EFFECT OF AFTERLOAD AND PRELOAD

       EFFECT OF AFTERLOAD AND PRELOAD

                                

                                Independent Effects of Afterload

If afterload is increased by increasing aortic pressure, the isovolumetric contraction phase is prolonged because the ventricle will need to generate a higher pressure to overcome the elevated aortic diastolic pressure. Therefore, ejection begins at a higher aortic diastolic pressure. If preload (end-diastolic volume) and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume (red loop in figure). Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected (see force-velocity relationship). A reduced stroke volume at the same end-diastolic volume results in reduced ejection fraction. If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases (green loop in figure).

                                     Independent Effects of Preload

To examine the independent effects of preload, assume that aortic systolic and diastolic pressure (afterload), and inotropy are held constant. The left ventricle is filled with blood from the pulmonary veins. If pulmonary venous flow is increased, the ventricle will fill to a greater extent (end-diastolic volume is increased; red loop in figure). As the ventricle contracts, it will eject blood more rapidly because the Frank-Starling mechanism will be activated by the increased preload. With no change in afterload or inotropy, the ventricle will eject blood to the same end-systolic volume despite the increase in preload. The net effect will be an increase in stroke volume, shown by an increase in the width of the PV loop (100 compared to 75 ml in figure). Ejection fraction (EF) will increase slightly from 60 to 67%. This ability to contract to the same end-systolic volume is a property of cardiac muscle that can be demonstrated using isolated cardiac muscle and studying isotonic (shortening) contractions under the condition of constant afterload.  When muscle preload length is increased, the contracting muscle shortens to the same minimal length as found before the preload was increased (see Effects of Preload on Cardiac Fiber Shortening). If pulmonary venous flow decreases, then the ventricle will fill to a smaller end-diastolic volume (decreased preload; green loop in figure). This will cause stroke volume to decrease (from 75 to 50 ml in figure) and EF to decrease from 60 to 50%, but the end-systolic volume will be unchanged. To summarize, changes in preload alter the stroke volume; however, end-systolic volume is unchanged if afterload and inotropy are held constant.

CONTENT DEVELOPER: Vinayak chalia

EDEMA

 EDEMA 

Edema is the presence of excess fluid in the body, typically in the extracellular fluid space but sometimes involving the intracellular fluid space also

• Intracellular Edema

• Two conditions lead to intracellular swelling

1. Depression of metabolic systems of the tissues

2. Inadequate nutrient delivery to the cell

• Extracellular Edema

• Much more predominant

• Two general conditions lead to extracellular edema

1. Abnormal leakage of fluid from the plasma through the capillary wall and into the

interstitial space

2. Failure of the lymphatics to return fluid from the interstitium back into the blood

Causes of edema

Edema can occur in tissues adjacent to other volumes - potential spaces that can also collect fluid in

• Pleural cavity
• Pericardial cavity
• Peritoneal cavity
• Synovial cavities

• Potential spaces are “filled” by capillaries and “drained” by lymphatics in a manner similar to other tissues

When edema occurs with fluid collection in a potential space, it is called effusion

cavities

INFLAMMATION

Inflammation

figure source ; janeways immunolgy

Macrophages sense bacteria and other types of microorganisms in tissues these bacteria  triggered to release cytokines (vasodilator) that increase the permeability of blood vessels, allowing fluid and proteins to pass into the tissues. Macrophages also produce chemokines which direct the migration of neutrophils to the site of infection this phenomenon is known as chemotaxis . The stickiness of the endothelial cells of the blood vessel wall is also changed, so that circulating cells i.e neutrophils of the immune system adhere to the wall and are able to crawl through it this phenomenon of passage of blood cells through the intact walls of the capillaries is known as diapedesis first neutrophils and then monocytes  enter the tissue from a blood vessel The accumulation of fluid and cells at the site of infection causes the redness, swelling, heat, and pain known collectively as inflammation. neutrophils and macrophages are the principal inlammatory cells. Later in an immune response,activated lymphocytes can also contribute to inflammation

TYPES OF MUSCLE FIBRE

MUSCLE FIBRE TYPES

Two criteria to consider when classifying the types of muscle fibers are

    1.   how fast some fibers contract relative to others  
    2.  how fibers produce ATP.                                                                                   

 Considering above criteria there are three main types of skeletal muscle fibers. 

