Take Heart
Chapter 18, The Heart
The heart pumps the same amount of blood to the lungs and the body, about 5 liters/minute at rest. The heart is a "double pump"- the right side pumps blood to the lungs and the left side pumps to the body. About the size of a fist, it lies in a space called the mediastinum with its apex pointing to the left side. See p. 678, 7th ed.; p. 662. -
HEART ANATOMY
1. Pericardium - the heart is enveloped in the pericardial sac. A serous (watery lubricant) secretion reduces friction between the visceral pericardium covering the heart and the parietal pericardium lining the sac. Pericarditis is an inflammation of the sac, usually caused by a virus. After a myocardial infarction (death of heart muscle) due to the blocking of a coronary artery, cardiac tamponade may occur when blood from a ruptured heart aneurysm accumulates in the pericardial sac - the weakened wall looks like a bubble that will burst. The accumulation of blood compresses the heart, reducing the volume of blood ejected.
2. Myocardium consists of cardiac muscle. There are two types of cardiac muscle cells: pacemaker cells and contractile cells.
Pacemaker cells have autorhythmicity - they depolarize at a set rate of approximately 70-80 beats/minute. You may want to review neuron membrane depolarization in the muscle chapter of BIOL 1611. Gap junctions are tubular channels connecting adjacent cells. This allows for more synchronous depolarization. Striations of stacked actin and myosin protein myofilaments provide for moderately strong, but fatigue resistant contractions. Your heart beats typically approximately 100,000 times a day or more!
Cardiac muscle has a long absolute refractory period and will not undergo tetany, the state of continuous contraction that occurs in striated skeletal muscle cells. See pg. 691, 7th ed.; 672, 8th ed..
The slow Ca++ channels allow for this long refractory period. Ca++ slowly bonds to troponin to start the ratcheting of actins and myosins. See the Biology 1611 Study Guide on Muscle. Some drugs are Ca++ channel blockers. What would then happen if Ca++ channels are partially blocked? Special neuromuscular cells called Purkinje fibers conduct electrical impulses to cardiac muscle.
PATH OF CIRCULATION THROUGH THE HEART, LUNGS AND BODY - (See p. 682, 7th ed; p. 672-673, 8th ed.)
Deoxygenated blood returns from the body via the superior and inferior vena cavae and the coronary sinus which collects venous blood draining from the heart wall, sending blood to the right atrium. Most blood trickles down into the right ventricle but 25% is moved by the right atrium which contracts and forces the blood through the tricuspid or right atrioventricular valve to the right ventricle; then the right ventricle contracts and blood is pumped through the pulmonary semilunar valve to the pulmonary trunk and arteries, and thus to the lung capillary bed; oxygenated blood returns through the pulmonary veins to the left atrium, then through the left atrio-ventricular valve (mitral or bicuspid) to the left ventricle, the most muscular chamber of the heart; the left ventricle contracts ("lubb" sound and QRS) and sends blood through the aortic semilunar valve to the aorta and to the main systemic arteries and the body tissue capillary beds.
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Label Vessels and chambers of the hearts above. - Superior view of the heart valves. Label the bicuspid, tricuspid, pulmonary and aortic valves.
ELECTRICAL STIMULATION OF THE HEART (See p. 694-698, 7th ed., p. 676-677, 8th ed.)
The heart has intrinsic rate control through the Pacemaker, atrio-ventricular node, bundles and Purkinje fibers. Extrinsic rate control acts upon the pacemaker and contractile cells through secretions of the Sympathetic Nervous System (Ep, NE) to increase heart rate or secretions of the Parasympathetic N.S. (Ach) to decrease rate.
Would the heart stop beating if all nerve connections with the CNS were severed?
Why do many older people need electrical Pacemakers?
What methods are used to restore the regular beat of a fibrillating heart?
Clinical Comments: Ectopic foci may induce extra beats by acting like the SA or AV nodes. Third degree or total heart block occurs if the AV node is damaged so that the SA can't communicate with the AV node. Then the atria and ventricles beat at different and uncoordinated rates, the ventricles beating at 40/MIN, the atria beat at a higher rate of 70. An artificial pacemaker may be surgically implanted to correct for heart blocks.
