Cardiovascular System BSFCR Case #1: 58-yo male teacher notices the sudden onset of “chest tightness” when he walks across

the parking lot to and from school. The pain, which is localized over the sternum goes away when he sits down. He does not experience any pain or discomfort at other times. He has mild hypertension, for which he is on therapy. His cholesterol level is elevated. He does not smoke. 1) What is the most likely diagnosis. ANGINA PECTORIS: all 3 diagnostic criteria are met: • • • Substernal chest pain/discomfort Aggravated by exertion (or emotional stress) Relieved by rest (or nitroglycerine)

2) Describe fat absorption process starting at the intestine through the formation of chylomicrons. I) Chylomicrons transport dietary lipids (LCFA) from intestine to peripheral tissues Step 1: Nascent chylomicrons formed in intestinal mucosa are secreted into lymph and eventually into subclavian vein via thoracic duct.  Nascent chylo’s are rich in dietary TAGs (85%) and contain apoB-48, necessary for chylo assembly  Contain only minimal amount (<3%) dietary cholesterol Step 2: Addition of apoC-ll & apoE from HDL leads to formation of mature chylos Step 3: Capillary lipoprotein lipase is activated by apoC-ll and hydrolyzes TAGs in chylos  glycerol and FFA in blood
 Glycerol is phosphorylated in liver by glycerol kinase into glycerol-3-P  used to synthesize more

VLDL  FFA enter adipose tissue to produce TAGs for storage  In muscle, FAs oxidized to provide energy Step 4: apoC-ll returns to HDL Step 5: Chylo remnants that remain after removal of FFA attach to apoE R’s in liver and are endocytosed  Dietary cholesterol delivered to liver via chylo remnants used for bile acid synthesis and also depresses de novo cholesterol synth  XS cholest excreted in bile II) VLDL carries TAGs synthesized in liver to peripheral tissues

Step 1: in addition to TAGs, nascent VLDL particles formed in liver also contain some cholesterol (~17%) and apoB-100; these VLDL particles contain apoC-ll and apoE from HDL Step 2 & 3: conversion of circulating nascent VLDL particles into LDL particles proceeds via IDL  Degradation of TAGs by apoC-ll activated by capillary lipase converts nascent VLDL particles into IDL remnants which then converted to LDL particles  FAs & glycerol released into blood stream III) Step 4 & 5: LDL particles remaining after metabolism of VLDL & IDL are enriched in cholesterol (~45%), which they deliver to peripheral tissues or to the liver  apoB-100, major lipoprotein on LDL, binds to LDL R’s on cell membranes of target cells in the liver and other tissues o following R-mediated endocytosis, LDL is degraded in lysosomes, releasing free cholest for use in membrane synth, bile salt synth (liver), or steroid hormone synth (endocrine tissues, ovaries, testes) o XS cholest not needed by cells is esterified by acyl CoA:cholesterol acyltransferase (ACAT) & stored as cholest esters  Free cholesterol in the cytosol has the following regulatory functions: o Activates ACAT o Suppresses HMG CoA reductase; ↓ de novo synth of cholest o Suppresses further LDL-R synth; ↓ further uptake of LDL IV) Step 6: HDL, “good cholesterol” is synth in the liver and small intestine and carries out reverse transport of cholest from extrahepatic tissues to the liver  HDL also acts as repository of apolipoproteins (i.e. apoC-ll, apoE), which are required in the metab of VLDL and chylos.  Step 7: LCAT mediates esterification of free cholest removed from peripheral tissues by HDL o HDL is converted from a discoid shape to spherical shape when esterified cholest is xfr’d into center of molecule  HDL xfr’s cholest esters to VLDL in exchange for TAGs o Xfr is mediated by cholesteryl ester transfer protein
o

Xfr explains why and ↑in VLDL leads to ↓in HDL cholest levels

 Step 8: cholesteryl esters are returned to liver via R-mediated endocytosis of HDL  HDL is ↑ by estrogen (women have ↑ HDL levels), exercise, & red wine

