Chest Pain - Paramedic Guide PDF

CHEST PAIN EMRG 1230 N. Alaimo Heart Disease Major cause of mortality and morbidity Includes: Congenital heart defects Hypertensive heart disease...

CHEST PAIN EMRG 1230 N. Alaimo Heart Disease Major cause of mortality and morbidity Includes: Congenital heart defects Hypertensive heart disease Angina Heart attacks Arrhythmias Cardiac Stress Where circumstances force the heart to work harder to maintain cardiac output Not necessarily pathological There are fluxuations in cardiac output constantly dependent on the metabolic needs of the body Categorized as: 1. Direct stress 2. Indirect stress Direct/Indirect Stress Direct: Structural or functional alterations in the heart that reduce pump effectiveness Ischemia Infection Arrhythmias Congenital defects Indirect: Disorders external to the heart that increase the workload Anxiety Stress from an accident Atherosclerosis Thickening of the artery wall from accumulation of fatty material Chronic disease that can remain asymptomatic for decades Affects all arteries but predominantly coronary, renal, aortic, femoral, carotid and cerebral Chronic gradual narrowing of the arteries can eventually cause ischemia. Acute plaque rupture and subsequent thrombus formation can cause acute infarction. Creates issues as it leads to narrowing of the vessels and reduction of blood flow through them  2 Mechanisms: 1. Chronic gradual narrowing of the arteries can cause ischemia from reduced blood flow 2. Acute infarction can be caused by an acute plaque rupture and subsequent thrombus formation and occlusion of coronary arteries (MI) Typically begins in childhood as small amounts of fatty material are left in the vessel walls Over years, this buildup hardens and becomes plaque Narrows artery lumen size and decreases vessel elasticity Predisposing Factors Factors that cannot be changed: Age- more common after 40, especially in men Gender- women are protected by HDL (High Density Lipoprotien) until after menopause Genetics- affects fat levels, metabolism etc. Factors that CAN be changed: Obesity- high levels of LDL Cigarette Smoking- decreases HDL, increases LDL, promotes platelet adhesion, increases vasoconstriction Sedentary Lifestyle- sluggish blood flow Uncontrolled HTN- causes vessel wall damage Angina Pectoris Also known as Chest Pain Occurs when there is a deficiency of O2 for the heart muscle Can occur when the heart is working harder then usual and needs more O2 or when blood supply to the myocardium is impaired Usually, the heart can adjust its required levels of O2 with vasodilation, however with CAD this function is altered “Choking in the chest” Stable Angina Typically follows the same pattern for the pt. Predictable pain, location, severity etc. Insufficient O2 supply- anaerobic metabolism and accumulation of lactic acid and CO2 Typically lasts 1-5 mins and is relieved by rest Supply and demand: At rest, supply is OK in a person with Heart Disease despite the narrowed arteries, enough to meet the sedentary needs As soon as this same person exercises or experiences any type of stress, blood flow is not enough to meet the hearts needs Angina results Unstable Angina Same etiology as stable, however, the pain is more severe, different feeling and is not as easily relieved by rest or meds. Typically lasts > 15 mins Often indicative of Pre-MI angina Does not follow the same pattern as their usual Angina Unstable Angina Greater degree of obstruction of the coronary arteries High risk of imminent MI Benefits from early and aggressive treatment to prevent infarction Symptoms of Angina Recurrent, intermittent episodes of substernal chest pain, usually triggered by physical or emotional stress Tightness or pressure in the chest that often radiates into the neck or left arm Pallor, diaphoresis and nausea Can last a few seconds to much longer Angina Treatment Full Assessment, detailed questioning Try and rule in/out differential diagnosis What are some possible differentials? Assess for need for O2 ASA 12 Lead Nitro IV therapy Vitals should be done every 5 mins. Minimum Acute Coronary Syndrome Results from a prolonged cardiac disorder causing myocardial ischemia or infarction STEMI, Non-STEMI and unstable angina Typically caused by a rupture of the plaque in the arteries and subsequent thrombosis of the coronary artery Acute Myocardial Infarction (AMI) Part of the coronary muscle is deprived of blood flow until that part subsequently dies (infarcts) Most common cause is plaque rupture and thrombus formation Can also occur from spasm of a coronary artery with angina- arteries are already narrowed 3rd cause is the thrombus size blocks the artery Classified as either STEMI or Non STEMI Clinical presentation is the same, only an ECG differentiates them Blood work- troponin is typically the distinguishing factor AMI Location and size of the MI depends on which coronary artery is blocked Infarcted tissue area is inevitably surrounded by a ring of ischemic tissue. This is relatively deprived of O2 but is still viable Ischemic tissue often is electrically unstable, this causes cardiac arrhythmias Of all deaths from MI’s- 90% are due to arrhythmias Usually V-Fibb AMI Prehospital 12-lead ECGs are crucial in recognizing STEMI. Location and size of an MI depend on Which coronary artery is blocked Where along its course the blockage occurred Majority of infarcts involve the left ventricle. 