EMS, Field Identification Of CHF


Article Author:
Connor Bounds


Article Editor:
Scott Goldstein


Editors In Chief:
Mitchell Farrell
Brian Froelke


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Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
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Daniyal Ameen
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Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
2/27/2019 9:08:22 PM

Introduction

Congestive heart failure (CHF) can arise from multiple causes, all resulting in decreased perfusion of body tissues. CHF may result from a drug overdose, infection of the myocardium, myocardial infarction, chronic hypertension, and numerous other causes. It may also be acute or chronic. Regardless of either the acute or chronic nature of CHF, it can range from mild symptoms to a serious emergency.[1][2][3][4]

Etiology

The beginning of CHF arises from failing compensatory mechanisms. To understand the pathophysiology of CHF, one must first look at the mechanisms used in patients to maintain cardiac output in the failing heart.

Epidemiology

Nearly 5.7 million people in the United States suffer from CHF and is the fastest growing cardiac disease in the United States, according to the American Heart Association. Though the body has multiple compensatory strategies to maintain cardiac output (CO) and end-organ perfusion, they may fail. These compensatory mechanisms consist primarily of neurohormonal systems.

Pathophysiology

One such mechanism is the renin-angiotensin-aldosterone system. Initial insult to the heart via any one of the mechanisms listed in the previous section may result in a decreased systolic blood pressure. Hypotension acts to release renin in the kidney, which cleaves the prohormone angiotensinogen, producing angiotensin I. This protein is released into circulation, where it is converted by angiotensin-converting enzyme (ACE) to angiotensin II. Angiotensin II has strong vasoconstrictive properties, raising arterial pressure. Angiotensin II acts on the kidney to reduce excretion of salt and water, increasing arterial pressure further. This mechanism occurs over the span of approximately 20 minutes.

Another mechanism is the sympathetic nervous system (SNS), whereby systolic blood pressure is rapidly regulated. The sympathetic nervous system measures systolic blood pressure via baroreceptors located in large systemic arteries, specifically in the internal carotid artery and the wall of the aortic arch. When this occurs, the central nervous system acts to constrict peripheral vessels. Regarding the heart, a specific region of the brain stem transmits sympathetic nervous system impulses to the heart, increasing heart rate and contractility (positive chronotropic and inotropic effects). These effects are accomplished primarily via the release of epinephrine (from adrenal glands) and norepinephrine (released from sympathetic nerves near the heart).

Another mechanism is the release of atrial natriuretic peptides (ANPs) from the atria. As heart failure produces increased atrial stretching via decreased cardiac output, Atrial natriuretic peptides are released from the atria. The second type of natriuretic peptide is known as brain natriuretic peptide (BNP). These peptides act to promote water and salt loss in the kidneys, as well as inhibit the renin-angiotensin-aldosterone system, promoting overall fluid loss, and decreasing the work of the failing heart. Additionally, both atrial natriuretic peptides and brain natriuretic peptide serve as a sympatholytic, promoting a down regulation of the sympathetic nervous system.

Each of the above mechanisms fails or undergo changes in heart failure, resulting in a low cardiac output state.

As mentioned previously, the renin-angiotensin-aldosterone system is down-regulated when brain natriuretic peptides and atrial natriuretic peptides are released in heart failure. Overall, this promotes more fluid and salt retention in the kidneys, increasing the workload of the heart.

The means by which the sympathetic nervous system acts to promote heart failure is through an uncoupling of beta-1 adrenergic receptors from actual cardiomyocytes. Though beta-2 adrenergic receptors and alpha-1 adrenergic receptors do function to maintain inotropy, it is the beta-1 receptors that play a key role in the progression of heart failure. More specifically, as the disease progresses, beta-1 receptors decrease in number, and various enzymes important in cardiac contraction begin to decrease in function.

Ultimately, blood return to the right atrium is slowed. As blood return slows, this results in a damming up of blood in the pulmonic circulation. As blood remains stagnant, capillary hydrostatic pressure increases, becoming greater than both the interstitial hydrostatic and interstitial osmotic pressures. This produces filtration of plasma out of the alveolar capillaries and into the alveoli themselves, filling them with fluid.

History and Physical

Certain hallmarks for CHF include jugular venous distention (JVD), dyspnea/tachypnea, tachycardia, crackles in lungs, and pitting pedal edema. JVD is due to decreased venous return to the heart via the right atrium. As blood continues to back up in the system circuit, the superficial vessels of the neck may become swollen with blood. Dyspnea arises from decreased gas exchange at alveoli flooded with fluid. Tachypnea is a compensatory mechanism by which the body attempts to exhale excess carbon dioxide, and tachycardia acts to return blood to the lungs as quickly as possible to accomplish gas exchange. As plasma is filtered into the alveoli, crackles begin to be heard bilaterally. These crackles often are first noticed in the lower lung fields, as filtered plasma is affected by gravity. Waveform capnography may show normal end-tidal carbon dioxide levels and waveform, as opposed to elevated carbon dioxide and abnormal waveform found in bronchospasm.