and ovaries are major contributors to body’s cholest pool Cholesterol synth & regulation: Enzymes in both cytosol and SER participate I) Step 1: HMG CoA is formed by condensation of three molecules of acetyl CoA -.3) Describe cholesterol biosynthesis. an allosteric inhibitor of gene expression of HMG CoA reductase. provides rapid feedback control of cholest synth w/in cells  STATIN drugs. act as competitive inhibitors w/ mevalonate for binding to HMG CoA reductase  Hormones control cycling b/w active/inactive forms of HMG CoA reductase via phosphorylation and dephosph. HMG CoA is also produced in the mitochondrial matrix  serves as intermediate in synth of ketone bodies II) Step 2: HMG CoA reductase conversion of HMG CoA to mevalonate is the rate-limiting step  Cholesterol. adrenal cortex. such as Atorvastatin. liver. intestinal mucosa. respectively  Sterol-mediated decrease in expression of HMG CoA reductase provides long-term regulation o Delivery of cholest to liver and other tissues via plasma lipoproteins. such as LDLs and HDLs leads to ↓ in de novo cholest synth and ↓ in synth of LDL R’s III) Step 3: Isopentenyl (farnesyl) pyrophosphate is formed in several rxns from mevalonate and is the key 5Carbon isoprenoid intermed in cholest synth  Isopentenyl pyrophosphate is also a precursor in the synth of Coenzyme Q (ubiquinone) and dolichol. include its regulatory step and the use of statin group of drugs Almost all tissues synthesize cholest. Simvastatin.in liver. 30-C molecule. & Pravastatin. testes. which functions in the synth of CHO side chains in glycoproteins IV) Step 4: Squalene. is formed by several condensation rxns involving isopentenyl pyrophosphate V) Step 5: Conversion of squalene to cholesterol requires several rxns and involves NADPH reduction VI) Step 6: Choles is excreted in bile or used to synth bile acids and salts  XS cholest in bile &/or deficiency of bile salts may lead to gall stones .

increases in myocardial contractility are accompanied by ↑ demand for O2. After the period of occlusion. blood flow increases to repay the O2 debt (reactive hyperemia) sympathetic nerves play a minor role • • . compensatory vasodilation of coronary vessels occurs and both blood flow and O2 delivery to contracting heart muscle increase (active hyperemia) during systole.***Synthesis occurs in the liver **HMG-CoA reductase is the rate limiting step 4) Describe coronary circulation anatomy • • • • • is controlled almost entirely by local metabolic factors exhibits autoregulation exhibits active and reactive hyperemia the most important local metabolic factors are hypoxia and adenosine for ex. mechanical compression of the coronary vessels reduces blood flow. To meet this demand.

inferior wall (** IN RIGHT DOMINANCE) Right Ventricle Posterior septum and inferior wall RCA & LCA arise in root or aorta. posterior septum. local metabolites and hormones to the activity of coronary blood vessels in the heart. Anterior septum SA & AV nodes. Right Ventricle. posterior LV. . just above aortic valve orifice Coronary arteries run along the epicardial surface & send arterioles into the myocardium LCA quickly divides into LAD & LCX RCA divides into AMA and PD Coronary blood flow is maximally during ventricular diastole and least during isovolumetric contraction Blood flow mainly controlled by local metabolic autoregulation Sympathetic stimulation does not cause significant vasoconstriction 5) Apply your knowledge about neurotransmitters. Anterior LV.ARTERY Left Circumflex (CFX) Left Anterior Descending (LAD) Right Coronary (RCA) Acute Marginal (AMA) Posterior Descending/ interventricular (PD) • • • • • • • SUPPLY Lateral free wall of left ventricle (LV) **IN LEFT DOMINANCE -Posterior Descending will branch off CRX & supply posterior wall of LV & Apex Apex.

