In this lesson we will explore the phenomenon of reactive hyperemia including the natural purpose it serves as well as how it is used as a diagnostic tool for Peripheral Vascular Disease.
Reactive Hyperemia
I'm sure you've had your blood pressure taken before. The nurse had you roll up your sleeve and put an inflatable cuff around your arm that she inflated until it felt really tight. You probably started to notice that your hand may have felt a little cool, like it was starting to get a little numb, or maybe it throbbed. Then, as she slowly deflated the cuff, you felt the blood surge back to your hand. Voila! That was reactive hyperemia in action. Ok, so what why did you feel that surging rush of blood? Well, let's take a closer look at why we experience reactive hyperemia.
What is Reactive Hyperemia
Reactive hyperemia refers to the temporary increase ('hyper') of blood flow ('emia') to an area as a result of (or reaction to) ischemia, or an arterial blockage ('isch', meaning to stop or block, 'emia', meaning blood flow). This occlusion (blockage) can take the form of any outside force, like a tourniquet wrapped around the arm during a blood draw or a clamp placed on a vessel during surgery, or internal, like a buildup of plaque or a blood clot within the vessel that impedes or interrupts blood flow.
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Ok, so reactive hyperemia might sound like a pretty obvious phenomenon- not so special, you occlude blood flow to an area, the blood pressure builds behind the point of the blockage and then, when you remove the occlusion, blood rushes to the area, temporarily increasing blood flow. Ok, that makes perfect sense but, what purpose does it serve? Well, it's actually a really important process that reduces further damage to the occluded tissue. During occlusion, cells are deprived of vital oxygen and metabolic wastes buildup; normally these wastes would've been washed away by the constant flow of blood. Now, this temporarily high surge of blood actually ensures that all cells receive enough oxygen immediately and that any dead cells and metabolic wastes are swiftly flushed from the area to reduce continued damage.
What's interesting is that this temporary surge of blood isn't just because blood flow builds up behind the clot but because your body actually responds to the reduced blood flow by secreting chemicals, calledvasodilators, that dilate (open) the deprived vessels. This dilation increases the size of the vessels thereby enabling a higher volume of blood to rush to the deprived area once the clot or blockage is cleared. In turn, this increased flow flushes the area of the vasodilators, causing the vessels to return to their normal size, thus reestablishing normal blood flow to the area.
Ok, so now that we understand what reactive hyperemia does, let's take at how it can be used to diagnose vascular diseases.
Peripheral Vascular Disease (PVD)
_Peripheral Vascular Disease (PVD) is actually a general term used to describe a progressive and chronic narrowing of your veins, lymph vessels, or arteries although, in the case of arterial damage the disease is referred to as Peripheral Arterial Disease (PAD). Now, PVD and PAD may not sound like a big deal, but they can be life threatening. Consider for a moment that your blood brings oxygen and nutrients to every cell and tissue of your body and, in the process, flushes away normal metabolic wastes. Now, consider interrupting or impeding that blood supply, thereby essentially starving, suffocating, and poisoning your tissues in one fall swoop. Yikes!
Now, PVD and PAD aren't actually primary disorders; they're known as secondary diseases, meaning that they're caused by some other disease affecting either the muscle of your heart or the vessels of your body. In actuality, the primary cause of PVD/PAD could really be any of a host of other disease like blood clotting within veins (known as deep vein thrombosis) or an enlargement of venous vessel (known as varicose veins) in the case of PVD, while atherosclerosis (hardening of the arteries due to plaque buildup) is the most common cause of PAD. Both PVD and PAD have associated risks of stroke and heart attack so they're certainly no laughing matter.
So, how is reactive hyperemia used to diagnose PVD/PAD you ask? Well, since PVD and PAD both result in reduced blood flow either to the limbs (in other words arterial) or from the limbs (venous), a reactive hyperemia test, can be used to essentially compare blood pressures between the legs to identify any differences that might indicate vessel narrowing.
Reactive Hyperemia & Diagnostic Testing
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The naturally occurring phenomenon of reactive hyperemia is utilized in various ways to diagnose the restriction of blow flow to particular limbs. In the case of PVD and PAD a test called an Ankle Brachial Index Evaluation (ABI) is utilized to compare the flow of blood between the lower limbs. An ABI evaluation is conducted by placing blood pressure cuffs around both of the patient's arms and legs while an ultrasound device measures and tracks the pulse in all four regions. The systolic pressure (or the blood pressure when the heart is contracting) is calculated for all four limbs and, since healthy individuals have higher systolic pressures in their legs than their arms, a simple calculation (dividing the systolic pressure of each ankle by the higher of the two found in the arms) can provide a quick assessment. ABIs above 0.90 are considered normal, anything in the 0.70-0.90 range indicates mild PVD, 0.50-0.70 indicates moderate PVD, and anything less than 0.50 indicates severe PVD.
