Question

In: Anatomy and Physiology

the class is Exercise physiology How to calculate CO, PP, MAP, DP, Fick. the equations Different...

the class is Exercise physiology

  1. How to calculate CO, PP, MAP, DP, Fick.
    1. the equations
  2. Different types of hemoglobin
    1. Oxy-, deoxy-, and carbamino-hemoglobin
  3. Pulmonary ventilation & lung volumes and capacities
  4. What are the responses and mechanisms of venous return during exercise
  5. Differences between hemoglobin and myoglobin
    1. Responses of these proteins under lower PO2
    2. Gender difference in Hb
  6. Acids and bases
    1. How to control (increase/decrease) acidity and alkalinity
  7. What are causes of acidosis and alkalosis
  8. Frank-Starling mechanism what is it

Solutions

Expert Solution

Cardiac Output (CO): CO describes the volume of blood being pumped by the heart, by the left and right ventricle, per unit time. Cardiac output (CO) is the product of the heart rate (HR), i.e. the number of heartbeats per minute (bpm), and the stroke volume (SV), which is the volume of blood pumped from the ventricle per beat; thus,

CO = HR × SV

Pulse Pressure (PP): Pulse pressure is the difference between systolic and diastolic blood pressure. It represents the force that the heart generates each time it contracts. Resting blood pressure is normally approximately 120/80 mmHg, Hence, the pulse pressure is 120-80 = 40 mmHg.

PP = SBP - DBP

Fick's Principle: CO is calculated as oxygen consumption divided by the arteriovenous oxygen concentration difference (in milliliters of oxygen)

cardiac output (CO) = (rate of O2 consumption) / (arterial O2 content- venous O2 content)

Mean Arterial Pressure (MAP): MAP is defined as the average pressure in a patient's arteries during one cardiac cycle. To calculate a mean arterial pressure, double the diastolic blood pressure and add the sum to the systolic blood pressure.

MAP = SBP + 2 (DBP)

Double Product (DP): DP is the systolic blood pressure (SBP) multiplied by the pulse rate (PR), is an index of myocardial oxygen consumption

DP = SBP x PR

Hemoglobin types:

Oxyhemoglobin is formed during physiological respiration when oxygen binds to the heme component of the protein hemoglobin in red blood cells. This process occurs in the pulmonary capillaries adjacent to the alveoli of the lungs

Deoxygenated hemoglobin is the form of hemoglobin without the bound oxygen.

Carbaminohemoglobin: When carbon dioxide binds to hemoglobin, a molecule called carbaminohemoglobin is formed. Binding of carbon dioxide to hemoglobin is reversible. Therefore, when it reaches the lungs, the carbon dioxide can freely dissociate from the hemoglobin and be expelled from the body.

Also, Humans have three hemoglobin types: hemoglobin A, hemoglobin A2 and hemoglobin F. Hemoglobin A is the common type of hemoglobin, which is encoded by HBA1, HBA2, and HBB genes. The four subunits of hemoglobin A consist of two α and two β subunits (α2β2). Hemoglobin A2 and hemoglobin F are rare and consist of two α and two δ subunits and two α and two γ subunits, respectively. In infants, the hemoglobin type is Hb F (α2γ2).

Hemoglobin is a multi-subunit globular protein with a quaternary structure. It is composed of two α and two β subunits arranged in a tetrahedral structure. Hemoglobin is an iron-containing metalloprotein. Each of the four globular protein subunits is associated with non-protein, prosthetic haem group, which binds with one oxygen molecule. The production of hemoglobin occurs in the bone marrow. Globin proteins are synthesized by ribozomes in the cytosol. Haem part is synthesized in the mitochondria. A charged iron atom is held in the porphyrin ring by covalent binding of iron with four nitrogen atoms in the same plane. These N atoms belong to the imidazole ring of the F8 histidine residue of each of the four globin subunits. In hemoglobin, iron exists as Fe2+, giving the red color to red blood cells.

Myoglobin is the oxygen-binding protein in muscle cells of vertebrates, giving a distinct red or dark gray color to muscles. It is exclusively expressed in skeletal muscles and cardiac muscles. Myoglobin constitutes of 5-10% of cytoplasmic proteins in muscle cells. Since the amino acid changes in the polynucleotide chains of hemoglobin and myoglobin are conservative, both hemoglobin and myoglobin bear a similar structure. Additionally, myoglobin is a monomer, composing of a single polynucleotide chain, composed of a single haem group. Therefore, it is capable of binding with a single oxygen molecule. Thus, no cooperative binding of oxygen occurs in myoglobin. But, the binding affinity of myoglobin is high when compared to that of hemoglobin. As a result, myoglobin serves as the oxygen-storing protein in muscles. Myoglobin releases oxygen when the muscles are functioning

Gender-related differences in hemoglobin concentration begin to emerge in adolescence. In females, the hemoglobin level reaches a plateau during early puberty, while in males the hemoglobin level continues to rise throughout puberty to higher levels characteristic of adult men. Hemoglobin is found to be higher in males as compared to the females may be due to the reason that testosterone effects on the kidneys to produce more erythropoietin that accelerates the erythropoiesis

Ventilation is described as the volume of air that is moved into and out of the lungs and airways over a period of time. Physiologically, lung volumes are subdivided into the categories of either dynamic lung volumes or static lung volumes. Clinically, dynamic lung volumes are used in the diagnosis and management of obstructive lung disease. These dynamic lung volumes are related to the rate of airflow. Static lung volumes, however, are important both in restrictive ventilatory defects and in obstructive lung disease. Static lung volumes are further broken down into standard lung volumes (tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume) and standard capacities (inspiratory capacity, functional residual capacity, vital capacity, and total lung capacity).

Exercise causes the heart to pump blood into the circulation more efficiently as a result of more forceful and efficient myocardial contractions, increased perfusion of tissues and organs with blood, and increased oxygen delivery. Aerobic exercise trains the heart to become more efficient. During exercise, the cardiac output increases more than the total resistance decreases, so the mean arterial pressure usually increases by a small amount. Rhythmical contraction of limb muscles occurring during normal locomotory activity (walking, running, swimming) promotes venous return by the muscle pump mechanism. During exercise, skeletal muscle contractions compress venous vessels, forcing blood centrally and supplementing venous return. The resulting decrement in intramuscular venous pressure increases the arterial–venous pressure gradient and aids arterial inflow into the muscle

The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism) represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The Frank-Starling mechanism occurs as the result of the length-tension relationship observed in striated muscle, including for example skeletal muscles, arthropod muscle and cardiac (heart) muscle.

Acidosis: Causes can include chronic alcohol use, heart failure, cancer, seizures, liver failure, prolonged lack of oxygen, and low blood sugar. Even prolonged exercise can lead to lactic acid buildup. Renal tubular acidosis occurs when the kidneys are unable to excrete acids into the urine.

Alkalosis: The most common causes are volume depletion (particularly when involving loss of gastric acid and chloride (Cl) due to recurrent vomiting or nasogastric suction) and diuretic use. Metabolic alkalosis involving loss or excess secretion of Cl is termed chloride-responsive.


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