a sympathetic neurotransmitter the body uses to increase blood pressure. Agonists of alpha-receptors. and the Purkinje system have stable resting membrane potentials (~ -90 mV). activates a Purinergic Receptor Vasorelaxation 1.Activates a Purinergic Receptor leading to release of NO Metabolic Changgs that Cause Vasodilation in the systemic Circulation. and increased Adenosine in the interstium. Histamine 6. Vasoactive Peptive 4. Endothelium Derived Hyperpolarizing Factor (EDHF). Phase 0 • Is the upstroke of the AP . Epinephrine 3. elicit very little constriction in the coronary circulation. The majority of vasculature in the body constricts to norepinephrine.The coronary circulation possesses unique pharmacologic characteristics. • Ventricles. This value approaches the K+ equilibrium potential Action potentials are of long duration.NO. increase Calcium entry 2. Local factors that play an important role to this end are: Adenosine.an agonist for Receptor Operated Calcium Channels (ROC). Endothelin-Derived Constricting Factor 1 and II 6) Describe the ionic basis of different phases of the ventricular action potential.Endothelin. K+. Increased PCO2. Molecular Mechansims Underlying the Contracton and Relaxation of Vascular Smooth Muscle VasoConstriction Molecular Mechanisms 1. (dominate pathway) Decreased P02. Beta II Agonists. Prostacyclin (PGI2) 5. atria. Vasoactive Agents produced by the Endothellial Cells VasoDilates. lactic acid. and other agonists at the Alpha 1 Receptors 3. ATP. NE. ANGII 5. NO 2. such as phenylephrine. increased Lactic Acid levels. norepinephrine elicits vasodilation. these are the best vasodilators if the coronary circulation. due to the predominance of beta-adrenergic receptors in the coronary circulation. In the coronary circulation. Prominent among these is its reactivity to adrenergic stimulation. esp in Purkinje fibers  300 msec • a. Decreased pH. and Prostacylin VasoConstricts. Adenosine. Adenosine. increased ATP in intestitium. Endothelin 4. ↑ O2 (high ATP) is to ↑ perfusion  coronary vasodilation b/c demand may ↑ up to 20x’s in situations such as exercise.

Phase 2 • • • Is the plateau of the AP Is caused by a transient ↑ in Ca2+ conductance  inward Ca2+ current. Phase 3 • • • Is repolarization Ca2+ conductance ↓. This ↑ results in an inward Na+ current that depolarizes the membrane At the peak of the AP. Phase 4 • • Resting membrane potential Period during which inward/outward currents (Ik1) are equal and membrane potent’l approaches the K+ equilibrium potential. in part b/c of K+ ion movement (favored by both chemical and electrical gradients) out of the cell and in part b/c of ↓ in Na+ conductance c. and by ↑ in K+ conductance Outward/inward movements are ~ equal so memb pot’l is stable d. the mem potential  Na+ equilibrium pot’l • b. and K+ conductance ↑ and therefore predominates High K+ conductance results in large outward K+ current (IK) which hyperpolarizes the membrane back toward the K+ equilib pot’l e.• Is caused by a transient increase in Na+ conductance. . Phase 1 • Is brief period of initial repolarization  caused by outward current.

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V1 and V2. only the Myoglobin will be elevated.Case 2 A 59-year old man complains of tight chest pressure and shortness of breath after lifting several boxes in his garage approximately 2 hours ago. What is the diagnosis? ST Elevation Myocardial Infarction of Right ventricle DIFF: Acute MI. PE. muscle-skeletal. His medical history is significant to hypertension. heart rate is 102 beats/min and regular. Questions: 1. Biomarker Myoglobin CK-MB isoforms cTnI ** specific ** cTnT LD-I Time to Initial Elevation 1-2 hrs 4-6 hrs 4-6 hrs 4-6 hrs 10-12 hrs Time to Peak Elevation 8-10 hrs 18 hrs 12 hrs 12-48 hrs 48-72 hrs Time to Return to Normal 24 hrs <24 hrs 3-10 days 7-10 days 7-10 days . and his lungs are clear to auscultation. 2. He says he is having feeling of doom. Unstable angina (ST Depression). hypercholesterolemia and cigarette smoking. As it is only 2 hours after the acute MI. An electrocardiogram shows tachycardia with ST-segment elevation and T inversion in multiple leads including the anterior leads. Describe the biomarkers profile of this patient. On examination.

Which coronary arteries are most likely affected in this case? ST-segment elevation and T inversion in multiple leads including the anterior leads. left leg positive Lead III – Left arm negative. 6.3. Though this patient will benefit from taking metoprolol for a long time. it is not advisable to give a B1 blocker right after an MI. therefore. 5. left leg positive Lead aVR – right arm positive. he will not receive this medication immediately. What is the rationale for prescribing aspirin and what is the relevant mechanism of action? Post MI. inhibiting platelet aggregation. it is the most likely artery to be affected. left arm + left leg negative Lead aVL – left arm positive. right of sternum to mid axillary. This anticoagulant effect is beneficial to patients post MI. 4. right arm + left arm negative Lead V1-V6 – Horizontal plane 4-5th intercostal. right arm + left leg negative Lead aVF – left leg positive. However. This blocks formation of Thromboxane A2 in platelets. Lead I – Right arm negative. segments and intervals and their associations with heart function. Aspirin irreversibly inhibits cyclooxygenase (COX 1 & 2) by acetylating serine in the active site thereby inhibiting the formation of prostaglandin and thromboxane. left arm positive Lead II – Right arm negative. This medication should not be given immediately because it causes a drop in cardiac output. Why? Metoprolol is a B1 selective blocker. peripheral perfusion is already compromised. in the long term management to reduce the pressure on the heart and to prevent remodeling of heart it is beneficial to give a B1 blocker to reduce the cardiac output of the patient so the workload of the heart is reduced thus reducing oxygen demand and preventing another MI. Since the RV is supplied by the RCA. After an MI. V1 and V2 indicates a Right Ventricular infarction. . patients are at an increased risk of subsequent thromboembolitic events. Describe the normal EKG waves.

