Cardiac History:
In addition to the standard NOPQRST-ASPN, SAMPLE questions, there are some important questions we want to ask in the setting of possible cardiac chest pain:
Where is the pain located?
Does the pain increase with deep inspiration or coughing?
Has the patient had an increase in the number of falls or dizzy spells lately?
Does the patient have palpitations?
How long has the pain lasted?
Is the patient SOB?
Angina, NSTEMI, and STEMI (The ACS):
ACS, or Acute Coronary Syndrome, is a bundle term that is meant to describe a group of pathologies that present with acute cardiogenic effects; primarily and mot notably: chest pain.
Angina: Angina occurs when arteriosclerosis and athersosclerosis cause the narrowing of one or more coronary artery. This leads to a decrease in coronary blood flow to the region(s) perfused by the affected vessel(s). In general, the patient is asymptomatic at rest. However, increased physical exertion, or physiological stressors lead to an increase in cardiac output. As the heart must increase its workload to meet physical demands, so to do its oxygen requirements increase. Unfortunately, the narrow and hardened coronary arteries do not permit enough blood flow to meet the oxygen requirements the heart now has. This results in ischemic chest pain. This is ultimately a transient phenomena, that can be relieved if the patient rests or uses nitroglycerine to allow for increased perfusion, and a decrease in preload. Angina presents with the following complex: -Retro-sternal chest pain, usually described as “Squeezing” or “heavy”. -Exertional dyspnea -Tachycardia -A HISTORY OF ANGINA (this is a condition that has already been diagnosed. Otherwise consider it a possible acute MI). Treatment is aimed at increasing cardiac perfusion, and reducing cardiac workload. To accomplish this we have nitroglycerine, and we need to reduce anxiety.
NSTEMI and STEMI: These are the traditional “heart attacks”. Both are conditions of ischemia and necrosis of cardiac tissue. The difference between the 2 is the degree of vascular occlusion occurring. In NSTEMI, a platelets aggregate to form a thrombus that partially occludes a coronary artery. In STEMI, the same process occurs, however there is a complete blockage of the coronary artery. Between the 2, STEMI is the more critical situation. While an NSTEMI causes ischemia, there is still a degree of blood flow occurring in the affected area. This means that damage takes much longer to occur and there is a longer timeline for treatment. In STEMI, the occlusion causes ischemia that rapidly progresses to necrosis of affected tissues, and irreversible damage to cardiac tissues. Both present with the same symptom complex: -Retro-sternal chest pain. Squeezing or heaviness, that may or may not radiate. -Dyspnea not relieved with rest. -Tachycardia or bradycardia depending upon the location of the injury. -Hypotension (RVI) or hypertension (anterio-lateral infarcts) -Diaphoresis -Pallor -Nausea -Dizziness or weakness A 12-lead ECG is the only way to determine STEMI in the prehospital environment. In the ED, Troponin testing can be used to definitively rule-in/out NSTEMI. Treatment for the PCP involves:
Early recognition and administration of ASA.
Acquisition of 12-lead ECG.
Providing Nitroglycerine unless the patient has evidence of an inferior infarct (Elevation in II, III, and aVF, with confirmation in V4R).
IV fluid management of hypotension.
Aortic aneurism:
A history of hypertension, smoking, or genetic predisposition (ie: Marfan's syndrome) can lead to the weakening of the wall of the aorta, typically in the arch. This ballooned area can eventually tear, and may begin to dissect. When this occurs there is a very good chance the patient will rapidly deteriorate and exsanguinate into the thoracic cavity. These patients usually present with:
-Sudden onset, “Tearing” chest pain that often is felt through into the mid scapula.
-Tachycardia (Baroreceptors in the carotid arteries detect the decrease in pressure because they are right next to the area of rupture. They signal an increase in HR to improve cardiac output).
-Hypertension until rupture occurs, then hypotension.
-Possible differences in blood pressure between both arms (If the tear is before one of the subclavian arteries, the limb on that side will receive less blood, and therefor have a lower pressure).
