Physiology PBL Module 5

School of Medicine Saint Louis University

Exercises on Cardiovascular Physiology

LABORATORY ACTIVITY ON CARDIAC PHYSIOLOGY HEART SOUNDS: Draw and Label:

GREEN: AORTIC AREA-Second

intercostal space, Right sternal border

BLUE: PULMONIC AREA- Second

intercostals space, Left sternal border

RED: ERBS POINT- Third intercostal

space, Left sternal border

YELLOW: TRICUSPID AREA- fourth or fifth intercostal space, Left sternal border ORANGE: MITRAL AREA OR APEX- Fifth intercostal space, Left
midclavicular line

Why does the second heart sound have a high frequency than the first heart sound? The second heart tone (key to auscultation of the heart). The second heart sound is shorter duration and higher frequency than the first heart sound. It has two audible components, the aortic closure sound (A2) and the pulmonic closure sound (P2), which must be separated by more than 20 msec (0.20 sec) in order to be differentiated and heard as two distinct sounds. It is composed of components A2 and P2 in which normally A2 precedes P2 especially during inspiration when a split of S2 can be heard. Why the second heart sound is normally split in inspiration? It is caused by the sudden block of reversing blood flow due to closure of the aortic valve and pulmonary valve at the end of ventricular systole, beginning of ventricular diastole. As the left ventricle empties, its pressure falls below the pressure in the aorta, aortic blood flow quickly reverses back toward the left ventricle, catching the aortic valve leaflets and is stopped by aortic (outlet) valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary (outlet) valve closes.

Normally the aortic closure sound (A2) occurs prior to the pulmonic closure sound (P2), and the interval between the two (splitting) widens on inspiration and narrows on expiration. With quiet respiration, A2 will normally precede P2 by 0.02 to 0.08 second (mean, 0.03 to 0.04 sec) with inspiration. Differentiate the following: a. Physiologic splitting of s2 Physiological S2 splitting is exaggerated by inspiration which lowers intrathorasic pressure causing more blood to be drawn from the superior and inferior vena cava; the increase of venous return to the right ventricle means takes longer to empty, leading to an additional delay in closure of the pulmonary valve. b. Fixed splitting of s2 Fixed splitting denotes absence of significant variation of the splitting interval with respiration remains unchanged during inspiration and expiration.

c. Reverse or Paradoxical splitting of s2 Paradoxical or reversed splitting is the result of a delay in the aortic closure sound. Splitting is maximal on expiration and minimal or absent on inspiration. Identification of the reversed order of valve closure may be possible by judging the intensity and transmission of each component of the second sound. The paradoxical narrowing or disappearance of the split on inspiration is a necessary criterion for diagnosing reversed splitting by auscultation.

Give conditions which causes fixed and reverse splitting of s2? Atrial septal defect, with either normal or high pulmonary vascular resistance, is the classic example of fixed splitting of the second sound. The audible expiratory splitting in these patients is primarily a reflection of changes in the pulmonary vascular bed rather than selective volume overload of the right ventricle prolonging right ventricular systole. Severe right heart failure can lead to a relatively fixed split. This occurs because the right ventricle fails to respond to the increased volume produced by inspiration and because the lungs are so congested that impedance to forward flow from the right ventricle barely falls during inspiration.

Paradoxical splitting occurs more commonly with hypertrophic cardiomyopathy. Paradoxical splitting of the second sound may occur during the first few days after an acute myocardial infarction or secondary to severe left ventricular dysfunction. How are murmurs described? Give the grading of intensity of cardiac murmurs. Murmur refers to a sound originate within blood flow through or near the heart. Murmurs are extra heart sounds that are produced as a result of turbulent blood flow that is sufficient to produce audible noise. Rapid blood velocity is necessary to produce a murmur. Most heart problems do not produce any murmur and most valve problems also do not produce an audible murmur.