**Interval = beginning to end . Increased preload. leads to increased myocardial stretching (increased tension) and increased cardiac output. Changes in either variable result in movement along the Starling curve (control) while addition of either a positive or negative inotropic agent shifts the curve up or down. segment = end to beginning*** P wave – Atrial depolarization (SA to AV. . mainly due to venous return. Explain with the help of the Starling curves positive and negative inotropic effects. Inotropic effects are those that change myocardial contractility either weaker (negative) or stronger (positive). Start of QRS complex to end of T wave (300-440 ms) PR segment – End of the P wave to start of the QRS complex Isovolumetric ventricular contraction ST segment – Ventricular cells in Phase 2 End of ventricular contraction End of QRS complex to start of the T wave (80-120 ms = 2-3 small boxes) 7. Right atrium to Left Atrium) T wave – Ventricular repolarization QRS complex – Ventricular depolarization (60-100 ms) PR interval – Atrial depolarization plus normal delay at the AV node Start of P wave to start of QRS complex (120-200 ms = less than 5 small boxes) QT interval – Total time needed for ventricles to depolarize and repolarize. The Starling curves show the relationship between cardiac output and left ventricular end diastolic volume (preload).

The contraction process accounts for 75% of MVO2 with the other 25% being consumed by other cellular mechanisms.8. What is myocardial oxygen consumption and its importance to ischemia. A-V difference  Oxygen conductance = Aterial O2 – venous O2 . Angina and ischemia result when this compensation fails to deliver adequate oxygen supply. Myocardial contraction is the primary factor determining myocardial oxygen consumption (MVO2). Ischemia is an imbalance between the supply of oxygen by the coronary arteries and the demand by the myocytes. Oxygen uptake here is near maximal and the only way to increase supply is to increase blood flow. Myocytes require oxygen to use ATP to function.

which would decrease the ventricular pressure during systole. pitting edema in both lower extremities. tender hepatomegaly. crepitant rales over both lower lobes. To maintain the cardiac output. She has also has noted increasing shortness of breath while walking as well as swelling of his ankles and legs. third heart sound. Capillary wedge pressure is the pressure in a pulmonary artery after occlusion of that artery as measured by a pulmonary artery catheter. However. or to direct injury to lung parenchyma. In the case of heart failure. Initially. She had a myocardial infraction 2 years ago and has a history of chronic hypertension. This is due to either failure of the heart/circulatory system to remove fluid from lung circulation. cold extremities. Physical exam shows distention of neck veins. increase the diastolic pressure and end systolic volume. Normal physiological values range from 6-12mmHg. 2) Compare and contrast normal contractility with this disease. This is an indirect measurement of left atrial pressure and is the gold standard for determining the cause of acute pulmonary edema. lower lung fields are dull on percussion bilaterally.Case 3 A 65-year-old white female complains of requiring three pillows in bed in order to breathe comfortably and having to open window to gasp for air at night. This patient also had a MI. Describe normal capillary wedge pressure and the genesis of lung edema. excessive elongation of the heart results in weaker contractions and the geometry . stretching of the heart muscle leads to a stronger contraction of the heart. Chronic hypertension leads to a chronic pressure overload on the heart. Lung edema is swelling and/or fluid accumulation in the lungs. increased release of catecholamines and hypertrophy of cardiac muscle w/ dilation of the chambers and a more globular geometry. This results in a decrease in stroke volume and an increase in end systolic volume. grade III/VI crescendo aortic systolic murmur. This change in Starlings forces pushes fluids out of the vasculature and into the lungs. Questions: 1. There is an increase in afterload on the LV. where it accumulates as edema. the heart responds by compensatory mechanisms which include: increased preload (Frank Starling relationship). and further decrease the stroke volume. Be sure to use the Starling capillary pressures in your description. there is a backup and congestion of pulmonary vasculature leading to increased blood volume and increased hydrostatic pressure. resulting in a loss of myocardium .

