Alterations in Cardiac Function

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Alterations in Cardiac Function
2014-10-06 03:34:29

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  1. What are the most common alterations in Cardiac Function?
    • Coronary Heart Disease (CHD) 
    • Endocardial and valvular diseases 
    • Myocardial Diseases
    • Pericardial Diseases 
    • Congenital Heart Disease (CHD)
  2. What are the layers of the heart?
    • Endocardium. 
    • Myocardium. 
    • Visceral pericardium (epicardium) 
    • Pericardial space. 
    • Pariental Pericardium. 
    • Fibrous Layer. 
  3. What is the period of ventricular contraction in each heartbeat called?
  4. What is diastole in the heartbeat?
    ventricular relaxation.
  5. What causes the first heart sound, s1?
    Closure of the AV valves (tricuspid and bicuspid)
  6. Closure of the semi-lunar valve causes?
    Second heart sound, S2.
  7. What does the p-wave mean? QRS? T-wave?
    • P-wave: initiation of construction. 
    • QRS: The amount of time that too for the bundle of his and the purinje fibers to proceed a ventricle contraction.
    • t-wave: relaxation.
  8. What is stroke volume? End-diastolic volume? end-systolic volume? Ejection fraction? CO? Which one is the most important?
    • Stroke Volume: is the amount of blood ejected with each contraction of the ventricle (SV = EDV - ESV) 
    • End-diastolic Volume (EDV): It is the volume of blood in the ventricle prior to ejection. 
    • End-systolic Volume (ESV): It is the amount of blood that remains in then ventricle after ejection. 
    • Ejection Fraction: SV/ EDV. (usually a healthy heart can eject 70%) 
    • CO = HR x SV. CO is the most important variable in cardiac function.
  9. What do coronary arteries do? Where are they located? what are the main 3?
    • Coronary arteries: are the ones that supply blood to the heart muscle. 
    • Location: they are located just beyond the aortic valve. 
    • 3 main: Rt coronary artery, Lt anterior descending, Lt cincumflex.
  10. What are the factors that effect cardiac performance?
    • Preload. 
    • Afterload. 
    • HR. 
    • Myocardiacl contractility.
  11. What is Frank-starling law of the heart?
    Increased preload increases force of contraction. If I increase volume of the blood, then increases the contraction.
  12. what increases afterload? What happens to SV when afterload increases?
    • Increase of resistance to ejection, such as: Increased in SVR, increased diastolic BP, and Aortic stenosis. 
    • SV: decreases
  13. what are the main clinical Manifestation of Coronary Heart Disease (CHD)/Ischemic Heart Disease (IHD)/ Coronary artery disease (CAD)?
    • Angina Perctoris. 
    • Myocardial Infarction. 
    • Ischemic cardiomyopathy. 
    • Sudden Cardiac Death.
  14. What is the main characteristic for CAD/CHD?
    Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries.
  15. What are CAD risk factor?
    • Coronary atheriosclerosis: Thicking of the vessels reduce lumen size. This cause inflammation, which make it worse.
    • Other risk factors: age, family history, abnormal lipids, smoking, HTN, diabetes, and obesity.
  16. When does cellular ischemia usually occur?
    • Increased of O2 demand. 
    • Or an absolute reduction in oxygen supply.
    • That is why MI usually occur when exercising or after a big meal.
  17. What is angina pectoris? what are the 3 patterns?
    • It is chest pain associated with intermittent myocardial ischemia. (not necrosis)
    • May result in inefficient cardiac pumping with result an pulmonary congestion and shortness of breath.
    • 3 patterns: Stable or typical angina, Prinzmetal (variant) angina, and unstable or crescendo angina.
  18. Characteristics of stable angina (classic/typical)
    • It is the most common form. 
    • Characterized by stenotic atherosclerotic coronary vessels that reduce coronary blood flow. 
    • Caused by a specific amount of activity
    • relieved by rest and nitrates. 
