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2012 cardiac lecture 2 pathologies


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cardiac lecture

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2012 cardiac lecture 2 pathologies

  1. 1. Lecture 2: Overview of cardiac pathologies Arrhythmias Cardiomyopathies Valvular problems Endocarditis Heart failure
  2. 2. Arrhythmias = dysrhythmias• What normally causes the presentation? – Syncope – Palpitations – Light-headedness – Cardiac Arrest – ?shortness of breath, fatigue, and chest pain
  3. 3. Identification by Location• Arrhythmias by location – Supraventricular – Nodal (Junctional) – Ventricular
  4. 4. Location? Supraventricular? Could be SA node• SA node is not coordinated……• atrial contraction not effective
  5. 5. Atrial Arrhythmias• Atrial fibrillation – >400bpm – Not immediately fatal – But… embolisation highly likely• Premature atrial contraction (PAC) – “Skips” – Caffeine, stress• SVT – Can be genetic, short spurts of rapid beats
  6. 6. Possible causes of AF• MI – 90% of pt with MI experience arrhythmia• Idiopathic?• Drugs – e.g. caffeine, nicotine, alcohol, pseudoephedrine• lots of other reasons, too!
  7. 7. Atrial Fibrillation Treatment Goals• Restore normal sinus rhythm – Drugs – antiarrhythmics – Cardioversion?• Control ventricular rate during AF – Drugs – antiarrhythmics• Prevention of blood clot formation. – Drugs – anticoagulants
  8. 8. Cardioversion vs defibrillation• Cardioversion refers to elective procedure to restore normal SA node control…common in AF not responsive to drugs• Defibrillation…….. Refers to emergent shock applied• Both will stop all electrical activity• Several YouTube videos available to see the procedure…..
  9. 9. Nodal? AV node• If the p wave is not always transmitted to the ventricles• “blocked” at the AV node• In third degree block: Ventricles have a separate pacemaker, 2 different rhythms going on…an atrial rhythm and a ventricular (slower) rhythm……• Must implant a mechanical pacemaker
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  11. 11. Location? Is it ventricular?• VT
  12. 12. VF• Fibrillation is an uncontrolled twitching or quivering of muscle fibers (fibrils).• During ventricular fibrillation, blood is not pumped.• Sudden cardiac death results.• The most common cause of VF is MI.• However, VF can occur whenever the heart does not get enough oxygen or if a person has other heart disorders…• electrocution!
  13. 13. Emergency! Call a code!• VF
  14. 14. Asystole!
  15. 15. Cardiac myopathies• Many types....... many causes• Dilated… most common• Hypertrophic• Restrictive
  16. 16.
  17. 17. Causes & effects• often secondary to MI• 2/3 idiopathic • ↓ contractility• valvular disorders • ↓ stroke volume• DM • ↓ cardiac output• renal failure • ..... failure• Alcohol use• nutritional deficiencies• drug toxicity• post- infection..viral..sudden• Hyperthyroid• genetic
  18. 18. Valvular dysfunctions• Causes: • Which valve?• Inflammation• Ischemia • What’s wrong?• Trauma • Stenosis• Degenerative/age • Regurgitation• Infections (insufficiency) • Prolapse (esp. mitral)
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  20. 20.
  21. 21.
  22. 22. Common in women! 6%
  23. 23. Picture of clot• age009.jpg
  24. 24.
  25. 25. scabies Endo Bacterialcarditis Skin Sore infection throat Rheumatic fever Heart Valve damage Rheumatic Heart Disease