Digitalis has a very low therapeutic index. congestion of the hepatic veins w/ formation of ascites which produces restricted diaphragmatic movements and dyspnea. so that the heart rate decreases and myocardial oxygen demand diminishes. List two additional characteristics of RHF. Describe the therapeutic index of digitalis. 1. During the plateau of the action potential. Vagal tone is also enhanced. Digitalis inhibits the Na+/K+ ATPase in the myocardial cell membrane increase in intracellular [Na+]  diminished Na+ gradient across the cell membrane  decreased Na+/Ca2+ exchange (a mechanism that extrudes Ca2+ from the cell)  increase in intracellular [Ca2+]  increased force of contraction  increased cardiac output  improved circulation leads to reduced sympathetic activity which then reduces peripheral resistance. these effects cause a reduction in heart rate. **contraction is inotropic…so starling law doesn’t play a role.due to right ventricular hypertrophy. The action potential spreads from the cell membrane into the T tubules. The only compensation is via starling 3) List the characterstics of this patient that are related to right HF. or reduced right sided Cardiac output leading to acidosis. e) Sustained systolic heave of the sternum. and tropomyosin is moved out of the way. *Inhibits Na/K atpase pump  ca2+ active pump affected 5) Explain excitation contraction coupling in ventricle myocardium. Together. Ca2+ binds to troponin C. a) shortness of breath. The compensatory mechanisms increase the work of the heart and contribute to further decline in cardiac performance. Sustained hepatojugluar reflex and asicetes. removing the inhibition of actin and myosin binding. 2. hypoxia. and air hunger b) pitting pedal edema – due to elevated right sided pressure which causes accumulation of fluid in the systemic veins and venous congestion  dependent edema c) Distension of Neck Veins – due to elevated atrial pressures caused by decreased ventricular function . Ca2+ conductance is increased and Ca2+ enters the cell from the extracellular fluid (inward Ca2+ current) 3. This results in a ventricle being unable to pump effectively. There is only a small difference between a therapeutically effective dose and doses that are toxic or even fatal. This Ca2+ triggers the release of even more Ca 2+ from the sarcoplasmic reticulum (Ca-induced Ca release) increase in intracellular [Ca2+] 4.diminishes the ability to eject blood. venous congestion 4) Describe the mechanism of action of Digitalis. existing pulmonary diseases.could be due to: LVF causing pulmonary edema. . myocardial contractility is lost. Additional characteristics of RVF: d) Abdominal pain.due to expansion of the liver from fluid accumulation which can cause distention of the liver capsule with accompanying right upper quadrant abdominal pain.

based on the drug’s mechanisms of action? Enalapril is an ACE inhibitor which will inhibit the formation of Angiotensin II (AGTII) from Angiotensin I so that there is ↓ AGTII. the thick and thin filaments slide past each other and the myocardial cell contracts. Bradykinin is a vasodilator so an ↑ in bradykinin due to a ↓ in its degradation will result in vasodialation which will further ↓ preload and afterload. It is pathognomic in patients over 40 for ventricular failure. Finally.5. ↓ of afterload and preload are desirable consequences for a patient in hear failure. S3 is best heard in the lateral decubitus position and when the patient is exhaling (exhalation brings the venticle close to the chest wall) 7. S3 is thought to be due to the rapid deceleration of blood in a failing ventricle that is already full. ↓ AGTII will also lead to ↑ bradykinin because AGTII normally inactivates bradykinin. as well as allowing for greater capacitance of the veins and ↓ VR thus ↓ preload. 6. The lack of vasoconstriction will ↓ BP and afterload on the heart. or S3 may be due to the wall of the dilated ventricle hitting the chest wall on filling in diastole. Describe how an S3 sound is produced? S3 is an extra heart sound heard in early diastole. The magnitude of the tension htat develops is proportional to the intracellular [Ca2+]. AGTII is a vasoconstrictor and since it is not present there in no vasoconstriction from this chemical. AGTII promotes the secretion of aldosterone from the adrenal cortex which will result in ↓ of water and Na retention which ↓ Blood volume and will ↓ preload and afterlaod . Describe how Enalapril would contribute to improve her condition. Actin and myosin bind. Relaxation occurs when Ca2+ is reaccumulated by the SR by an active Ca2 ATPase pump and Ca2+ is also extruded out of the cell by a Na+/Ca2+ exchange reaction across the cell membrane 6.