Lesson Summary
Reactive hyperemia refers to a temporary increase in blood flow to an area after a period of arterial occlusion. Vasodilators secreted by blood deprived cells dilate deprived vessels ensuring that, post occlusion, blood will experience minimal resistance when resupplying the area. Reactive hyperemia ensures that, post occlusion, all cells will receive enough oxygen quickly and any dead cells and/or metabolic wastes will be swiftly flushed from the area to reduce continued damage. This phenomenon can be used to test for _Peripheral Vascular Disease (PVD) (a progressive narrowing of veins or lymph vessels) as well as Peripheral Arterial Disease (PAD) (narrowing of arteries) by way of a Ankle Brachial Index Evaluation (ABI). ABI values greater than 0.90 are normal, while values below that indicate some degree of PVD.
Side Lesson from the University Moodle Website
Hyperemia and congestion are the terms used for increased volume of blood within dilated vessels of an organ or tissue the increased volume from arterial and arteriolar dilatation being referred to as hyperemia or active hyperemia, whereas the impaired venous drainage is called venous congestion or passive hyperemia. The capillaries and veins are dilated paralytically and filled with blood.
Arterial or active hyperemia is caused by an increased supply of blood from arterial system. The affected tissue or organ is pink or red in appearance (erythema).
I. Common arterial or active hyperemia is a result
• Of increasing volume of circulating blood (pletora).
• Of increasing of amount of erythrocytes.
• Vacatic (lat. – vacuum) because of decreased atmospheric pressure.
II. Local arterial hyperemia can be
• Angioneurotic – because of dilatation of arteries and arterioles.
• Collateral.
• Hyperemia after anemia.
• Vacatic.
• Inflammatory.
• In arterio-venous fistula.
Venous, or passive hyperemia, or congestion is caused by impediment to the exit of blood through venous pathway. The dilatation of veins and capillaries due to impaired venous drainage results in passive hyperemia or venous congestion, commonly referred to as congestion. Congestion may be acute or chronic, the latter being more common and called chronic venous congestion.
I. Common congestion or Systemic (General) venous congestion is engorgement of systemic veins. It can be a result of
• left-sided and right-sided heart failure
• diseases of the lungs which interfere with pulmonary blood flow, like pulmonary fibrosis, emphysema, etc.
• cardiac decompensation.
II. Local congestion can be a result of
• venous obstruction because of its thrombosis,
• compression of venous vessel with tumor or ingrowth of connective tissue,
• development of collateral blood circulation.
Morphology of congestion
Because of the increase in venous blood, organs become swollen and purplish. With long continued over-distension, the wall of the venules shows reactive thickening and there is mild intestinal fibrosis of the organs, giving them a very firm consistency. These changes are seen typically in the kidney and spleen. Important additional changes are found in the lungs and liver.
Lungs. The lungs are burcly, congested and brownish in color. Pulmonary venous engorgement leads to alveolar hemorrhage. Hemoglobin from intra-alveolar blood is transformed into hemosiderin, which is then phagocytized by macrophages. These macrophages are known as heart failure cells. Phagocytes full of brown pigment migrate into intestinal tissue and to the lymph nodus. The sectioned surface is dark brown. It process in lungs is named as “brown induration” of the lungs.
Spleen. Chronic venous congestion of the spleen occurs in right heart failure and in portal hypertension from cirrhosis of liver. The spleen in early stage is moderately enlarged while in long-standing cases there is progressive enlargement and may weigh up to 500 g to 1000 g. The organ is deeply congested, tense and cyanotic (“cyanotic induration of the spleen”). Sectioned surface is gray tan. The red pulp shows congestion and marked sinusoidal dilatation with areas of recent and old hemorrhages. These hemorrhages may get organized. This advanced stage seen more commonly in hepatic cirrhosis is called congestive splenomegaly and is the commonest cause of hypersplenism.
