Module 5 CARDIAC PHYSIOLOGY

Case No. 1 Melvin Rodriguez was admitted at the intensive care unit. On the first hospital day, he developed hypotension, BP of 70/40, cardiac rate of 100 beats per minute, rales all over lung fields, respiratory rate of 24 breaths per minute. Pertinent physical examination showed patient was dyspneic, distented neck vein. Patient was on left ventricular failure with pulmonary congestion. Objectives General The medical students should be able to explain Frank Starling law of the heart Specific Questions 1. What is the Frank starling law of the heart? The FrankStarling law of the heart (also known as Starling's law or the FrankStarling mechanism or Maestrini heart's law) states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume). The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank-Starling mechanisms). The stroke volume may also increase as a result of greater contractility of the cardiac muscle during exercise, independent of the enddiastolic volume. The Frank-Starling mechanism appears to make its greatest contribution to increasing stroke volume at lower work rates, and contractility has its greatest influence at higher workrates. This allows the cardiac output to be synchronized with the venous return, arterial blood supply and humeral length without depending upon external regulation to make alterations. To be able to draw Frank starling left ventricular volume curve To be able to discuss types of heart

2. Draw the normal Frank starling left ventricular volume curve; then superimpose the above findings of left ventricular failure using dotted lines.

3. What is the type of this heart? Hypereffective? Hypoeffective? Or normoeffective? It is a hypoeffective heart, meaning the heart has a decreased level of ability to pump blood. This is because his left ventricle is not pumping blood out of his lungs/pulmonary vein sufficiently. So, the lungs get over saturated with blood - the pressure from the right side causes a shift of fluid from the intravascular space into the lungs causing distension of neck veins, rales upon auscultation and dyspnea due to impaired gas exchange.

4. Enumerate at least 5 causes of this type of heart. Coronary artery blockage, causing a heart attack Inhibition of nervous excitation of the heart Pathological factors that cause abnormal heart rhythm or rate of heart beat Valvular heart disease Increased arterial pressure against which the heart must pump, such as in hypertension Congenital heart disease Myocarditis

Case No. 2 Rafael Aquino is a 52 year old manager who is significantly overweight. Enjoyed despite his doctors repeated admonitions; Rafael ate rich diet that include red meats and high calorie desserts. He enjoyed unwinding a few beer each evening. He had occasional chest pains that were relieved by Nitroglycerin. One evening, he went to bed early because he wasnt feeling well. He awakened at 2 am with crushing pressure on his chest and pain radiating down his left arm that was not relieved by Nitroglycerin. He was nauseated and sweating profusely. He also had difficulty of breathing especially when he was recumbent. His breathing was also noisy. He was then brought to the hospital and initial BP was 105/ 80. Inspiratory rales were present. His skin was cold. ECG and cardiac enzymes were suggestive of a left ventricular wall myocardial infarction. His ejection fraction on 2D echo was 0.35 (Normal was 0.55). He was then brought to the intensive care unit and was treated with thrombolytic agent digitalis and furosemide. After 7 days in the hospital, he was sent home on a low fat sodium diet. Objectives General The medical students should be able to explain cardiovascular condition of the patient Specific To be able to expound on ejection fraction and orthopnea To be able to discuss the mechanism of action of Digitalis and low sodium diet in response to the patients condition

Questions 1. What is the meaning of the decreased ejection fraction of Rafael Aquino? Ejection fraction is widely used as an index of contractility so the decreased ejection fraction of our patient would indicate a decreased contractility of his heart. Ejection fraction is the ratio of the volume of blood ejected from the left ventricle per beat (stroke volume) to the volume of blood in the left ventricle at the end of diastole (end-diastolic volume). Rafaels ejection fraction was 0.35 (35%) which is considered low compared to the normal value of 0.55 (55%). 2. Why did he experience difficulty of breathing and orthopnea? The patient experienced difficulty of breathing and dyspnea because of the development of pulmonary edema. The etiology of dyspnea in pulmonary edema is not entirely clear but the following factors play a role: (1) Juxtacapillary receptors are stimulated by the accumulation of

interstitial fluid, and trigger reflexes that stimulate rapid, shallow breathing. (2) Bronchial congestion stimulates the production of mucus. As a result, resistance of the bronchi is increased, causing wheezing and respiratory distress. (3) Accumulation of edema fluid leads to decreased pulmonary compliance, which increases the work of breathing. Orthopnea is dyspnea that is precipitated by lying clown. When a person lies down, venous return from the lower extremities back to the heart is increased. In left ventricular failure, increased venous return compounds the pulmonary venous congestion that is already present. 3. Why was his skin cold? Marvin's skin was cold and clammy because the stress of the myocardial infarction produced a massive outpouring of catecholamines (epinephrine and norepinephrine) from the adrenal medulla. The circulating catecholamines activated alpha 1 adrenergic receptors in cutaneous vascular beds and reduced cutaneous blood flow.

