NEET MDS Lessons
Physiology
Contractility : Means ability of cardiac muscle to convert electrical energy of action potential into mechanical energy ( work).
The excitation- contraction coupling of cardiac muscle is similar to that of skeletal muscle , except the lack of motor nerve stimulation.
Cardiac muscle is a self-excited muscle , but the principles of contraction are the same . There are many rules that control the contractility of the cardiac muscles, which are:
1. All or none rule: due to the syncytial nature of the cardiac muscle.There are atrial syncytium and ventricular syncytium . This rule makes the heart an efficient pump.
2. Staircase phenomenon : means gradual increase in muscle contraction following rapidly repeated stimulation..
3. Starling`s law of the heart: The greater the initial length of cardiac muscle fiber , the greater the force of contraction. The initial length is determined by the degree of diastolic filling .The pericardium prevents overstretching of heart , and allows optimal increase in diastolic volume.
Thankful to this law , the heart is able to pump any amount of blood that it receives. But overstretching of cardiac muscle fibers may cause heart failure.
Factors affecting contractility ( inotropism)
I. Positive inotropic factors:
1. sympathetic stimulation: by increasing the permeability of sarcolemma to calcium.
2. moderate increase in temperature . This due to increase metabolism to increase ATP , decrease viscosity of myocardial structures, and increasing calcium influx.
3. Catecholamines , thyroid hormone, and glucagon hormones.
4. mild alkalosis
5. digitalis
6. Xanthines ( caffeine and theophylline )
II. Negative inotropic factors:
1. Parasympathetic stimulation : ( limited to atrial contraction)
2. Acidosis
3. Severe alkalosis
4. excessive warming and cooling .
5. Drugs ;like : Quinidine , Procainamide , and barbiturates .
6. Diphtheria and typhoid toxins.
Respiration involves several components:
Ventilation - the exchange of respiratory gases (O2 and CO2) between the atmosphere and the lungs. This involves gas pressures and muscle contractions.
External respiration - the exchange of gases between the lungs and the blood. This involves partial pressures of gases, diffusion, and the chemical reactions involved in transport of O2and CO2.
Internal respiration - the exchange of gases between the blood and the systemic tissues. This involves the same processes as external respiration.
Cellular respiration - the includes the metabolic pathways which utilize oxygen and produce carbon dioxide, which will not be included in this unit.
Ventilation is composed of two parts: inspiration and expiration. Each of these can be described as being either quiet, the process at rest, or forced, the process when active such as when exercising.
Quiet inspiration:
The diaphragm contracts, this causes an increase in volume of the thorax and the lungs, which causes a decrease in pressure of the thorax and lungs, which causes air to enter the lungs, moving down its pressure gradient. Air moves into the lungs to fill the partial vacuum created by the increase in volume.
Forced inspiration:
Other muscles aid in the increase in thoracic and lung volumes.
The scalenes - pull up on the first and second ribs.
The sternocleidomastoid muscles pull up on the clavicle and sternum.
The pectoralis minor pulls forward on the ribs.
The external intercostals are especially important because they spread the ribs apart, thus increasing thoracic volume. It's these muscles whose contraction produces the "costal breathing" during rapid respirations.
Quiet expiration:
The diaphragm relaxes. The elasticity of the muscle tissue and of the lung stroma causes recoil which returns the lungs to their volume before inspiration. The reduced volume causes the pressure in the lungs to increase thus causing air to leave the lungs due to the pressure gradient.
Forced Expiration:
The following muscles aid in reducing the volume of the thorax and lungs:
The internal intercostals - these compress the ribs together
The abdominus rectus and abdominal obliques: internal obliques, external obliques- these muscles push the diaphragm up by compressing the abdomen.
Respiratory output is determined by the minute volume, calculated by multiplying the respiratory rate time the tidal volume.
Minute Volume = Rate (breaths per minute) X Tidal Volume (ml/breath)
Rate of respiration at rest varies from about 12 to 15 . Tidal volume averages 500 ml Assuming a rate of 12 breaths per minute and a tidal volume of 500, the restful minute volume is 6000 ml. Rates can, with strenuous exercise, increase to 30 to 40 and volumes can increase to around half the vital capacity.
Not all of this air ventilates the alveoli, even under maximal conditions. The conducting zone volume is about 150 ml and of each breath this amount does not extend into the respiratory zone. The Alveolar Ventilation Rate, AVR, is the volume per minute ventilating the alveoli and is calculated by multiplying the rate times the (tidal volume-less the conducting zone volume).
AVR = Rate X (Tidal Volume - 150 ml)
For a calculation using the same restful rate and volume as above this yields 4200 ml.
Since each breath sacrifices 150 ml to the conducting zone, more alveolar ventilation occurs when the volume is increased rather than the rate.
During inspiration the pressure inside the lungs (the intrapulmonary pressure) decreases to -1 to -3 mmHg compared to the atmosphere. The variation is related to the forcefulness and depth of inspiration. During expiration the intrapulmonary pressure increases to +1 to +3 mmHg compared to the atmosphere. The pressure oscillates around zero or atmospheric pressure.
