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CVP-GI Exam II
CVP-GI Exam 2 Dr. Virji Cleveland Chiropractic College Fall 2012
| Question | Answer |
|---|---|
| What is the normal weight of the heart for males and females? | Males- 300 grams Females- 250 grams |
| What is the weight of the heart largely dependent on? | Largely dependent on the Thickness of the Left Ventricle |
| What 9 things do they really look for during autopsy of an individual who has apparently died of sudden heart failure? | 1. The pericardium 2. Pericardial cavity 3. Size/weight of the heart 4. Myocardium 5. Atria & Ventricles 6. Endocardium 7. Valve Cusps 8. Valvular openings 9. Coronary arteries |
| Approximately, how many liters of blood are propelled through the body by the heart on a daily basis? | 6,000 Liters of blood per day |
| What is the thickness of the left and right ventricles? | Left Ventricle - 13-15mm or 1.3-1.5cm Right Ventricle- 3-5mm or .3-.5cm |
| Do both the right & the left ventricles undergo hypertrophy? | YES, both ventricles undergo hypertrophy. |
| Why do both ventricles undergo hypertrophy? | The ventricles hypertrophy when they have increased work to do. |
| Under what situation would left ventricle undergo hypertrophy? | The LEFT ventricle would undergo hypertrophy… In arterial hypertension With aortic valve stenosis Stenosis is the “narrowing of a vessel” |
| Under what situation would right ventricle undergo hypertrophy? | With Mitral Stenosis(Mitral Valve Disease which causes Pulmonary HTN) and Pulmonary Hypertension (due to Chronic Lung Disease) |
| What does greater heart weight or ventricular thickness indicate? | Indicates Hypertrophy |
| What does an enlarged chamber size indicate? | An enlarged chamber size indicates dilation. Valve not closing properly. |
| Why is it that wall thickness itself may not be a good measure of increased cardiac mass? | This is because an apparently normal (or less than normal) left ventricular thickness may be found in a markedly heavy, hypertrophied heart that has dilated BEFORE death |
| What is cardiomegaly? | An increase in cardiac weight or size is termed cardiomegaly |
| What is the function of the heart valves? | Heart valves prevent any admixture between arterial & venous blood In other words, circulation must be strictly ONE way! |
| How many valves are there in the heart? | There are FOUR valves in the heart |
| What are the four valves? | 1. Tricuspid Valve 2. Mitral Valve (Bicuspid Valve) (MV) 3. Pulmonic Valve (PV) 4. Aortic Valve (AV) |
| Where is the Tricuspid Valve located? | -Tricuspid valve has three cusps (leaflets) -It separates right atrium from right ventricle (hence called right atrioventricular valve) -It opens towards the right ventricle & closes towards the right atrium |
| Where is the Mitral Valve (Bicuspid Valve) (MV) located? | -Mitral valve (Bicuspid valve) has two cusps (leaflets) -It separates left atrium from left ventricle -It opens towards the left ventricle & closes towards the left atrium |
| Where is the Pulmonic Valve (PV) located? | -Pulmonic valve has THREE leaflets (cusps) -It is also known as the semilunar valve -It guards the opening of the pulmonary artery from the right ventricle -It opens away from the right ventricle & closes towards the right ventricle |
| Where is the Aortic Valve (AV) located? | •Aortic valve has THREE leaflets (cusps) •It is also known as semilunar valve •It guards the opening of the aorta from the left ventricle •It opens away from the left ventricle & closes towards the left ventricle |
| What is the size of valvular openings? | -Tricuspid valve (12 cm in circumference) -Mitral valve (10 cm in circumference) -Pulmonic valve (8.5 cm in circumference) -Aortic valve (7.5 cm in circumference) |
| What is ‘nodule of Arantius’? | Each aortic leaflet (3 leaflets total) has a small nodule in the center of the free edge, which facilitates closure—the nodule is known as nodule of Arantius Arantius (1530-1589) was an Italian anatomist & physician |
| What is chordae tendineae? | The free margins of atrioventricular (AV) valves (vis a vis mitral & tricuspid valves) are attached to the ventricular wall by many delicate tendon-like cords that attach to papillary muscles that are in contract with the underlying ventricular walls |
| What is mitral apparatus? | coordinated actions of: Annulus (in the old days “anulus” was spelled as “annulus”) or ring-like structure Leaflets Cords Papillary muscles Associated left ventricular wall |
| What sort of cells line the cardiac valves? | The cardiac valves are lined with endothelial cells (endothelium) |
| How are heart valves nourished? | In general, normal leaflets have very few blood vessels limited to the proximal portion because they are thin enough to be nourished by DIFFUSION from the heart’s blood |
| What is the pathologic significance of the points where the leaflets are joined together (known as “commissures”) particularly for the aortic valve? | Any widening of these commissures is an indications of disease, nearly always syphilis |
| Briefly describe the structure of the heart. | The heart is composed of: The endocardium—which lines the internal surfaces of the cardiac chambers and valves The myocardium The pericardium—composed of an inner visceral layer covering the heart & outer parietal layer completing the pericardial sac |
| Briefly describe the structure of the hearts conducting system. | A specialized conducting system consisting of: Sinoatrial node (SA) Atrioventricular node (AV) Bundle of His Purkinje fibers |
| What is myocardium? | Myocardium, the main component of the heart, forms the bulk of the cardiac chambers It consists of: Contractile myocardial cells (cardiac myocytes) Modified myocytes forming the conduction system |
| Myocardium | Myocytes are striated muscle cells forming a syncytium, meaning multinucleated protoplasmic mass formed by the secondary union of originally separate cells In short, it is continuous with the cytoplasm of other myocytes |
| What is the purpose of this syncytial arrangement of cardiac myocytes? | Syncytial arrangement of cardiac myocytes is essential for… The transmission of electrical impulses through the myocardium The synchronized contraction of cardiac chambers |
| Why is the heart often called “a miracle of constants”? | 2 ventricles contract together as do the 2 atria The same amount of blood passes out of the ventricles at the same time during systole (during contraction) The same amount of blood enters the heart at the same time during diastole(during relaxation) |
| What happens if the constants aren't constant? something is off? | Any discrepancy in the time or in the quantitative relations may ultimately cause HEART FAILURE |
| What are sarcomeres? | Sarcomeres are the functional units of each cardiac myocyte |
| What are sarcomeres composed of? | Sarcomeres are composed of: Contractile proteins actin & myosin A number of regulatory proteins, such as troponin, tropomyosin, etc. |
| What is a Z-Line? | By electron microscopy, one can see that the sarcomeres are separated from one another by a dense Z-line |
| What happens during the contraction of cardiac muscle? | Contraction of cardiac muscle occurs by the cumulative effort of sliding of the actin filaments between the myosin filaments toward the center of each sarcomere In other words, the sarcomeres shorten & elongate with each cardiac contraction |
| What governs the strength of cardiac contraction? | The lengths of sarcomeres range from 1.6 to 2.2 micrometers depending on the state of contraction Shorter sarcomeres have overlap of actin & myosin filaments,reduce in contractile force longer lengths enhance contractility (Frank-Starling mechanism) |
| What governs the strength of cardiac contraction, overall result? | Thus, moderate ventricular dilation increases the force of contraction; however, further elongation of the sarcomere is accompanied by weakening of cardiac contractions |
