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Cardiology 1 NotesAnne Messman, MD, MHPE, FACEPVice Chair of Education, Wayne State University, Department of Emergency Medicine amessman@med.wayne.eduCPR/ACLS review and updateBLS interventions (rapid defibrillation, high-quality CPR) are more important than ACLS interventions (medications, early intubation).BLS/ACLS guidelines were updated in 2015. Here is what has changed:For chest compressions, there is now an upper limit for how hard to compress. It is now recommended to compress the chest 5-6 cm (2-2.4 in).The prior recommendation was to compress at a rate > 100 compressions per minute. There is now an upper limit on that, so it is recommended to compress 100-120 times per minute. It is also imperative to allow full chest recoil between compressions. This allows for negative pressure, which increases the return of blood flow to the heart.>60% of the total resuscitation time should be spent doing chest compressions (this is called the “chest compression fraction”). Interruptions are to be minimized.Vasopressin was removed from the recommendations.Epinephrine should be given immediately following defibrillation in a shockable rhythm and ASAP in non-shockable rhythms.The 2015 AHA recommendations only addressed 1 specific toxicologic etiology of cardiac arrest: arrest secondary to regional anesthesia (most frequently involving bupivacaine). The AHA recommends consideration of IV lipid emulsions in addition to standard cardiac care for this circumstance.Because studies have definitely shown the benefit of good CPR and BLS, advanced airways are now somewhat de-emphasized. The recommendation is that advanced airway intervention (intubation) can be delayed for 3 cycles/6 minutes to focus on BLS interventions.Once an advanced airway is established, 1 breath should be given every 6 seconds (i.e. respiratory rate of 10). Do NOT overventilate.MOST IMPORTANT: MINIMIZE INTERRUPTIONS OF CPR! If you are given a question about CPR, the correct answer choice will probably have something to do with minimizing interruptions. This is critically important when performing pulse checks (should be less than 10 seconds), administering meds, and intubating. You can even continue CPR while the defibrillator is charging, just make sure everyone is clear prior to discharge of the defibrillator.Post-resuscitation careTherapeutic hypothermia is coming under more scrutiny and the recommendations have changed slightly. Prior guidelines suggested aggressive cooling to a temperature of 32-34?C but now the recommendation is 32-36?C.If a post-arrest patient has a STEMI on their post-arrest EKG, it is a level I recommendation to take that patient to the cath lab. PCI should be considered in all successfully resuscitated patients with suspected coronary syndromes.Avoid hyperoxia, avoid hypotension and monitor electrolytes.Review of BLS/ACLSConsider reversible causes, aka the “Hs and Ts”: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade (pericardial), toxins, thrombosis (coronary and pulmonary). This primarily applies to PEA arrest. VF/VT are usually secondary to primary cardiac etiologies.If the patient is not intubated, breaths should be given at a rate of 2 breaths for every 30 compressions. If the patient is intubated, give 10 breaths/min (i.e. 1 breath every 6 seconds). Insufflate enough to produce minimal chest rise. Do NOT overventilate.Ventilation can be accomplished via bag-valve mask, supraglottic airway or endotracheal intubation. The choice of airway management is up to you, no particular method of airway management has been proven to be superior.If defibrillation is performed, use 200J for a biphasic machine and 360J for a monophasic machine. Do NOT delay defibrillation to perform CPR beforehand.Vascular access: get access however it can be accomplished quickly and without impeding CPR efforts. It does not matter how access is achieved (peripheral, central, intraosseus) but it is important to MINIMIZE interruptions in CPR.MedsEpinephrine: it is unknown whether epinephrine is beneficial, harmful or neutral in cardiac arrest patients. The current recommendations state that epinephrine 1mg should be given every 3-5 minutes.Amiodarone: it is recommended that amiodarone be considered in patients with VF/VT that is refractory to CPR, defibrillation, and vasopressor therapy.If the rhythm strip is concerning for Torsade de Pointe, magnesium 1-2g IV push should also be considered in addition to defibrillation and epinephrine.If hyperkalemia is a possible cause of cardiac arrest (ex. dialysis patient), medical treatment should be initiated alongside standard ACLS care. This will include calcium chloride or calcium gluconate, sodium bicarbonate, insulin and D50.Post-arrest careAll comatose post-arrest patients should undergo therapeutic hypothermia with a target temperature of 32-36?C for at least 24 hours and should be monitored in an intensive care unit setting.Systolic blood pressures < 90mmHg should be promptly treated, although the AHA does not offer specific guidance regarding how to accomplish this goal. Most will use norepinephrine to increase the blood pressure.Arterial DiseaseAbdominal aortic aneurysmAortic aneurysms involve