NEET MDS Lessons
Physiology
Ventilation simply means inhaling and exhaling of air from the atmospheric air into lungs and then exhaling it from the lung into the atmospheric air.
Air pressure gradient has to exist between two atmospheres to enable a gas to move from one atmosphere to an other.
During inspiration: the intrathoracic pressure has to be less than that of atmospheric pressure. This could be achieved by decreasing the intrathoracic pressure as follows:
Depending on Boyle`s law , the pressure of gas is inversely proportional to the volume of its container. So increasing the intrathoracic volume will decrease the intrathoracic pressure which will allow the atmospheric air to be inhaled (inspiration) . As decreasing the intrathoracic volume will increase the intrathoracic pressure and causes exhaling of air ( expiration)
So. Inspiration could be actively achieved by the contraction of inspiratory muscles : diaphragm and intercostal muscles. While relaxation of the mentioned muscles will passively cause expiration.
Contraction of diaphragm will pull the diaphragm down the abdominal cavity ( will move inferiorly) , and then increase the intrathoracic volume ( vertically) . Contraction of external intercostal muscle will pull the ribs upward and forward which will additionally increase the intrathoracic volume ( transversely , the net result will be increasing the intrathoracic volume and decreasing the intrathoracic pressure.
Relaxation of diaphragm will move it superiorly during expiration, the relaxation of external intercostal muscles will pull the ribs downward and backward , and the elastic lungs and chest wall will recoil. The net result is decreasing the intrathoracic volume and increasing intrathoracic pressure.
All of this occurs during quiet breathing. During forceful inspiration an accessory inspiratory muscle will be involved ( scaleni , sternocleidomastoid , and others) to increase negativity in the intrathoracic pressure more and more.
During forceful expiration the accessory expiratory muscles ( internal intercostal muscles and abdominal muscles ) will be involved to decrease the intrathoracic volume more and more and then to increase intrathoracic pressure more and more.
The pressure within the alveoli is called intralveolar pressure . Between the two phases of respiration it is equal to the atmospheric pressure. It is decreased during inspiration ( about 1 cm H2O ) and increased during expiration ( about +1 cm H2O ) . This difference allow entering of 0.5 L of air into the lungs.
Intrapleural pressure is the pressure of thin fluid between the two pleural layers . It is a slight negative pressure. At the beginning of inspiration it is about -5 cm H2O and reachs -7.5 cm H2O at the end or inspiration.
At the beginning of expiration the intrapleural pressure is -7.5 cm H2O and reaches -5 cmH2O at the end of expiration.
The difference between intralveolar pressure and intrapleural pressure is called transpulmonary pressure.
Factors , affecting ventilation :
Resistance : Gradual decreasing of the diameter of respiratory airway increase the resistance to air flow.
Compliance : means the ease , which the lungs expand.It depends on both the elastic forces of the lungs and the elastic forces , caused by the the surface tension of the fluid, lining the alveoli.
Surface tension: Molecules of water have tendency to attract each other on the surface of water adjacent to air. In alveoli the surface tension caused by the fluid in the inner surface of the alveoli may cause collapse of alveoli . The surface tension is decreased by the surfactant .
Surfactant is a mixture of phospholipids , proteins and ion m produced by type II pneumocytes.
Immature newborns may suffer from respiratory distress syndrome , due to lack of surfactant which is produced during the last trimester of pregnancy.
The elastic fibers of the thoracic wall also participate in lung compliance.
Clinical Physiology
Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .
To understand the pathophysiology of the heart failure , lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume
Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .
Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .
Contractility : Reducing the power of contraction such as in myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .
Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.
Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff .
The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .
HEART DISORDERS
- Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.
