Acute Coronry Syndrome:
Acute coronary syndrome (ACS) is a blanket term to describe all chest pain (or its equivalents) resulting from a cardiac point of origin. In general, this encompasses Angina pectoris, NSTEMI, and STEMI.
ACS is the result of ischemia to the cells of the myocardium. The primary cause of cardiac ischemia is a reduction in perfusion to the tissues as a result of accumulation of arterial plaques; also known as atherosclerosis. Plaques develop as a result of damage to the internal lumen of the coronary arteries. High blood pressure, high cholesterol, and elevated blood glucose levels are common culprets here. When the lumen (tunica intima) is damaged, fibrolipid plaques develop at the area of injury. Over time these plaques cause significant narrowing of the coronary arteries. In patients where this is the primary problem, we see the development of Angina Pectoris. These patients are able to adequately perfuse the heart at normal levels (normal for them) of exercise and exertion, however an increase in oxygen demand will result in ischemic chest pain. Typically angina is managed well with nitroglycerine and management of chronic hypertension. When the pain associated with angina follows a predictable pattern associated with abnormal exertion, and is releived with nitro and rest, we call it STABLE angina. However, if there is a change in the factors that provoke and palliate the pain, such as pain at rest, during sleep, or inability to gain releif, we call this UNSTABLE angina. Unstable angina may represent further progression of atherosclerotic heart disease, or it can indicate that the patient is suffering a more severe cardiac event.
NSTEMI and STEMI are both names referring to what is classically known as a “heart attack” (myocardial infarction). In a myocardial infarction (MI), a plaque affixed to the tunica intima ruptures. Within the fibrolipid plaque are fibrin, and prothrombotic factors.When platelets in the blood come into contact with the area of rupture, they are activated and begin to form a clot in this area. The result is a partial (NSTEMI) or complete (STEMI) occlusion of the arterial lumen, and subsequent ischemia of the tissue beyond the clot. When this happens we see characteristic changes in the ecg of the patient. If there is still some degree of distal perfusion, we will see changes in the ST segment of the ecg associated with the affected area of the heart. Ischemia typically presents with ST segment depression, and T wave changes such as peaking or inversion. Repeat 12-lead ecgs may show these changes to be dynamic, meaning they will change over a period of time. If the occlusion is complete, and there is no perfusion beyond the clotted area of the artery (infarction), we see a characteristic ST segment elevation in the leads associated with the affected area of the heart. Generally we will also see ST segment depression in leads that are reciprocal to the leads in which we see elevation.
In EMS, we do not have the diagnostic ability to rule out myocardial infarction definitively. The only test that can do so is a blood test for elevated troponin levels. Troponin is a cardiac enzyme that is released when myocardial cells die. For this reason, we treat all chest pain that is suspected to be of cardiac origin, as though it is an MI. In EMS we have several tools for this purpose. First, these patients should receive ASA. ASA is a platelet aggregation inhibitor. What this means is that it prevents the formation of blood clots. ASA will not break up the existing clot, but it will prevent it from getting worse. Next we have nitroglycerine, which triggers vasodilation systemically. This reduces the preload and afterload to the heart, reducing the workload of the heart, Nitro also has vasodilatory affects on the coronary arteries themselves, and may allow additional perfusion to take place. We also have opioid pain medications such as morphine to address the sympathetic effects of epinephrine in the body that are brought on by pain. Ultimarely these patients need to be transported to a hospital capable confirming MI. In the case of STEMI, the patient needs to go to a hospital capable of cardiac catheterization, and stent placement.
Types of MI:
Just like ice cream, MI comes in a few flavours; namely ANTERIOR, INFERIOR, and POSTERIOR.
Anterior MI:
Occlusion of the left coronary artery, the left anterior descending, or the left circumflex arteries results in ischemia of the anterior portion of the left ventricle. This results in reduced ejection fraction, and difficulty overcoming afterload at the end of the cardiac cycle. Pressure in the left ventricle builds, and a backflow of blood occurs into the pulmonary veins, and into the vasculature of the lungs. Ultimately pulmonary edema can develop if the pressure is high enough. The anterior MI commonly presents with central chest pain, dyspnea, nausea, diaphoresis, hypertension, and tachycardia. Arrhythmias such as SVT, VTACH, and V-Fib may develop.