4. What was the rationale for treating him with Digitalis? Digoxin is one of the few positive inotropes that does not increase HR. Digoxin enhances myocardial inotropism and automaticity but slows impulse propagation through the conduction tissues. Digitalis reciprocally facilitates calcium entry into the myocardial cell by blocking the Na K adenosine triphosphatase pump. This calcium influx may account for its positive inotropic action because this inotropic response is not catecholamine- or beta receptor- dependent and is therefore effective in patients taking beta-blocking drugs. Digitalis was expected to increase contractility and return the Frank-Starling relationship toward that seen in a normal ventricle. 5. Why was he sent home on a low sodium diet? Sodium is usually limited to prevent fluid accumulation. A low sodium diet was recommended to reduce extracellular fluid volume and blood volume, and to prevent subsequent episodes of pulmonary edema.

Case No. 3 Theresa Camantiles was a 38 year old home maker and mother of 4 children. Keeping house and driving the children to activities kept her busy. To stay in the shape, she took aerobics classes at the local community center. The first sign that Theresa was ill was vague; she fatigued easily. However, within 6 months, Theresa was short of breath, both at rest and when she exercised, and she had swelling in her legs and feet. She then sought medical consult. On physical examination, she had distended jugular vein, liver was enlarged and had ascites in her peritoneal cavity and edema in her legs. A fourth heartsound was audible her right ventricle. Chest X- Ray revealed enlargement of right ventricle and pulmonary arteries. ECG was consistent with ventricular hypertrophy. She was manage as a case of primary pulmonary hypertension, a rare type of pulmonary hypertension that is caused by diffuse pathologic changes in the pulmonary arteries. Objectives General The medical students should be able to discuss physiologic bases of ventricular hypertrophy Specific Questions 1. Why does right ventricular failure cause right ventricular hypertrophy? Use the Law of Laplace to answer this question. Theresas right ventricular failure resulted to right ventricular hypertrophy because her right ventricle was obligated to perform increased work against an increased afterload. The right ventricular wall thickens as an adaptive mechanism for performing more work. This adaptive response is best explained by the Law of Laplace for a sphere (a sphere being the approximate shape of the heart). P= 2HT/ r Where P = ventricular pressure H = ventricular wall thickness (height) T = wall tension To be able to discuss the defining characteristics of the hypertrophy which are increased systemic venous pressure and jugular vein distention To be able to discourse audible fourth heart sound

r= radius of the ventricle Hence, ventricular pressure correlates directly with developed wall tension and wall thickness and inversely the radius. The thicker the ventricular wall, the greater the pressure that can be developed at a given tension. Theresas right ventricle hypertrophied adaptively so that it could develop the higher pressures required to eject blood against the increased pulmonary artery pressure. 2. Increased systemic venous pressure and jugular vein distention are the sine quanon (defining characteristics) of right ventricular failure. Why were Theresas jugular veins distended? Theresas jugular veins were distend with blood because the right ventricular failure caused blood to back up into the right ventricle and then into the right atrium and the systemic veins. 3. During what portion of the cardiac cycle is the fourth heart sound? What is the meaning of an audible fourth heart sound? A fourth heart sound is not normally audible in adults. However, it may occur in ventricular hypertrophy, where ventricular compliance is decreased. During filling of a less compliant ventricle, blood flow produces noise (the fourth heart sound). Thus, when it is present, the fourth heart sound is heard during artrial systole. 4. Why did right ventricular failure lead to edema on the systemic side of the circulation? (Example: ascites, edema on the legs) Would you expect pulmonary edema to be present in right ventricular failure? Right ventricular failure caused blood to back up into the systemic veins, which increased systemic venous pressure. The Starling forces that determine fluid movement across capillary walls can be used to explain why edema would form on the systemic side of the circulation such as ascites and edema in the legs when systemic venous pressure is increased. There are four Starling pressures (or forces) across the capillary wall: capillary hydrostatic pressure, capillary oncotic pressure, interstitial hydrostatic pressure, and interstitial oncotic pressure. In most capillary beds, the Starling pressures are such that there is a small net filtration of fluid that is returned to the circulation by the lymphatics. Jv = Kf [(Pc Pi) (c l)] where Jv = fluid movement Kf = hydraulic conductance Pc = capillary hydrostatic pressure Pi = interstitial hydrostatic pressure c = capillary oncotic pressure l = interstitial oncotic pressure

Edema occurs when filtration of fluid increases and exceeds the capacity of the lymphatics to return it to the circulation. Her increased systemic venous pressure in turn caused an increase in capillary hydrostatic pressure (Pc). Increases in Pc favor filtration. Pulmonary edema would not be expected to occur in right ventricular failure. Pulmonary edema occurs in left ventricular failure, where blood backs up behind the left ventricle into the left atrium and pulmonary veins. An increase in pulmonary venous pressure then leads to increased pulmonary capillary hydrostatic pressure and increased filtration of fluid into the pulmonary interstitium. Theresas left atrial pressure was normal, suggesting that she did not have left ventricular failure thus pulmonary venous pressure is not expected to have been elevated and pulmonary edema is not expected to have occurred.