- Renin release (Juxtaglomerular cells) Kidney
- Converts Angiotensinogen => Angiotensin I
- In lungs Angiotensin I Converted => Angiotensin II
- Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)
- stimulates thirst
- stimulates adrenal cortex to release Aldosterone
(Sodium retention, potassium loss) - stimulates kidney directly to reabsorb Sodium
- releases ADH from Posterior Pituitary
- Myocardial Infarction
- Myocardial Cells die from lack of Oxygen
- Adjacent vessels (collateral) dilate to compensate
- Intracellular Enzymes leak from dying cells (Necrosis)
- Creatine Kinase CK (Creatine Phosphokinase) 3 forms
- One isoenzyme = exclusively Heart (MB)
- CK-MB blood levels found 2-5 hrs, peak in 24 hrs
- Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction
- Serum glutamic oxaloacetic transaminase (SGOT)
- Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
- SGOT returns to normal after 3-4 days
- Creatine Kinase CK (Creatine Phosphokinase) 3 forms
- Myocardium weakens = Decreased CO & SV (severe - death)
- Infarct heal by fibrous repair
- Hypertrophy of undamaged myocardial cells
- Increased contractility to restore normal CO
- Improved by exercise program
- Prognosis
- 10% uncomplicated recovery
- 20% Suddenly fatal
- Rest MI not fatal immediately, 15% will die from related causes
- Congenital heart disease (Affect oxygenation of blood)
- Septal defects
- Ductus arteriosus
- Valvular heart disease
- Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
- Regurgitation = cusps, retracted, Do not close, blood moves backwards
The Body Regulates pH in Several Ways
- Buffers are weak acid mixtures (such as bicarbonate/CO2) which minimize pH change
- Buffer is always a mixture of 2 compounds
- One compound takes up H ions if there are too many (H acceptor)
- The second compound releases H ions if there are not enough (H donor)
- The strength of a buffer is given by the buffer capacity
- Buffer capacity is proportional to the buffer concentration and to a parameter known as the pK
- Mouth bacteria produce acids which attack teeth, producing caries (cavities). People with low buffer capacities in their saliva have more caries than those with high buffer capacities.
- Buffer is always a mixture of 2 compounds
- CO2 gas (a potential acid) is eliminated by the lungs
- Other acids and bases are eliminated by the kidneys
Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .
To understand the pathophysiology of the heart failure , lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume
Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .
Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .
Contractility : Reducing the power of contraction such as in myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .
Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.
Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff .
The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .
Typical Concentration Gradients and Membrane Potentials in Excitable Cells
The Na Pump is Particularly Important in the Kidney and Brain
- All cells have Na pumps in their membranes, but some cells have more than others
- Over-all Na pump activity may account for a third of your resting energy expenditure!
- In the kidney the Na pump activity is very high because it is used to regulate body salt and water concentrations
- Kidneys use enormous amounts of energy: 0.5% of body weight, but use 7% of the oxygen supply
- Pump activity is also high in the brain because Na and K gradients are essential for nerves
- The brain is another high energy organ; it is 2% of body weight, but uses 18% of the oxygen supply
In the Resting State Potassium Controls the Membrane Potential of Most Cells
- Resting cells have more open K channels than other types
- More K+ passes through membrane than other ions- therefore K+ controls the potential
- Blood K+ must be closely controlled because small changes will produce large changes in the membrane potentials of cells
- Raising K will make the membrane potential less negative (depolarization)
- High blood K+ can cause the heart to stop beating (it goes into permanent contraction)
During an Action Potential Na Channels Open, and Na Controls the Membrane Potential
- Whichever ion has the most open channels controls the membrane potential
- Excitable cells have Na channels that open when stimulated
- When large numbers of these channels open Na controls the membrane potential
Functional Divisions of the Nervous System:
1) The Voluntary Nervous System - (ie. somatic division) control of willful control of effectors (skeletal muscles) and conscious perception. Mediates voluntary reflexes.
2) The Autonomic Nervous System - control of autonomic effectors - smooth muscles, cardiac muscle, glands. Responsible for "visceral" reflexes