    • No change in cause, amount or duration of pain over time.
  19. Characteristics of unstable Angina?
    • Pain occurring with increase frequency, severity and duration over time. 
    • Unpredictable and occurs with decreasing levels of activity. 
    • high risk for myocardial infarction.
  20. Characteristics of Prinzmetal Angina (variant)?
    • Atypical form occurring without precipitation cause. 
    • Unpredictable attacks of pain. Onset of pain is unrelated to physical or emotional exertion. 
    • May occur at the same time each day or awaken pt from sleep. 
    • May intensify over year bye does not carry same concern as unstable angina. 
    • usual cause is Vasospasm.
  21. What are the common etiologies for angina pectoris?
    • CAD- artherosclerosis. 
    • Coronary Spasm. 
    • Thrombi (narrowing) 
    • imbalance b/t oxygen supply and demand -- anemia, exercise, stress.  (the pt can have angina, and be healthy, ex: when exercising) 
    • Cardiomyopathy. 
    • LVH (Lt ventricular hypertrophy) 
    • CHF (congestive heart failure)
  22. Angina pathophysiology?
    • Weak muscle pushing out blood. 
    • Results in inefficient cardiac pumping with pulmonary congestion and shortness of breath. 
    • Reduced O2 supply causes a switch from aerobic to anaerobic metabolism. 
    • Increased cell permeability releases histamine, bradykinis, and specific enzymes that stimulate the myocardium and send pain signals to the CNS.
  23. Clinical manifestations of angina pectoris?
    • Chest pain 
    • Sweating 
    • light-headedness
    • Hypotension 
    • Indigestion 
    • Pain may radiate to arms, jaw, abdomen (referred pain)
  24. What is an acute coronary syndrome?
    • Chest pain longer and more sever that angina.
    • Plaque rupture with acute thrombus
    • development. 
    • ECG and Biomarkers used for dx. 
    • unstable angina - Occlusion is partial. 
    • MI - Occlusion is complete
  25. MI characteristics?
    • Death of cells in the myocardium due to ischemia. 
    • MI leads to drop in CO and triggers compensatory responses including sympathetic activation.
    • SNS activation lead to increased myocardial workload by increasing: HR, Contractility, and BP
  26. MI etiology?
    • Ventricular Fibrillation, usually LVH (no time for ventricular filling. 
    • Embolus. 
    • Thrombosis. 
    • Atherosclerosis. 
    • Prolonged vasospasm. 
    • Arteritis (inflammation of the artery) 
    • Coronary anomalies (malformation of the arteries)
  27. MI pathophysiology:
    • Lack of O2 to the myocardium causes lack of contractibility. Results in decreased SV, CO, BP, and tissue perfusion. 
    • Coronary occlusion results in cell death distal to the occlusion. 
    • Ultimate size of the infarcted tissue depends on the extent, duration, and severity of ischemia. (the longer and higher up the ischemias, the longer the MI)
  28. MI Clinical Manifestations:
    • Pain in the midsternal not relieved by nitrogens or rest. 
    • Tachycardia. 
    • Diaphoresis. (sweating) 
    • tachypnea, dyspnea, Shortness of breath. 
    • Anxiety. 
    • Nausea and vomiting. 
    • ECG changes. 
    • Elevated cardiac enzymes (total CK, CK-MB, LDH, troponin I) 
    • Leukocytosis.
  30. MI treatment:
    • Decreasing myocardial oxygen demand: rest, HR controlled, pain relief, afterload reduction, sympathetic antagonists (decrease the pressure of the aorta) 
    • Increasing the myocardial oxygen supply: angioplasty, CABG, thrombolysis.
    • Monitoring and managing complications: dysrhythmias, EKG monitoring.
  31. Sudden Cardiac death (SCD) characteristics:
    • Defined as unexpected death from cardiac causes within 1 hr of the onset of symptoms. 