all three layers of the arterial wall97% are infrarenalRisk factorsAgeMale sexFamily history in a first-degree relativeHistory of smokingHistory of HTN and/or high cholesterolHistory of CAD or PVDPresentationThink of this in a patient with syncope AND sudden abdominal, back or flank painFlank pain may radiate to the groin and also be associated with hematuria, leading to the most common (and potentially fatal) misdiagnosis of renal colic. As far as the in-service is concerned, old people don’t get renal colic, they get ruptured AAAs.Other misdiagnoses include: musculoskeletal back pain because ruptured AAAs can present with dull lower back pain radiating in the legs or diverticulitis because ruptured AAAs can present with LLQ pain and guaiac-positive stools.Physical examination findingsPulsatile mass in the epigastriumBruits over the abdominal aorta or femoral arteriesSigns of distal extremity ischemiaDiagnosis and managementIf the diagnosis is obvious clinically, no further diagnostics are necessary and you can proceed immediately to management (and hopefully the OR). If the diagnosis is obvious, DO NOT delay immediate surgical management to get confirmatory studies.If the diagnosis is not as obvious:Ultrasound is great at detecting AAA but cannot tell you if the AAA is ruptured. However, if you are quite suspicious and your ultrasound shows a AAA, this may be all you need.CT with contrast in nearly 100% sensitive but requires IV contrast and the patient must leave the ED to go to the CT scanner.Angiography is the least desirable study because it has a high false positive rate, is time consuming and invasive, and requires exposure to IV contrast.Once the diagnosis is made or strongly suspected, IMMEDIATELY place 2 large-bore peripheral IVs, obtain pre-operative labs including coagulation studies and a type and cross for AT LEAST 10 units of blood, obtain an ECG and consult surgery (vascular surgery, if possible). If the patient is unstable, resuscitation with blood products and fluids will need to begin in the ED. Thoracic Aortic DissectionRisk factorsHistory of hypertension = MOST COMMON risk factorHistory of connective tissue disorders (ex. Ehlers-Danlos syndrome, Marfan syndrome, lupus erythematosus, giant cell arteritis, cystic medial necrosis)PregnancyCongenital heart disease (ex. bicuspid aortic valve, coarctation of the aorta)Turner syndromeCocaine and methamphetamine usageEpstein anomalyAortic valve stenosisInfectious disease (ex. syphilis, endocarditis)Tobacco usagePathophysiology: there is a tear in the intima that allows blood to leak into the media, which rips the media away from the adventitia. If the blood pressure is not well controlled, then the dissection will propagate.Classification systemsDeBakeyType I = ascending aorta and part of the distal aorta (most common)Type II = ascending aorta onlyType III = descending aorta onlyStanford classificationType A = ascending aorta is involvedType B = only the descending aorta is involvedPresentationPAIN is the most common symptom. It is abrupt, maximal at onset, and moves as the dissection propagates. It may be described as “tearing” or “ripping”.Patients may also present with an acute stroke, visual changes, a cool and pulseless extremity, CHF, abdominal pain, N/V, flank pain, hematuria, syncope, acute MI, aortic regurgitation.Be particularly mindful of acute strokes and acute MIs because giving these patients aspirin, heparin, tPA, etc would be catastrophic!DO NOT RELY ON THE PATIENT BEING HYPERTENSIVE!!! Patients can be hypertensive, normotensive or hypotensive. It is more important to look for a discrepancy in the blood pressure in the extremities as well as differences in pulses between the extremities.DiagnosisGet a chest x-ray immediately. There will usually be something abnormal although it may not always be obvious. Look for mediastinal widening > 8cm (most common finding), “eggshell” or “calcium” sign of the aorta = extension of the aortic shadow > 5mm beyond its calcified aortic wall, blurred aortic knob, “double density” appearance of the aorta, right-sided deviation of the trachea, elevation of the right mainstem bronchus, left pleuro-apical cap, depression of the left mainstem bronchus, left-sided pleural effusion.Obtain an ECG. Like the XR, this is usually abnormal also. May show acute ischemia or infarction (most commonly in the inferior leads), AV block, LVH.Definitive studies include:Transesophageal echo (TEE): almost 100% accurate and can be done quickly in the ED but you need the staff available to do this. If you have this option, choose this.Aortography: this is the traditional gold standard but it is invasive and time-consuming. It cannot be performed in the ED and exposes the patient to IV contrast.MRI: extremely accurate but obviously not available quickly, requires the patient to leave the ED for an extended period of time.Rapid-sequence CT with contrast: this is becoming the preferred diagnostic technique. Extremely sensitive and specific. It is less invasive and provides better images than aortography, but still requires the patient to leave the ED and be exposed to contrast. If TEE is not available, do this.Management: as with a ruptured AAA, get 2 large bore IVs and type and