EMT Heart Failure
EMT Heart Failure: everything you need to know and more to crush your National Registry, and impress your colleagues.
EMT Pathophysiology- Heart Failure
This article will address one of the more commonly found cardiac pathologies seen in many of our patients both prehospitally and in the ED. Regardless of whether Heart Failure is the pathologic process driving the Chief Complaint of our patient, often in the form of shortness of breath from acute pulmonary edema, or simply a comorbidity, understanding the pathophysiology of this disease is key to operating as an informed, and competent EMT or Paramedic.
Prior to reading this article if you are unfamiliar with either basic cardiac anatomy, or bloods pathway through the heart, both are key to understanding Congestive Hearty Failure. I highly recommend you view the articles linked if you feel there are gaps in your knowledge on either of these topics.
Heart Failure: Overview
Heart Failure is a disease process characterized by the hearts’ inability to adequately pump enough blood to the tissues of the body and/or lungs. Both the Right and Left sides of the heart can succumb to this pathologic process, and while heart failure can happen individually, for instance Left Sided Heart Failure vs. Right Sided Heart Failure, there is also the potential for Biventricular Heart Failure, in which both the Right and Left ventricles are failing to pump adequately to supply the pulmonary and systemic tissues.
Heart Failure most commonly arises as a result of Coronary Artery Disease (CAD) and Myocardial Infarction (MI) commonly referred to as a heart attack. After an MI, normal contractile heart tissue dies as a result of either lessened or absent perfusion from an occluded coronary vessel. Dead, rigid scar tissue replaces healthy contractile cardiac tissue that typically composes the heart in these areas, and lessens the contractility and contractile force of the heart. This lessens the hearts ability to keep up with metabolic demands of the body, and can lead to heart failure.
Other causes of heart failure include; Pulmonary Embolism, Hypertension, disorders of the valves within the heart, cardiomyopathy, congenital defects, or drug ingestion. Such pathologic processes typically either diminish the contractility of the heart, or increase vascular resistance, resulting in the hearts need to work harder to create enough pressure to push through the semilunar valves and into the vessels and tissues of the lungs and body.
Diminished contractility of the heart is often well illustrated in a decrease in Ejection Fraction, which is the percent of blood that is pumped out of the ventricle (nearly always left) with each contraction. This value is expressed as a percentage. For instance, an ejection fraction of a normal healthy left ventricle is typically 55%-70% meaning that if there is 100ml of blood in the ventricle with each ventricular contraction between 55 and 70ml of blood will be pushed out of the ventricle into the body.
Heart Failure: Left vs. Right
While the disease process that results in right and left heart failure is similar, the resulting signs and symptoms of right and left heart failure can vary significantly. Thinking first about the anatomy of the heart and the path that blood takes through the heart, the main difference in distinguishing between the right and left sides of the heart is what is being perfused and where this blood is coming from.
With the left side of the heart the left atrium receives blood from the pulmonary (or pulmonic) circuit through the pulmonary veins, and the left ventricle ejects blood that goes to the systemic circuit to perfuse the cells of the body. Now imagine that some of the blood that would normally be ejected into the systemic circuit is instead beginning to back up in the left ventricle as the ventricle cannot pump blood effectively. This collecting blood will soon not only be increasing pressure and backup within the left ventricle, but as blood continues to back up it will back up and affect the left atrium as well. This backup will continue to work its way up through the pulmonary veins and into the vessels of the lungs where the increase in pressure will begin affect the capillaries in the lungs and their relation to the alveoli.
This increase in oncotic pressure within the capillaries will result in their “leaking” fluid into the lungs. These capillaries play an important role in respiration, as they exchange CO2 and O2 with the alveoli within the lungs, allowing blood to become oxygenated, and allow waste products to be released. This increase in capillary pressure, as well as the accumulation of fluid around the capillaries creates an environment that is significantly less friendly for gas exchange, and decreases respiratory efficiency. This in turn can lead to hypoxia and shortness of breath. The fluid accumulation that results from this pathologic process is known as pulmonary edema, and is an indicator for a high index of suspicion for left sided heart failure.
The right side of the heart on the other hand receives blood from the systemic circuit via the inferior and superior vena cava, as well as the coronary sinus, all of which enter the heart via the right atrium. This blood is ejected into the pulmonary (pulmonic) circuit via the right ventricle through the pulmonary artery. While the backup in blood flow on the left side resulted in fluid accumulation and increased vessel pressure within the lungs, this backup on the right side will results in similar issues, but occur in the body or systemic circuit rather than within the lungs.
Heart Failure: Common Signs and Symptoms
Significant findings of left heart failure may include rales, commonly referred to as crackles, as well as cardiac wheezing. Either or both lung sounds will likely be present upon auscultation of the lung fields, and are a result of the fluid accumulation (rales) and bronchiole inflammation, most often found in chronic heart failure patients (cardiac wheezing).
Right-sided heart failure will commonly present with peripheral edema, commonly found in the ankles (pedal edema) and may pit or leave a prolonged indentation when sufficiently pressed upon. The liver and many other tissues of the body are also susceptible to becoming edematous, and abdominal swelling and right upper quadrant tenderness are not uncommon findings in right sided heart failure patients. Another sign of right-sided heart failure is jugular vein distention as blood begins to back up and engorge veins leading to the superior and inferior vena cava.