ELECTROCARDIOGRAPHY: 3. Draw and label properly the parts of a normal ECG tracing, also including the different intervals and duration. For the corresponding numerical values of each interval or duration, write them in a tabulated manner. Characteristics of a normal ECG

Rhythm: sinus Rate: 60-100 bpm Conduction: o PQ interval 120-200ms o QRS width 60-100ms o QTc interval 390-450ms (use the QTc calculator for this) Heart axis: between -30 and +90 degrees P wave morphology: o The maximal height of the P wave is 2.5 mm in leads II and / or III o The p wave is positive in II and AVF, and biphasic in V1 o The p wave duration is usually shorter than 0.12 seconds QRS morphology: o No pathological Q waves o No left or right ventricular hypertrophy o No microvoltage o Normal R wave propagation. (R waves increase in amplitude from V1-V5) ST morphology o No ST elevation or depression o T waves should be concordant with the QRS complex The ECG should not have changed from the previous ECG
Figure 1.Schematic representation of normal ECG trace (sinus rhythm), with waves, segments, and intervals labeled.

Figure 2.The qt-time is normal, when it is less than half the rr-time.

4. In the ECG tracing, which wave corresponds to the following: a. atrial depolarization b. atrial repolarization c. ventricular depolarization (base) d. ventricular depolarization (apex) e. ventricular repolarization

The P wave represents the wave of depolarization that spreads from the SA node throughout the atria, and is usually 0.08 to 0.1 seconds (80-100 ms) in duration. The brief isoelectric (zero voltage) period after the P wave represents the time in which the impulse is traveling within the AV node (where the conduction velocity is greatly retarded) and the bundle of His. Atrial rate can be calculated by determining the time interval between P waves. The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval, which normally ranges from 0.12 to 0.20 seconds in duration. This interval represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. If the P-R interval is >0.2 sec, there is an AV conduction block, which is also termed a first-degree heart block if the impulse is still able to be conducted into the ventricles. The QRS complex represents ventricular depolarization. Ventricular rate can be calculated by determining the time interval between QRS complexes. The duration of the QRS complex is normally 0.06 to 0.1 seconds. This relatively short duration indicates that ventricular depolarization normally occurs very rapidly. If the QRS complex is prolonged (> 0.1 sec), conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever a ventricular foci (abnormal pacemaker site) becomes the pacemaker driving the ventricle. Such an ectopic foci nearly always results in impulses being conducted over slower pathways within the heart, thereby increasing the time for depolarization and the duration of the QRS complex. The isoelectric period (ST segment) following the QRS is the time at which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the ventricular

action potential. The ST segment is important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated. The T wave represents ventricular repolarization and is longer in duration than depolarization (i.e., conduction of the repolarization wave is slower than the wave of depolarization). Sometimes a small positive U wave may be seen following the T wave (not shown in figure at top of page). This wave represents the last remnants of ventricular repolarization. An inverted or prominent U wave indicates underlying pathology or conditions affecting repolarization. The Q-T interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. This interval can range from 0.2 to 0.4 seconds depending upon heart rate. At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T interval. Because prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias, it is important to determine if a given Q-T interval is excessively long. There is no distinctly visible wave representing atrial repolarization in the ECG because it occurs during ventricular depolarization. Because the wave of atrial repolarization is relatively small in amplitude (i.e., has low voltage), it is masked by the much larger ventricular-generated QRS complex.

CASE 1: Cardiovascular Calculations 1. Mean arterial pressure is not the simple average of systolic and diastolic

pressures. Why not? How is mean arterial pressure estimated? From the information given in Table 1, calculate the mean arterial pressure in this case. Arterial pressure varies over the course of each cardiac cycle. Systolic pressure is measured when the heart is contracting such that blood is ejected from the left ventricle into the aorta. Diastolic pressure on the other hand is measured as blood flows from the arteries, into the veins and back to the heart. Mean arterial pressure is not the simple average of systolic and diastolic pressures because averaging the two pressures does not take into account that a greater portion of each cardiac cycle is spent in diastole which is approximately two-thirds than in systole (approximately one-third). Moreover, mean arterial pressure is closer to diastolic pressure than to systolic pressure. Pulse pressure is the difference between systolic and diastolic pressure. Mean arterial pressure can be calculated by using the formula: Mean arterial pressure = diastolic pressure + 1/3 pulse pressure Where: Diastolic pressure= lowest value for arterial pressure in a cardiac cycle Systolic pressure= highest value for arterial pressure in a cardiac cycle Pulse pressure= systolic pressure - diastolic pressure From the information given in Table 1, the mean arterial pressure in this case is: Mean arterial pressure = 82 rom Hg + 1/3 (124 mm Hg - 82 mm Hg) = 82 mm Hg + 1/3 (42 mm Hg) = 82 mm Hg + 14 mm Hg = 96mm

