1 / 62

Cardiac Review

Cardiac Review. Cardiac Monitoring, Leads, Identifying Ischemia, Infarction & Location, ACLS Algorithms, Other Cardiac Problems. Cardiac Monitoring – Lead I. Lead II. Lead III. MCL1. How it looks on a real chest. 12 Lead Electrode Placement.

newman
Télécharger la présentation

Cardiac Review

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Cardiac Review Cardiac Monitoring, Leads, Identifying Ischemia, Infarction & Location, ACLS Algorithms, Other Cardiac Problems

  2. Cardiac Monitoring – Lead I

  3. Lead II

  4. Lead III

  5. MCL1

  6. How it looks on a real chest

  7. 12 Lead Electrode Placement • Limb Leads – near ankles and wrists, but may be more proximal- just not on the trunk • aVR should be negative • If aVR is upright, check for reversal of the limb leads.

  8. 12 Lead Chest Leads • a.k.a. precordial leads • V1 – 4th intercostal space to the right of the sternum • V2 – 4th intercostal space to the left of the sternum • V3 – directly between V2 and V4 • V4 – 5th intercostal space at left midclavicular line • V5 – level of V4 at left axillary line • V6 – level with lead V5 at left midaxillary line

  9. How it looks on paper… plus right precordial leads

  10. The posterior leads

  11. A Normal 12 Lead EKG

  12. St Segment Elevation

  13. Identifying Ischemia and Infarct

  14. The 3 Is Ischemia - lack of oxygenation - ST depression or T wave inversion Injury - prolonged ischemia - ST elevation Infarct - death of tissue - may or may not show in Q wave

  15. Ischemia • Inadequate oxygen to tissue • Represented by ST depression or T wave inversion • May or may not result in infarct • > 1 mm ST depression one small box to right of J point in 2 or more anatomical leads/ T wave inversion if full thickness of myocardium

  16. Injury • Prolonged ischemia • Transmural • Represented by ST elevation • Usually results in infarct • > 1 mm ST elevation one small box to right of the J point or > 2 mm in the precordial leads in 2 or more anatomical leads

  17. Infarct • Death of tissue • Represented by Q wave • Not all infarcts develop Q waves • Non-Q wave MI looks like ST elevation and has elevated cardiac enzymes too • Q-wave MI indicates dead tissue- if duration more than one small box and >25% amplitude of R wave

  18. Infarct • EKG includes new or presumed new transient ST deviation ≥ 0.5 mm or T wave inversion ≥ 2 mm with symptoms, fixed Q waves • Cardiac markers include elevated troponin, elevated CK-MB

  19. ACS • All acute coronary syndromes suggest acute myocardial ischemia. • It is often not possible to determine which syndrome is present in the first hours of clinical presentation because they all have the same initiating events: -plaque rupture -thrombus formation -vasoconstriction

  20. Presumed AMI - STEMI • ST elevation of one or more millimeters in two or more contiguous leads • New or presumably new LBBB • Strongly suspicious for injury • May require repeat 12 leads • Treatment may include beta blocker, clopidogrel, heparin, reperfusion therapy (fibrinolysis or cath), ACE/ARB, statin

  21. Management - NSTEMI • ST depression or dynamic T wave inversion • Strongly suspicious for ischemia • High risk unstable angina • Treatment: Beta blocker, clopidogrel, heparin, glycoprotein IIa/IIIb inhibitor, cath within 48 hours, asa, ACE/ARB, statin

  22. Management – Unstable Angina • Normal or non-diagnostic changes in ST segment or T wave • Treatment: serial cardiac markers (including troponin), repeat 12 leads & continuous telemetry monitoring, consider stress test, discharge for follow-up if no evidence of ischemia or infarction

  23. Unstable Angina Not chronic stable angina if… -New onset -Lower exertion threshold -Change in pattern of relief -New or different associated symptoms

  24. Management • Story • Risk factors • EKG • Clinical presentation: classical anginal chest pain, atypical chest pain, anginal equivalents (dyspnea, palpitations, syncope or pre-syncope, general weakness, DKA)

  25. Management • Patients with severe or multiple risk factors should be evaluated with a high index of suspicion for ACS: diabetes, smoking, hypertension, age, family hx, obesity, stress, sedentary • Note re: age- males >35 & females >40; increasing age = increasing risk

  26. ST Elevation

  27. ST Elevation

  28. Evolution of AMI on the 12 Lead • Note Q wave measuring at least 40 ms wide (pathologic associated with cellular necrosis) • When Q waves first form, tissue may not yet be necrotic. Reperfusion may result in Q waves disappearing. • Presence of wide Q and absence of ST segment elevation = previous MI = age undetermined (rather than old MI)