90% of all deaths from AMI are due to dysrhythmias. Chest Pain- Most Common Sign Most common symptom is chest pain. Pain of MI typically felt just beneath the sternum or on the left side of the chest Described as heavy, squeezing, crushing, or tight Patient unconsciously clenches a fist when describing the pain (Levine sign). May also describe as pressure or discomfort Patient may mistake the pain for indigestion. S&S of ACS Cont… Not every AMI patient has chest pain—silent MI People with diabetes, older people, and heart transplantation patients Present with symptoms related to a drop in cardiac output: sudden dyspnea, pulmonary edema, hypotension, confusion, profound fatigue, or feeling weak and dizzy S&S of ACS Cont… Women may present differently from men. Nausea Light-headedness Epigastric burning Sudden onset of weakness or unexplained tiredness Many women may not recognize these symptoms as potentially cardiac. Heart disease accounts for one-third of all female deaths in Canada. Women are more likely to die of AMI than men. Other Signs of an MI (ACS) 1. Pain- sudden, sub sternal chest pain that can radiate into the jaw, neck and left arm. Usually described as severe, steady and crushing- no relief with vasodilators 2. Non pain- (Silent MI). Gastric discomfort, described as indigestion. Often in women. 3. Pallor 4. Diaphoresis 5. Dizziness, weakness 6. Anxiety and fear 7. Hypotension 8. Rapid and weak pulse 9. Dyspnea Remember… Many AMI patients have normal physical examination findings. Diagnosis in the field depends chiefly on the history and the 12-lead ECG findings. Specific physical exam findings can help detect the development of complications to AMI: General appearance Level of responsiveness Skin Vital signs Signs of left-side heart failure or right-side heart failure Prehospital Management of ACS On Arrival Assessment and management for possible ACS should occur simultaneously. Be calming and place the patient at rest. Determine the presence of possible ACS. How do we rule in/out possible ACS? Care must begin immediately. Limit the size of the infarct. Prehospital Management of ACS Confirm Possible ACS. Perform a 12-lead ECG, and assess for aspirin and oxygen administration. Rapid acquisition of the 12-lead ECG before the secondary assessment and before anti- ischemic therapy is preferred. Consider rapid transport now if your patient has evidence of a STEMI. Prehospital Management of ACS Confirm possible ACS. (continued) Early ECG prior to treatment can document ischemic ECG changes that may normalize after treatment is started. If aspirin has not been taken before your arrival, give the patient aspirin to chew and swallow. Oxygen should be administered only if needed (avoid hyperoxemia) Put the patient physically and emotionally at ease. Decrease the amount of work that the heart must do (semi-Fowler position or sitting up if there is pulmonary edema). Prehospital Management of ACS Perform cardiac monitoring. Document initial rhythm. Record vital signs. 12 leads- 1 vs. Serial. Defib Pads applied if STEMI is present Prehospital Management of ACS Secondary assessment Detailed history: find out if the patient has a history of cardiac disease, heart medications, or heart attack or heart surgery. Obtain a more complete description of the present symptoms (especially onset). OPQRST Do not delay transport to the hospital; do this en route to the hospital. Prehospital Management of ACS Secondary assessment (continued) If a serious arrhythmia or cardiac arrest occurs during transport, pull over and start treatment immediately. Look for other potential causes of the patient’s symptoms and for complications of ACS. While you are assessing the patient for further therapies, start an IV line. Assess for Nitro Pre-Hospital Treatment for MI Full assessment Vitals, detailed questioning Assess for ASA – Cardiac Ischemia Medical Directive Assess for O2- BLS standard 12 Lead- needs to be done prior to Nitro Why? Assess for Nitro- Cardiac Ischemia Medical Directive Transport to PCI if possible, otherwise closest ER Prehospital Medications for Cardiac Ischemia PCP Nitro ASA ACP Narcotics PRN ASA Platelet aggregating inhibitor (anticlotting) Interferes with the production of clotting factor Has been shown to significantly decrease mortality with MI Orally administered 160-162 mg Chewed and swallowed Antiplatelet vs. Anticoagulant Antiplatelet- impeded the ability of the blood to clot by e.g- ASA, Clopidogrel, preventing platelets from Ticagrelor sticking together to create clots Anticoagulant (Blood Thinner) – impedes the ability of the e.g- Warfarin, Enoxaparin, blood to clot by targeting the Apixiban, Xarelto thrombin Nitro Vasodilator that dilates the coronary vasculature Can relieve vasospasm and improve blood flow Relaxes peripheral vasculature and may reduce afterload to reduce the cardiac workload Typically won’t relieve the pain in an MI as it has little to no effect on the blockage Does not reduce mortality- not life-saving Side effects: hypotension, headache Should NEVER be used in patients with RVI Sublingually administered by EMS (can come in patches, tablets, creams for pt. use) Other Cardiac Medications Beta Blockers Decrease the rate and strength of cardiac contractions Prescribed for HTN, angina, and heart failure (-lol) Calcium Channel Block influx of calcium ions into cardiac muscle Prevent spasms of the coronary arteries and decrease Blockers (-ine) the force of cardiac contraction For patients with chronic fluid overflow Diuretics (Water Can be used for HTN Pills) (-ide) Tricks kidneys into excreting more sodium and water Antihypertensive Can combine diuretics and beta blockers