  26. 26. DefinitionsRheumatic Fever:• is a complication following Group AStreptococcus infection (sore throat)• damages collagen fibrils & ground substanceof connective tissue• affects mostly heart, joints, CNS, skin.• Outcomes include Rheumatic Heart Disease,Rheumatoid arthritis, and mental illness.(Franks, 2002; McCance & Huether, 2002).
  27. 27. Streptococcus Infection• Reservoirs of infection – Group A Streptococcus pyogenes – endogenous in oral cavity (5% of ATSI) – Group A Streptococcus pyoderma – endogenous in skin (70% of ATSI) – dried (months) in dust & mucus• Portal of Entry – Pharyngeal mucous membranes – Skin damage • Scratched pimples or scabies (esp. low socioeconomic communities, living with animals, rural)(Currie & Brewster, 2001; Franks, 2002; McCance & Huether, 2002).
  28. 28. Rheumatic Fever• Streptococcus antibodies• Once the immune system has removed the bacteria, antibodies may attack normal “self” tissue – Collagen fibrils – Connective tissues – Basement substances (under endothelium)
  29. 29.
  30. 30. Results: – Valvular Stenosis; – Valvular Regurgitation; – Valvular Adhesion – Valvular Turbulence
  31. 31. Picture of vegetation
  32. 32. http://www.heart-valve- valve-operation-image.jpg
  33. 33. What is Heart Failure?• Heart cannot circulate enough blood to supply organs with sufficient oxygen, nutrients to support cells• Common end-point for many cardiac diseases• Long-term, slow decline of Cardiac Output• Compensatory mechanisms• Eventual failure
  34. 34. What Causes Heart Failure? Any health condition that either damages the heart or makes it work too hard Coronary artery disease > ischemia Myocardial infarction Hypertension (↑ peripheral resistance) Abnormal heart valves Cardiomyopathy Heart inflammation (myocarditis & pericarditis)3/28/2012 35
  35. 35. • What Causes Heart Failure? Severe lung disease (COPD > cor pulmonale) Diabetes (↑ CAD) Severe anemia Hyperthyroidism Arrhythmias Congenital heart defects3/28/2012 36
  36. 36. Stages in the Evolution of Heart Hypertension Diabetes, Failure Hypercholesterolemia A Heart disease (any) B Asymptomatic LV dysfunction Systolic / Diastolic C Dyspnea, Fatigue Reduced exercise tolerance D Marked symptoms at rest despite max. therapyAHA guidelines 2001
  37. 37. Left heart failureForward failure Backward failure Ischemia, Myocarditis, ↓ cardiac output Residual blood in left ventricle Valvular heart diseases et cetera! Tissue anoxia  Left atrial pressure and volume  Pressure in pulmonary venous circulation↓ renal perfusion Pulmonary arterial hypertensionActivation of RAAS Right heart failure  Right ventricular pressureNa+, H2O retention SYSTEMIC VENOUS CONGESTION and PULMONARY PERIPHERAL OEDEMA CONGESTION and OEDEMA
  38. 38. Diastolic versus SystolicDiastolic- “can’t fill” Systolic– “can’t pump” Mitral valve Stenosis Aortic valve Stenosis, Tamponade Insufficiency Hypertrophy HTN (↑ PR) Infiltration Mitral valve Regurgitation Fibrosis (stiff wall) Muscle Loss Ischemia Fibrosis Infiltration3/28/2012 39
  39. 39. DIASTOLIC SYSTOLIC HEART FAILURE HEART FAILURE “can’t fill” “can’t pump”3/28/2012 40
  40. 40. Lt. VENTRICULAR FAILURE Rt. VENTRICULAR FAILURE• Ischemia, Myocarditis, Valvular • Pulmonary HTN, Valvular heartheart disease disease COMPENSATORY MECHANISMSActivation ofSympathetic NS Activation of RAAS Activation of Sym NS > mechanism  Myocardial contractilityTachycardia  cardiac workload Na+ and water retention Cell stretchingFurther stress on myocardium COMPENSATORY CONGESTIVE HYPERTROPHY and HEART FAILURE DILATATION
  41. 41. Treatment Options The more common forms of heart failure cannot be cured, but can be treated/managed Lifestyle changes Medications Surgery Heart transplant3/28/2012 42