| Are atrial myocytes different from ventricular myocytes? | Atrial myocytes are generally smaller in diameter & less structured than their ventricular counterparts |
| What are specific atrial granules? | Some atrial cells differ from ventricular cells in having distinctive electron dense granules in the cytoplasm called specific atrial granules |
| What is the function of specific atrial granules? | Specific atrial granules are the site of storage of atrial natriuretic peptide |
| Where is atrial natriuretic peptide synthesized? | Atrial natriuretic peptide is synthesized in the atrial muscle cells & secreted into the blood under conditions of atrial pressure elevation & distension |
| What is the role of atrial natriuretic peptide? | Atrial natriuretic peptide can produce a variety of physiological effects: -Vasodilation -Natriuresis (meaning enhanced sodium excretion) -Suppression of the renin-angiotensin-aldosterone axis -A fall in arterial pressure Beneficial to HN & Heart fa |
| What is the pericardial sac? | The heart is located inside the pericardial sac—a cavity that shares some features with the pleural & abdominal cavities -surface covering the heart itself is called epicardium, whereas the surface facing it is called pericardium |
| Are the Epicardium and the Pericardium the same Mesothelial Cells? | Yes, both the endocardium and the pericardium have the same mesothelial cells |
| What are the main components of the cardiac conducting system | Sinoatrial Node (SA) Atrioventricular Node (AV) Bundle of His Purkinje Fibers |
| Congestive Heart Failure | Powerpoint |
| What is congestive heart failure? | occurs when the ventricular muscle is incapable of maintaining a circulation adequate for the needs of the body (usually evaluated in terms of oxygen requirements)—producing symptoms during exercise & at rest |
| What is the difference between forward & backward heart failure? | --Forward heart failure is characterized by diminished cardiac output (reduced systolic output) --Backward heart failure is characterized by damming back of blood in the venous system due to inadequate emptying at the heart chambers |
| What is the importance of forward & backward heart failure clinically? | In most clinical conditions, there are signs of both forward & backward failure |
| Is it possible to classify diseases causing heart failure? | It is useful to classify heart failure into two main groups… 1.Diseases affecting the myocardium (pump) leading to primary muscle failure 2.Diseases of other cardiac & circulatory components leading secondarily to muscle failure |
| Diseases affecting the myocardium (pump) leading to primary muscle failure (3) | 1.Ischemic Heart Disease most common The primary disease vis a vis atheroma & thrombosis in the coronary arteries leads to myocardial damage, fibrosis or infarction 2.Inflammation & toxic degeneration of the myocardium (myocarditis) 3.Cardiomyopathies |
| Disease 1 of other cardiac & circulatory components leading secondarily to muscle failure | 1.Control Mechanism Defects Valvular disease increases work load Electrical disorders involving SA, AV nodes, & Bundle of His as in cardiac arrhythmias leading to inefficient pumping action |
| Disease 2 of other cardiac & circulatory components leading secondarily to muscle failure | Distribution Defects Systemic hypertension Chronic lung disease causing pulmonary hypertension |
| Disease 3 of other cardiac & circulatory components leading secondarily to muscle failure | Increased work load |
| How can we explain the initiation of compensatory mechanisms? | heart failure is preceded by cardiac hypertrophy compensatory response of myocardium to increased work rate of protein synthesis increases in cell protein in each cell increases size of myocytes increases number of sarcomeres & mitochondria increases |
| How can we explain the initiation of compensatory mechanisms final parts? | The mass & size of the heart increases Up-regulation of several immediate early response genes & embryonic forms of contractile & other proteins ALL OF THESE CHANGES INITIALLY MEDIATE ENCHANCED FUNCTION, BUT IT EVENTUALLY LEADS TO HEART FAILURE |
| How can we explain the failure of compensatory mechanism? | Proteins related to contractile elements may be significantly altered through production of different isoforms that may be dysfunctional or may be reduced or increased in amount |
| How can we explain the failure of compensatory mechanism? | Alterations of intracellular handling of calcium ions may also contribute to impaired contraction & relaxation There is reduced adrenergic drive There is decreased calcium availability There is impaired mitochondrial function |
| How we explain the failure of compensatory mechanism | increased loss of myocytes through apoptosis most often associated with dividing cells that reactivate the fetal growth program in cardiac myocytes, presumably because such cells are no longer capable of progressing through the cell cycle to mitosis |
| How we explain the failure of compensatory mechanism | There is decreased capillary-to-myocyte ratio There is increased fibrous tissue Myocardial hypertrophy leads to increased metabolic requirements of the enlarged muscle mass There is an increased wall tension |
| How we explain the failure of compensatory mechanism, what ultimately happens? | Ultimately the primary cardiac disease & the superimposed compensatory burdens further encroach on the myocardial reserve At autopsy, the hearts of patients having CHF are Increased weight Chamber dilation Thin walls microscopic changes of hypertroph |
| What are the most common causes of heart failure? | Pump Failure Valvular Failure Restrictive/Constrictive Diseases |
| Describe the Pump Failure type of Heart Failure. | This category includes numerous diseases that damage the myocardium & reduce its contractility, such as… Ischemic coronary heart disease Electrical disorders (e.g. ventricular fibrillation) Myocarditis Cardiomyopathies (e.g. metabolic, hereditary, etc |
| Describe the Valvular Failure type of Heart Failure. | Diseases affect the valves & cardiac skeleton to which the valves are attached include: Endocarditis (bacterial, immunologic diseases) Degenerative diseases (calcific aortic stenosis of old age) Metabolic disorders(Marfan syndrome, floppy mitral valve) |
| Describe the Restrictive/Constrictive diseases of Heart Failure. | They prevent dilation of cardiac chambers in diastole & include… Myocardial infiltration with amyloid, endomyocardial fibrosis, etc. Pericarditis |
| What is left-sided heart failure? | primarily result from progressive damming of blood within the pulmonary circulation (increased pulmonary venous pressure) & the consequences of diminished peripheral blood flow |
| What are the causes of left-sided heart failure? | Ischemic heart disease Hypertension Aortic & mitral valvular disease Non-ischemic myocardial diseases |
| What are the morphological changes observed in left ventricular failure? | Hypertophied, unless blockage of mitral valve etc. Dilated Secondary enlargement of left atrium with uncoordinated atrial fibrillation which increase risk of Embolic Stroke |
| Where is the most prominent extra-cardiac effect manifested in left ventricular failure? | LUNGS!!!! The result is pulmonary congestion & edema, with heavy, wet lungs |
| What other organs are affected (besides the lungs) by the left ventricular failure? | The kidneys & brain are also affected by left ventricular failure |
| How the Kidneys are affected by the left ventricular failure | *Azotemia means nitrogen retention resulting from something other than primary renal disease Azotemia is reflected in elevated Plasma urea & creatinine |
| How the Brain is affected by the left ventricular failure | In far-advanced CHF, cerebral hypoxia may give rise to hypoxic encephalopathy, which results in… Irritability Loss of attention span Restlessness It may progress to stupor & coma |
| What is right-sided heart failure? | occurs in only a few diseases Pure right-sided failure most often occurs with: 1. Chronic severe pulmonary hypertension & thus is called “cor pulmonale” 2.Acute severe decrease in output 3.Cardiac Tamponade |