2. Calculate the stroke volume, cardiac output, and ejection fraction of the left ventricle. Stroke volume can be calculated by using the formula: Stroke volume = end-diastolic volume - end-systolic volume Where: Stroke volume = volume ejected by the ventricle during systole (ml) End-diastolic volume = volume in the ventricle before ejection (ml) End-systolic volume = volume in the ventricle after ejection (ml)

Cardiac outputcan be calculated by using the formula: Cardiac output =stroke volume x heart rate Where: Cardiac output = volume ejected by the ventricle per minute (ml/lmin) Stroke volume = volume ejected by the ventricle (ml) Heart rate = beats/min

Ejection fraction can be calculated by using the formula: Ejection fraction = stroke volume/end-diastolic volume Where: Ejection fraction := fraction of the end-diastolic volume ejected in one stroke

Based from the mentioned equations, the calculations for stroke volume, cardiac output, and ejection fraction of the left ventricle are calculated as follows:

Stroke volume = left ventricular end-diastolic volume - left ventricular endsystolic volume = 140 ml - 70 ml = 70 ml

Cardiac output is referred as the volume ejected by the left ventricle per minute. It is equal to the the product of stroke volume, which was calculated as 70 ml and heart rate. Heart rate is the number of heart beats per minute and can be calculated from the R-R interval which is the time elapsed from one R wave to the next. This R-R interval is also known as the cycle length or the time elapsed in one cardiac cycle.

Heart rate= l/ cycle length = 1/800 msec = 1/0.8 sec = 1.25 beats/sec or 75 heats/min

Cardiac output = stroke volume x heart rate = 70 ml x 75 beats/min = 5250 ml/min Ejection fraction= stroke volume/end-diastolic volume = 70 mIl 140 mi = 0.5 or 50% 3. Calculate cardiac output using the Fick principle. The Fick principle of conservation of mass is used to measure cardiac output. It has two basic assumptions. First, it states that Pulmonary blood flow or the cardiac output of the right ventricle is equal to the systemic blood flow or the cardiac output of the left ventricle) in the steady state. Secondly, the rate of oxygen utilization by the body is equal to the difference between the amount of oxygen leaving the lungs in pulmonary venous blood and the amount of oxygen returning to the lungs in the pulmonary arterial blood. This principle can be mathematically stated as:

Oxygen consumption= cardiac output x [O2]pulmonary vein - cardiac output x cardiac output x [O2]pulmonary artery

Such that cardiac output =[ Where:

Cardiac output = cardiac output (ml/min) O2 consumption = O2 consumption by the body (ml O2/min) [O2]pulmonary vein = O2 content of pulmonary venous blood (ml O2 /ml blood) [O2]pulmonary artery = O2 content of pulmonary arterial blood (ml O2 /ml blood)

It is also important to note that the systemic arterial blood is equal to the pulmonary venous blood. Cardiac output is then calculated as: Cardiac output = 250 ml/ min__________________ 0.20 ml O2 /ml blood 0.152 ml O2 /ml blood

250 ml/ min__________ 0.048 ml O2 /ml blood

5208 ml/min

The value for cardiac output using the product of stroke volume and heart rate yielded a close cardiac output value using the Fick principle.

4. What is the definition of total peripheral resistance (TPR)? What equation describes the relationship between TPR, arterial pressure and cardiac output? What is the value of TPR in this case? TPR is described as the collective resistance of blood flow that is provided by all the blood vessels in the systemic side of the circulation which include the aorta, large and small arteries, arterioles, capillaries, venules, veins, and vena cava. Arterioles are known to be the site of highest vascular resistance.