for a synergistic effect Agents (-pril) Watch for hypotension BLS PCS Chest Pain Standard Pg. 80-84 ALS PCS Cardiac Ischemia Medical Directive Pg. 52-54  Note the order of the MD- Why is this Important in your treatment decisions? OTHER CARDIAC EMERGENCIES Aortic Emergencies Hypertensive Emergencies Aortic Emergencies Dissecting Aortic Aneurysm Aorta is subjected to massive hemodynamic forces, leads to degenerative changes in the middle layer of the aorta These are more dominant in older people, people with HTN and patients with connective tissue disorders Over time, these changes in the middle layer lead to an “ungluing” of the inner layer of the aorta, tears Once this is torn, dissection often begins Blood gets pumped into the unnatural layer between the inner and middle layer, this then chronically stretches and weakens the vessel If it dissects into the valves, may prevent the valve from closing and results in blood entering back into the left ventricle during systole Signs and Symptoms Middle aged or older- chronic HTN Main complaint is chest pain- often described as “the worst pain I have ever felt”, “ripping or tearing” , “like a knife” Pain usually comes on suddenly Located in the anterior chest or the back, between the shoulder blades- can radiate into the back or abdomen Difference in BP between the 2 arms- disruption of blood flow through the brachiocephalic or left subclavian artery Signs and symptoms depend on the site of the tear and extent of the dissection. How to Differentiate AMI vs. Dissection? Acute Dissection of the Aorta Disruption of blood flow into the left common carotid artery may produce signs and symptoms of a stroke. Death is nearly always a result of aortic rupture into the pericardium and resultant cardiac tamponade. Occurs more commonly in older patients with a history of hypertension Management of Aortic Dissection Main objective is pain relief- Consider ALS Calm and reassure the pt. O2 IV Cardiac Monitor Transport without delay- nothing can be done prehospital to stabilize the condition Hypertensive Emergencies Hypertension Afflicts nearly 1 in 4 Canadians Yet almost one-half of those with hypertension do not know it because they have no symptoms Major contributing cause in many cases of MI, heart failure, and stroke Most often the result of advanced atherosclerosis or arteriosclerosis Most common complications include renal damage, stroke, and heart failure. Blood pressure at rest consistently greater than 130/80 mm Hg Hypertension By the time symptoms start to occur, hypertension is already in a more advanced stage and has probably produced at least some damage to organs such as the heart, kidneys, and brain. Hypertension S&S Vary pt. to pt. Vary based on severity Common S&S: Headache Dizziness Blurred vision Buzzing in the ears Chest pain Altered LOC Management of Hypertension Supportive treatment Keep the pt. supine Measure BP in both arms often (min. q 5 mins) Ensure you do manual BP check APPLY You are the Paramedic…  You receive a call for “unknown medical.” The patient is a 55- year-old woman who was awakened at approximately 0500 hours with jaw pain. The patient has a history of diabetes. It is now 0830 hours. You find the patient lying in bed. She looks pale and diaphoretic. The patient tells you that she has an awful pain in her jaw that she cannot explain. You ask the patient if she is having pain anywhere else, to which she replies, “No.” What is your initial impression of this patient’s condition? What initial history do you need for your assessment of this patient? What are some of the questions you need to ask the pt? What types of physical assessments do you need to do?  (continued) You and your partner begin your assessment. Your partner obtains vital signs while you complete the primary and secondary assessment. You ask for OPQRST and SAMPLE history, which indicate nothing unusual except for the pain in the patient’s jaw. The patient says the pain feels like a dull ache that she rates “about a 5 out of 10” on a scale with 10 being the worst pain possible. Your partner reports that the patient’s pulse feels irregular at a rate of 64 beats/min. You start an intravenous (IV) line of normal saline. What are the differences between the presentations of cardiac problems in men and women? At this point in time, what is your initial differential diagnosis? What are some potential other differentials? How would you proceed now?  (continued) You ask your partner to place electrodes on the patient’s chest to assess her cardiac rhythm. Lead II of the ECG shows a sinus rhythm with multifocal premature ventricular complexes (PVCs) tracing at 8 to 10 per minute. Your partner performs a 12-lead ECG, which shows no apparent ST-segment elevation. What are PVCs, and what does multifocal mean? What is your first-line treatment for PVCs?  (continued) You and your partner place the patient on the stretcher and move her to the truck for transport. You notice that the PVCs have dropped from 8 to 10 per minute to 2 per minute, and they appear to be unifocal. The patient states that she is feeling a little bit better, but she still reports pain in her jaw. She says it is “still a 5 out of 10.” The remainder of the transport is uneventful, with no change in her condition, and you transfer care to the hospital staff on arrival. What is the most life-saving medication you can administer? What other therapies and investigations will you consider next? What is your final differential diagnosis and what evidence do you have to support this?