| What is cor pulmonale? | Cor pulmonale is dilation & hypertrophy of the right heart in response to pulmonary hypertension |
| Acute severe decrease in output | Acute right heart failure occurs most commonly when a massive pulmonary embolus becomes impacted in & obstructs the outflow tract of the right ventricle & main pulmonary artery This results in arrest of the circulation & sudden death |
| What is Cardiac Tamponade? | Cardiac Tamponade means compression of venous return to the heart due to increased volume of fluid in the pericardium |
| What is Cardiac Tamponade another form of? | This is another form of acute right heart failure -A sudden increase in pericardial cavity pressure due to fluid accumulation interferes with right ventricular diastolic filling, resulting in decreased right ventricular output |
| What is the most common cause of right sided heart failure? | most common cause of right-sided heart failure is a secondary consequence of left-sided heart failure the causes of right-sided failure must then include all those causes that induce left-sided heart failure |
| Why is right sided heart failure secondary to left sided heart failure? | This is because any increase in pressure in the pulmonary circulation incident to left-sided failure, inevitably produced an increased burden on the right side of the heart |
| Main Causes of Right-Ventricular Failure? | Lung Disease Mitral Stenosis Congenital Heart Disease, usually as a result of LV failure |
| What are the morphological changes observed in right-sided heart failure? | engorgement of the systemic & portal venous systems may be pronounced respiratory symptoms may be absent or quite insignificant in right-sided failure, |
| What organs are affected by right-sided CHF? | The liver & the portal system Kidneys Brain Pleural and pericardial spaces Subcutaneous Tissue (Edema) |
| What is Anasarca? | Generalized massive edema is called anasarca |
| As a result of chronic failure of the left ventricle, what are the 4 major consequences of increased pressure in the alveolar capillaries? Number 1 | Microhemorrhages release erythrocytes into the alveolar spaces, where they are engulfed & degraded by alveolar macrophages. The released iron, in the form of hemosiderin, remains in the macrophages, which are then called “heart failure cells”. |
| Number 2 | The increased hydrostatic pressure forces fluid from the blood into the alveolar spaces, resulting in pulmonary edema—a dangerous condition that interferes with gas exchange in the lung |
| Number 3 | The increased pressure along with other poorly understood factors, stimulates fibrosis in the interstitial spaces of the lung. The presence of fibrosis & iron is viewed grossly as a firm, brown lung. |
| Number 4 | The increased capillary pressure is transmitted to the pulmonary arterial system, a condition labeled pulmonary hypertension. This may lead to right-sided heart failure & consequent generalize systemic venous congestion. |
| What are the clinical features of CHF? Depends upon which ventricle is failing—recognizing that both may be in failure simultaneously | Patients with left-sided CHF complain of shortness of breath (dyspnea) on exertion & when recumbent (orthopenia) |
| CHF Clinical features continued | They may be awakened from sleep by sudden episodes of shortness of breath (paroxysmal nocturnal dyspnea) Physical examination reveals distended jugular veins |
| Patients with right-sided CHF have: | Pitting edema of the lower extremities Enlarged & tender liver The abdomen is distended |
| Define Cardiac Failure | Cardiac failure is the inability to maintain a cardiac output for tissue metabolic needs despite normal venous return Cardiac output also falls below normal if venous return is reduced, as in the noncardiogenic types of shock |
| What are the common causes of left-sided heart failure? | Ischemic heart disease Hypertensive heart disease Aortic valve disease(stenosis, incompetence) Mitral valve disease(stenosis, incompetence) Myocarditis Cardiomyopathy Cardiac amyloidosis High-output states (thyrotoxicosis, anemia, arteriovenous fis |
| What are the common causes of right-sided heart failure? | Chronic pulmonary disease(cor pulmonale) Pulmonary valve stenosis Tricuspid valve disease(stenosis, incompetence) Congenital heart disease (ventricular septal defect,patent ductus arteriosus) Pulmonary hypertension (both) Massive pulmonary embolism |
| Is Left-sided heart failure also a common cause of right sided heart failure? | YES, Left-sided heart failure often causes right-sided heart failure |
| Define high-output cardiac failure: | Inability to maintain an abnormally high cardiac output because of demand for increased blood flow Normal = 5 L/min Increased Demand = 7 L/min Failure = 3 to 4 L/min |
| Common causes of High output cardiac failure: | Valve incompetence Anemia Thyrotoxicosis (hyperthyroidism) Fever Arteriovenous malformation Paget’s disease of bone Plasma volume overload Beriberi |
| Define low-output cardiac failure: | Inability to maintain a normal systemic cardiac output Normal = 5 L/min Failure = 3 to 4 L/min |
| Common causes of low output cardiac failure: | Myocardium disorders: Ischemic Heart Disease Myocarditis Cardiomyopathy Amyloidosis Arrhythmias Increased pressure load… Systemic hypertension Valve stenosis All causes of right ventricular failure secondary to lung disease (cor pulmonale) |
| What is “Ischemic Heart Disease” (IHD)? | IHD is the generic designation for a group of closely related syndromes resulting from myocardial ischemia |
| What is myocardial ischemia? | In short, it means “to keep back or hold back blood due to mechanical obstruction” In ischemia there is an imbalance between the supply (perfusion) & the demand of the heart for oxygenated blood |
| What happens in ischemia? | Ischemia is characterized by: Insufficiency of oxygen Reduced availability of nutrient substrates Inadequate removal of metabolites |
| Why is it that isolated hypoxemia induced by cyanotic congenital heart disease, severe anemia, or advanced lung disease is less deleterious than ischemia? | This is because in the above mentioned scenario… Perfusion Metabolic substrate delivery And waste removal are all maintained |
| What is the cause of Ischemic Heart Disease (IHD)? | More than 90% of cases of IHD are caused by narrowing of one or more of the three major coronary artery branches: Left coronary artery—Anterior descending branch Right coronary artery Left coronary artery—Circumflex branch |
| Why do these 3 arteries affect IHD? | These are functional end arteries & sudden occlusion of any one lead to infarction in the area of supply |
| What conditions can aggravate ischemia? | Increase in cardiac energy demand (e.g. hypertrophy) Lowered systemic blood pressure as in shock Hypoxemia Increased heart rate |
| What is the major cause of IHD? | Atherosclerosis accounts for 98% of the cases of IHD Therefore, the risk factors for IHD are those for atherosclerosis |
| What are the other rare causes of IHD? | Coronary artery spasm (Prinzmetal angina) Coronary artery embolism (most commonly in infective endocarditis) Coronary ostial narrowing (in syphilis & Takayasu’s aortitis) NOTE: “Ostial” means “small opening” |
| What are the risk factors for IHD? | Non-modifiable Age Gender (Male) Familial predisposition Modifiable Hypertension Smoking Obesity Diabetes Sedentary lifestyle |
| What is the mneumonic for IHD risk factors? | “HAS LIPIDS” H-ereditary A-ge S-ex (male) L-ipidemia I-ncreased weight (obesity) P-ressure (arterial) I-nactivity (sedentary lifestyle) D-iabetes S-moking |
| What are the main clinical features of ischemic heart disease? | Myocardial infarction Angina pectoris Sudden death Cardiac arrhythmias Cardiac failure |
| What is the anatomic distribution of myocardial infarcts? | Myocardial infarction involves principally: The left ventricle Interventricular septum Conducting system NOTE: The atria & right ventricle are rarely involved |