Inferior MI:
Occlusion of the right coronary artery causes ischemia of the inferior right ventricle. The ability of the RV to pump is compromised, and the stroke volume is reduced. The RCA also feeds the SA node in many people, so we see the problem compounded as bradycardia may also be present, meaning the heart is unable to compensate for reduced stroke volume with an increase in heart rate. We see acute right heart failure, hypotension, chest pain, diaphoresis, altered LOA, and nausea with these patients.
Posterior MI:
When there is occlusion of the circumflex artery we can see ischemia affect the posterior portion of the heart. This physically presents as an anterior MI would, however, ECG changes will be slightly different. Rather than having ST segment elevation in the anterior leads, we will see uniform ST segment depression. A 15 lead ECG will reveal elevation in V8 and V9.
Nitro and the inferior STEMI:
Because the inferior STEMI causes hypotension with a compromised ability to compensate due to SA node interference, we do not want to give nitrates. Doing so will cause further drop in systolic blood pressure, and could potentially prove to be fatal.
Heart Failure:
Heart failure can be acute or chronic, and results from structural changes to the cardiac muscle due to ischemia. The causes of ischemia can vary from inflammatory conditions, and long term coronary artery disease to cardiac infection, to acute ischemia. Even respiratory conditions such as COPD can cause remodelling of the myocardium due to long term pulmonary hypertension (Cor Pulmonale). Regardless of the underlying cause, heart failure can be divided into left sided heart failure, and right sided heart failure, although both tend to occur together to some degree. When heart failure is sufficient to cause backflow of blood into the lungs and systemic circulation, we call it congestive heart failure (CHF).
Left Sided Heart Failure (LSHF):
In LSHF the left ventricle is unable to pump effectively, resulting in a reduced ejection fraction (the % of blood that exits the left ventricle during each beat). Because the stroke volume of the heart is reduced, and is insufficient to meet systemic oxygen demands, the body responds by increasing heart rate. While this effective over a period of time, there is an upper limit to which the body can raise the rate without negative results. When the increase in heart rate becomes insufficient to overcome afterload (the pressure in the aorta against which the heart must pump), there is backflow of blood into the pulmonary vasculature, pulmonary hypertension, and pulmonary edema.
Right Sided Heart Failure (RSHF):
The right ventricle is smaller than the left, as it relies on preload (Starlings law) in order to overcome pressure in the pulmonary artery and vasculature of the lungs. When the right ventricle fails, there is a reduced ability to generate sufficient pressure to overcome pulmonary afterload. The right ventricle may be able to hypertrophy to a degree in order to overcome this, but it lacks the musculature of the LV and has limited ability to compensate. The result is that blood backs up into the vena cava, and into systemic circulation. We see this manifest as peripheral edema, and ascites. The most common cause of RSHF is LSHF. The second most common is pulmonary hypertension that results from COPD.
In congestive heart failure (CHF) we see failure of both ventricles. The left ventricle is unable to overcome afterload in the aorta, and dilates as a result. Back-pressure causes pulmonary edema. Increased pulmonary pressure causes right sided heart failure. The cardiac septum shifts left, further reducing LS ejection fraction. Blood from the right side pools in the extremities and the core. Ultimately cardiac function deteriorates into a condition where the heart cannot perfuse itself, or the tissues of the body sufficiently to sustain life. This is called cardiogenic shock, and there is little that can be done to address it in the prehospital environment.
Common treatments for heart failure include:
Digoxin: Reduces heart rate and increases the force of contraction.
Furosemide (Lasix): A loop diuretic that removes excess circulating fluid volume through the kidneys.
HCTZ: Another diuretic.
Aldactone: A potassium sparing diuretic.
Beta blockers and calcium channel blockers.