  29. Reciprocal Changes - Those leads that look at the infarct site from the opposite perspective tend to produce the opposite changes. - When a lead sees the AMI directly, the ST segment becomes elevated in that lead. - When a lead sees the infarct from the opposite perspective, the ST segment may be depressed in that lead. - Reciprocal changes – not necessary to presume infarction, strong confirming evidence when present

  30. Reciprocal Changes • Because of the way the leads are oriented on the patient’s body, II, III, and aVF are on the bottom looking up. • All other leads are on top looking in. • Therefore, when AMI produces elevations in II, III, and aVF, it tends to produce depression in the opposing leads. II, III, aVF I, aVL, V leads

  31. 12 Lead EKG – Related Groups • Each lead has only one positive electrode. • The positive electrode is like the eye. • The view is from the positive electrode to the negative electrode. • All 6 chest leads are positive electrodes. • The 4 limb leads provide another 6 views of the heart.

  32. Contiguous Leads in the ECG

  33. Lateral Wall • I, aVL, V5, V6 • When ST segment elevation is noted in Leads I, aVL, V5 and v6 lateral wall infarction should be considered.

  34. LCA Occlusions • Consider bundle branches supplied by LCA • Serious infranodal heart blocks may occur • Proximal occlusions of LCA = “widow maker” – with evidence in septal, anterior, and lateral leads; complications are common • With normal BP do fibrinolysis, if signs of shock do PTCA or CABG • LCA dominance with 10% of population • Inferolateral MI

  35. Left Coronary Artery • Left anterior descending (LAD) = anteroseptal area of heart • Left circumflex (LCX) = lateral wall of heart, supplies posterior descending artery • Left Main (proximal LCA) = anterior wall of heart

  36. Inferior Wall MI

  37. Anterior Wall • V3 and V4 – left anterior chest • The positive electrode for these two leads is on the anterior wall of the left chest. • ST segment elevation in V3 and V4 implies an anterior wall infarction.

  38. Anterior Wall MI

  39. Pacemaker Leads

  40. Ventricular Pacemaker Rhythm

  41. Ventricular Pacer – Demand Mode

  42. Atrial Pacer

  43. AV Sequential Pacer

  44. AV Sequential Pacer

  45. ACLS Algorithms • Bradycardia • Tachycardia • Ventricular fibrillation/Pulseless VT • PEA/ Asystole

  46. CHF • The heart is unable to pump effectively to meet metabolic demands of the body or may require elevated filling pressures to meet this demand. • Systolic dysfunction is most common and occurs when the ejection fraction is less than 50%.

  47. CHF – Systolic Dysfunction • Systolic dysfunction is the inability of the right ventricle to effectively pump blood to the pulmonary bed resulting in right sided heart failure. • Stroke volume decreases and the body compensates by retaining water and sodium. • That leads to an increase in stroke volume and results in pulmonary congestion. • The right ventricle enlarges resulting in peripheral edema and elevated JVD. • If you press on the patient’s right abdomen and see an increase in JVD when the patient is at a 30-45 degree angle, it is positive test for heart failure.

  48. CHF – Diastolic Dysfunction • EF is normal or greater than 50-55% • The left ventricle is unable to fill because it is unable to completely relax (stiff or non-compliant)– most commonly as a result of hypertension. • Left sided heart failure is diastolic heart failure that results in inadequate filling pressures and rising diastolic pressures. This results in increased left atrial, pulmonary venous, and pulmonary capillary pressures. Systolic function may be normal or hyperdynamic. • Causes: mitral stenosis, constrictive pericarditis, hypertrophic cardiomyopathy, or restrictive cardiomyopathy.

  49. Causes of Heart Failure • Most common – CAD, hypertension, valvular dysfunction, idiopathic • Least common – viral, anemia, dysrhythmias (atrial fibrillation), peripartum, endocrine (diabetes & thyroid), restrictive (amyloid, sarcoid, hemochromatosis), cardiotoxic (alcohol, chemotherapy, cocaine)

  50. HF Signs & Symptoms • Signs – JVD, rales or crackles, tachypnea, unexplained weight gain, ascites, edema, nocturia, pallor, diminished peripheral pulses, hepatomegaly, extra heart sounds, RUQ tenderness • Symptoms – orthopnea, paroxysmal nocturnal dyspnea, fatigue, DOE, depression, cough, anxiety, palpitations, N/V, abdominal fullness, chesst pain, anorexia

More Related