| Why is it that the atria & right ventricle are rarely involved in the anatomic distribution of myocardial infarcts? | This is most likely because their thin muscle walls derive a considerable part of their nutritional supply directly from the blood in the cardiac lumen The distribution of infarction depends on which vessel is occluded |
| What is paradoxic infarction? | Remember…collaterals develop in a chronically narrowed coronary circulation This means that the blood supply may traverse circuitous routes (meaning going around), leading to infarcts in unusual sites (i.e. paradoxic infarction) |
| How is myocardial infarct defined? | Transmural infarcts “Transmural infarcts” means “through any wall” They involve the entire thickness of the ventricular wall from the endocardium to the subepicardial fat tissue |
| What are Transmural infarcts usually caused by? | These infarcts are usually (90%) caused by occlusive thrombi forming in the atherosclerotic coronary arteries In a small number of cases, they are related to thromoemboli, vasospasm or their causes remain unknown (idiopathic) |
| Transmural infarcts | Occlusion, due to thrombus, thromboemboli, vasospasm or idiopathic origin involves the entire wall of the ventricle, from endocardium to the subepicardial fat tissue |
| What are Subendocardial infarcts ?(non-transmural) | Involves an area of necrosis limited to the inner one-third or, at most, one-half of the ventricular wall It may extend laterally beyond the perfusion territory of a single coronary artery |
| What causes Subendocardial infarcts? | In short, these infarcts are caused by hypoperfusion of the myocardium & are not caused by coronary occlusion Typically these infarcts occur in hypotensive shock |
| How long does it take before severe ischemia leads to striking loss of contractility of the heart? | It takes bout 60 seconds before severe ischemia leads to striking loss of contractility of the heart & can precipitate acute heart failure |
| Is myocardial cell death immediate after severe ischemia? | It has been demonstrated experimentally in dogs that only severe ischemia lasting at least 20 to 40 minutes or longer leads to irreversible damage (necrosis) of some cardiac myocytes |
| Is cardiac myocyte injury due to severe ischemia reversible? | Yes…if restoration of myocardial blood flow (known as reperfusion) follows briefer periods of flow deprivation (less than 20 minutes in the most severely ischemic myocardium), loss of cell viability does not occur!* |
| What is the importance of the above discussed fact? | Rationale for the early detection of acute myocardial infarction to permit early therapy such as thrombolysis to establish reperfusion of the area at risk, salvage as much ischemic,but not yet dead myocardium as possible,& minimize infarct size |
| What are the various techniques employed for reperfusion? | 1.Thrombolysis By the use of thrombolytic or fibrinolytic drugs 2.Angioplasty 3.Coronary bypass graft surgery |
| What is the difference between anticoagulant/anti-platelet drugs & thrombolytic drugs? | Anticoagulant/anti-platelet drugs are administered to prevent the formation of clots Thrombolytic drugs are used to lyse already formed clots |
| How do these thrombolytic or fibrinolytic drugs act? | Fibrinolysis=breakdown fibrin that holds clot together Fibrinolysis-initiated by activation of plasminogen to plasmin Plasmin-catalyzes degradation of fibrin Activation of plasminogen initiated by plasminogen activators |
| What do the Thrombolytic drugs do then? | Thrombolytic drugs are the Plasminogen activators!!! |
| What is the first generation of plasminogen activators? | The first generation The first generation of drugs (steptokinase & urokinase) convert all plasminogen to plasmin throughout the plasma! |
| What is the second generation of plasminogen activators? | The second generation The second generation of drugs tissue-type plasminogen activator (t-PA) selectively activate plasminogen bound to fibrin! In fact, t-PA’s selectively appear to be quite limited (Alteplase; Reteplase) |
| Are there any complications associated with reperfusion? | YES- number of ischemic cells are in tact but lose integrity, Apoptosis may occur after |
| Are there any complications associated with reperfusion? Part 2 | injury may be mediated by the generation of oxygen free radicals Ischemic &/or reperfusion injury is associated with the production of Cytokines Increased expression of adhesion molecules |
| Part3 | These recruit circulating polymorphonuclear leukocytes to reperfused tissue This leads to inflammation causes additional injury |
| What is important to help prevent further injury in reperfusion? | of neutrophil influx in reperfusion injury has been demonstrated by experimental studies that have used anti-inflammatory interventions, such as antibodies to either cytokines or adhesion molecules, to reduce the extent of the injury |
| What are the consequences & complications of myocardial infarction? (8) | 1. Arrythmias 2. Sudden Death 3. Cardiogenic shock (contractile dysfunction) 4. Myocardial Rupture 5. Rupture of the free wall of the left ventricle 6. Rupture of the papillary muscles 7. Mural Thombosis 8.Extension of the myocardium or reinfarctio |
| Does autonomic stimulation occur during the myocardial infarction? | Yes…in fact, it is quite common in acute MI It produces either: Tachycardia (sympathetic stimulation) Bradycardia (vagal or parasympathetic stimulation) |
| What is the major function of neutrophils? (Myocardial Rupture) | They constitute the body’s first line of defense when tissue is damaged or foreign material gains entry Neutrophils phagocytize & degrade particles of many types |
| What is another major function of neutrophils? (Myocardial Rupture) | They are capable of releasing enzymes into their own cytoplasm or into the surrounding medium Alkaline phosphatase is an enzyme present in late-developing granules of neutrophils, whereas peroxide-reacting enzymes are present in earlier granules |
| What is the mneumonic for the consequences & complications of myocardial infarction? | Arrhythmias Pump Failure Pericarditis Extension of infarct Asystole(heart block or ventricular fibrillation Rupture(free wall of ventricle,septum or papillary muscle Aneurysms of ventricle Nervousness Coagulation problems(mural thrombosis Emboli |
| How can we classify the various types of cardiac arrhythmias | 1. Altered activity of the SA Node 2. Ectopic Rhythms 3. Heart Block |
| What are altered activities of the SA Node involved in Cardiac arrythmias? | Sinus tachycardia Sinus bradycardia Sinus arrhythmia |
| What are the Ectopic Rhythms involved in cardiac arrythmias? | -Supraventricular (atrial or AV nodal) Supraventricular extra-systoles Paroxysmal supraventricular tachycardia Atrial flutter Atrial fibrillation -Ventricular Ventricular extra-systoles Ventricular tachycardia Ventricular fibrillation |
| What are the Heart Blocks involved in Cardiac Arrythmias? | Sinoatrial block (partial or complete) Atrioventricular block (partial or complete) Bundle branch block |
| Look at effects of cardiac arrythmias on pp3 slides 106 & 107 | slide 106 and 107 |
| What is Dressler Syndrome? | Dressler syndrome is a compilation of transmural myocardial infarcts clinically presenting with pericardial pain associated with friction rub |
| What is the pathogenesis of chronic ischemic heart disease after an infarction? | pp3 slide 111 |
| What are the pathologic findings in sudden cardiac death? | The most common findings is thrombosis of coronary arteries |
| What are the pathologic findings in sudden cardiac death? Other causes | Coronary disease such as… Vasculitis Coronary artery aneurysm Cardiac diseases not clinically recognized Cardiomyopathies Myocarditis Valvular disease Mitral valve prolapse Aortic stenosis |
| What is cardiomyopathy? | Cardiomyopathy literally means “an ailment of the heart” In response to injury, the heart may undergo dilation or hypertrophy |