The EKG (also called the ECG) See p. 696-697, 7th ed.; p. 681, 8th ed.
SELECTED ABNORMAL EKG INDICATIONS 1. Increased time of P-Q (PR) or first degree heart block) - P-R intervals 0.2+ seconds can be due to coronary artery disease (atherosclerosis), rheumatic fever, or lyme myocarditis - all may result in an increase of scar tissue which slows transmission between the SA and AV nodes. If the P-R gets longer with successive beats, Type I Second degree heart block is present: when the p waves must signal twice or more before the QRS happens, with an increased P-R, Type II Second degree heart block is the diagnosis. If the SA and AV are disconnected entirely, you have Third degree heart block. See above. 2. S-T may be elevated by acute MI. It may be below the baseline if ischemia is occurring. The T wave may be elevated by high K+. What conditions could cause high blood K+? 3. Elevated P waves can indicate enlarged atria. 4. An elevated R wave can indicate an enlarged ventricle. 5. Multiple P waves indicate atrial tachycardia. If they increase even further, atrial fibrillation is indicated. 6. Ventricular tachycardia and fibrillation occur as heart rate increases greatly. The rapid QRS waves obscure the P and T waves. Blood flow practically ceases. 7. Premature Ventricular contraction (PVCs) show the QRS "stepping on" the P wave. 8. Inverted U wave - infarction and unstable angina See http://medstat.med.utah.edu/kw/ecg/image_index/ and http://www.ecglibrary.com/ecghome.html Compare an atrial tachycardia to atrial fibrillation. Compare a ventricular tachycardia to ventricular fibrillation. What is sinus bradycardia? CARDIAC CYCLE SYSTOLE is the phase of contraction and DIASTOLE is the period of heart relaxation. PHASES - See page 701//697//699. 1. Relaxation - the heart muscle repolarizes. Isovolumetric Relaxation - As the heart relaxes, it expands. The volumes of the ventricles increase until ventricular pressure is lower than atrial pressure, the AV valves open and ventricular filling (by trickling) begins. The diastole lasts 0.4 seconds at rest. 2. Completion of Ventricular filling. The atria send the final 25% of blood by contracting. Then 130 ml of blood (END VENTRICULAR DIASTOLIC VOLUME) is present in each ventricle at rest. 3. Isovolumetric contraction - the ventricles begin to contract and the semilunar valves have not opened. 4. Ventricular ejection - 70 ml of the 130 E.D.V. is ejected, 70 ml is the stroke volume. The end systolic volume is 60 ml. Atrial and ventricular contractions last 0.4 seconds. How many heart beats a minute is a cardiac cycle lasting 0.8 seconds? Blood Pressure and Sounds The systolic pressure is the pressure read at the first sound heard in a stethoscope when the blood pressure cuff, which has closed off flow of the brachial artery, is released and the first spurt of blood comes through the artery below the cuff. The diastolic pressure is read when the last sound is heard. The numbers, e.g., 120 systolic/80 diastolic, are normal for an adult. During ventricular contraction, the atrio-ventricular valves make turbulence which makes the 'lubb' sound; semilunar valves snap shut and produce turbulence which makes a 'dupp' sound. Elevation of B.P. above 140 systolic indicates arteriosclerosis or other problems which cause increased blood volume or heart rate. See p. 699, th ed.; p. 681, 8th ed. Echocardiography can diagnose valve leakage by hearing the turbulence of blood flow through the heart and great vessels. A similar technology is used in a sonogram of the fetus. CARDIAC OUTPUT - See p. 700, 7th ed.; p. 682, 8th ed. At rest CO = stroke volume (70ml) X = heart rate (75/min) = 5250 ml/min STRESS (EXERCISE) CO = 140ml/beat (x) 150 beats/min = 21,000 ml/min The four fold rise in cardiac output is due to an increased rate of ventricle filling and increased contractile force due to additional stretching of muscle fibers. Cardiac reserve is that extra (above resting) capacity of cardiac output. The cardiac reserve of athletes may be seven or eight times the resting output. REGULATION OF STROKE VOLUME - 3 Factors 1. Preload factors increase stretch and contractility. Rapid filling and the stretching of the cardiac muscle of the ventricles during diastole by larger volumes of blood increases the force of the contracting muscle fibers. This is called the FRANK- STARLING LAW OF THE HEART. When heart rate exceeds 160/min. heart efficiency declines. Why? Remember the outputs of the right and left ventricles are the same normally. 