Blood flow is calculated by using the formula: Q= Where: Q = blood flow (ml/min) = pressure difference (mm Hg) R = resistance (mm Hg/ml/min) In the systemic circulation, the pressure difference ) is measured as the difference in

pressure at the inflow and outflow points wherein the inflow pressure is the aortic pressure and the outflow pressure is the right atrial pressure. The mean aortic pressure was calculated as 96 mm Hg and the right atrial pressure was given on table 2-1 which is equal to 2 mm Hg. Thus, the pressure difference, mm Hg - 2 mm Hg, or 94 mm Hg. Total peripheral resistance (TPR)is then equal to mean arterial pressure - right atrial pressure)/cardiac output. Hence, Total peripheral resistance (TPR) = (96 mm Hg - 2 mm Hg)/5229 ml/min , across the systemic circulation is then equal to 96

= 94 mm Hg/5229 ml/min = 0.018 mm Hg/ml/min 5. How is the pulmonary vascular resistance calculated? What is the value of pulmonary vascular resistance in this case? Compare the calculated values for pulmonary vascular resistance and TPR and explain any difference in the two values. In calculating for the pulmonary vascular resistance, the values of pulmonary blood flow or the cardiac output of the right ventricle and the pressure difference across the pulmonary circulation must be known. In the steady state, the cardiac output of the right ventricle is equal to the cardiac output of the left ventricle, which in this case has a value of 5229 ml/min. Across the pulmonary circulation, the pressure difference is calculated as inflow pressure minus the outflow pressure. inflow pressure = mean pulmonary artery pressure = 15 mm Hg outflow pressure = atrial pressure = 5 mm Hg Pulmonary vascular resistance therefore is: R = P/Q = (mean pulmonary artery pressure - left atrial pressure)/cardiac output = (15 mm Hg - 5 mm Hg)/5229 ml/min = 10 mm Hg/5229 ml/min = 0.0019 mm Hg/ml/min Pulmonary blood flow is equal to systemic blood flow. However, the pulmonary vascular resistance is only one-tenth the value of systemic vascular resistances. Pulmonary pressures are also known to be much lower than systemic pressures. Pulmonary blood flow can be exactly equal to the systemic blood flow since pulmonary vascular resistance as well as pulmonary vascular pressures are proportionately lower than the systemic vascular resistance and pressures.

Case 2: Conduction Block Patients profile: Name: Deither Campos Age: 68 Sex: Male Occupation: Retired middle management position from an automotive industry Diagnosis: Acute Myocardial Infarction Events before ECG: a. Recovering in the hospital. b. Fainted twice in the hospital. Events after ECG: a. PR interval longer than normal. b. QRS complex normal. c. Occasional P wave (not followed by QRS complexes) (non conductive P waves). d. Possible MI was caused by an AV block. e. ECG returned to normal. f. No more fainting. g. Sent home

Questions: 1. What does the PR interval on the ECG represent? What units are used to express the PR interval? What is the normal value?

a. Represents the time from initial depolarization of the atria to initial depolarization of the ventricles. PR interval includes the P wave (atrial depolarization) and the PR segment, an isoelectric portion of the ECG that corresponds to conduction through the AV node

b. Seconds or in Milliseconds c. 120-200 msec (average, 160 msec)

2. What does the term "conduction velocity" mean, as applied to myocardial tissue? What is the normal conduction velocity through the AV node? How does conduction velocity in the AV node compare with conduction velocity in other portions of the heart?

a. Speed at which action potentials are propagated within the tissue from one site to the next. b. Slowest of all of the myocardial tissues (0.01-0.05 m/sec). The slow velocity ensures that the ventricles will not be activated "too soon" after the atria are activated, thus allowing adequate time for ventricular filling prior to ventricular contraction. c. Conduction velocities in atria and ventricles (1 m/sec) and in His-Purkinje tissue (2-4 m/sec).

3. How does AV nodal conduction velocity correlate with PR interval? Why were Mr. Doucette's PR intervals longer than normal?

a. The slower the conduction velocity through the AV node, the longer the PR interval because the length of the PR segment is increased). b. The faster the conduction velocity through the AV node, the shorter the PR interval. c. The conduction velocity through the AV node was decreased, presumably because of tissue damage caused by the myocardial infarction.

4. What does the QRS complex on the ECG represent what is implied in the information that the QRS complexes on Mr. Doucette's ECG hac1 a normal configuration?

a. Electrical activation of the ventricles. b. The normal configuration of Mr. Doucette's QRS complexes implies that his ventricles were activated in the normal sequence (i.e., the spread of activation was from the AV node through the bundle of His to the ventricular muscle).