| What are the three different forms of cardiomyopathy? | 1. Dilated cardiomyopathy 2. Hypertrophic cardiomyopathy 3. Restrictive cardiomyopathy |
| Discuss infections of the myocardium leading to myocarditis: | caused by viruses, such as coxsackie B virus, or parasites, such as Toxoplasma gondii or Trypanosoma cruzi Cause cell death that weakends myocardium and contribute to heart failure |
| What else occurs in infections of the myocardium? | myocardium is invaded by T lymphocytes that are attracted by the virus/parasite T lymphocytes secrete cytokines, such as TNF & interleukins which are supposed to kill the virus or parasite—that means parasite or virus-infected myocardial cells as well |
| What are the symptoms of myocarditis? | The symptoms of myocarditis are vague, & the diagnosis of this disease cannot be easily made Symptoms include: Mild fever Shortness of breath Other signs of heart failure (e.g. tachycardia, peripheral cyanosis, pulmonary edema & precardial pressure pa |
| What are the common symptoms of myocardial infarct? | Substernal pain persisting for more than 30 min,not relieved by nitroglycerin Pain may occur at rest,but is often caused by work/exercise pain often in the morning(catecholamine burst awakening) Severe distress marked by nausea,sweating & vomiting Dys |
| What are the common symptoms of myocardial infarct? | severe episodes, the patient becomes apprehensive & may develop a sense of impending doom Patients with MI have rapid, weak pulse & are often diaphoretic (meaning perspiring) Blood pressure is variable unless cardiogenic shock is developing |
| What percent of myocardial infarctions are silent? | Approximately 20% of cases of myocardial infarction occur without pain—”silent infarction” |
| Which tests are helpful for the diagnosis of myocardial infarcts? | EKG changes are found in 85% of cases, but often they are nonspecific Diagnostic EKG changes are found in 50 to 65% of cases during the first two days of onset of the infarction |
| Which tests are helpful for the diagnosis of myocardial infarcts? | Necrotic myocardial fibers release a variety of enzymes into the bloodstream |
| What enzyme is used in the tests for myocardial infarctions? Where is it concentrated at? | Creatine Kinase (CK) is highly concentrated in: Brain Myocardium Skeletal muscle |
| What is Creatine Kinase composed of? | Creatine kinase is composed of two dimers designated as M & B: CK-MM: Skeletal muscle & heart CK-BB: Brain, lung, & many other tissues CK-MB: Principally from myocardium, although variable amount of MB are also present in skeletal muscle |
| Diagnosis of Myocardial infarct with Creatine Kinase | An absence of a change in levels of total CK & CK-MB during the first two days of chest pain essentially excludes the diagnosis of MI |
| What type of proteins are used in tests for myocardial infarcts? And what are they? | Troponins Troponins are proteins that regulate calcium-mediated contraction of cardiac & skeletal muscle |
| Are Troponins normally detected in the blood? | Troponin I (TnI) & troponin T (TnT) are not normally detected in the blood Therefore, serum elevations are abnormal! Cardiac & skeletal muscle forms can be distinguished by specific antibodies that also permit quantitative immunologic assays |
| What is the time line like for creatine kinase and both forms of troponin? (Troponin I (TnI) & troponin T (TnT) | Creatine Kinase, rises within 4-8 hrs peaks at 18 hours, and dissappears by 48-72 hrs. TnI-rises within 4-8 hrs, peaks at10-24 hrs, and dissappears in 4-6 days TnT-rises within 4-8 hrs, peaks in 10-24 hrs, and dissappears in 10 days or more |
| What are the 3 types of Creatine Kinase and what tissues do they go too? | CK-MM: Skeletal muscle & heart CK-BB: Brain, lung, & many other tissues CK-MB: Principally from myocardium, although variable amount of MB are also present in skeletal muscle |
| End powerpoint 3 | Begin powerpoint 4 Angina Pectoris |
| How is a symptom complex of ischemic heart disease (IHD) characterized? | By sudden: Constricting Squeezing Chocking Knifelike It is caused by transient (15 seconds to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines infarction |
| What are the three overlapping patterns of angina pectoris? | Stable or typical angina Prinzmetal or variant angina Unstable or crescendo angina |
| What causes angina? | Anginas are caused by varying combinations of increased myocardial demand & decreased myocardial perfusion, due to: Fixed stenosing plaques Disrupted plaques Vasospasm Thrombosis Platelet aggregation Embolization |
| Angina: | Insufficient blood flow to the heart muscle from fixed stenosing plaques, disrupted plaques, vasospasm, thrombosis, platelet aggregation, & embolization |
| What is silent ischemia? | It is being recognized that not all ischemic events are perceived by patients, even though such events may have adverse prognostic implications |
| What is stable angina? | The most common form & often known as typical angina pectoris It appears to be caused by the reduction of coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis |
| What does Stable Angina leave the heart more vulnerable too? | This renders the heart vulnerable to further ischemia whenever there is increased demand, such as: That produced by physical activity Emotional excitement Any other cause of increased cardiac workload |
| How is the attack of Stable/Typical angina pectoris relieved? | It is usually relieved by: Rest (thereby decreasing demand) Nitroglycerin (a strong vasodilator thereby increasing myocardial perfusion) |
| How does nitroglycerin work? | relax vascular smooth muscle through conversion into nitric oxide Therefore, they dilate vessels in a manner similar to endogenously produced nitric oxide By the way, the so-called endothelium-derived relaxing factor (EDRF) is probably nitric oxide |
| What is the principle physiologic effect of low doses of nitroglycerin (nitrates)? | Dilation of the veins which causes a diminished (or reduced) preload & reduced cardiac output |
| What is the effect of high doses of nitrates? | Arterioles become dilated which leads to: A decrease in peripheral resistance A decrease in blood pressure |
| What are the additional minor effects of nitrates? | Dilation of collateral coronary vessels in spasm |
| What is myocardial oxygen demand dependent upon? | Preload—diastolic filling pressure Afterload—peripheral vascular resistance Heart rate Wall tension |
| Name four major classes of drugs used to treat angina | 1.Nitrates 2.Calcium channel blockers (drugs of choice for Prinzmetal’s angina) 3.Beta blockers 4.Aspirin |
| What is Prinzmetal variant angina? | It is an uncommon pattern of episodic angina that occurs at rest & has been documented to be due to coronary artery spasm Usually there is elevation of the ST segment of the electrocardiogram (ECG), indicative of transmural ischemia |
| Prinzmetal angina is unrelated to what? and responds to what? | the anginal attacks are unrelated to: Physical activity Heart rate Blood pressure Prinzmetal angina generally responds promptly to: Vasodilators such as nitroglycerin Calcium channel blockers |
| What is common with Prinzmetal anginas? | Prinzmetal anginas occur often with arrythmias and at certain times of the day |
| What is unstable angina? | It is characterized by pain that is becoming more & more severe & is precipitated by less & less effort & attacks tend to be of more prolonged duration |
| Unstable angina is caused by what? | Unstable angina is caused by coronary atheromas prone to rupture Rupture results in intimal defects which are covered with thrombi causing severe narrowing of the lumen Peripheral emboli from ruptured atheromas also contribute to the ischemia |
| Describe the ischemia that occurs with unstable angina: | NOTE: Ischemia that occurs in stable angina falls precariously short of inducing clinically detectable infarction. Approximately, 30% of patients with unstable angina will suffer an MI within 3 months of onset! |