Heart Failure: Systolic vs. Diastolic
Beyond right versus left sided, heart failure can be further broken up into systolic and diastolic heart failure. As you recall from my bloods pathway article diastole is the stage at which the heart is at rest and the atria and ventricles are passively filling with blood. During diastolic heart failure, there is an insufficiency in the hearts ability to fill with blood adequately. This failure often results from scar tissue, which has resulted from a previous MI, reducing the elasticity of the heart, and preventing the blood from filling the chambers to their normal capacity.
Systole on the other hand is characterized by cardiac contraction and the ejection of blood from a chamber. Simply put systolic heart failure is the hearts inability to pump adequately, and heart function during contraction is decreased.
Diastolic heart failure can be thought of as a stroke volume problem, as less volume is allowed to accumulate. Systolic heart failure can be thought of as an ejection fraction problem, as less blood as a percentage is pushed out with every contraction.
Heart Failure vs. Congestive Heart Failure
While seemingly a complex problem, heart failure can simply be viewed as a hearts inability to pump adequately. This failure of the heart to adequately do its job can lead to a backup and pooling of fluid in places that fluid should not be. This fluid pooling, described in numerous pathologic processes above, are what divide normal heart failure from Congestive Heart Failure (CHF). This fluid, or congestion, will typically pool in the lungs during left sided heart failure, and in the susceptible areas of the body during right-sided heart failure. As such CHF can be viewed as simply heart failure that has continued uncontrolled until fluid has begun to accumulate.
Paramedic Heart Failure: ALS Treatment and Recent Studies
Prehospitally, my county in California relies solely on non-invasive positive pressure ventilation through CPAP and pharmacologic vasodilation with both transdermal and sublingual Nitroglycerine in treating shortness of breath of cardiac origin. While many counties follow the LMNOP algorithm, providing Lasix, Morphine, Nitro, Oxygen, and Positioning/Positive pressure I believe my counties protocol is sufficient, and potentially more beneficial. The thought process behind such treatment is as follows.
CPAP has been proven to “decrease work of breathing, stent open alveoli during the entire respiratory cycle, and decrease afterload.” Treatment of patients with non-invasive positive pressure ventilation has been proven in studies to decrease ICU admission in patients with acute pulmonary edema, reduce hospital mortality, and intubation rates.
Nitroglycerine decreases both preload and afterload, which in turn leads to an increase in cardiac output and decreases vascular resistance. Both of which are extremely beneficial to patient outcome.
Furosemide (Lasix), while an NREMT approved medication, is not currently used within my county, and I have no experience with it prehospitally. As a Tech however I have seen physician prescribed loop diuretics as a nearly ubiquitous treatment for patients who present with acute exacerbations of CHF. Lasix has recently come under scrutiny however for its universal application in patients with acute pulmonary edema.
For a more in depth look into the physiology and pharmacology associated with furosemide in acute pulmonary edema I strongly suggest you view the article by Dr. Anand Swaminath linked below in my references section. Briefly stated this article articulates how acute pulmonary edema is not a byproduct of fluid overload but rather fluid shifting. Dr. Swaminath cites a 2007 study showing that only 50% of patients have a weight gain of over 2 lbs. Dr. Swaminath states that a more evidence based approach does not require diuresis but rather the treatment of improving vascular resistance, and preload through positive pressure and vasodilation.
Dr. Swaminath also discussing the negative effects of Lasix, which results in diminished left ventricular function, and increases in ventricular filling pressure, mean arterial pressure and systemic vascular resistance. While I highly recommend viewing his article on the topic, I cannot advocate against the use of furosemide in a prehospital setting if it is what your local protocol mandates, but rather am mentioning it as an interesting point of discussion, and something that you may seem moved away from in your future in medicine.
EMT Heart Failure: BLS Treatment:
If the patient has physician prescribed Nitroglycerine, is experiencing chest pain, and is having cardiac based shortness of breath as an EMT-B according to national registry you can assist the patient in administering one, 0.4mg dose of their own nitroglycerine medication every 3-5 minutes to a total of three doses given their systolic blood pressure is greater than 90. Always check a blood pressure before every dose of medication administration and always follow local protocol regarding medication administration. Nitroglycerine has numerous contraindications, and remaining thorough in your understanding of Nitroglycerines pharmacological effects, as well as your patients history, will allow you to safely assist your patient to improve their symptoms.
These patients often times have orthopnea, or difficulty breathing while lying down, so sitting these patients in a semi-fowlers or high fowlers position may greatly improve patient comfort, and reduce the sensation of drowning, and reduce anxiety in these patients. Positive pressure is ideal, but oxygen can be delivered via nasal cannula or NRB mask if o2 saturation dips below 94%, and should be titrated to maintain a reading of over 94%.
I hope you found this article regarding heart failure useful, and wish you all the best of luck in your future exploits in medicine. If you have any questions, comments, or disagree with anything posted on this article please use the contact me form to get in touch with me. Also, please sign up for my newsletter for infrequent and informative articles regarding emergency medicine. Cheers.
Swaminathan, Anand MD( 2016) Myths in Emergency Medicine: Rethinking Furosemide in Acute Pulmonary Edema