2. Contractility - the sympathetic accelerator neurotransmitters, NE from the sympathetic cardiac accelerator nerves, and NE and EP from the adrenal medulla increase the rate of Ca++ movement through the slow Ca++ channels of the Pacemaker cells. Parasympathetic Vagus nerve secretions of Ach have the opposite effect. Ep and NE bind to beta receptors to increase heart rate. Why are beta blockers like inderal used for heart patients with irregular and high beat patterns and rates? 3. Afterload factors - the pressures of blood in the pulmonary trunk and the aorta must be exceeded before blood can move out of the heart. Arteriosclerosis increases afterload pressures. Baroreceptors detect pressure in the carotid arteries and aorta. Sensory inputs are carried to the cardiovascular center of the medulla. Increased pressure decreases heart rate and vice versa. The inverse relationship between BP in the carotid arteries leading to the brain and heart rate is called Marey's Law of the Heart. Increased pressure in the right atrium is relayed to the cardiovascular center, then, specifically, the cardioaccelerator center that increases heart rate and force of contraction - this is called the right heart or Bainbridge atrial reflex. What is the effect of Carotid massage? Clinical comments: Left ventricular failure produces pulmonary edema. Why? Right ventricular failure causes peripheral edema in the feet and ankles. Excess K+ can block impulse generation. Could injections of KCl kill a patient? VERTEBRATE HEARTS: SEQUENCE OF EMBRYONIC DEVELOPMENT See pg. 700//703//not in 7th ed. Vertebrate Heart # chambers design FISH-LIKE 2 (atrium and ventricle) blood flow from the aortic arches to the body; is sluggish AMPHIBIAN-LIKE 3 (2 A, 1 common V) blood flow from lung loop is repressurized in the left atrium and common ventricle, oxygenated blood mixes in with deoxygenated in ventricle REPTILE-LIKE 3, V with partial septum partial interventricular septum divides ventricles; mixing largely prevented MAMMALIAN 4 (2 A & 2 V) completed septum; R of heart pumps blood to lungs. L side pumps to body. Two chambers, 3 chambers, four chambers! The fetal heart features a ductus arteriosus which conducts blood from the pulmonary trunk to the aorta. Also, there is a hole, the foramen ovale, with a "swinging door" between the right and left atria (the "door" opens into the left atrium) . Why? A ductus venosus conducts blood from the umbilical vein through the fetal liver to the inferior vena cava, bypassing the fetal hepatocytes. Why? There are two umbilical arteries, but one umbilical vein. Label the fetal vessels and by-passes seen below. The developmental pattern of the heart is interrupted by the following conditions: 1. Patent Ductus Arteriosus produces a heart murmur. 2. Patent Foramen Ovale or Atrial Septal Defect (ASD) - Some adults tolerate this well. 3. Tetralogy of Fallot - See p. 708, 7th ed.; p. 688, 8th ed. A. Patent interventricular septum or ventricular septal defect (VSD) - oxygenated and deoxygenated blood from both ventricles mix and flow into the aorta; "blue babies" can result. B. Pulmonary semilunar valve stenosis (narrowing) causes ... C. Enlargement of the right ventricle. In the 1980s, "Baby Faye" in Florida received a baboon heart; it was rejected and she died. D. A common opening of the pulmonary trunk and aorta (goes with the VSD). What do you think about the ethics of this experiment? Coronary Arteries serving heart muscle can become blocked by fatty plaque (atherosclerosis) and/or platelet clots forming on the surface of plaque; the muscle tissues become starved for oxygen and nutrients (ischemia). The first symptom is chest pain called angina pectoris. As the cardiac muscle cells die, the heart attack occurs. If the attack causes a loss of the regular heart contraction rhythm, ventricular twitching or fibrillation will occur and the patient dies unless