    • Lethal dysrhythmia (such as ventricular fibrillation) is usually the primary cause. 
    • Use of external defibrillators and CPR has increased survival. 
    • Associated with CAD.
  32. Valvue Disorders characteristics? what is stenosis? what is regurgitation?
    • Abnormalities of valve function caused by inflammation, scarring, calcification, congenital malformation. 
    • Stenosis: failure of the valve to open completely results in extra pressure work for the heart. 
    • Regurgitation: Inability of a valve to close completely results in extra volume work for the heart.
  33. Mitral stenosis? etiology? Clinical Manifestations?
    • Impaired flow from Lt atrium to Lt Ventricle during ventricular diastole (relaxation) 
    • Can led to: Chronic pulmonary HTN, atrial hypertrophy, Rt ventricle hypertrophy, and rt-sided heart failure. 
    • Etiology: almost always the result of rheumatic fever with a latency period of 10-20 yrs. 
    • CM: include diastolic murmur, pulmonary edema, dyspnea, palpitation, fatigue, hemoptysis (cough up blood), chest pain, PND, and recumbent cough.
  34. Mitral regurgitation? pathophysiology? etiology? clinical Manifestations?
    • Backflow of blood from Lt ventricle to Lt atrial when ventricular systole (contraction). 
    • May lead to Lt-sided Heart Failure. 
    • etiology: Usually occurs with chord tendinae rupture secondary to a MI or chronic rheumatic fever. 
    • Clinical Manifestations: dyspnea, PND, chest pain, palpitation and high-pitched, pansystolic blowing murmur.
  35. What are Mitral valve prolapse?
    • It is a very common pathology in women when they are pregnant. 
    • Most ppl are asymptomatic. 
    • Displacement of the mitral valve leaflets into the Lt atrium during ventricular systole.
  36. Aortic stenosis pathophysiology? etiology? Clinical Manifestations?
    • results in obstruction of aortic outflow form the Lt ventricle into the aorta during systole. 
    • May result in Ischemia and Lt-sided HF. 
    • Eitology: Predominant cause is age-related calcium deposits on the aortic cusps. 
    • CM: Crescendo-decrescendo murmur during ventricular systole with prominent S4. fatigue, angina, syncope.
  37. Aortic regurgitation pathophysiology? etiolgy? CM?
    • incompetent aortic valve allows blood to leak back into the Lt ventricle during diastole (relaxation). 
    • Leads to Lt ventricule hypertrophy, eventually Lt-sided HF. 
    • Etiology: High volume workload. 
    • CM: palpitations, high systolic and low diastolic BP, High-pitched blowing murmur during ventricular diastole.
  38. Rheumatic heart disease? etiolgy? Clinical manifestations?
    • Disease of the endocardium. Primarly occurs in children.  
    • Etiology: Consequence of RF (rheumatic fever). 
    • CM: Causes valvular deformity (stenosis or regurgitation 10 or 20 yrs after). 
    • Chest discomfort, tachycardia, CHF, pericardial friction rub, murmur.
  39. infective endocarditis? etiology? CM?
    • inflammation of the lining of the heart.
    • Scarring and embolization may occur. 
    • Etiology: Infection in the endocardium caused by streptococcus, or staphylococcus. 
    • CM: murmur, cough, SOB, anorexia, abdominal pain, fever, chills, night sweats, joint pain, and petechiae (red and purple dots) 
    • * most common pts are the ones using IV drugs.
  40. Myocarditis? pathophysiology? Etiology? CM?
    • Inflammatory disease causes dead heart muscle cells causes Lt ventricle dysfunction
    • May lead to cardiomyopathy (weak heart muscle). 
    • Etiology: causes include microbial agents, immune-mediated diseases, physical agents. sequela of Viral infection is most common
    • CM: signs of inflammation and signs of heart failure.
  41. Cardiomyopathy? etiology? types? CM?
    • Disease of the myocardium, usually resulting of underlying cardiovascular disorder. (like myocarditis) 
    • Pt. is not oxygenating. 