Case No. 4 ESSENTIAL CARDIOVASCULAR CALCULATIONS This case is designed to take you through important basic calculations involving the cardiovascular systems. Use the information below to answer the questions. Part of the challenge in answering these questions will be in deciding which information you need in order to perform each calculation. Systolic pressure (aorta) Diastolic pressure (aorta) R-R interval Left ventricular end- diastolic volume Left ventricular end- systolic volume Mean pulmonary artery pressure Right atrial pressure Left atrial pressure O2 consumption (whole body) O2 content of systemic arterial blood O2 content of pulmonary arterial blood Objectives General The medical students should be able to perform essential cardiovascular calculations Specific To be able to explain different cardiovascular calculations such as mean arterial pressure, stroke volume, cardiac output, ejection fraction, total peripheral resistance and blood flow 124 mmHg 82 mmHg 800 msec 140 ml 70 ml 15 mmHg 2 mmHg 5 mmHg 250 ml/ min. 0.20 ml O2 / ml blood 0.152 ml O2 / ml blood

Questions 1. Mean arterial pressure is not simple average of systolic and diastolic pressures. Why not? How is mean arterial pressure estimated? From the information given above, calculate the mean arterial pressure in this case. Mean arterial pressure is determined by two major physical factors: arterial blood volume and arterial compliance. These physical factors in turn are affected by certain physiological factors, namely, cardiac output (heart rate x stroke volume) and peripheral resistance.

It is estimated by means of the following formula:

Pa = Pd + (Ps- Pd) 3 Where: Pa = mean arterial pressure Pd = diastolic volume Ps = systolic value Therefore, Pa = 82 mmHg + 124 mmHg- 82 mmHg 3 = 82 mmHg + 42 mmHg 3 = 82 mmHg + 14 mmHg = 96 mmHg

2. Calculate the stroke volume, cardiac output and ejection fraction of the left ventricle. a. Stroke volume- amount of blood put out by the left ventricle of the heart in one contraction SV = EDV- ESV = 140 ml- 70 ml = 70 ml Where: SV = Stroke Volume EDV = End Diastolic Volume ESV = End Systolic Volume b. Cardiac Output- amount of blood the heart pumps through the circulatory system in a minute HR (Heart Rate) = 60/ R-R interval = 0/ 0.8 = 75 BPM CO = SV x HR = (EDV - ESV) x HR = (140 ml- 70 ml) x 75 BPM = 5250 ml/min. c. Ejection Fraction EF = (LV diastolic volume- LV systolic volume) (WO) LVdiastolic volume Therefore,

3. Calculate the cardiac output using the Fick principle. Fick principle: CO = 2.50 ml/ min. 0.2 ml- 0. 152 ml = 5, 208 ml/ min. Fick principle states that the rate if diffusion is proportional to the difference in concentration. Similarly, the volume of O2 consumed per unit time is proportional to the difference in O2 content between atrial one venous blood, the degree of proportionality depends on the volume of blood pumped per unit time or cardiac output. Therefore, cardiac output can be calculated from the equation: VO2 = CO (CaCv) where VO2 is the volume O2 consumed/ unit time, Ca and Cv are the arterial and venous O2 concentration. Experimentally, the volume of O2 consumed and O2 concentration in the blood can be calculated. 4. What is the definition of total peripheral resistance? What equation describes the relationship between TPR, arterial pressure and cardiac output? What is the value of TPR in this case? TPR is the collective resistance to blood flow that is provided by all of the blood vessels on the systemic side of the circulation. These blood vessels include the aorta, large and small arteries, arterioles, capillaries, venules, veins, and vena cava. Most of this resistance resides in the arterioles. TPR = (mean arterial pressure right atrial pressure)/cardiac output = (96 mmHg 2 mmHg)/5229 ml/min = 0.018 mmHg/ml/min

5. What is total blood flow in ml/ min. through all of the pulmonary capillaries? BF= (mean pulmonary artery pressure left atrial pressure) / CO = (1.5 mmHG 5 mmHg) / 5, 229 ml/min = 0. 0019 mmHg / ml/ min