revived by CPR. The dead tissue or myocardial infarct will become a scar in time if the patient survives. HEART DISEASE Risk factors 1. High blood cholesterol and/or concomitant high blood steroid hormone levels lead to atherosclerosis. Cholesterol is carried by lipoprotein "vehicles." These include dietary fat-carrying chylomicrons, made in the lacteal of the intestinal villi, and VLDLs that are large "taxi" particles made by the liver that carry fats and cholesterol to cells for use and storage. See p. 943, 8th ed.High density lipoproteins or HDLs are "garbage trucks" that carry oxidized cholesterol (the real 'bad' cholesterol) to the liver for excretion as a part of bile. Low density lipoproteinsor LDLs ("taxis") carry cholesterol and fat to the hepatic cells for recycling also, but more generally to cells that use cholesterol for building cell membranes and steroid hormones. They form by splitting off VLDLs. An LDL/HDL ratio of more that 4/1 is a risk factor for atherosclerosis and CHD: 2/1 or lower is ideal,a lower ratio puts one at risk for sudden death! A total cholesterol of above 220 is viewed as a risk factor, as well as a total LDL above 160 or an HDL below 35. In the familial (inherited) hypercholesterolemia that killed the Olympic skater Grinkov; there are too few LDL receptors on the hepatic cells. Therefore the LDLs and their fats and cholesterol end up in the internal layer of arteries. Recently, smaller than normal LDL particles have been implicated as a risk factor, along with gum recession and exposure to Chlamydia pneumoniae infections of the upper respiratory tract.. Know the Friedewald equation:In mg/dl: LDL cholesterol = (approx.) total cholesterol – HDL cholesterol – (0.2 × triglycerides) | Why is LDL/HDL ratio a better measure of risk that total cholesterol? 2. High blood pressure leads to an enlargement of the heart and increased chances for strokes due to emboli or blowouts of aneurysms. 3. Smoking - CO and HCN in smoke are thought to cause lesions on the surface of arteries leading to thrombi and plaque formation. Nicotine also increases NE and Ep secretion and therefore increased heart rate and blood pressure. 4. Sedentary lifestyles - exercise increases cardiac reserve and makes vessels more flexible. Steroids are used up instead of deposited in vessel walls. 5. Diabetes mellitis - blood sugar may help drive steroids into plaques? 6. Inheritance - If you want to live a long time, do a better job of picking your parents! 7. Obesity - increased fat tissue lead to increased blood vessel length which leads to the heart having a heavier load. 8. Being male or a Kentucky football fan - in other words stress! 9. Peridontal (gum) disease - bacterial infections that follow from peridontal disease present a stronger risk than hypertension according to one published study. Atherosclerosis (See p. 718, 7th ed.; p. 687, 8th ed.) - this is usually classified as a type of arteriosclerosis. Macrophages phagocytize (eat) low density lipoproteins and migrate into lesions (perhaps caused by carbon monoxide), in the internal layer the increased number of smooth muscle cells (increased in number by PDGF) fill with fats and cholesterol and die. Platelet clots or thrombi tend to form on the irregular surfaces because collagen is exposed to the blood. The vasoconstrictors released by platelets may make things worse by causing vasospasms. Heart attacks occur when the coronary arteries are blocked and the heart muscle dies. As cells rupture, free radicals are released which perfuse through the myocardium and nodal conduction systems causing further damage. Coronary artery spasms can also block arteries. Why are spasms more likely if atherosclerotic plaque is present (see the blood chapter)? Ventricular fibrillation will kill the patient if CPR is unsuccessful. Arteriosclerosis/Mineralosclerosis - hardening of the arteries due to the build up of minerals and collagen. It is a natural result of long term high blood pressure. High blood pressure leads to hardening of the arteries which leads to more high blood pressure. What is the relationship between high salt and sugar levels in the blood and high blood pressure? Why are arteries more flexible