    • Etiology: genetic, environmental (alcohol), pregnancy, post viral myocardium. 
    • Primary: dysfunction of unknown causes. 
    • Secondary: Known cause. 
    • Types: Dilated, hypertrophic, restrictive.
    • CM: Palpitations, fatigue, edema, the major complication is the Lt ventricular dysfunction.
  42. Dilated Cardiomyopathy? hypertrophic cardiomyopathy? restrictive cardiomyopathy?
    • Dialeted: Ventricle enlarges and it becomes harder for the myocardium to contract.
    • Etiology: usually seen in alcoholics (don't know why), post viral myocarditis, pregnancy, etc. 
    • Hypertrophic: thickening of the myocardium, reduction of volume pump. usually in the Lt ventricle. 
    • Usually seen in kids and need a transplant. 
    • Restrictive: The fiber of the muscle become tight, and they don't dilate. This reduces the volume in diastole (relaxation). 
    • Very rare form.
  43. Pericardial effusion? PP? CM?
    • Any abnormal collection of fluids in a sac. 
    • They could be life-threating if the sac formed will not let the ventricles to dilate well. 
    • CM: distended neck veins, muffle heard sounds, increased chamber pressure.
  44. Cardiac tamponade? etiology? CM?
    • A large amount of fluid in the pericardium space (could be blood) that is compressing the ventricles and not letting them dilate. 
    • It is life-threating. 
    • CM: reduce SV, tachycardia, hypotension.
  45. pericarditis? Etiology? CM?
    • Inflammation in the pericardium that causes rubbing with the visceral and could cause destruction of the pericardium sac. 
    • Etiology: usually viral. 
    • CM: pericardial friction rub, back pain or esophageal pain, dyspnea, cough, and fever.
  46. Acyanotic congenital defects? examples?
    • Disorder that results in the Left - to - Right shunting of blood or obstruction to flow are generally acyanotic.
    • Examples: atrial septal defect, Ventricular septal defect, Patent ductus arteriosus, Coarctation of the aorta.
  47. Atrial Septal defect (ASD)
    • Left to right shunt (acyonatic). usually at the foramen ovale. 
    • Long term can cause pulmonary HTN.  
  48. Ventricular Septal Defect (VSD)
    • Left to right shunt (acyonatic) 
    • Most common congenital cardiac anomaly. 
    • It depends on the size of the hole to know if it is repairable. 
    • Could cause pulmonary HTN, Rt ventricle hypertrophy, and reversal of the shunt. 
  49. Patent Ductus arterious
    • The ductus arterious usually closes soon after birth (48 hrs), but if it remains opened, a Lt to Rt shunt develops (acyonatic)
    • Results in Pulmonary HTN, and Rt to Lt hear failure.
  50. Coarctation of Aorta
    • Narrowing of the aorta lumen (proximal if infant, distal if adult) 
    • CM: hypertension. 
  51. Cyanotic Congenital defects
    • Disorders that result in Right-to-left shunting of blood. 
    • EX: Tetralogy of fallot, transposition of the great arteries, Truncus arteriosus.
  52. Tetralogy of Fallot
    • Ventricular septal defect 
    • Aorta positioned above the ventricular septal opening. 
    • Pulmonary stenosis that obstructs right ventricular outflow. 
    • Rt ventricular Hypertrophy. 
  53. transposition of great arteries
    • It is incompatible with life unless mixing of blood occurs through other defects (ASD or VSD, and PDA)
    • Very difficult to repair. 
    • Aorta arises from the Rt ventricle, and Pulmonary artery from the Lt. 
    • Cyonatic Right to left shunt. 
  54. Truncus Arteriosus
    • Failure for the pulmonary artery and the aorta to separate. 
    • systemic cyonatic Rt to Lt shunting. 
    • Could cause pulmonary HTN, and Rt ventricular hypertrophy.