cross the patient for 10-15 units of blood.If the patient is hypertensive and/or tachycardic, the pulse rate and blood pressure MUST be controlled immediately. The traditional therapy is an IV beta-blocker (esmolol, propranolol, metoprolol, atenolol) first to control HEART RATE. Once the heart rate is 60-80 bpm, then start nitroprusside IV to get the SBP down to 100-110 mmHg.If the patient is hypotensive, give small boluses of IVF or blood.Treat the pain with IV narcotics.Be aware that some people are walking around with known dissections. If the dissection only involves the descending aorta, treatment (long-term) is with medical management and surgery is only performed if there are complications.Arterial Embolism (specifically arterial emboli to the extremities)Emboli usually originate from the heart. 2/3 of cases are due to atrial fibrillation, making it the most common cause. Second most common is from a mural thrombus, usually in a patient with a recent MI. The average amount of time that it takes to form a mural thrombus s/p MI is 14 days so consider a mural thrombus if given a patient with a recent MI. Non-cardiac sources include thrombi from aneurysms and atheromatous plaques. A venous clot could also embolize if the patient has a PFO.Classic presentation is with the 6 “Ps”: pain, pallor, paralysis, pulselessness, paresthesias, and polar (i.e. cold). The onset will be sudden and the opposite limb is typically normal. On physical examination, check capillary refill and pulses (including using the Doppler to check pulses that are not palpable). If a pulse is Dopplerable but not palpable, check ABIs.Diagnosis: can use duplex ultrasound, arteriography or CT with contrast. If you suspect a mural thrombus, you could ultrasound the heart. Irreversible changes occur within 6 hours so prompt diagnosis and treatment is extremely important.Treatment: get vascular surgery on board immediately, even prior to obtaining confirmatory imaging. If there are no contraindications, the patient should receive heparin (80 units/kg bolus then 18 units/kg/hr) and aspirin 325mg.CardiomyopathiesGeneral information: “cardiomyopathy” is a general term that describes a disease of the heart muscle that causes damage to the structure and function of the myocardium. In general, patients will present with signs and symptoms of systolic and/or diastolic dysfunction. Cardiomyopathies can be primary or secondary. There is not a perfect classification system of cardiomyopathies and there can be significant overlap between the categories but here is a general breakdown of the different types of cardiomyopathies:Idiopathic/dilated: all 4 chambers will be dilated and there will be myocardial hypertrophy. Systolic pump failure will be present, therefore patients will present with signs and symptoms consistent with congestive heart failure. Patients may also present with symptoms of systemic or peripheral embolization, including focal neurological deficits, a pulseless extremity, flank pain + hematuria, etc.Physical exam: CHF findings, S3 and S4 gallop, may hear a murmur and the patient may be tachycardic.Work-up: get an EKG, CXR (will show cardiomegaly with enlargement of all 4 chambers), echo.Treatment: treat as you would CHF. If there is an intracardiac thrombus, chronic AFib or peripheral embolism, give anticoagulants.Restrictive: characterized by a diastolic restriction of ventricular filling. Think of a heart that is more rigid and not as elastic as it should be. It can be secondary to systemic disease but is more commonly idiopathic. Presentation is identical to idiopathic dilated CM. The diagnostic evaluation is also identical, but the findings will be different. The EKG may be low-voltage and the chest x-ray can have a normal-sized heart early on in the disease process. Treatment is aimed at symptom reduction and may include diuretics and digoxin.Hypertrophic: this is probably the most testable cardiomyopathy for the in-service/boards. There is LVH but it disproportionately affects the septum more than the wall of the LV. In the majority of cases, it is inherited via an autosomal dominant transmission pattern. Presentation: dyspnea on exertion = most common complaint, atypical chest pain, palpitations, syncope/presyncope (usually exertional), sudden death (think of the young athlete who drops dead while playing a sport). On physical exam, listen for a systolic murmur that worsens with Valsalva or exercise and improves with squatting, hand grip and passive leg elevation.The ECG is almost always abnormal so be on the lookout for these things: Q waves in the septal leads, dagger-like (deep and narrow) Q waves in the lateral leads, giant inverted T waves in the lateral leads.Work-up: ECG, chest x-ray (usually normal), echo.Treatment: follow ACLS algorithms if the patient is unstable. For stable patients, beta-blockers are the mainstay of therapy and help with symptom control and decrease myocardial oxygen consumption. Calcium-channel blockers are used in those who cannot tolerate beta-blockers. Amiodarone is 3rd line and helps with ventricular dysrhythmias.Antibiotic prophylaxis prior to dental procedures is not necessary. ................
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