than veins? Coronary artery bypass is done with a graft from the saphenous vein and/or (and, in my case!) the internal mammary artery. Why is the arterial graft more long lasting? Balloon angioplasty also clears soft, fatty plaques from coronary artery lumens by pressing it against the wall. Spring-like stents may be used to keep vessels open. Hard plaques accumulate Calcium deposits that harden them: they can be removed by surgery. Study Questions 1. List the chambers, valves, organs and vessels encountered in the flow of the blood from the heat to the lungs and back. 2. Explain how heart attacks occur and how they kill. 3. Explain CPR. 4. How is the heart sped up and slowed down. 5. Explain the segments of the EKG. What does an increased P-R mean? Contrast v-fib and v-tac. 6. Criticize the term "bad cholesterol" used commonly for LDL. 7. How did HDL get the "good cholesterol" label? john.aliff @ gpc.edu
SELECTED ABNORMAL EKG INDICATIONS
1. Increased time of P-Q (PR) or first degree heart block) - P-R intervals 0.2+ seconds can be due to coronary artery disease (atherosclerosis), rheumatic fever, or lyme myocarditis - all may result in an increase of scar tissue which slows transmission between the SA and AV nodes. If the P-R gets longer with successive beats, Type I Second degree heart block is present: when the p waves must signal twice or more before the QRS happens, with an increased P-R, Type II Second degree heart block is the diagnosis. If the SA and AV are disconnected entirely, you have Third degree heart block. See above.
2. S-T may be elevated by acute MI. It may be below the baseline if ischemia is occurring. The T wave may be elevated by high K+. What conditions could cause high blood K+?
3. Elevated P waves can indicate enlarged atria.
4. An elevated R wave can indicate an enlarged ventricle.
5. Multiple P waves indicate atrial tachycardia. If they increase even further, atrial fibrillation is indicated.
6. Ventricular tachycardia and fibrillation occur as heart rate increases greatly. The rapid QRS waves obscure the P and T waves. Blood flow practically ceases.
7. Premature Ventricular contraction (PVCs) show the QRS "stepping on" the P wave.
8. Inverted U wave - infarction and unstable angina
See http://medstat.med.utah.edu/kw/ecg/image_index/ and http://www.ecglibrary.com/ecghome.html
Compare an atrial tachycardia to atrial fibrillation. Compare a ventricular tachycardia to ventricular fibrillation. What is sinus bradycardia?
CARDIAC CYCLE
SYSTOLE is the phase of contraction and DIASTOLE is the period of heart relaxation.
PHASES - See page 701//697//699.
1. Relaxation - the heart muscle repolarizes. Isovolumetric Relaxation - As the heart relaxes, it expands. The volumes of the ventricles increase until ventricular pressure is lower than atrial pressure, the AV valves open and ventricular filling (by trickling) begins. The diastole lasts 0.4 seconds at rest.
2. Completion of Ventricular filling. The atria send the final 25% of blood by contracting. Then 130 ml of blood (END VENTRICULAR DIASTOLIC VOLUME) is present in each ventricle at rest.
3. Isovolumetric contraction - the ventricles begin to contract and the semilunar valves have not opened.
4. Ventricular ejection - 70 ml of the 130 E.D.V. is ejected, 70 ml is the stroke volume. The end systolic volume is 60 ml.
Atrial and ventricular contractions last 0.4 seconds. How many heart beats a minute is a cardiac cycle lasting 0.8 seconds?
Blood Pressure and Sounds
The systolic pressure is the pressure read at the first sound heard in a stethoscope when the blood pressure cuff, which has closed off flow of the brachial artery, is released and the first spurt of blood comes through the artery below the cuff. The diastolic pressure is read when the last sound is heard. The numbers, e.g., 120 systolic/80 diastolic, are normal for an adult. During ventricular contraction, the atrio-ventricular valves make turbulence which makes the 'lubb' sound; semilunar valves snap shut and produce turbulence which makes a 'dupp' sound. Elevation of B.P. above 140 systolic indicates arteriosclerosis or other problems which cause increased blood volume or heart rate. See p. 699, th ed.; p. 681, 8th ed.