In the EMS setting, patients with acute heart failure should be assessed for ischemic causes, as MI is frequently associated with LSHF. We may find ourselves treating for cardiac ischemia, as well as addressing cardiogenic pulmonary edema. Lets talk a bit more about Acute Cardiogenic Pulmonary Edema (ACPE).
ACPE:
Sometimes calle SCAPE (Sympathetic Crashing Acute Pulmonary Edema), ACPE is the accumulation of blood and plasma in the alveoli as a result of acute left sided heart failure, OR exacerbation of existing heart failure. These patients present with dyspnea, cough (typically with frothy sputum that may or may not be pink tinged), hypertension (think SBP >180mmHg), and rales auscultated (typically globally). If the ACPE is in an early stage, the patient may also present with wheezing, similar to that heard in asthma and COPD (Cardiac Wheeze).
Treatment should involve establishing IV access, provision of nitrates to reduce afterload, application of CPAP/BIPAP, and acquisition of 12-lead ecg to assess for evidence of ischemia. These patients will need to be transported rapidly to an appropriate facility, for what will likely be an inpatient stay.
Pulmonary Embolism:
While sometimes considered a respiratory problem, pulmonary embolism (PE) is actually a problem of the pulmonary vasculature, and affects the heart. In pulmonary embolism, a thrombus breaks loose from a distal site (usually a deep vein in the leg) and travels as an embolus, through the right side of the heart. The embolus then lodges in a branch of the pulmonary artery. The lung tissue distal to the blockage is no longer perfused, and does not participate in gas exchange, causing V:Q mismatch. This leads to retention of CO2 in the bloodstream and reduced oxygen saturation. More significant, however, is the effect on the right side of the heart. The embolus occludes a pulmonary artery branch, which significantly raises afterload against which the right ventricle must pump. The only way the body can compensate is to raise preload through systemic vasoconstriction, and increasing heart rate. Unfortunately, the blockage is not going anywhere, and there is a limit to how much the heart can compensate. This results in RSHF, peripheral edema, hypoxia, hypercarbia, acidosis, and cell death. Eventually the heart will fail; entering dysrhythmia. Death is the result unless treatment is reached.
These patients typically present with sharp, well localized, pleuritic chest pain, diminished SPO2 with clear breath sounds, diminished ETCO2 (because gas exchange cannot occur), hyperventilation, diaphoresis, pallor, and DVT or a history of risk factors suggestive of DVT. Common prothrombotic conditions include: Pregnancy, oral contraceptive use, age >60, prolonged immobilization, recent long distance travel, and cancer.
EMS treatment is aimed at rapidly identifying the situation, providing supplemental oxygen, establishing IV access and maintaining normotension, and ruling out MI with 12-lead ECG. The only definitive treatment is available in hospital, so rapid transport is crucial.
Pericarditis:
The pericardial sac surrounds the heart and contains fluid that allows for smooth, lubricated, contraction and expansion of the heart muscle. Occasionally infection can cause inflammation of the pericardial sac, and accumulation of cellular debris in the area between the visceral and parietal layers. This inflammation of the pericardial sac is known as “Pericarditis”. If the infection causes excess fluid or pus to form in the pericardial fluid space, the patient is said to have a pericardial effusion. Depending on the severity of the effusion, the patient may develop tamponade; a dangerous condition in which the heart is unable to expand properly during the diasolic phase, and fill volumes in the ventriles are reduced, dropping cardiac output.
Pericarditis is often cited as a STEMI mimic because it too presents with ST segment elevation when 12-lead ecg is performed, however, the ST elevation has a characteristic coved shape, and is present in all or nearly all leads. Pericaditis presents with central cehst pain, usually described as burning in character. The pain is typically exacerbated by lying flat and reduced by leaning the patient forward. Patients are generally febrile, and auscultation may reveal a pleural rub. Depending on the progression of the illness, you may see electrical alternans present on the ecg as well.
Treatment of pericarditis involves identification of the condition, establisment of IV access and potentially fluid support. While you arent wrong to treat for potential cardiac ischemia, the patient will ultimately have little benefit from such protocols. What the patient requires is transport to the ED for antibiotic therapy.
Comments