Case Study 2 Your patient is a 56-year-old office manager who is significantly o
ID: 51364 • Letter: C
Question
Case Study 2
Your patient is a 56-year-old office manager who is significantly overweight. His diet consists of fatty foods that included red meats and high-calorie desserts. He had occasional chest pains that were relieved by nitroglycerin. One night, he went to bed early because he wasn't feeling well. He awakened at 4:00 A.M. with crushing pressure in his chest and pain radiating down his left arm that was not relieved by nitroglycerin. He was nauseated and sweating profusely. He also had dyspnea, especially when he was in the recumbent position. His wife stated his breathing was "noisy." He called 911. The paramedics arrived and transported him to the nearest hospital. In the emergency department, his blood pressure was 105/80. Inspiratory rales were present, consistent with pulmonary edema, and his skin was cold and clammy. Successive electrocardiograms and lab results of cardiac enzymes (creatine phosphokinase and lactate dehydrogenase) suggested a left ventricular wall myocardial infarction. His heart rate was variable during the sequential ECGs. His heart rate was 116 bpm during the first recording and 80 during the last recording. During cardiac catheterization, pulmonary capillary wedge pressure was 32 mm Hg (normal, 5 mm Hg). His ejection fraction, measured was 0.35 (normal, 0.55). His stroke volume was measured at 38 mL (normal range is 50-80 mL).
1. Why did he suffer orthopnea (difficulty breathing while recumbent)? Why would pulmonary edema be worse while lying supine compared to sitting or standing?
2. Why did pulmonary edema develop? Elaborate on the major Starling forces involved.
3. Which information in the case tells you that his stroke volume was decreased?
Explanation / Answer
1. Why did he suffer orthopnea (difficulty breathing while recumbent)? Why would pulmonary edema be worse while lying supine compared to sitting or standing?
Orthopnea is a sign of heart failure. It is caused by congestion in the lungs -- and perhaps accompanied by accumulation of excess fluid in the lungs (pulmonary edema) -- that occurs as a result of left-sided heart failure.
Orthopnea is shortness of breath (dyspnea) which occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair. It is the opposite of platypnea. It is commonly seen as a late manifestation of heart failure, resulting from fluid redistribution into the central circulation, causing an increase in pulmonary capillary pressure. It is also seen in cases of abdominal obesity or pulmonary disease.
Main Cause:
Orthopnea is due to increased distribution of blood to the pulmonary circulation while recumbent, but usually can be attributed to a more fundamental cause.Orthopnea is often a symptom of left ventricular heart failure and/or pulmonary edema.Orthopnea is caused by the accumulation of too much fluid in the lungs (pulmonary congestion or fluid overload) when a person lies down. In a prone position, blood volume from the feet and legs redistributes to the lungs, which doesn't cause a problem for people whose hearts are pumping normally. However, in people with heart failure, excess blood in the lungs can cause breathing problems or shortness of breath.
2.Why did pulmonary edema develop? Elaborate on the major Starling forces involved.
Pulmonary edema is an abnormal buildup of fluid in the lungs. This buildup of fluid leads to shortness of breath.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs.
As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This fluid reduces normal oxygen movement through the lungs. These two factors combine to cause shortness of breath.
Congestive heart failure that leads to pulmonary edema may be caused by:
Pulmonary edema may also be caused by:
Major Starling forces involved:
Imbalance of Starling forces - Ie, increased pulmonary capillary pressure, decreased plasma oncotic pressure, increased negative interstitial pressure
increased pulmonary capillary pressure:
Pulmonary capillary pressure is a primary determinant of fluid flux across the pulmonary capillary wall. Increasing pulmonary capillary pressure increases fluid flux out of the capillaries into the interstitium and in the extreme induces pulmonary edema. Pulmonary capillary pressure is itself determined by the mean pulmonary artery pressure, pulmonary vascular resistance, and total blood flow. The distribution of the pulmonary vascular resistance from precapillary arterial to postcapillary venous compartments varies. Accordingly, at any given blood flow rate the hydrostatic pressure in the pulmonary capillaries depends on the magnitude of the resistance to blood flow across the pulmonary circulation and its distribution between precapillary and postcapillary vessels.
Oncotic pressure, is a form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel's plasma (blood/liquid) that usually tends to pull water into the circulatory system. It is the opposing force tocapillary filtration pressure and interstitial colloidal osmotic pressure. It has a major effect on the glomerular filter pressure.
The large majority of oncotic pressure in capillaries is generated by the presence of high quantities of albumin, which can be identified as a protein, and constitutes approximately 80% of the total oncotic pressure exerted by blood plasma on interstitial fluid. The total oncotic pressure of an average capillary is about 28 mmHg with albumin contributing approximately 22 mmHg of this oncotic pressure. Because blood proteins cannot escape through capillary endothelium, oncotic pressure of capillary beds tends to draw water into the vessels. It is necessary to understand the oncotic pressure as a balance; because the blood proteins reduce interior permeability, less plasma fluid can exit the vessel.
increased negative interstitial pressure :
Interstitial fluid or tissue fluid is a solution that bathes and surrounds the tissue cells of multicellular animals.interstitial fluid pressure is the main component of the extracellular fluid, which also includes plasma and transcellular fluid. pressure exerted by the free interstitial fluid; if the pressure is negative this tends to suck fluid out of the vascularsystem and into the tissue space; if the pressure is greater than the intravascular pressure fluid tends to move out of thetissue space.
3. Which information in the case tells you that his stroke volume was decreased?
Its value is obtained by subtracting end-systolic volume (ESV) fromend-diastolic volume (EDV) for a given ventricle.
SV=EDV-ESV
The patient had stroke volume of 38 mL (normal range is 50-80 mL).which is clearly indicate us that stroke volume is not in the noraml range and had decread.