The only significant cardiovascular disease that is increasing with regularity in our society is heart failure. Heart failure is a common cause of premature death and poor quality of life. There are 5 million people in the United States diagnosed with it, and we add almost 550,000 new cases a year. Four years after symptom onset, heart failure results in 50% mortality.
As you can see from these numbers, we need to have a good understanding of heart failure and how it affects our patients. In this article we will give you an overview into the pathophysiology of how pulmonary edema occurs during heart failure.
There are many different types of heart failure. The two main categories are systolic and diastolic. Systolic heart failure occurs when the heart’s ability to contract decreases—the heart cannot pump with enough force to push a sufficient amount of blood into the circulation. Diastolic heart failure occurs when the heart has a problem relaxing—the heart cannot properly fill with blood because the muscle has become stiff, losing its ability to relax.
One of the biggest misconceptions of heart failure is that there is always pulmonary edema associated with symptoms. Though pulmonary edema is a common problem with heart failure, they are not one and the same. Strong assessment skills will aid you in the proper recognition of its signs and symptoms, which will lead you to appropriate treatment and management of your patient.
Blood Flow Through the Heart
Before examining how pulmonary edema occurs, let’s look at the normal process of blood flow. The heart and lungs are a closed system; the same amount of blood circulates throughout the system with each heartbeat. As long as nothing restricts or impedes the flow of blood, we have a normal course of blood flow. In this progression, deoxygenated blood flows into the right atrium from the superior and inferior vena cava, and then flows through the tricuspid valve. The tricuspid valve closes when the right ventricle is full and begins to contract. From the right ventricle the blood flows through the pulmonary valve into the pulmonary artery and on into the lungs. Once in the lungs, it travels through capillary vessels and into the alveoli. It’s here that blood is oxygenated and waste is removed. Once this process is complete, blood travels through the pulmonary veins to the left atrium, through the mitral or bicuspid valve, which closes when the left ventricle is full and contracts. Blood leaves the left ventricle via the aortic valve and enters the aorta. The aorta is the main artery of the body.
Left Ventricular Failure
As seen from above, there are different types of heart failure. For the purpose of our discussion, let’s look at left heart failure and how it relates to pulmonary edema. Medical conditions that can cause the left ventricle to weaken and eventually fail include coronary artery disease, cardiomyopathy, myocardial infarction, hypertension and heart valve problems. As the left ventricle begins to fail, the heart’s ability to pump effectively is decreased. The normal blood volume returning from the lungs through the left atrium and into the left ventricle becomes unable to enter the aorta, thus reducing cardiac output.
Look at this in terms of a kitchen sink: Under normal circumstances, when we go to the kitchen sink and turn on the faucet, water flows into the basin and down the drain. If there is a clog somewhere in the drain, however, we begin to have water back up into the basin. If we cannot clear the clog and continue to add water, the sink will keep backing up until the clog is cleared. In this example the water would be the blood coming back from the lungs, the sink represents the left ventricle, and the clog is the failing of the ventricle. As the left ventricle fails to eject all the blood into the aorta, this leaves some blood behind with each heartbeat, causing the ventricle to stay constantly loaded with blood. This reaches a point where heart muscle contraction becomes less efficient, causing further reduction in cardiac output. This will eventually cause a backup of the blood volume returning from the lungs.
As the failure of the left ventricle worsens, blood will continue to back up throughout the system. Pressure consequently increases in the left atrium and eventually in the veins and capillaries in the lungs; this will eventually cause fluid to be pushed against the capillary walls. This pressure will cause fluid to leak out of the capillary and into the space between the capillary and the alveoli, which will begin to reduce O2 -CO2 exchange. To counteract fluid leaking from the capillary, the lymph system increases its workload in an attempt to pull fluid back into the vascular or lymphatic space. When the flow of fluid from the capillary exceeds the lymphatic system’s ability to remove it, it results in further movement of fluid into the interstitial space and now the alveoli, causing an increase in pulmonary edema.
In an attempt to maintain homeostasis and resolve the problem, some major compensatory mechanisms kick in. These include the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). These systems may help initially, but eventually these mechanisms will make the problem worse. The sympathetic nervous system will try to compensate for low cardiac output by elevating the heart rate and blood pressure and increasing peripheral vasoconstriction. Think about our kitchen sink comparison—increasing the heart rate sends more blood to the heart, causing more of a backup; this is like adding more water to an already-clogged basin. Vasoconstriction is like making the pipes of the sink even smaller, which will further increase the backup. Activation of the RAAS will actually promote fluid retention, which will worsen the problem. In a future article we will look at the pathophysiology of the renin-angiotensin-aldosterone system and how this powerful vasoconstrictor works.
When dealing with patients in heart failure, it is important to ensure rapid transport to the appropriate treatment facility and treatment based on local protocols. This treatment should focus on improving cardiac output, decreasing systemic vascular resistance, and increasing contractility and the management of fluid overload. Understanding the pathophysiology of pulmonary edema hopefully gives you a better understanding of what the cardiovascular and pulmonary systems go through in heart failure and puts you on a good track to treat and manage these sick patients.
Chris Cebollero, NREMT-P, is chief of EMS for Christian Hospital in St. Louis, host of the EMS Leadership podcast and a member of the EMS World editorial advisory board.