficiently pump blood to meet one’s metabolic demands. Causes of heart weakening include prolonged alcohol or cocaine use, prolonged chemotherapy agents use, or, in most cases, myocardial infarctions (MI) and hypertension.

           When heart muscles, or myocardial tissues, sustain necrotic injuries from drug use or a MI, they will never be fully recovered and will be replaced by scar tissues. Because the injured myocardial tissues have sclerotized, they lose their ability to contract. When more than 40% of the ventricles of the heart are damaged, cardiogenic shock develops. Cardiogenic shock is when the heart is no longer able to meet the body’s metabolic demands, as oppose to in heart failure when the heart can still meet the body’s demands but inefficiently and to a limit.

           There are different stages to heart failure as the condition develops and worsens. To begin, heart failure can develop from either side of the heart, distinguished as left heart failure (LHF) and right heart failure (RHF), all depending on the location of the injury and pre-existing comorbidities. For instance, if the left side of the heart is sufficiently injured, left heart failure will likely develop, and so on.

           (To keep the article brief, only left heart failure will be expanded upon.)

           Now, if a patient has chronic hypertension, which side of the heart will be affected overtime? Before being proficient in answering that question, some notions of the cardiovascular system and the heart must be understood. Firstly, the cardiovascular system is composed of three main components: Blood, blood vessels, and the heart as a pump. To circulate blood efficiently, the heart must be strong enough and blood vessels must be closed. Because the cardiovascular system is a closed system, where blood is enclosed in a circuit and can only move towards the path of least resistance, it means the heart can only pump out as much blood as it receives. In other words, the cardiac output, the amount of arterial blood pumped out of the heart into the systemic circulation in a minute, is equal to the venous return, the amount of venous blood that enters the heart from the systemic circulation, in a minute. With that in mind, if the venous return is decreased due to physiological changes, the cardiac output is subsequently decreased as well.

           Secondly, other factors, such as the heart rate (HR) and stroke volume (SV), will also influence the cardiac output (CO). Briefly, the heart rate is the number of ventricular contractions in a minute whereas the stroke volume is the amount of blood pumped out by the left ventricle in one contraction. HR, measured in beats per minute, and SV, measured in liters per beats, are used to calculate the cardiac output, measured in liters per minute, in the following equation: HR x SV = CO.  Thus, an increase of the HR or SV will as a result increase the CO.  

           Thirdly, for the pathophysiology of heart failure, one more factor is crucial in the weakening of the heart: The afterload. The afterload is defined as the amount of force and pressure the heart must overcome to pump blood into the systemic circulation. In other words, the afterload is a pressure in the systemic circulation that works against the cardiac output, meaning an increase in the afterload decreases the cardiac output. Without overcoming the afterload, blood will not exit the left ventricle. Therefore, the greater the afterload is the faster and stronger must the left ventricle work to pump blood forward into the systemic circulation.

           At last, if a patient has chronic hypertension, which side of the heart will be affected overtime? The answer is the left side of the heart because of the increase resistance in the systemic circulation, which increases the afterload. To overcome the increased afterload, heart rate and stroke volume are increased to improve cardiac output. Overtime, the left ventricle is overworked and becomes enlarged, a condition known as left ventricular hypertrophy. As a result of its enlargement, the left ventricle is weakened and has become inefficient in producing a sufficient cardiac output against the elevated afterload. As consequence, the blood pressure in the systemic circulation is now greater than the blood pressure in the left ventricle, the opposite of what the heart is supposed to accomplish. Because the tables have turned, so to speak, a fraction of blood will move from the left side of the heart into the pulmonary circulation, going backward into the pulmonary arteries instead of forward into the aorta. This phenomenon occurs due to the cardiovascular system being a closed system, where blood is enclosed in a circuit and can only move from an area of high pressure to an area of low pressure.

           The backflow of blood  in the pulmonary circulation due to left heart failure pushes against capillary walls around the alveoli. As a result, pulmonary blood pressure increases and causes fluid of low-protein content to move from the blood into lung tissues, due to the pressure variant. The lung tissues will eventually reach its threshold to contain the fluid in itself, which leads the fluid to leak into the alveoli, causing severe dyspnea. When the accumulation of fluid develops into the alveoli due to heart failure, the condition is referred as cardiogenic pulmonary edema, or congestive heart failure.

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