Liver. Chronic venous congestion of the liver occurs in right heart failure and sometimes due to occlusion of inferior vena cava and hepatic vein. The liver is enlarged and tender and the capsule is tense. Cut surface shows characteristic “nutmeg liver” due to red and yellow mottled appearance. The changes of congestion are more marked in the centrolobular zone due to severe hypoxia than in the peripheral zone. The centrolobular hepatocytes undergo degenerative changes, and eventually centrolobular hemorrhagic necrosis may be seen. The peripheral zone of the lobule is less severely affected by chronic hypoxia and shows some fatty change in the hepatocytes. If the patient has periods of remission, the remaining liver cells may undergo compensatory hyperplasia. This results in small, irregular, pale nodules alternating with areas of fibrosis – so-called cardiac cirrhosis. It’s not true cirrhosis and does not causes hepatic failure.
Outcomes of congestion:
• Edema.
• Stasis.
• Hemorrhage.
• Thrombosis.
• Induration of organs.
• Atrophy of organs.
Arterial or active hyperemia is caused by an increased supply of blood from arterial system. The affected tissue or organ is pink or red in appearance (erythema).
I. Common arterial or active hyperemia is a result
• Of increasing volume of circulating blood (pletora).
• Of increasing of amount of erythrocytes.
• Vacatic (lat. – vacuum) because of decreased atmospheric pressure.
II. Local arterial hyperemia can be
• Angioneurotic – because of dilatation of arteries and arterioles.
• Collateral.
• Hyperemia after anemia.
• Vacatic.
• Inflammatory.
• In arterio-venous fistula.
Venous, or passive hyperemia, or congestion is caused by impediment to the exit of blood through venous pathway. The dilatation of veins and capillaries due to impaired venous drainage results in passive hyperemia or venous congestion, commonly referred to as congestion. Congestion may be acute or chronic, the latter being more common and called chronic venous congestion.
I. Common congestion or Systemic (General) venous congestion is engorgement of systemic veins. It can be a result of
• left-sided and right-sided heart failure
• diseases of the lungs which interfere with pulmonary blood flow, like pulmonary fibrosis, emphysema, etc.
• cardiac decompensation.
II. Local congestion can be a result of
• venous obstruction because of its thrombosis,
• compression of venous vessel with tumor or ingrowth of connective tissue,
• development of collateral blood circulation.
Morphology of congestion
Because of the increase in venous blood, organs become swollen and purplish. With long continued over-distension, the wall of the venules shows reactive thickening and there is mild intestinal fibrosis of the organs, giving them a very firm consistency. These changes are seen typically in the kidney and spleen. Important additional changes are found in the lungs and liver.
Lungs. The lungs are burcly, congested and brownish in color. Pulmonary venous engorgement leads to alveolar hemorrhage. Hemoglobin from intra-alveolar blood is transformed into hemosiderin, which is then phagocytized by macrophages. These macrophages are known as heart failure cells. Phagocytes full of brown pigment migrate into intestinal tissue and to the lymph nodus. The sectioned surface is dark brown. It process in lungs is named as “brown induration” of the lungs.
Spleen. Chronic venous congestion of the spleen occurs in right heart failure and in portal hypertension from cirrhosis of liver. The spleen in early stage is moderately enlarged while in long-standing cases there is progressive enlargement and may weigh up to 500 g to 1000 g. The organ is deeply congested, tense and cyanotic (“cyanotic induration of the spleen”). Sectioned surface is gray tan. The red pulp shows congestion and marked sinusoidal dilatation with areas of recent and old hemorrhages. These hemorrhages may get organized. This advanced stage seen more commonly in hepatic cirrhosis is called congestive splenomegaly and is the commonest cause of hypersplenism.
Liver. Chronic venous congestion of the liver occurs in right heart failure and sometimes due to occlusion of inferior vena cava and hepatic vein. The liver is enlarged and tender and the capsule is tense. Cut surface shows characteristic “nutmeg liver” due to red and yellow mottled appearance. The changes of congestion are more marked in the centrolobular zone due to severe hypoxia than in the peripheral zone. The centrolobular hepatocytes undergo degenerative changes, and eventually centrolobular hemorrhagic necrosis may be seen. The peripheral zone of the lobule is less severely affected by chronic hypoxia and shows some fatty change in the hepatocytes. If the patient has periods of remission, the remaining liver cells may undergo compensatory hyperplasia. This results in small, irregular, pale nodules alternating with areas of fibrosis – so-called cardiac cirrhosis. It’s not true cirrhosis and does not causes hepatic failure.
Outcomes of congestion:
• Edema.
• Stasis.
• Hemorrhage.
• Thrombosis.
• Induration of organs.
• Atrophy of organs.
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