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numbness. Stable (Typical) Angina: associated with increased demand. Omega-s also will lead to a decrease in inflammatory response which will decrease plaque formation. awakens the patient from sleep . Vasospastic. This is the result of an increased predisposition of these patients to develop arethomas because of the high LDL content in their blood. 5. LDL>190 mg/dL is considered very high. Combination of diet and lipid lowering drugs is used to treat patients. and emotional excitement due to critical stenosis. transmural ischemia. He has a history of smoking two packs of cigarettes aday for 25 years. Describe familial hypercholesterolemia. LDL plasma concentration is increased due to the inability for the tissue to clear it form the plasma. Smoking increases risk for atherosclerosis. CVA or blood clot in any other part of the arterial system. What is the anatomical basis of the symptoms presented in this case? Atherosclerosis: if it is atherosclerosis. Patient may experience problems such as atrophy. If there is occlusion of the vessels the blood would not adequate travel to the extremities. Complications include MI. it is occluding the vessels and decreasing blood supply to the extremities. his symptoms have been occurring for a year and are relieved by rest. atrophy of calf muscles. His labs show elevated LDL and decreased HDL and elevated total serum cholesterol. 4. The carotid and femoral bruits show problems with blood flow. carotid and femoral arterial bruits. loss of hair over dorsum of feet and hands. towards the lower extremities would be the usual place that would be affected. Pathology based on the body reaction to nicotine. This will result in a decreased risk of MI and CVA. physical activity. Sometimes even the nerves could also be affected. and been smoking heavily for many years. decreased temperature in hands and feet. 3. A history reveals that the patient has also been impotent for two years. What is the diagnosis? Arterial insufficiency 2° to atherosclerosis 2.Case 4 A 59-year-old man complained of pain in the calf muscles during exercise along with coldness and numbness in both legs. so an increase in omega-3 fatty acids will result in decreased LDLs. Describe the significance of omega-3 acids in the diet. Questions: 1. Describe the different types of angina. If the LDLs are decreased than there is less to incite the formation of atherosclerotic plaques. Omega-3 fatty acids lower LDLs. Berger’s disease: Patient would be at risk because he is a male smoker. Seen as crushing or squeezing substernal pain radiating down left arm relieved by rest Prinzmetal variant angina: associated with st elevation. In addition. His blood pressure is150/100 with diminished peripheral pulses bilaterally. A type of dyslipidemia in which there is a co-dominant genetic mutation resulting in non-functional LDL-receptors. LDL<100 mg/dL is considered optimal. Occurs at rest.

Unstable (crescendo) angina. So there would be more blood left over. After isovolumetric relaxation. What are the likely changes seen in Pressure-Volume loop in patients with systemic hypertension? A person who has systemic hypertension would have increased after load. isovolumetric contraction would increase so the height would be higher. During the cycle. there would be more blood left over. superimposed thrombosis. Next phase systolic ejection would not have too much ejected. disruption of plaque. Pain that occurs with progressively increasing frequency and precipitated by progressively less effort 6. Volume loop would be more to the right. Describe the relationship between vascular resistance and blood flow. reorganization. Directly proportional to viscosity and inversely proportional to the radius to the 4th power 7. .

