>> Understand why rapid intervention of cardiac emergencies is important.
>> Recognize signs and symptoms of the different types of cardiac emergencies.
>> Learn how to treat patients suffering from a cardiac-related problem.
Angina pectoris: Chest pain caused by oxygen deprivation to the heart.
Atherosclerosis: A disorder in which plaques of cholesterol and fats are deposited in the walls of arteries. The vessel walls become thick and hardened, which lessens circulation to areas normally supplied by the artery.
Cardiogenic shock: A sudden mental or physical disturbance caused by poor tissue perfusion as a result of decreased cardiac output.
Perfusion: Supplying an organ or tissue with nutrients and oxygen via the circulatory system.
Medic 1 and Medic-Engine 1 are dispatched to the Silver Hotel at 7545 Fourth Avenue, a residential hotel known for the elderly indigent, many with significant medical problems.
The EMS team is escorted to a seventh-floor room where they encounter a disheveled, unshaved and moderately emaciated 68-yearold male. He’s sitting upright in a lounge chair, slumped slightly to one side. He doesn’t have a shirt on and he’s visibly breathing, although shallow. His skin looks pale and mottled, and his hands and feet are cyanotic. He’s also noted to have circum-oral cyanosis.
When asked his name, he’s barely able to whisper “Abe” and it’s clear he’s not able to provide any further verbal assistance. The team quickly applies an ECG and oxygen saturation monitoring, and vital signs are achieved. Heart rate is 62 and Lead II ECG appears to be a junctional rhythm with a widened QRS complex. Cardiac defibrillation/pacing pads are applied. Blood pressure is 76/44 mechanically, and when auscultated, Korotkoff sounds can be heard from 74 systolic to complete cuff deflation.
Oxygen saturation is 84%. Lung sounds are mildly congested in the upper lobes, almost a mix of rhonchus and rales, and there’s notably not enough air movement to hear any lower lobe sounds. As soon as this is recognized, bagvalve mask (BVM) ventilatory support is initiated, with a high-flow oxygen reservoir. End tidal carbon dioxide (EtCO2) is applied to the BVM. Capnometry is measured at 68 mmHg and capnography is unrevealing.
Nearby prescription medication bottles are found to be empty, most notably beta-blockers, antihypertensives and cholesterol controllers.
IV access is established. A small bolus of 250 mL of normal saline (NS) solution is given and a dopamine dose is prepared with 400 mg dopamine mixed with 250 mL NS. An updated blood pressure reading of 74/66 is noted, with heart rate remaining in the 60s. Appropriate dopamine IV therapy is established.
Cardiac emergencies, including ischemic episodes, myocardial infarction (MI), and cardiac pump failure leading to circulatory collapse, require efficient and rapid interventions to help return cardiac perfusion, with the ultimate goal of survival. Cardiac emergency care and treatment are solely a matter of survival. When the bell rings, the fuse has already been lit and the clock is ticking. It’s time to act.
In the United States, approximately 1.5 million people suffer an MI each year—of these, almost 500,000 will die.1 Genesis of EMS care and training has evolved from this epidemiology, and although interventional care has become exceedingly successful, it still relies on EMS providers doing the right things at the right times and delivering these patients to the right resourced medical facilities.
There’s a wide range of cardiac emergencies that can develop into rapidly evolving life-threatening situations, including ischemic events, evolving or migrating cardiac circulation events, chronic exacerbation problems and cardio circulatory collapse issues. The EMS provider should hone in on recognition and treatment for any of these, and others, to help the patient survive. The maintenance of perfusion, especially cardiac perfusion, is the key to survival of cardiac emergencies.
Basically, the heart is a hollow muscular organ in the center of the thorax, known as the mediastinum, between the right and left lung. There are four chambers with four valves, and although it’s one organ, it acts as two pumps. The right side receives blood from the body and pumps blood to the lungs, and the left side receives blood from the lungs and pumps blood to the body.
The atria (upper) and the ventricles (lower) chambers are like muscular pump. The left ventricle seemingly has the largest mass, as it tends to require more energy to pump blood to the entire peripheral circulatory system. The bicuspid valve leads out of the left atrium to the left ventricle, where the aortic valve leads out of the left ventricle into the systemic circulatory system. The tricuspid valve leads out of the right atrium into the right ventricle and the pulmonic valve leads out of the right ventricle into the pulmonary circulatory system. (See Figure 1, above.)
The entire pump system is orchestrated by the cardiac conduction circuit, where impulses are generated and conducted through various pathways that produce each heartbeat. The human body can regulate these impulses with regards to excitability, automaticity and conductivity (timing). The autonomic nervous system regulates the cardiac conduction circuit, as well as other factors affecting the entire cardiac cycle.
The sinus (SA) node, located in the atrium, releases an impulse that causes depolarization of the atrium. The impulse then travels to the atrial-ventricular (AV) node, where the conduction of the impulse is delayed long enough to allow mechanical movement of the blood volume into and out of the varying chambers. The impulse, once released from the AV node, travels through the Purkinje network, depolarizing the ventricular cardiac cells, and creating pumping action to the systemic circulatory system and the pulmonary circulatory system.