Echocardiography can diagnose valve leakage by hearing the turbulence of blood flow through the heart and great vessels. A similar technology is used in a sonogram of the fetus.
CARDIAC OUTPUT - See p. 700, 7th ed.; p. 682, 8th ed.
At rest
CO = stroke volume (70ml) X = heart rate (75/min) = 5250 ml/min
STRESS (EXERCISE)
CO = 140ml/beat (x) 150 beats/min = 21,000 ml/min
The four fold rise in cardiac output is due to an increased rate of ventricle filling and increased contractile force due to additional stretching of muscle fibers.
Cardiac reserve is that extra (above resting) capacity of cardiac output. The cardiac reserve of athletes may be seven or eight times the resting output.
REGULATION OF STROKE VOLUME - 3 Factors
1. Preload factors increase stretch and contractility. Rapid filling and the stretching of the cardiac muscle of the ventricles during diastole by larger volumes of blood increases the force of the contracting muscle fibers. This is called the FRANK- STARLING LAW OF THE HEART.
When heart rate exceeds 160/min. heart efficiency declines. Why?
Remember the outputs of the right and left ventricles are the same normally.
2. Contractility - the sympathetic accelerator neurotransmitters, NE from the sympathetic cardiac accelerator nerves, and NE and EP from the adrenal medulla increase the rate of Ca++ movement through the slow Ca++ channels of the Pacemaker cells. Parasympathetic Vagus nerve secretions of Ach have the opposite effect. Ep and NE bind to beta receptors to increase heart rate. Why are beta blockers like inderal used for heart patients with irregular and high beat patterns and rates?
3. Afterload factors - the pressures of blood in the pulmonary trunk and the aorta must be exceeded before blood can move out of the heart. Arteriosclerosis increases afterload pressures.
Baroreceptors detect pressure in the carotid arteries and aorta. Sensory inputs are carried to the cardiovascular center of the medulla. Increased pressure decreases heart rate and vice versa. The inverse relationship between BP in the carotid arteries leading to the brain and heart rate is called Marey's Law of the Heart.
Increased pressure in the right atrium is relayed to the cardiovascular center, then, specifically, the cardioaccelerator center that increases heart rate and force of contraction - this is called the right heart or Bainbridge atrial reflex.
What is the effect of Carotid massage?
Clinical comments: Left ventricular failure produces pulmonary edema. Why? Right ventricular failure causes peripheral edema in the feet and ankles. Excess K+ can block impulse generation. Could injections of KCl kill a patient?
VERTEBRATE HEARTS: SEQUENCE OF EMBRYONIC DEVELOPMENT See pg. 700//703//not in 7th ed.
Two chambers, 3 chambers, four chambers!
The fetal heart features a ductus arteriosus which conducts blood from the pulmonary trunk to the aorta. Also, there is a hole, the foramen ovale, with a "swinging door" between the right and left atria (the "door" opens into the left atrium) . Why?
A ductus venosus conducts blood from the umbilical vein through the fetal liver to the inferior vena cava, bypassing the fetal hepatocytes. Why? There are two umbilical arteries, but one umbilical vein. Label the fetal vessels and by-passes seen below.
The developmental pattern of the heart is interrupted by the following conditions:
1. Patent Ductus Arteriosus produces a heart murmur.
2. Patent Foramen Ovale or Atrial Septal Defect (ASD) - Some adults tolerate this well.
3. Tetralogy of Fallot - See p. 708, 7th ed.; p. 688, 8th ed.
A. Patent interventricular septum or ventricular septal defect (VSD) - oxygenated and deoxygenated blood from both ventricles mix and flow into the aorta; "blue babies" can result.
B. Pulmonary semilunar valve stenosis (narrowing) causes ...
C. Enlargement of the right ventricle. In the 1980s, "Baby Faye" in Florida received a baboon heart; it was rejected and she died.