| What are pathological findings in the myocardium caused by Stable and Prinzmetal angina? | Stable angina & Prinzmetal angina do not cause any significant myocardial cell necrosis Therefore, there are no microscopic changes in the heart |
| What are pathological findings in the myocardium caused by Unstable angina? | Unstable angina my be accompanied by focal myocyte necrosis, which is repaired by fibrosis |
| End powerpoint 4 | Begin powerpoint 5 Valvular Heart Disease |
| What is endocarditis? | It means inflammation of the endocardium or lining membrane of the heart It may involve: Only the membrane cover the valves (valvular endocarditis) (OR) the general lining of the chambers of the heart (mural endocarditis) |
| What are the main causes of valvular endocarditis? | Rheumatic endocarditis (or immunologically mediated endocarditis) Valvular degeneration caused by calcification Congenital heart disease |
| What are the minor causes of valvular endocarditis? | Inherited deficiencies of the ground substance of the valve |
| What is rheumatic endocarditis? | Rheumatic endocarditis is an aspect of rheumatic fever (RF) The incidence of RF has decreased dramatically in the U.S. & most industrialized countries because of widespread use of antibiotics |
| What is rheumatic fever (RF)? | caused by group A beta hemolytic streptococci In most cases, the infection involves the oropharynx (“strep throat”), but it may also affect the connective tissues at many sites, of which the heart is most important! |
| What is the evidence that rheumatic fever (RF) is an immunologically mediated disease? | In the current theory,the inflammation is regarded as being due to immunological cross-reaction in genetically predisposed individuals since streptococci are not found at the various local sites & the disease follows some 2-4 weeks after throat infection |
| Antibodies to streptococcal antigens includ what 3 antibodies? | Steptolysin O (ASO)Widely used test DNAase Hyaluronidase |
| What are Aschoff Bodies? | Aschoff bodies are granulomas of a peculiar form found in the heart of most patients with RF |
| What are granulomas? | An indefinite term applied to nodular inflammatory lesions, usually small or granular, firm, persistent, & containing compactly grouped mononuclear phagocytes |
| What are the non-cardiac manifestations of rheumatic fever (RF)? | Fever with sweating & malaise Raised ESR (erythrocyte sedimentation rate) Raised C-reactive protein Neutrophil leukocytosis Indications of inflammation at local sites |
| What are the cardiac manifestations of rheumatic fever (RF)? | inflammation is widespread throughout the heart; that is, there is pancarditis |
| What is pericarditis? | during the acute phase of the illness,is important cause of pericardial effusion Pain aggravated by thoracic motion,cough,&respiration NOTE:Ischemic pain is not aggravated by thoracic motion alot of Pericardial fluid may muffle heart sounds |
| What is Myocarditis? | It is common during acute phase & is usually mild It is rarely severe enough to cause cardiac failure The histological picture is striking & the presence of the Aschoff body is characteristic |
| What is Endocarditis? | gross changes are seen usually on the endocardial sites subject to the greatest pressure & traumas; that is, in the left side of the heart at the points of the valve closure & at any sites of jet effect in the blood flow |
| In Endocarditis basic inflammation is complicated by what? | is complicated by ulceration of the valve surface followed by platelet & fibrin thrombosis in the form of small “vegetations” |
| What is the progression of pericarditis, myocarditis, & endocarditis? | Florid Acute=Pericarditis-->Recovery or Myocarditis--> Death (Rare) usually Recovery Low grade Grumbling and latent or very very mild=Epicarditis Left side valves-->healing with scarring and valve deformities |
| Which heart valves are mainly involved in valvular heart disease? | The mitral & the aortic valves are subject to much greater pressures & are more susceptible to damage than the tricuspid & pulmonic valves |
| Which disease is likely to cause valvular damage? | Rheumatic mitral disease but, calcific aortic disease is now much more common |
| How is rheumatic disease diagnosed clinically? | RF is diagnosed clinically using Jones criteria, which are divided into two groups: Major & Minor The diagnosis is established when: Two major & one minor (or) One major & two minor criteria are present |
| What are the major criteria in the Jones Criteria to diagnose Rheumatic Disease? (5) | Major Criteria- Carditis (35%) Polyarteritis (75%) Chorea (5%) Erythema marginatum (10%) Erythema nodosum (10%) |
| What are the minor criteria in the Jones Criteria to diagnose Rheumatic Disease? (3) | Minor Criteria- Fever Arthralgia - Increase of ESR or CRP - EKG changes (prolonged P-R) Preceding attack of RF |
| Is there a useful mnemonic for remembering the features of rheumatic fever (RF)? | Yes—the mnemonic is: CARDIAC RF C-arditis A-rthritis R-andom (involuntary) movements (chorea) D-ematologic signs I-nflammatory lab indices (ESR & CRP increased levels) A-rthralgia C-ardiogram (EKG) R-ecurrent attack (previous RF) F-ever |
| What are the most important features of chronic rheumatic carditis? | Deformities of the cusps Shortening & fusion of chordae tendinae Residual fibrinous vegetations, which can become infected with bacteria Superimposed infection may cause ulceration of the cusps, perforation of valves,rupture of chordae tendinae |
| What is meant by the term “fibrinous vegetations”? | The endocardial abnormality is apt to be the formation of sterile fibrin & platelet thrombi on the surface of non-bacterial thrombotic endocarditis |
| Where do Fibrinous vegetations occur? | Such sterile thrombi occur in areas of endocardial trauma,are found Over scarred valves In areas of turbulent flow & high pressure jet effects associated with valvular defects & congenital lesions In patients with debilitating chronic diseases (Cancer) |
| The meaning of the term “fibrinous vegetations” | Bacteria that adhere to platelets & fibrin have an advantage; however, the adhesion factors are not well understood |
| The meaning of the term “fibrinous vegetations” What does entry of the organism to the thrombus allow? | permits multiplication & further deposition of fibrin & platelets, causing an enlarging thrombus (vegetation) |
| What are the functional consequences of valvular deformities in chronic rheumatic carditis? | Valvular dysfunctions are classified as: Valvular stenosis The orifice is narrowed because the valves cannot open completely Valvular insufficiency valves dont close completely,thus permitting reflow of blood from one chamber into another (regurgitati |
| What is the etiology of mitral valve stenosis? | It is almost always the result of chronic rheumatic heart disease |
| Is mitral valve stenosis more common in males or females? | Females are affected more than males in a ration of 7:1 |
| What are the consequences of mild mitral valve stenosis? | In mild mitral stenosis, the pressure across the valve rapidly equalizes, & the murmur is restricted to the mid-diastolic part of the cycle |
| What occursin Mitral Valve Stenosis | Mitral valve stenosis causes resistance to blood flow through the open mitral valve during diastole |
| What are the consequences of increasing mitral valve stenosis from mild mitral valve stenosis? | the length of the diastolic murmur increases;murmur is accentuated by atrial systole;Closure of the abnormal valve is often loud (loud first heart sound); |
| When does a normal mitral valve open? what happens when it is stenosed? | Normally, the mitral valve opens silently soon after aortic valve closure; however, an abnormal stenotic mitral valve opens with a clicking sound |
| What happens to sounds if the mitral valve becomes rigid as a result of calcification? | the opening “snap” disappears |
| Is left ventricular filling and cardiac output normal or increased in mild mitral valve stenosis? | They are both Normal |