 A.Type 1 Slow oxidative (SO) fibers contract relatively slowly and use aerobic respiration (oxygen and glucose) to produce ATP.      
                                   

 B. Type 2A  Fast oxidative (FO) fibers have fast contractions and primarily use aerobic respiration, but because they may switch to anaerobic respiration (glycolysis), can fatigue more quickly than SO fibers.                                           

C.Type 2B Fast glycolytic (FG) fibers have fast contractions and primarily use anaerobic glycolysis. The FG fibers fatigue more quickly than the others. Most skeletal muscles in a human contain(s) all three types, although in varying proportions.                                                                                                             

 figure source   https://www.teachpe.com

1. The speed of contraction is dependent on how quickly myosin’s ATPase hydrolyzes ATP to produce cross-bridge action. 
2. Fast fibers hydrolyze ATP approximately twice as quickly as slow fibers, resulting in much quicker cross-bridge cycling (which pulls the thin filaments toward the center of the sarcomeres at a faster rate). 
3. The primary metabolic pathway used by a muscle fiber determines whether the fiber is classified as oxidative or glycolytic.
4.  If a fiber primarily produces ATP through aerobic pathways it is oxidative. More ATP can be produced during each metabolic cycle, making the fiber more resistant to fatigue.
5.  Glycolytic fibers primarily create ATP through anaerobic glycolysis, which produces less ATP per cycle. As a result, glycolytic fibers fatigue at a quicker rate.

    The oxidative fibers contain many more mitochondria than the glycolytic fibers, because aerobic metabolism, which uses oxygen (O2) in the metabolic pathway, occurs in the mitochondria. 

 Slow oxidative fibres

• The SO fibers possess a large number of mitochondria and are capable of contracting for longer periods because of the large amount of ATP they can produce, but they have a relatively small diameter and do not produce a large amount of tension. 
• SO fibers are extensively supplied with blood capillaries to supply O2 from the red blood cells in the bloodstream. 
• The SO fibers also possess myoglobin, an O2-carrying molecule similar to O2-carrying hemoglobin in the red blood cells. The myoglobin stores some of the needed O2within the fibers themselves (and gives SO fibers their red color). All of these features allow SO fibers to produce large quantities of ATP, which can sustain muscle activity without fatiguing for long periods of time.
• The fact that SO fibers can function for long periods without fatiguing makes them useful in maintaining posture, producing isometric contractions, stabilizing bones and joints, and making small movements that happen often but do not require large amounts of energy. They do not produce high tension, and thus they are not used for powerful, fast movements that require high amounts of energy and rapid cross-bridge cycling.

fast oxidative fibres

• FO fibers are sometimes called intermediate fibers because they possess characteristics that are intermediate between fast fibers and slow fibers. They produce ATP relatively quickly, more quickly than SO fibers, and thus can produce relatively high amounts of tension. They are oxidative because they produce ATP aerobically, possess high amounts of mitochondria, and do not fatigue quickly. 
• However, FO fibers do not possess significant myoglobin, giving them a lighter color than the red SO fibers. FO fibers are used primarily for movements, such as walking, that require more energy than postural control but less energy than an explosive movement, such as sprinting. 
• FO fibers are useful for this type of movement because they produce more tension than SO fibers but they are more fatigue-resistant than FG fibers.
• FG fibers primarily use anaerobic glycolysis as their ATP source. They have a large diameter and possess high amounts of glycogen, which is used in glycolysis to generate ATP quickly to produce high levels of tension. Because they do not primarily use aerobic metabolism, they do not possess substantial numbers of mitochondria or significant amounts of myoglobin and therefore have a white color
• . FG fibers are used to produce rapid, forceful contractions to make quick, powerful movements. These fibers fatigue quickly, permitting them to only be used for short periods. Most muscles possess a mixture of each fiber type. The predominant fiber type in a muscle is determined by the primary function of the muscle. 

         

       SUMMARY