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Semelhante a 2012 cardiac lecture 2 pathologies
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2012 cardiac lecture 2 pathologies
- 1. Lecture 2: Overview of cardiac pathologies Arrhythmias Cardiomyopathies Valvular problems Endocarditis Heart failure http://thumbs.dreamstime.com/thumblarge _336/1227476058tNtio3.jpg
- 2. Arrhythmias = dysrhythmias • What normally causes the presentation? – Syncope – Palpitations – Light-headedness – Cardiac Arrest – ?shortness of breath, fatigue, and chest pain
- 3. Identification by Location • Arrhythmias by location – Supraventricular – Nodal (Junctional) – Ventricular
- 4. Location? Supraventricular? Could be SA node • SA node is not coordinated…… • atrial contraction not effective http://lysine.pharm.utah.edu/netpharm/netpharm_00/gifs/arrhythmia_gifs/atrial_fib.gif
- 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. 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. 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. 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. 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
- 11. Location? Is it ventricular? • VT
- 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! http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004467/
- 13. Emergency! Call a code! • VF
- 15. Cardiac myopathies • Many types....... many causes • Dilated… most common • Hypertrophic • Restrictive
- 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. Valvular dysfunctions • Causes: • Which valve? • Inflammation • Ischemia • What’s wrong? • Trauma • Stenosis • Degenerative/age • Regurgitation • Infections (insufficiency) • Prolapse (esp. mitral)
- 22. Common in women! 6% http://gearwestbike.files.wordpress.com/2010/01/mitral-valve.jpg
- 23. Picture of clot • http://sitemaker.umich.edu/medchem4/files/Cephalosporin%20project_im age009.jpg
- 25. scabies Endo Bacterial carditis Skin Sore infection throat Rheumatic fever Heart Valve damage Rheumatic Heart Disease
- 26. Definitions Rheumatic Fever: • is a complication following Group A Streptococcus infection (sore throat) • damages collagen fibrils & ground substance of connective tissue • affects mostly heart, joints, CNS, skin. • Outcomes include Rheumatic Heart Disease, Rheumatoid arthritis, and mental illness. (Franks, 2002; McCance & Huether, 2002).
- 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. 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)
- 31. Results: – Valvular Stenosis; – Valvular Regurgitation; – Valvular Adhesion – Valvular Turbulence http://www.biomed.metu.edu.tr/courses/term_papers/MuratGuvendiren_files/image003 .gif
- 32. Picture of vegetation http://health.yahoo.com/media/mayoclinic/images/image_popup/r7_endocardi tis.jpgvegetation
- 33. http://www.heart-valve- surgery.com/Images/cardiac-replacement- valve-operation-image.jpg http://groups.bme.gatech.edu/groups/cfmg/gr oup/MV%20Mechanical%20Valve.jpeg
- 34. 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
- 35. 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
- 36. • What Causes Heart Failure? Severe lung disease (COPD > cor pulmonale) Diabetes (↑ CAD) Severe anemia Hyperthyroidism Arrhythmias Congenital heart defects 3/28/2012 36
- 37. 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. therapy AHA guidelines 2001
- 38. Left heart failure Forward 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 hypertension Activation of RAAS Right heart failure Right ventricular pressure Na+, H2O retention SYSTEMIC VENOUS CONGESTION and PULMONARY PERIPHERAL OEDEMA CONGESTION and OEDEMA
- 39. Diastolic versus Systolic Diastolic- “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 Infiltration 3/28/2012 39
- 40. DIASTOLIC SYSTOLIC HEART FAILURE HEART FAILURE “can’t fill” “can’t pump” 3/28/2012 40
- 41. Lt. VENTRICULAR FAILURE Rt. VENTRICULAR FAILURE • Ischemia, Myocarditis, Valvular • Pulmonary HTN, Valvular heart heart disease disease COMPENSATORY MECHANISMS Activation of Sympathetic NS Activation of RAAS Activation of Sym NS > mechanism Myocardial contractility Tachycardia cardiac workload Na+ and water retention Cell stretching Further stress on myocardium COMPENSATORY CONGESTIVE HYPERTROPHY and HEART FAILURE DILATATION
- 42. Treatment Options The more common forms of heart failure cannot be cured, but can be treated/managed Lifestyle changes Medications Surgery Heart transplant 3/28/2012 42