-Possible Stroke-like symptoms if the dissection affects a carotid artery.
-Possible symptoms of cardiac tamponade if the dissection occurs anterograde into the myocardium itself.
Treatment is very limited in this particular case. Our goals are essentially to recognize the symptoms, and to attempt to reduce the patient's anxiety. Early recognition and pre-alerting the hospital are essential as this patient needs surgery.
WE DON'T want to give this patient Nitroglycerine. They are in a state of shock, and we want to ensure the heart has sufficient preload to continue to compensate for blood loss. ASA is not recommended either, as we do not want to increase bleeding.
Congestive Heart Failure:
CHF is a condition that results in a decrease in SV and ultimately a decrease in CO. CHF is usually a problem that develops secondary to other underlying conditions, and it can affect the left side of the heart, the right side, or both sides. If CHF affects the left side of the heart, blood backs up into the lungs. If it affects the right side of the heart, blood backs up into the vena cava, and the peripheral circulation. For this reason, LS CHF usually presents with pulmonary edema, whereas RS CHF presents with pedal edema, JVD, and ascites. If untreated CHF eventually leads to death by cardiogenic shock. In CHF, the inability of the heart to effectively pump sufficient blood to maintain MAP, leads to hypoperfusion of the kidneys. This causes the release of Renin and the activation of the RAAS. This is actually counterproductive because increasing the preload and afterload on the heart actually adds more work to its already failing pump mechanism. It becomes a vicious cycle where the body is ultimately placed in a state of complete fluid overload. Both LS and RS HF have similar pathology with slightly different initial causes. The most common cause of RS HF is actually LS HF. LS HF is most commonly precipitated by ischemic heart disease or CAD. The left ventricle is damaged and cannot pump blood effectively because it loses contractility. As the left side fails it causes back pressure into the lungs causing pulmonary edema, and increasing the afterload that the right ventricle must pump against. The right ventricle hypertrophies in response, losing the volume it is able to pump with each beat (SV), and fluid backs up into peripheral circulation. Ultimately these patients need medications such as Digoxin to improve contractility, and diuretics like lasix to reduce systemic fluid volume. In the prehospital setting, we can address their needs with nitrates and CPAP.
Anterior MI: The acute anterior MI occurs due to a blockage of the LAD, and is usually seen presenting with:
Substernal chest pain
HTN
Tachycardia
Other associated symptoms such as nausea, dizziness, and diaphoresis.
The presence of an occlusion in the LAD causes infarction of the septal wall and anterior/anteriolateral left ventricle. This leads to loss of contractility of cardiac myocytes as necrosis occurs. The loss of SV from the LV causes a drop in cardiac output, with baroreceptors detect in the carotid arch. The only way for the heart to compensate is through increasing SVR with vasoconstriction, and to increase HR, in order to prevent hypotension and maintain MAP. Unfortunately increasing the afterload also puts more strain on the damaged LV which will eventually fail, resulting in death. Additionally, as seen in CHF, there is an acute onset of pulmonary edema due to the loss of LV SV. This is why all patients with ACPE should get a 12 lead even if they have a Hx of CHF. Treatment includes ASA administration, and administration of nitrates to reduce SVR and improve coronary artery perfusion.
Inferior MI: The inferior portion of the heart and the right ventricle are perfused by the RCA in 80% of people, and may be perfused by the LCX in 20%. As the RV is responsible for maintaining preload, infarction here causes a significant decrease in cardiac output, leading to hypotension. If the SA node is affected, the patient will also be bradycardic. If the SA node is not affected we will see compensatory tachycardia. Unfortunately, LS tachycardia is not sufficient to raise BP systemically without preload from the RV. As a result the heart will eventually fail and death will occur. Treatment includes ASA administration, and fluid resuscitation to improve preload. Nitrates can prove deadly for these patients as they will drop preload further and may cause sudden cardiac death. These patients are in a state of cardiogenic shock. Symptoms include:
Substernal chest pain
Hypotension
Bradycardia or tachycardia
Diaphoresis
Pallor
Possible altered mental status
Cardiac dysrhythmias:
Supraventricular Tachycardia (SVT): In SVT a regular, rapid, narrow complex, tachycardia occurs. This is due to a re-entry mechanism, where impulses are generated above the bundle branch bifurcation, causing both ventricles to depolarize simultaneously (hence the narrow complex). P waves are buried in the preceding QRS complex, however T waves are present. The rate is typically between 140 and 250 BPM. This may be persistent SVT, or come in periodic runs and be known as Paroxysmal Supraventricular Tachycardia (PSVT).
