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Physiology II
Cardiovascular Case I

aortic stenosis 

the patient: a 53-year-old man 

principal complaint: fatigue and chest pain on exertion

history: When the patient was 31 years of age, a heart murmur was detected during a routine physical examination for insurance purposes, but no follow-up occurred. About a year prior to the present admission, the patient began to note chest pain during vigorous physical activity, and the condition has progressed to the point where chest pain is present during even slight exertion. On one occasion, the patient temporarily lost consciousness.

clinical examination: The patient appeared to be chronically ill. His arterial blood pressure was 95/80 mm Hg, his heart rate was 85 beats/min, and his respiratory rate was 21 breaths/min. A harsh systolic ejection murmur was present. Palpation revealed an arterial pulse that was decreased in intensity with a slow rate of rise (prolonged upstroke). The electrocardiographic findings suggested left ventricular hypertrophy but no evidence of myocardial infarction was found. X-ray examination of the chest confirmed that the heart was enlarged and that the lungs were clear. Evidence of calcification was noted in the region of the aortic valve. Coronary angiography findings included no evidence of impairment of coronary blood flow, an aortic pressure of 90/50 mm Hg, and an upstroke time for the arterial pressure pulse of 0.25 sec (normal, 0.05-0.1 sec). There were no other significant physical findings.


1. This patient appears to be suffering from ANGINA PECTORIS despite the presence of an adequate coronary circulation. Which hemodynamic and mechanical factors may be responsible for the INADEQUACY OF MYOCARDIAL OXYGENATION in this patient?  The heart is bigger due to the hypertrophy so the heart muscle is using much more oxygen than a normal sized heart does.  This has increased the demand.  Also because there is a prolonged systole, the heart is using more oxygen to keep the myosin cross-bridges cycling.  With the prolonged systole, there is a shorter diastole.  The only time that the heart can feed itself through the coronary arteries is during diastole.  So the heart is demanding more oxygen but there is less time to bring oxygen to the myocardium.

2. What is the status and importance of METABOLIC CONTROL of coronary blood flow in this patient? of NEURAL CONTROL?  The neural control doesn't have a huge effect on the coronary blood flow because the coronaries both dilate AND constrict with neural stimulation.  On the other hand, the metabolic contribution is very important.  During systole blood is not flowing through the coronary arteries because the contraction of the cardiac muscle has collapsed them.  During this time, the O2 decreases, and  CO2, H+, K+ and Adenosine increases,  causing vascular dilation so that when the heart is in diastole, blood can flow very quickly into the coronary vessels.

3. What are the major factors determining STROKE VOLUME in this patient? How is stroke volume being maintained? or is it?  The aortic stenosis is causing less blood to flow out of the ventricles.   To maintain the stroke volume the body has done a few things to compensate.  It has increased the SNS stimulation (increased HR to 85).  It has remodeled the heart to create more muscle (ventricular hypertrophy) to squeeze out the blood.  The body may also be retaining fluid to help increase the blood volume to help increase the preload (to help increase SV).  The original BP of 95/80 (PP=15) indicates that the body at that time was not maintaining an adequate SV.

4. What would be the pattern of CARDIAC ENLARGEMENT in this patient, and what would be the effect of this enlargement on MYOCARDIAL OXYGEN REQUIREMENTS? Please include in your answer a discussion of the SURFACE TENSION LAW of LaPlace as it would apply to a cardiac chamber such as the left ventricle.  Since the stenosis is on the aorta, the heart has remodeled the left ventricle to have more muscle.  The stenosis is making it harder for the blood to leave the left ventricle (more pressure to push against).  The body wants to normalize the tension that is exerted (T=P*r/thickness) so it has remodeled the heart to be more "thick" to compensate for the increase in ventricular pressure.  The increased muscle mass has greatly increased the O2 requirements.  This kind of makes a double-whammy.  The heart needs more O2 BUT it isn't ejecting as much blood as it used to.  Vicious circle.


Reasons For Decreased O2 Supply Reasons For Increased O2 Demand
  • Decreased Perfusion Pressure Gradient
  • Prolonged Systole which = Increased cardiac compression = decreased diastole perfusion
  • ? Collateral Supply
  • Vigorous physical activity
  • HR is 85
  • Hypertrophy of ventricle (increased mass = more area to oxygenate)
  • Prolonged systole (more myosin crossbridge cycling)
  • Increased afterload

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