. hemoptysis. The pulmonary hypertension manifests itself in dyspnea.In MS. left atrial enlargement may impinge on recurrent laryngeal n. When the pressure in the ventricle decreases below the pressure in the aorta. atrial arrhythmia leading to embolus formation.Pulmonary hypertension. This decreased the overall work of the ventricle as blood is not filling it up completely. and causing a cerebral vascular accident. 3. Blood is then forced into the aorta.Mitral stenosis 2. Questions: 1. She describes a serious illness she had as a child. What is the most likely diagnosis? . causing pulmonary hypertension. typically Atrial fibrillation. . The stroke volume is decreased as well as cardiac output. This causes an increased pressure in all phases of the cycle in the atrium. rash. This is the peak of pressure in the atria. As the pressure in the ventricle decreases below the pressure in the aorta. The ventricle begins to contract and when the pressure increases. and a diastolic rumble. . What are the complications of this disorder? . This back pressure enlarges the LA causing atrial arrhythmias. She complains of occasional palpitations.[O2]pulmonary artery O2 consumption for the body is measured Pulmonary vein is measured in a peripheral artery Pulmonary artery is measured in systemic mixed venous blood . there is initial rapid filling which then slows and ends with the atrial ‘kick’. . The atrium is working harder to expel the extra blood past the constriction. and the cycle begins again. and orthopnea. an opening snap. This causes a build up of blood in the LA and the build up of back pressure. How do you determine cardiac output by using oxygen consumption as a marker? (Fick principle) Cardiac output = O2 consumption [O2]pulmonary vein . joint pains. She recovered after approximately a month. As the pressure increases. as well as back pressure into the pulmonary vein and lungs. the left atrium is having to work harder to force blood past the mitral valve. with fever. Define preload and explain how it affects stroke volume and cardiac output. A chest radiograph shows an enlarged left atrium. The stretching of the myocytes before contraction. the aortic valve closes and volumetric relaxation begins. 4.In mitral stenosis: The left atrium never relaxes fully. the mitral valve opens. the atria is slowly filled shown by the v wave. causing hoarseness. This forces the last volumes of blood into the ventricle. isovolumetric contraction takes place until the pressure in the ventricle exceeds the pressure in the aorta and the aortic valve opens. Cardiac examination reveals a loud S1. hemoptysis. The atrial fibrillation also increases the risk of embolism which can enter the systematic circulation. Explain the hemodynamic changes in mitral stenosis. 5. When the valve opens.In a normal person: The left atrium contracts towards the end of diastole in an atrial ‘kick’. the mitral valve closes. 6. As blood is expelled from the ventricle. orthopnea.Case 5 A 42-year-old woman develops fatigue and dyspnea that have been worsening over approximately 6 months. Describe the pressure profile of the left ventricle and left atrial pressure in normal and a patient with mitral stenosis.Preload is the pressure from blood that is stretching the ventricle.

As a result. 3. This feature of the arterial pulse wave is also called “parvus et tardus”. crescendo-decrescendo murmur. in aortic stenosis. In the normal cardiac cycle. Compare normal after load with the after load associated with this disease. a pressure versus time graph would show that the left ventricular pressure and the aortic pressure coincide as soon as the aortic valve opens during systole and continues in this manner until the aortic valve closes in the early stages of diastole. Describe the consequences on heart performance. and the paradoxical splitting of the S2 heart sound are all indicative of an aortic valve problem and decreased blood flow into the aorta itself. 4. These two pressures do not coincide between the opening and the closure of the aortic valve because there is not enough blood being pushed into the aorta to create a pressure that matches the ventricular pressure once the aortic valve opens. S2 sound is generated by aortic and pulmonary valve closure. increase in ventricular pressure leading to ventricular hypertrophy to compensate and increase in EDP . In other words. However. Describe how an S2 sound is produced.Case 6 1. the initial rise of the pulse is much slower than normal and the fall of the pulse is much faster than normal. when the pressure in the aorta/pulmonary artery is higher than in the ventricles. the arterial pulse wave is described as anacrotic. It is loudest at the left sternal border . Heart performance will decrease. Afterload in left ventricle with AS is increased due to the increase force of contraction needed to push blood through the stenosed aortic valve 5. the pressure versus time graph shows a higher ventricular pressure and a lower aortic pressure during systole. these all contribute to decrease SV and CO 6. The dyspnea may be from the increased pressure load on the left ventricle and subsequent blood back up to the left atrium and pulmonary veins and capillaries that lead to pulmonary edema. due to the increase in ESP from the stenosis . or “decreased and late”. Compare and contrast normal left ventricle and aortic pressure with this disease. What is the diagnosis? Aortic stenosis – This patient most likely has aortic stenosis based on the symptoms and findings presented in the case history. the normal pressure versus time graph shows a big difference between the ventricular pressure and the aortic pressure. 2. The fatigability is probably due to a lack of adequate amounts of blood reaching the peripheral tissues. A normal arterial pulse wave shows an initial rapid rise in the arterial pulse followed by a relatively slow decline. The soft. In aortic stenosis. Compare and contrast normal arterial pulse wave with this disease process.