The heart’s circulatory system is composed of a network of arteries and veins. The arteries are referred to as coronary arteries—the two main are the right and the left—which originate at the base of the aorta and funnel into the right and the left sides of the heart.
Any disease process that affects any human body system or component undoubtedly has a role in altering any or all parts of the cardiac cycle, either acutely or subtlety. One of the most common (and probably the most silent) disease processes is atherosclerosis. (See Figure 2, above.) This is the accumulation of various types of fats inside the arteries, causing narrowing of the arteries and varying degrees of blockages that create a decrease in oxygen- rich circulation to the downstream tissues.
Many people develop conditions related to circulatory insufficiency, including cardiac ischemia, both chronic and acute, and MI. Dependent on the ensuing damage caused by these conditions, varying levels of other acute conditions may develop.
BLS and ALS assessments are critical, especially primary assessment practices. Evaluation of initial provider impression should include the presence of chest pain. The PQRST method is a popular tool:
P – Provoke
Q – Quality
R – Region, radiation, recurrence
S – Severity
T – Time
The method also looks for dyspnea, syncope, abnormal heart rate or palpitations, and past medical history.
Coronary insufficiency created by the effects of atherosclerosis can be associated with the primary symptom of angina pectoris. This literally means squeezing pain in the thorax, and is a result of an oxygen supply and demand deficit. Angina can be classified as stable or unstable. Modern technology and treatment, primarily cardiac angioplasty, has resulted in a decrease of stable angina pectoris patients being sent home with the chronic condition. The initial care provider should be highly suspicious of an unstable development should this issue arise in the patient’s history evaluation.
These patients, both BLS and ALS, should be treated as if an acute MI is suspected. The overall goal is to reduce the oxygen supply and demand deficit. A good deal of concern should be focused on emotionally calming the patient and helping to decrease anxiety. Physical exertion should be held to a minimum, and the patient shouldn’t be allowed to ambulate or strain to move. A 12-lead ECG should be accomplished and, dependent on protocol, the patient should be considered for transport to a known ST elevation MI (STEMI) receiving facility.
If oxygen saturation measurement is available, supplemental oxygen should be titrated to the reading, and if not, applied with a device that provides the best level of comfort for the patient and avoids hyperoxygenation.
If appropriate, the patient should be allowed and assisted to take prescribed nitroglycerin, or paramedics should administer nitroglycerin according to local protocol. IV access should be established should the need arise to deliver other medications, including morphine for vasodilatation and pain control
Vital signs should be closely monitored, as well as the level of pain, and continued therapies should be employed during transport to the hospital.
Your patient’s acute coronary syndrome (ACS) event may continue to worsen if coronary artery occlusion persists beyond the ischemic phase. The symptoms of myocardial injury will thus continue, as they had for ischemia, with chest pain, shortness of breath, jaw pain and fatigue. You may notice the T wave becomes wider and more peaked in shape. The ST segment will now begin to elevate as the J point moves above the isoelectric line. Once the J point is elevated by 1 mm or more, the patient is now considered to have an acute MI. If this occurs in two or more anatomically contiguous leads, the patient is considered to have a STEMI.
STEMI patients benefit most from percutaneous coronary intervention, also known as a cardiac cath. During an MI, the affected cells begin to die and no longer conduct impulses. Over the next few hours to days the ECG will begin to develop a widened Q wave that can be viewed as the first downward deflection following the P wave. If the Q wave is greater than four milliseconds, it’s considered to be indicative of infarction.
In the wake of an MI and the subsequent pathological damage inflicted on the heart, the pumping action and the cardiac cycle can become acutely weaker and begin to fail. Dependent on the amount of damage and the area of the damage, a patient may develop acute signs and symptoms of cardiogenic shock, which has a high degree of likelihood of progressing to full cardiac arrest. Recognition and treatment of this condition is paramount to avoiding terminal complications.
Inclusive of signs and symptoms of MI or a patient suffering cardiogenic shock will display significant and profound hypotension (with systolic blood pressure usually less than 80 mmHg), pulmonary congestion, tachypnea, altered level of consciousness and poor skin conditions.
Treatment includes appropriate positioning with supporting ventilator support. This can often be in the form of CPAP or BVM ventilations with an increased oxygen concentration. An IV line should be established with dopamine or other favorable inotropic agents should be given. This patient should be transported as rapidly and safely as possible to a STEMI receiving facility. New therapies now exist that have been shown to help the weakened heart pump more effectively, including left ventricular assist devices and other implantable biomechanical aids.