Case 3: Ventricular Pressure-Volume Loops

I. Answers to Questions: 1. Describe the events that occur in the four segments between numbered points on the pressure-volume loop. Correlate each segment with events in the cardiac cycle. The figure above is a graphic representation of the events in the cardiac cycle, showing how blood enters and is ejected from the left ventricle. The events are as follows, point 1 to point 3, or 2accounts for ventricular filling. This process occurs because the increase of pressure in the right atria causes the mitral valve to open, which is represented by point 1. Because the ventricle is relaxed, ventricular pressure increases only slightly as ventricular volume increases. Rapid ventricular filling is followed by diastasis then atrial systole (left atrium contracts to give an additional 25% to the volume of blood). Point 3 to point 5 or fragment 4 represents isovolumic or isometric contraction. The increased blood volume in the ventricle also increases the pressure, besides the fact that the ventricle is also contracting. The mitral valve has already closed and the aortic

valve is also closed. Hence, no blood is ejected and left ventricular volume remains constant (i.e., is isovolumetric). This implies that there is increase in tension but no emptying. The increase in tension leads to the opening of the aortic valve at point 5 and the start of the next phasethe period of ejection (fragment 6). The ventricle is still contracting, causing ventricular pressure to increase further. Blood is ejected from the left ventricle into the arteries, which causes ventricular volume to decrease. The last phase, isovolumetric or isometric relaxation (fragment 8) marks the relaxation of the left ventricle and ventricular pressure decreases. This is due to the closing of the aortic valve at point 7. Again, both the aortic and the mitral valves are closed, and ventricular volume remains constant. The cycle then repeats itself every lab-dab of the heart.

2. Define left ventricular-end diastolic volume and end-systolic volume. End-diastolic volume is the volume present in the ventricle after filling is complete, but before any blood is ejected into the aorta. Therefore. end-diastolic volume is present at points 3 to 5. End-systolic volume is the volume that remains in the left ventricle after ejection is complete, but before the ventricle fills again and is represented at point 7 to 1.

3. Define stroke volume and ejection fraction? Stroke volume is the amount of blood pumped during each cardiac contraction; quantitatively, the diastolic volume of the left ventricle minus the volume of blood in the ventricle at the end of systole. The proportion of blood ejected out of the left ventricle during each heartbeat. It is equal to the stroke volume divided by the end diastolic volume. The ejection fraction is usually expressed as a percentage. It averages about 60% at rest.

4. Which portions of the pressure loop correspond to systole, to diastole? Diastole is the rhythmic period of relaxation and dilation of the ventricles of the heart during which it fills with blood. It can also be referred to as the period after the contraction of the heart muscle, during which the aorta releases the potential energy stored in its elastic tissue. The pressure measured at this period is the lowest attained during the cardiac pumping cycle and is called the diastolic pressure. In the loop above, the Diastole corresponds to segment 8 (isovolumetric relaxation) and 2 (ventricular filling). Systole is the period of contraction of the ventricles of the heart. It occurs with the first heart sound. The pressure from the systolic contractions is taken up and stored as potential energy by the elastic properties of the aorta and other great vessels of the arterial system. It also be referred to as the pressure recorded at the height of the ventricular contraction. In the loop above, the systole corresponds to segment 4 (isovolumetric contraction) and 6 (ventricular ejection). 5. Which portions of the pressure loop are isovolumetric? By definition, isovolumetric portions of the ventricular cycle are those in which ventricular volume is constant (i.e., the ventricle is neither filling with blood nor ejecting blood). Isovolumetric segments are 4 and 8. 6. At which numbered point does the aortic valve open and close? At which numbered point does the mitral valve open? The aortic valve opens at point 5, when ventricular pressure exceeds aortic pressure. Opening of the aortic valve is followed immediately by ejection of blood and a decrease in ventricular volume, the aortic valve closes at point 7, and ejection of

blood ceases. The mitral valve opens at point 4, it marks the beginning of ventricular filling. 7. At which numbered point or segment will the 1st heart sound be heard? The first heart sound is produced by closure of the two atrio-ventricular valves, wh h .I f d b d b h S1 h d. This closure occurs at the end of ventricular filling and just before contraction of the ventricle. Thus, the first heart sound occurs at point 3. 8. At which numbered point or segment will the 2nd heart sound be heard? The second heart sound is produced by closure of the aortic and pulmonary valves (b w h d h ), d f d b d d S2 heart sound and corresponds to point 7.