| What are the first 2 consequences of obstruction to blood flow in severe mitral valve stenosis? | Obstruction to blood flow through the mitral valve opening leads to left atrial dilation & hypertrophy Blood tends to stagnate in the left atrium, predisposing to thrombus formation, especially if atrial fibrillation develops,common |
| What are the last 2 consequences of obstruction to blood flow in severe mitral valve stenosis? | Left atrial thrombi may cause a systemic embolism—(OR) it may obstruct the narrowed mitral orifice, causing sudden death (“Ball valve thrombus”) |
| Sever mitral valve stenosis may result in sudden death, what is that called? | Left atrial thrombi may obstruct the narrow mitral orifice and cause sudden death= Ball Valve Thrombus!!! |
| What are 2 things severe mitral valve stenosis leads to? | to increased pulmonary venous pressure & features of left heart failure |
| What happens in Acute Mitral valve stenosis if there is severe mitral valve stenosis obstruction of blood? | In acute mitral valve stenosis, pulmonary edema & pulmonary hemorrhage may occur |
| What happens in Chronic Mitral valve stenosis if there is severe mitral valve stenosis obstruction of blood? | In chronic mitral valve stenosis, there is chronic venous congestion, pulmonary arterial hypertension, & right ventricular hypertrophy |
| How can we briefly summarize all the anatomic changes in the heart as a result of mitral valve stenosis? | Left atrial hypertrophy & dilation With or without atrial fibrillation With or without thrombi Pulmonary venous congestion Right ventricular hypertrophy Small left ventricle |
| What is mitral valve insufficiency (also called mitral valve regurgitation)? | A mitral valve that cannot close during diastole is considered to be insufficient |
| What is the etiology of mitral valve insufficiency? | Rheumatic heart disease account for about 40% of cases of mitral valve insufficiency Please note that rheumatic heart disease is usually associated with mitral valve stenosis |
| Is mitral valve insufficiency more common in males or females? | Males & females are equally affected |
| What is mitral valve prolapse (“floppy valve syndrome”)? | It is a degenerative change that is present in about 1% of the population (especially young women) It is the result of accumulation of mucopolysaccharides in the valve leaflet |
| What other abnormality of the Mitral Valve is similar to floppy vlave syndrom (mitral valve prolapse) | A similar abnormality of the mitral valve is present in patients with MARFAN'S SYNDROME |
| What are the other causes of mitral valve insufficiency? | Chronic left ventricular failure with dilation of the mitral valve ring may cause functional mitral regurgitation |
| Acute mitral regurgitation may occur with | Rupture of the chordae tendinae due to infective endocarditis or trauma Rupture of papillary muscles due to myocardial infarction Perforation of the valve leaflet may also occur in infective endocarditis |
| Acute Mitral regurgitation may also occur with one other thing but is very rare, what is it? | Rarely, calcification of the valve ring in the elderly may lead to mitral regurgitation |
| What are the consequences of mitral valve insufficiency (mitral valve regurgitation)? | left ventricle to the left atrium occurs throughout the systole, producing a typical pansystolic murmur;During diastole, regurgitant blood flows back across the mitral valve, producing a third heart sound & a diastolic flow murmur; |
| What happens to the left ventricle as a consequence to Mitral valve insufficiency? | Left ventricular volume is greatly increased, being the sum of the cardiac output & the regurgitant flow; the left ventricle, therefore, is dilated & hypertrophied |
| How can we briefly summarize all the anatomic changes in the heart as a result of mitral valve insufficiency (mitral valve regurgitation or mitral valve incompetency)? | Left atrial hypertrophy & dilation Pulmonary venous congestion Right ventricular hypertrophy Left ventricular hypertrophy & dilation NOTE: This differs from mitral valve stenosis |
| What is aortic insufficiency (or aortic regurgitation)? | Aortic valves are supposed to be closed during diastole If the valves cannot close properly (completely), blood regurgitation will occur during diastole |
| What is the etiology of aortic insufficiency (or aortic regurgitation)? | Rheumatic heart disease Accounts for about 50% of cases In most of these cases, there is associated mitral valve disease as well as aortic stenosis NOTE: Rheumatic heart disease rarely causes isolated aortic regurgitation |
| What are 3 other etiologies associated with aortic insufficiency? | Ankylosing Spondylitis (AS) Rupture of Aortic Valve Myxomatous degeneration |
| Describe Ankylosing Spondylitis: | AS is a chronic inflammatory joint disease of vertebrae & sacroiliac joints This occurs predominantly in males Begins usually after an infection & is presumed to be of immunogenetic origin, with autoantibodies directed at joint elements |
| How does Ankylosing Spondylitis progress in general? | It follows a chronic progressive course, with extension to hips, knees, & shoulders in one-third of all patients (HLA-B27 & RF) |
| What 2 things is Ankylosing Spondylitis associated with? | HLA-B27 & (RF) Rheumatic Fever |
| Ankylosing Spondylitis is responsible for what two conditions? | AS involve mitral valve insufficiency. AS also involves the root of the aorta—this is important, through uncommon cases (5% of cases) of isolated aortic regurgitation |
| What are the symptoms of Ankylosing Spondylitis? | Recurrent back pain that is often nocturnal of varying intensity Early morning stiffness that is relieved by activity (more frequent in men than women) |
| What can cause Rupture of the Aortic valve and result in aortic insufficiency? | Blunt chest trauma Infective endocarditis (the most common cause) |
| What can cause Myxomatous degeneration and result in aortic insufficiency? | This is due to accumulation of mucopolysaccharides, similar to that seen in mitral valve prolapse This is being recognized as a possible important cause of aortic regurgitation |
| What are the consequences of aortic valve insufficiency (or aortic regurgitation)? | Regurgitation of blood across the incompetent aortic valve occurs in diastole The pressure gradient across the valve is greatest in early diastole—it is the phase that the murmur is the loudest |
| Regurgitation of blood from the aorta in diastole causes: | Decreased diastolic BP, sometimes to zero At the same time, the systolic BP is elevated as a result of increased cardiac output (normal volume & regurgitant volume) |
| What is the result of the previous answer? | causes greatly increased pulse pressure,the typical bounding pulse (known as water-hammer pulse)& capillary pulsations are characteristic of aortic regurgitation Massive dilation & hypertrophy of left ventricle is typical L ventricular failure is commo |
| What is cardiac myxoma? | It is a benign neoplasm of the endocardium |
| How common is cardiac myxoma? | It is rare; however, it is by far the most common primary neoplasm of the heart Approximately, 5% have an inherited basis |
| Where is cardiac myxoma derived from? | from endocardial mesenchymal cells & usually forms a firm gelatinous mass that protrudes into the lumen of the heart |
| Is there a special site where cardiac myxoma occurs? | They occur almost exclusively in the atria—particularly the left atrium |
| What are the clinical features of cardiac myxoma? (3) | Systemic effects are: Irregular, prolonged fever Weight loss Anemia Increased plasma globulin levels The reason for these systemic symptoms is unknown |
| What are the additional clinical features of cardiac myxoma? (3) | 1.Systemic embolism resulting from detachment of fragments of the neoplasm 2.Mitral valve orifice obstruction: turbulence of blood around the tumor produces a mid-diastolic murmur that resembles the murmur of mitral valve stenosis |