ALS CASE STUDY CONTINUED
Abe is transported to a STEMI receiving facility, supine with slight incline of the head. Repeat vital signs indicate a heart rate of 72, still junctional with widened QRS. Blood pressure has improved to 78/66, and Abe is now opening his eyes and tracking, but still not able to speak well. SpO2 has improved to 92% with BVM support continuing. A 12-lead ECG obtained during transport indicates junctional rhythm, with evidence of left bundle branch block. Suggestive evidence of old inferior and septal infarcts is also present. The patient doesn’t have anterior thorax surgical scars, possibly suggesting previous angioplasty intervention care.
Abe is transferred to the ED team with BVM support continuing, a capnometric reading of 44 mmHg and a capnographic reading that shows a delayed expiratory period with slow return to baseline. IV is patent and dopamine remains at the desired rate.
Two days later, follow up was obtained from the paramedic base station and found that Abe had suffered another MI, had been noncompliant with his medications and follow-up medical care, and was difficult to stabilize after admission to the coronary intensive care unit, where he succumbed the following day.
Learn more from Fran Hildwine at the EMS Today Conference & Expo, Feb. 25–27, in Baltimore, Md. EMSToday.com
1. Roger VL, Go AS, Lloyd-Jones DM, et al. Executive summary: Heart disease and stroke statistics—2012 update: A report from the American Heart Association. Circulation. 2012;125(1):188–197.
- Bledsoe BE, Anderson E, Hodnick R, et al. Low-fractional oxygen concentration continuous positive airway pressure is effective in the prehospital setting. Prehosp Emerg Care. 2012;16(2):217–221.
- Hargarten KM, Aprahamian C, Stueven H, et al. Limitations of prehospital predictors of acute myocardial infarction and unstable angina. Ann Emerg Med. 1987;16(12):1325–1329.
- Morrison LJ, Long J, Vermeulen M, et al. A randomized controlled feasibility trial comparing safety and effectiveness of prehospital pacing versus conventional treatment: ‘PrePACE’.Resuscitation. 2008;76(3):341–349.
- Quintero-Moran B, Moreno R, Villarreal S, et al. Percutaneous coronary intervention for cardiac arrest secondary to ST-elevation acute myocardial infarction. Influence of immediate paramedical/medical assistance on clinical outcome. J Invasive Cardiol. 2006;18(6):269–272.
- Schwartz B, Vermeulen MJ, Idestrup C, et al. Clinical variables associated with mortality in out-of-hospital patients with hemodynamically significant bradycardia. Acad Emerg Med. 2004;11(6):656–661.
- Stub D, Smith K, Bernard S, et al. Air versus oxygen in ST-segment-elevation myocardial infarction. Circulation. 2015;131(24):2143–2150.
- Zughaft D, Harnek J. A review of the role of nurses and technicians in ST-elevation myocardial infarction (STEMI). EuroIntervention. 2014;10(Suppl T):T83–T86.
BLS CASE STUDY: CHF & CPAP
Ambulance 17, your BLS unit, is dispatched to 301 Main Street for a female with respiratory distress. After entering your response mode on the mobile data computer you’re advised the caller requests a silent approach and they’ve called EMS four times in the past year for the same problem.
As you arrive on scene you recognize the ranch style home and tell your partner about the last time you responded to this address: the patient wouldn’t tolerate the non-rebreather oxygen mask and the paramedic was preparing for intubation when you finally arrived at the ED. You also note that the closest three ALS units aren’t available tonight due to a rash of heroin overdoses, so you begin your silent prayer that the patient won’t be too sick.
As you approach the front door you notice it’s cracked open and you hear a weak, breathy, “Come in.”
“EMS!” you call out as you cautiously open the door. Your patient is sitting upright on the living room sofa with sweat pouring off her forehead and a productive cough. You think she looks a little pink.
“Please help me,” she whimpers. “I can’t breathe.”
Your partner obtains initial vital signs: pulse is 112, respirations are 32, blood pressure is 168/104 and oxygen saturation is 88% on room air. Your partner also notes the lung sounds are crackles to the nipple line, and the skin is pale, cool and diaphoretic as the patient is placed on 15 Lpm O2 via non-rebreather mask.
“Don’t talk. Save your energy and focus on your breathing,” you calmly tell the patient. You wish ALS was available because she could use some meds. “I’ll ask you some questions and I just need you to nod your head yes or no. Understand?” The patient nods her head yes.
“Has this ever happened to you before?” Yes, she nods.
“Have you ever been on a ventilator before?” She shakes her head no.
Your partner has been reading your mind and returns from the ambulance with the litter and the continuous positive airway pressure (CPAP) unit, which was placed in-service just a few months ago.
“Have you ever used CPAP?” You’re relieved when she enthusiastically nods her head yes.
You and your partner get the CPAP unit set up to provide a pressure of 10 cm water and 100% oxygen. As you turn on the unit, the patient readily holds the mask to her face as you position and tighten the head straps. After a few minutes you note she’s more relaxed and her skin is starting to dry. After you transfer the patient to the ambulance her repeat vital signs show a pulse of 96, respirations of 22, blood pressure 154/94 and oxygen saturation of 95% on 100% O2 via CPAP.