Case 4: Right Ventricular Failure Patients profile: Name: Nida Blanco Age: 38 Sex: Female Occupation: Home maker # of Children: three (ages 12, 14, and 15) Educational attainment: Vocational graduate

Diagnosis: Acute Myocardial Infarction Activities prior to death: a. House keeping b. Driver c. Took aerobics classes Past medical history: a. Easy fatigability. b. Shortness of breath during rest or exercise for 6 months. c. Swelling in her legs and feet.

Present medical history: a. Jugular veins distention. b. Enlarged liver c. Ascitis and edema in her legs. d. Fourth heart sound was noted over her right ventricle. e. Chest x-ray: Enlarged Right ventricle and pulmonary arteries. f. ECG: Ventricular hypertrophy. g. Cardiac catheterization results: mean pulmonary artery pressure (35 mm Hg), Right ventricular pressure (increased), Right arterial pressure (Increased), Pulmonary capillary wedge pressure (normal).

Diagnosis: Primary Pulmonary Hypertension A rare type of pulmonary HPN that is caused by diffuse pathologic changes in the pulmonary arteries that leads to increased pulmonary vascular and pulmonary HPN, which causes Right ventricular failure. Treatment: Vasodilators, Heart transplant but did not make it. Questions: 1. Why did increased pulmonary vascular resistance cause an increase in pulmonary artery pressure (pulmonary hypertension)?

Pressure difference= blood flow x resistance If blood flow (pulmonary) increases, the pressure difference also increases. Because pressure in the pulmonary artery increases or because pressure in the pulmonary vein decreases.

Decrease in pulmonary vein pressure would have little impact on pressure difference, because its value is normally very low.

Increased Pressure difference because her pulmonary arterial pressure increased. As pulmonary vascular resistance increased, resistance to blood flow increased, and blood "backed up" proximal to the pulmonary microcirculation into the pulmonary arteries. Increased blood volume in the pulmonary arteries caused increased pressure.

2. What values are needed to calculate pulmonary vascular resistance?

Resistance= Pressure difference/blood flow Blood flow= Cardiac output of right ventricle Blood flowin its steady state= Cardiac output of the left ventricle The values needed to calculate pulmonary vascular resistance are pulmonary artery pressure, pulmonary vein pressure (or left atrial pressure), and cardiac output.

3. Discuss the concept of "afterload" of the ventricles. What is the afterload of the left ventricle? What is the afterload of the right ventricle? Wl1at is the effect of increased afterload on stroke volume, cardiac output, ejection fraction, and endsystolic volume? How did Celia's increased pulmonary artery pressure lead to right ventricular failure?

Afterload of the ventricles= pressure against which the ventricles must eject blood. Afterload of the left ventricle= aortic pressure. Right ventricular pressure must increase above artery pressure. Right ventricular pressure must increase above pulmonary artery pressure. Increased pulmonary artery pressure had a devastating effect on the function of her right ventricle.

Much more work was required to develop the pressure required to open the pulmonic valve and eject blood into the pulmonary artery.

Right ventricular stroke volume, cardiac output, and ejection fraction were decreased. Right ventricular end-systolic volume was increased, as blood that should have been ejected into the pulmonary artery remained in the right ventricle.

Case 5: Left Ventricular Failure I. Demographic Data: Patient's Name: John Lloyd Cruise Gender: Male Age: 52 years old Occupation: Construction manager II. History of Illness: The patient is significantly overweight because of eating a rich diet that included red meats and high-calories desserts. He also enjoyed drinking beer each evening. He had occasional chest pains (angina) that were relieved by nitroglycerin. III. Signs and Symptoms: The evening of his myocardial infarction, he went to bed early for not feeling well. He awakened with crushing pressure in his chest and pain radiating down his left arm that was not relieved by nitroglycerine. Nausea, profuse sweating, dyspnea (especially when he was recumbent), and noisy breathing were noted. IV. Physical / Laboratory Examination Results:

The patient's blood pressure was 105/80. Inspiratory rales were present, consistent with pulmonary edema and his skin was cold and clammy. Sequential electrocardiograms and serum levels of cardiac enzymes (creatinine, phosphokinase and lactate dehydrogenase) suggested a left ventricular wall myocardial infarction. Pulmonary capillary wedge pressure was 30 mmHg, and his ejection fraction was 0.35. He was treated with a thrombolytic agent to prevent another M.I., digitalis, and furosemide.