Causes: Several causes exist including:
Heart failure
Hyperthyroid
Heart disease
Lung conditions
Caffeine use or other stimulant drugs (cocaine, amphetamines, etc).
Symptoms:
Palpitations/fluttering in the chest
Dyspnea
Dizziness/light headedness
Syncope
Treatment: Unlike ischemic blockages to the heart, the symptoms of SVT are due to rate related perfusion deficits. This means that ASA is not effective as a tool for these patients. Obtaining an accurate BP, and a 12-lead ECG to confirm the rhythm should be first steps. If the patient's perfusion is low enough that SPO2 drops, administer supplemental O2. If IV certified, consider cannulation. There is nothing in the PCP scope to treat SVT, however ACP may consider Valsalva maneuver, Adenosine, or synchronized cardioversion if protocols are met.
Atrial Fibrilation (A-Fib):
A-Fib occurs when multiple foci in the atria generate impulses in a chaotic fashion. The result is quivering of the atria, and an inefficient ejection of blood into the ventricles. The result is the formation of micro-clots in the atria, which can become emboli if the patient is not on anticoagulation therapy. This presents as a rhythm that is irregularly irregular, with no discernible P waves. At high rates it may look like SVT, however the rhythm will not be regular.
Symptoms:
Dizziness/light-headedness
Syncope
Dyspnea
Weakness
Possibly chest pain
Causes:
MI
CAD
HTN
Congenital defects
Hyperthyroid
Stimulant use
Treatment: Depending upon patient presentation, ASA may be considered if MI is suspected as a causative event. 12-lead ECG should be obtained to get a full picture of the patient's cardiac conduction status. PCP scope does not have specific protocols for rapid A-Fib, however symptoms such as hypotension can be managed via IV bolus.
Atrial Flutter:
Atrial Flutter is caused by the same mechanism as A-Fib but presents with a regularly irregular, narrow complex, tachycardia. In slower rates, a saw tooth P wave pattern may be noted, however at faster rates (>150BPM) it may be indistinguishable from SVT. Treatment is not specific for PCP scope, other than obtaining 12 lead ECG, and managing hemodynamic stability. ACP may treat for narrow complex tachycardia under that protocol.
Ventricular Tachycardia (conscious):
V-Tach occurs when ectopic foci in the ventricles generate a repeating impulse to fire. This results in a wide complex, tachycardia that is usually >120bmp. V-Tach may be monomorphic, polymorphic, or a combination (Torsades).
Symptoms:
Dizziness
Dyspnea
Chest pain
Causes:
Heart disease
CAD
Electrolyte imbalance (K+)
Stimulant use
Medications (TCAs)
Treatment:
V-Tach is a critical rhythm that can rapidly deteriorate into fibrillation. Obtaining an 12-Lead ECG to confirm QRS duration and an accurate pressure are priority tasks. ASA may or may not be administered if the paramedic suspects ischemic causes. Defibrillator pads should be placed rapidly as a precaution. IV therapy should also be considered. PCP do not have a protocol for V-Tach, however ACP may consider protocols for wide complex tachycardia (amiodarone).
Top 5 Killer differentials for Chest Pain:
Aortic Aneurism
Myocardial Infarction
Tachydysrhythmia
Pulmonary Embolism
Pneumothorax
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