AD trait . Hypertrophic cardiomyopathy is attributed to mutations in one of a number of genes that encode for one of the sarcomere proteins including: 7. 45% of these mutations occur in the â myosin heavy chain gene on chrom 14 q11. most common congenital cause of pansystolic murmur.Case 7 During a routine athletic physical. tangled and hypertrophied myocardial fibers. while approx.4 3p 2q24.1 11p11. systolic murmur that is best heard at the site of the thrill but it does not radiate to carotids.1 Type CMH1 CMH2 CMH3 CMH4 CMH5 CMH6 CMH7 CMH8 CMH9 CMH10 CMH11 CMH12 6. The three types include: ostium secundum. Mutation identified in at least 1 of 9 sarcomeric genes. or edema. 5. May result in left ventricular outflow obstruction . What is left to right shunt and what are the consequences? Abnormal flow of blood from the left heart to the right heart. heart size is normal . He is asymptomatic and has no evidence of hypertension. thrills and systolic mumor. leading to syncope and sudden death in young athletes 2. anemia. Approx. AV fistula. An electrocardiogram and a chest radiograph are normal. cyanosis. The patient often presents with a collapsing pulse and sinus tachycardia. Other answer: Hypertrophic cardiomyopathy . disoriented. What is the most likely diagnosis? VSD = age. etc 4.2-3. Gene MYH7 TNNT2 TPM1 MYBPC3 ? PRKAG2 TNNI3 MYL3 TTN MYL2 ACTC1 CSRP3 Locus 14q12 1q32 15q22. a 15-year-old boy is found to have a systolic thrill that is palpable at the lower left sternal border accompanied by a harsh. 35% involve the cardiac myosin binding protein C gene. What is the embryologic explanation of a ASD? Failure of the two ends of the interatrial septum to fuse. Greater obstruction occurs when preload is decreased during standing and valsalva’s maneuver (both decrease venous return) and the murmur becomes intense. ostium primum and sinus venosus. What is hyperdynamic circulation and what are the causes? Increase in pulse pressure and blood pressure caused by certain physiological and psychiatric illnesses. Possible causes are renal disease volume expansion. the shunt reverses from L-> R to R->L which causes late cyanosis. What are potential sequelae if this condition remains untreated? Possible shunt reversal [R->L] -> cyanosis. Consequences include compensatory vascular hypertrophy which results in progressive pulmonary hypertension and as pulmonary resistance increases. hepatic failure. Describe the changes in the HOCM murmur with different maneuvers'? HOCM is normally manifested by a systolic murmur noted on physical examination. 50% Familial AD. What is the genetic basis of hypertrophic cardiomyopathy? Hypertrophic cardiomyopathy is an autosomal dominant disease.3 12q23-q24 15q14 11p15. .2 ? 7q36 19q13. 1. hypertrophy of the septum . Also could cause CHF -> pulmonary HTN 3.

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He regains consciousness without any treatment. What is the diagnosis? 3rd degree block: Complete AV block. 5. jugular venous pressure 6 cm. What is Torsades de pointes? Name any drug which can cause this complication? Torsades de pointes is a ventricular tachycardia with a twist of the QRS complex which usually degrades into ventricular fibrillation. What is the most likely cause of sudden death in myocardial infarction? Arrhythmia 6. respiratory rate 14 breaths/minute. Physical exams reveals the following: blood pressure 90/60 mm Hg. heart rate 46 beats/minute. The patient has normal electrolytes and complete blood count. Quinidine can cause this complication. Chest is clear to auscultation and no murmurs are detected. He had similar episodes few times before. •Action potential originates at the SA node •Action potential conducts to the AV node rapidly •AV delay occurs and at the same time spreads over the atria slowly •Spreads rapidly to the apex through bundle of His and bundle branches •Spreads rapidly over both the ventricles from apex to base through the Purkinje fibers 3. Myocardial infarction of which part of the heart leads to bradycardia and hypotension and why? Infarction of the AV node causes bradycardia and hypotension because it causes an AV block which leads to the Bundle of His taking over as the intrinsic pacemaker. There is no history of any abnormal movements. His past history is significant for hypertension and diabetes. 4. His current medications include lisinopril. What is the basis of narrow and wide QRS complex? A wide QRS denotes ventricular origin whereas a narrow QRS denotes atrial origin. Describe the conduction system of the heart. EKG shows P waves unrelated to QRS complex. and hydrochlorothiazide. Questions: 1. glyburide.Case 8 A 60-year-old man complains of sudden loss of consciousness for few seconds. This episode was associated with racing of heart and lightheadedness. Signs pointing to this diagnosis: •loss of consciousness •slow heart rate •EKG showing P waves unrelated to QRS complex 2. temperature 37°C. .

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