V.

Answers to Questions: 1. Draw the normal Frank-Starling relationship for the left ventricle. Superimpose a second curve showing the Frank-Starling relationship after the M.I., and use this relationship to predict the changes in stroke volume and cardiac output. The Frank-Starling law of the heart (also known as Starling's law or the FrankStarling mechanism) states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice-versa.

The Frank Starling principle is based on the length-tension relationship within the ventricle. If ventricular end diastolic volume is increased it follows that the ventricular fiber length is also increased, resulting in an increased tension of the muscle. In this way, cardiac output is directly related to venous return, the most important determining factor of preload. When heart rate is constant, cardiac output is directly related to preload. An increase in preload will increase the cardiac output until very high end diastolic volumes are reached. At this point cardiac output will not increase with any further increase in preload, and may even decrease after a certain preload is reached. Also, any increase or decrease in the contractility of the cardiac muscle for a given end diastolic volume will act to shift the curve up or down, respectively.

2. Which information provided in the case tells you that John Lloyd's stroke volume was decreased? Stroke volume (SV) is the volume of blood pumped from one ventricle of the heart with each beat. It is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat (end-systolic volume) from the volume of blood just prior to the beat (end-diastolic volume). Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate, and is also used to calculate ejection fraction, which is stroke volume divided by end-diastolic volume. Therefore, the information that the patient's ejection fraction was 0.35 (normal, 0.55) indirectly shows that his stroke volume was decreased. In addition to, stroke volume is the most important determinant of pulse pressure, wherein a decrease in pulse pressure means a decrease in the stroke volume. In the case, it is seen that the patient's stroke volume decreased because his pulse pressure was also decreased to 25mmHg (normal, 40mmHg), by subtracting his diastole from his systole (105-80).

3. What is the meaning of John Lloyd's decreased ejection fraction? Ejection fraction is the fraction of blood pumped out of ventricles with each heart beat. Healthy individuals typically have ejection fractions between 50% and 65%.However, normal values depend upon the modality being used to calculate the ejection fraction, and some sources consider an ejection fraction of 55-75% to be normal. Damage to the muscle of the heart (myocardium), such as that sustained during myocardial infarction or in cardiomyopathy, impairs the heart's ability to eject blood and therefore reduces ejection fraction. A decrease in the ejection fraction also means that the patient's stroke volume and cardiac output are reduced because of reduced contractility of the heart muscles especially that of the left ventricle. This reduction in the ejection fraction can manifest itself clinically as heart failure.

4. Why was John Lloyd's pulmonary capillary wedge pressure increased? It is important to measure Pulmonary capillary wedge pressure (PCWP) to diagnose the severity of left ventricular failure and to quantify the degree of mitral valve stenosis. Both of these conditions elevate Left Atrial Pressure (LAP) and therefore PCWP. LAP is the outflow or venous pressure for the pulmonary circulation and increases in LAP are transmitted almost fully back to the pulmonary capillaries thereby increasing their filtration of fluid.

5. Why did pulmonary edema develop? Why is pulmonary edema so dangerous? As the heart fails, pressure in the veins going through the lungs starts to rise. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. Pulmonary congestion and edema develop from back pressure of accumulated blood in the left ventricle. The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts of the balance of forces in favor of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in pulmonary edema (fluid build-up) in the lungs. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. Therefore, pulmonary edema is so dangerous that it can be lethal in less than 30 minutes if the pulmonary capillary pressure rises 25 to 30 mmHg above the safety factor level.

6. Why did John Lloyd have dyspnea and orthopnea? Dyspnea and orthopnea are both consequences and manifestations of pulmonary edema. Dyspnea, usually the earliest and the cardinal complaint of patients in left-sided heart failure, is an exaggeration of the normal breathlessness or shortness of breath that follows exertion. Dyspnea is due to the impaired contractility of the ischemic myocardium. With further impairment, there is orthopnea, which is dyspnea on lying down that is relieved by sitting or standing. Thus the orthopneic patient must sleep while sitting upright. This is due to the reduced efficiency of gas exchange consequently to pulmonary edema.