The intrapleural pressure is always negative compared to the atmosphere. This is necessary in order to exert a pulling action on the lungs. The pressure varies from about -4 mmHg at the end of expiration, to -8 mmHg and the end of inspiration.
The tendency of the lungs to expand, called compliance or distensibility, is due to the pulling action exerted by the pleural membranes. Expansion is also facilitated by the action of surfactant in preventing the collapse of the alveoli.
The opposite tendency is called elasticity or recoil, and is the process by which the lungs return to their original or resting volume. Recoil is due to the elastic stroma of the lungs and the series elastic elements of the respiratory muscles, particularly the diaphragm.
Blood is a liquid tissue. Suspended in the watery plasma are seven types of cells and cell fragments.
- red blood cells (RBCs) or erythrocytes
- platelets or thrombocytes
- five kinds of white blood cells (WBCs) or leukocytes
- Three kinds of granulocytes
- neutrophils
- eosinophils
- basophils
- Two kinds of leukocytes without granules in their cytoplasm
- lymphocytes
- monocytes
- Three kinds of granulocytes
Gonadotropin-releasing hormone (GnRH)
GnRH is a peptide of 10 amino acids. Its secretion at the onset of puberty triggers sexual development.
Primary Effects
FSH and LH Relaese
Secondary Effects
Increases estrogen and progesterone (in females)
testosterone Relaese (in males)
Growth hormone-releasing hormone (GHRH)
GHRH is a mixture of two peptides, one containing 40 amino acids, the other 44. GHRH stimulates cells in the anterior lobe of the pituitary to secrete growth hormone (GH).
Corticotropin-releasing hormone (CRH)
CRH is a peptide of 41 amino acids. Its acts on cells in the anterior lobe of the pituitary to release adrenocorticotropic hormone (ACTH) CRH is also synthesized by the placenta and seems to determine the duration of pregnancy. It may also play a role in keeping the T cells of the mother from mounting an immune attack against the fetus
Somatostatin
Somatostatin is a mixture of two peptides, one of 14 amino acids, the other of 28. Somatostatin acts on the anterior lobe of the pituitary to
- inhibit the release of growth hormone (GH)
- inhibit the release of thyroid-stimulating hormone (TSH)
Somatostatin is also secreted by cells in the pancreas and in the intestine where it inhibits the secretion of a variety of other hormones.
Antidiuretic hormone (ADH) and Oxytocin
These peptides are released from the posterior lobe of the pituitary
Chemical Controls of Respiration
A. Chemoreceptors (CO2, O2, H+)
1. central chemoreceptors - located in the medulla
2. peripheral chemoreceptors - large vessels of neck
B. Carbon Dioxide Effects
1. a powerful chemical regulator of breathing by increasing H+ (lowering pH)
a. hypercapnia Carbon Dioxide increases ->
Carbonic Acid increases ->
pH of CSF decreases (higher H+)- >
DEPTH & RATE increase (hyperventilation)
b. hypocapnia - abnormally low Carbon Dioxide levels which can be produced by excessive hyperventilation; breathing into paper bag increases blood Carbon Dioxide levels
C. Oxygen Effects
1. aortic and carotid bodies - oxygen chemoreceptors
2. slight Ox decrease - modulate Carb Diox receptors
3. large Ox decrease - stimulate increase ventilation
4. hypoxic drive - chronic elevation of Carb Diox (due to disease) causes Oxygen levels to have greater effect on regulation of breathing
D. pH Effects (H+ ion)
1. acidosis - acid buildup (H+) in blood, leads to increased RATE and DEPTH (lactic acid)
E. Overview of Chemical Effects
Chemical Breathing Effect
increased Carbon Dioxide (more H+) increase
decreased Carbon Dioxide (less H+) decrease
slight decrease in Oxygen effect CO2 system
large decrease in Oxygen increase ventilation
decreased pH (more H+) increase
increased pH (less H+) decrease
Neural Substrates of Breathing
A. Medulla Respiratory Centers
Inspiratory Center (Dorsal Resp Group - rhythmic breathing) → phrenic nerve→ intercostal nerves→ diaphragm + external intercostals
Expiratory Center (Ventral Resp Group - forced expiration) → phrenic nerve → intercostal nerves → internal intercostals + abdominals (expiration)
1. eupnea - normal resting breath rate (12/minute)
2. drug overdose - causes suppression of Inspiratory Center
B. Pons Respiratory Centers
1. pneumotaxic center - slightly inhibits medulla, causes shorter, shallower, quicker breaths
2. apneustic center - stimulates the medulla, causes longer, deeper, slower breaths
C. Control of Breathing Rate & Depth
1. breathing rate - stimulation/inhibition of medulla
2. breathing depth - activation of inspiration muscles
3. Hering-Breuer Reflex - stretch of visceral pleura that lungs have expanded (vagal nerve)
D. Hypothalamic Control - emotion + pain to the medulla
E. Cortex Controls (Voluntary Breathing) - can override medulla as during singing and talking
Function of Blood
- transport through the body of
- oxygen and carbon dioxide
- food molecules (glucose, lipids, amino acids)
- ions (e.g., Na+, Ca2+, HCO3−)
- wastes (e.g., urea)
- hormones
- heat
- defense of the body against infections and other foreign materials. All the WBCs participate in these defenses