D. A common opening of the pulmonary trunk and aorta (goes with the VSD).
What do you think about the ethics of this experiment?
Coronary Arteries serving heart muscle can become blocked by fatty plaque (atherosclerosis) and/or platelet clots forming on the surface of plaque; the muscle tissues become starved for oxygen and nutrients (ischemia). The first symptom is chest pain called angina pectoris. As the cardiac muscle cells die, the heart attack occurs. If the attack causes a loss of the regular heart contraction rhythm, ventricular twitching or fibrillation will occur and the patient dies unless revived by CPR. The dead tissue or myocardial infarct will become a scar in time if the patient survives.
HEART DISEASE
Risk factors
High density lipoproteins or HDLs are "garbage trucks" that carry oxidized cholesterol (the real 'bad' cholesterol) to the liver for excretion as a part of bile. Low density lipoproteinsor LDLs ("taxis") carry cholesterol and fat to the hepatic cells for recycling also, but more generally to cells that use cholesterol for building cell membranes and steroid hormones. They form by splitting off VLDLs.
An LDL/HDL ratio of more that 4/1 is a risk factor for atherosclerosis and CHD: 2/1 or lower is ideal,a lower ratio puts one at risk for sudden death! A total cholesterol of above 220 is viewed as a risk factor, as well as a total LDL above 160 or an HDL below 35. In the familial (inherited) hypercholesterolemia that killed the Olympic skater Grinkov; there are too few LDL receptors on the hepatic cells. Therefore the LDLs and their fats and cholesterol end up in the internal layer of arteries. Recently, smaller than normal LDL particles have been implicated as a risk factor, along with gum recession and exposure to Chlamydia pneumoniae infections of the upper respiratory tract..
Know the Friedewald equation:
In mg/dl: LDL cholesterol = (approx.) total cholesterol – HDL cholesterol – (0.2 × triglycerides)
|
Atherosclerosis (See p. 718, 7th ed.; p. 687, 8th ed.) - this is usually classified as a type of arteriosclerosis. Macrophages phagocytize (eat) low density lipoproteins and migrate into lesions (perhaps caused by carbon monoxide), in the internal layer the increased number of smooth muscle cells (increased in number by PDGF) fill with fats and cholesterol and die. Platelet clots or thrombi tend to form on the irregular surfaces because collagen is exposed to the blood. The vasoconstrictors released by platelets may make things worse by causing vasospasms. Heart attacks occur when the coronary arteries are blocked and the heart muscle dies. As cells rupture, free radicals are released which perfuse through the myocardium and nodal conduction systems causing further damage. Coronary artery spasms can also block arteries. Why are spasms more likely if atherosclerotic plaque is present (see the blood chapter)? Ventricular fibrillation will kill the patient if CPR is unsuccessful.
Arteriosclerosis/Mineralosclerosis - hardening of the arteries due to the build up of minerals and collagen. It is a natural result of long term high blood pressure. High blood pressure leads to hardening of the arteries which leads to more high blood pressure. What is the relationship between high salt and sugar levels in the blood and high blood pressure?
Coronary artery bypass is done with a graft from the saphenous vein and/or (and, in my case!) the internal mammary artery. Why is the arterial graft more long lasting? Balloon angioplasty also clears soft, fatty plaques from coronary artery lumens by pressing it against the wall. Spring-like stents may be used to keep vessels open. Hard plaques accumulate Calcium deposits that harden them: they can be removed by surgery.
Study Questions
1. List the chambers, valves, organs and vessels encountered in the flow of the blood from the heat to the lungs and back.
2. Explain how heart attacks occur and how they kill.
3. Explain CPR.
4. How is the heart sped up and slowed down.
5. Explain the segments of the EKG. What does an increased P-R mean? Contrast v-fib and v-tac.
6. Criticize the term "bad cholesterol" used commonly for LDL.
7. How did HDL get the "good cholesterol" label?
john.aliff @ gpc.edu