Evaluation

Field evaluation involves careful history and physical exam. Further testing in the field is not available.

Treatment / Management

Reducing the workload of the failing heart is the primary goal of treating CHF. This goal is accomplished by increasing oxygenation through supplemental oxygen, increasing airway pressures, and decreasing pre-load. A nasal cannula,  a non-rebreather, or (preferably and if tolerated) by continuous positive airway pressure or CPAP may deliver supplemental oxygen may. CPAP acts to provide continuous pressure to the alveoli, thereby opening any alveoli that have collapsed (a condition known as atelectasis), and increasing the pressure within the alveoli, forcing fluid back into the alveolar vasculature. Additional medications like nitroglycerin or other vasodilators act to dilate blood vessels. Vasodilation promotes a decrease in capillary hydrostatic pressure, which allows the increased alveolar pressure of CPAP to force the filtrate (essentially blood plasma) from the alveolar sac back into pulmonic circulation. Both vasodilators and CPAP should be judiciously used, if not withheld entirely, in the patient with low systolic blood pressure (usually considered less than 90 mmHg to 100 mmHg) and/or recent erectile dysfunction drugs. Follow local protocol or contact medical direction if any question about CPAP or nitroglycerin use exists.

Another important tool in monitoring the efficacy of CHF treatment is waveform capnography. In the case of determining CHF, asthma, or chronic obstructive pulmonary disease (COPD) as a cause of a patient’s respiratory distress, capnography is extremely useful. Both the pulmonary edema associated with CHF and the bronchospasm from asthma may produce wheezing in patient’s, the actual end-tidal carbon dioxide waveforms are different. A normal capnograph is rectangular in nature, indicating normal exhalation of carbon dioxide. As carbon dioxide is soluble in water, CHF patient’s will have a normal capnograph, even if they present to emergency medical services providers with wheezing. This is different from the shark fin appearance of a bronchospastic waveform.

Enhancing Healthcare Team Outcomes

The management of CHF is with a multidisciplinary team that includes an emergency department physician, nurse practitioner, cardiologist, internist, and intensivist. On the field, EMS can only assess the vital signs but cannot confirm the presence of CHF. The key is to keep the patient upright, provide oxygen and limit IV fluids. These patients need immediate transport to a medical facility. the role of EMS is not to make a diagnosis but to safely transport the patient without delay.[1][5][6]


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EMS, Field Identification Of CHF - Questions

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A 65-year-old male calls 911 for a complaint of dyspnea. Upon arrival, you are directed to a back bedroom where you find the patient propped up on several pillows. His respiratory rate is 30 per minute and shallow in nature. His blood pressure is 150/85 with a strong, regular heart rate of 120. Upon laying him flat upon your stretcher for transport, which of the following changes to his clinical condition would you expect to arise?



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A patient activates emergency medical services for a complaint of difficulty breathing. Upon arrival, the crew finds a 67-year-old male in severe respiratory distress. Vitals are blood pressure 156/102 mmHg, heart rate 140 bpm, respiratory rate 32/minute, and pulse oximetry of 82% on room air. The patient’s family states that he has a history of previous myocardial infarction treated with a stent, and insulin dependent diabetes mellitus. Which of the following should be administered to reduce pre-load on the patient’s potentially failing heart?



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What is the expected waveform and relative carbon dioxide levels on waveform capnography in the patient with congestive heart failure?



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Which of the following is a contraindication to continuous positive airway pressure (CPAP) in patients experiencing congestive heart failure exacerbation?



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Which of the following is the most specific physical exam finding in the patient with congestive heart failure (CHF)?



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EMS, Field Identification Of CHF - References

References

Mosesso VN Jr,Dunford J,Blackwell T,Griswell JK, Prehospital therapy for acute congestive heart failure: state of the art. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors. 2003 Jan-Mar;     [PubMed]
Brill AK,Pichler Hefti J,Geiser T,Ott SR, The SERVE-HF safety notice in clinical practice - experiences of a tertiary sleep center. Sleep medicine. 2017 Sep;     [PubMed]
Thoonsen B,Engels Y,van Rijswijk E,Verhagen S,van Weel C,Groot M,Vissers K, Early identification of palliative care patients in general practice: development of RADboud indicators for PAlliative Care Needs (RADPAC). The British journal of general practice : the journal of the Royal College of General Practitioners. 2012 Sep;     [PubMed]
Archacki S,Wang Q, Expression profiling of cardiovascular disease. Human genomics. 2004 Aug;     [PubMed]
Sze S,Pellicori P,Zhang J,Weston J,Clark AL, Identification of Frailty in Chronic Heart Failure. JACC. Heart failure. 2019 Feb 4;     [PubMed]
Yineng Zheng,Xingming Guo, Identification of chronic heart failure using linear and nonlinear analysis of heart sound. Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference. 2017 Jul;     [PubMed]

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