| 3.Prolapse of the neoplasm into the mitral valve orifice may obstruct circulation & is a rare cause of sudden death | |
| End powerpoint 5 Valvular Heart disease | Start Powerpoint 6 Infective Endocarditis |
| What is infective endocarditis? | It is an infection associated with formation of vegetations on the endocardial surface, usually on a valve |
| What are vegetations? | Infected thrombi are called “vegetations” |
| What is meant by the term “Friable”? | This term is often employed in bacteriology It denotes a dry & brittle culture falling into powder when touched or shaken |
| Is infective endocarditis age related? | Most cases occur in adults Patients developing disease in their native valves tend to be over 50 years old |
| Is endocarditis likely to occur in particular groups of people? | Yes… Intravenous drug abusers tend to develop disease in the second & third decades Endocarditis also occurs in patients with prosthetic valves |
| Why doesn’t host immune system prevent endocarditis? | The colonies of organisms within the vegetations are relatively protected from host defenses |
| In what ways are the colonies within the vegetations protected? | 1.The valves are avascular & cannot mount an adequate acute inflammatory response 2.the surface of vegetation is covered by dense fibrin & platelets, which limits access of leukocytes or antimicrobial agents (including antibiotics) |
| What are the characteristics of the vegetations of infective endocarditis? | The vegetations of infective endocarditis are multiple, large, & friable & commonly become detached from the valve as emboli |
| Are vegetations different in acute & in subacute endocarditis? | Yes… Vegetations tend to be larger & more friable in acute than in subacute endocarditis |
| Do vegetations occur at particular sites in the heart? | Yes… Vegetations occur principally on the valves of the left side of the heart, following the distribution of chronic rheumatic heart disease: Mitral > Aortic > Tricuspid > Pulmonary |
| Right sided endocarditis is rare but what may it occur with? | IV drug abusers, in whom tricuspid valve is commonly affected Patients with indwelling venous catheters extending into the right atrium; gonococcal endocarditis;ventricular septal defect the jet of shunted blood cause endocardial injury to right ventric |
| What are the clinical features of infective endocarditis? | Bacteremia (or Fungemia) Fever is the most common symptom; low grade & persistent in subacute endocarditis & high with rigors (chill) in acute disease Weight loss & chronic anemia also occur in subacute disease Finger clubbing is a common but late sign |
| What test is used to diagnose Infective Endocarditis? | Blood culture is positive in over 95% of cases & is the most important diagnostic test |
| Why is it necessary to collect multiple blood culture samples drawn at intervals before the patient is given antibiotics? | Because most patients have constant bacteremia & some have a few intermittent bacteremia |
| Chronic Bacteremia causes what? | Chronic bacteremia causes phagocytic & endothelial cell hyperplasia in the spleen leading to spleomegaly |
| Small pinpoint to pinhead size red dots as a result of bacteremia are what? | Petechial hemorrhages (minute hemorrhagic spots, of pinpoint to pinhead size in the skin) in the skin, retina (Roth spots—named after Moritz Roth who was a Swiss physician & pathologist) & nails (“splinter hemorrhages”) |
| When infection is caused by virulent pyogenic organisms what occurs? | miliary abscesses are produced all organs of the body |
| What symptoms are present in subacute endocarditis | Weight loss & chronic anemia also occur in subacute disease |
| What is meant by the term “miliary”? | “Miliary” means marked by the presence of nodules of millet seed size which is about 2 mm |
| What is meant by the term “abscess”? | It is a circumscribed collection of pus appearing in acute or chronic, localized infection, & associated with tissue destruction, &, frequently, swelling |
| 4 Clinical features of Infective Endocarditis? | 1. Bacteremia 2. Immune Complexes 3. Valvular Dysfunction 4. Embolism |
| How can one classify etiology of infective endocarditis? | 1. Infectious agent 2.Acute versus Subacute Infective Endocarditis 3.Patient Groups |
| how do these infectious agent(s) reach the heart in infective endocarditis? | Following oral & dental procedures (viridans streptococci are the most common agents) Following urologic procedures enterococcus faecalis & gram-negative-bacilli are common causes) |
| what is another way infectious agent(s) reach the heart in infective endocarditis? | Following skin infections associated with IV drug use (staphylococcus aureus is a common cause) During surgery, particularly prosthetic valve replacement |
| What is Acute Infective Endocarditis caused by? | It is caused by virulent agents (S. aureus, group A streptococci) which frequently infect previously normal valves |
| What is the progression like in Acute Infective Endocarditis? | The course is fulminant(Fast)severe destruction of the valve, commonly causing acute valvular regurgitation, severe bacteremia associated with abscesses in the myocardium & throughout the body |
| Does Acute Infective Endocarditis have a high or low mortality rate? | High |
| What is Subacute Infective Endocarditis caused by? | Commonly caused by less virulent agents, such as… Viridans streptococci Staphylococcus epidermidis |
| What type pf patients present with Subacute endocarditis? | Almost always occurs in a patient with a preexisting cardiac (usually valvular) abnormality |
| What is the progressionlike for Subacute Infective Endocarditis? | Subacute endocarditis has a more chronic course not characterized by severe valve destruction or abscess formation |
| Etiology- Patient groups is associated with what type of endocarditis? | Native valve endocarditis 60-80% of patients in this group have a previously damaged cardiac valve |
| What are prior problems for people with Native Valve Endocarditis? | Chronic rheumatic valvular diseases—most commonly mitral regurgitation & aortic valve disease (30%) Congenital heart disease—most commonly ventricular septal defect, coarctation of the aorta, & bicuspid aortic (15%) |
| Native valve endocarditis patient groups | Mitral valve prolapse (20%) In the elderly, calcific aortic stenosis (??%) NO UNDERLYING CARDIAC DISEASE IDENTIFIABLE (20-40%) |
| Patient Group- Intravenous Drug users | Consists of mainly young males (80%) with no preexisting cardiac lesions S. aureus is the infecting agent (50%) The tricuspid valve is affected in over 50% of cases |
| Patient Group- Prosthetic valve endocarditis | Accounts for 15-20% of cases of endocarditis Early-onset endocarditis Occurring within 2 months after surgery 50% of cases are due to staphylococci & are associated with a fulminant course with valvular failure |
| Patient Group- Prosthetic Valve endocarditis-- Late onset endocarditis | Late-onset endocarditis Occurring 2 months after surgery Resembles (or behaves like) native valve endocarditis in etiology (viridans streptococci is the most common agent) & course is usually subacute |
| Why is it important to classify etiology of infective endocarditis? | Because it is of utmost importance in understanding & treating disease |
| What is Libman-Sacks endocarditis? | feature of system lupus erythematosus (SLE) |
| How is Libman-Sacks endocarditis presented? | It presents in the form of multiple small war-like outgrowths (known as excrescences) from the surface of the mitral & less commonly tricuspid valve |
| What do the vegetations in Libman-Sacks endocarditis result from? | These vegetations result from immune complex mediated injury of the valvular endocardium followed by thrombus formation |
| How can we identify the vegetations in patients with Libman-Sacks endocarditis? | by echocardiography, but usually these lesions are clinically of limited significance |
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