Dr.waleed mahaftha

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Renal transplant
Causes of chronic graft failure more than 6 monthschronic allograft nephropathyureteric obstruction recurrence of original renal disease MCGN more than IgA more than FSGS

Renal transplant
Managment of acute graft failure less than 6 monthsgive steroid ,if resestent use monoclonal antibodies

Renal transplant
Hyperacute graft rejectiondue to antibodies against donor HLA type 1antigensrarely seen due to matching

Renal transplant :
Graft failureacute rejectioncyclosporin toxicityATN of graftvascular thrombosisurine leakageUTI

Indication for urgent dialysissevere acidosispulmonary edema due to volume overloadhyperkalemiauremic pericarditis sever uremic symptoms
*Encephalopathy
*Vomiting

Physiology, Tidal Volume
Hallett S, Toro F, Ashurst JV.

Publication Details

Introduction
Tidal volume is the amount of air that moves in or out of the lungs with each respiratory cycle. It measures around 500 mL in an average healthy adult male and approximately 400 mL in a healthy female. It is a vital clinical parameter that allows for proper ventilation to take place. When a person breathes in, oxygen from the surrounding atmosphere enters the lungs. It then diffuses across the alveolar-capillary interface to reach arterial blood. At the same time, carbon dioxide continuously forms as long as metabolism takes place. Expiration occurs to expel carbon dioxide and prevent it from accumulating in the body. The volume of inspired and expired air that helps keep oxygen and carbon dioxide levels stable in the blood is what physiology refers to as tidal volume.[1]

Issues of Concern
Tidal volume is vital when it comes to setting the ventilator in critically ill patients. The goal is to deliver a tidal volume large enough to maintain adequate ventilation but small enough to prevent lung trauma. Initially, mechanical ventilation involved delivering tidal volumes of 10 mL/kg of ideal body weight or higher. The rationale was to reduce hypoxemia, prevent airway closure, and increase functional residual capacity. However, ventilation with large tidal volumes causes volutrauma due to alveolar overdistension and repetitive opening of collapsed alveoli. The result is the initiation of an inflammatory cascade characterized by increased lung permeability, pulmonary edema, alteration of surfactant, and production of cytokines that injure the lungs. It was not until 1974 that Webb and Tierney described this phenomenon, called volutrauma when they demonstrated pulmonary edema in rats after exposure to high inflation pressures. Lung injury during mechanical ventilation can be caused by ventilating with large tidal volumes in healthy lungs, though also with small tidal volumes in injured lungs.

Ventilation with large tidal volumes might as well cause barotrauma, a condition characterized by alveolar rupture and subsequent accumulation of air in the pleural cavity or the mediastinum. In mechanically ventilated patients, monitoring plateau pressure is a reliable way to predict the risk of barotrauma. Plateau pressure is the pressure imposed on the small airway and alveoli during mechanical ventilation. It mainly depends on compliance and tidal volume. As compliance decreases, plateau pressure increases, and so does the risk of barotrauma. Therefore, an increase in plateau pressure necessitates lowering the tidal volume to decrease the risk of alveolar rupture. Due to continuing research in lung-protective mechanical ventilation, using tidal volumes of 6 mL/kg of predicted body weight is the common practice nowadays.[2][3][4]

Organ Systems Involved
The lungs are responsible for delivering a tidal volume capable of maintaining adequate ventilation. However, producing precise tidal volumes relies on complex coordination between the respiratory center in the brain and the muscles of respiration. The respiratory pacemaker in the brainstem determines the rate and depth at which breathing occurs. In response to changes in blood oxygen and carbon dioxide levels, central and peripheral chemoreceptors send information to the brainstem to modulate the pacemaker's firing rate and pattern. The diaphragm, and other inspiratory muscles, respond by altering tidal volume and respiratory rate. The aim is to maintain adequate levels of oxygen and carbon dioxide in the blood. During exercise, for example, oxygen consumption increases, and carbon dioxide accumulates. As a result, respiratory rate and tidal volume rise to meet the increasing demand.[5]

Function
Functionally, the respiratory tract consists of the conducting airways, extending from the nose down to the terminal bronchioles, and the gas-exchanging airways, which extend from the respiratory bronchioles to the alveoli within the lungs. Dead space refers to the portions of the lungs that fill with air but do not participate in gas exchange. The primary determinant of dead space is the anatomical dead space, which refers to air in the conducting airways. Alveolar dead space, on the other hand, refers to alveoli that fill with air but do not participate in gas exchange. It constitutes a minor contributor to dead space. Together, the anatomical and alveolar dead space form the physiological dead space, which represents the total amount of air in the lungs that does not participate in gas exchange.

Tidal volume is essentially every breath a person takes. It is one of the main determinants of minute ventilation and alveolar ventilation. Minute ventilation, also known as total ventilation, is a measurement of the amount of air that enters the lungs per minute. It is the product of respiratory rate and tidal volume. Alveolar ventilation, on the other hand, takes physiological dead space into account. It represents the volume of air that reaches the respiratory zone per minute.

Minute ventilation = respiratory rate x tidal volume
Alveolar ventilation = respiratory rate x (tidal volume - dead space)
Since alveolar ventilation considers dead space, it represents actual ventilation. Generally, there is an equal contribution from tidal volume and respiratory rate to minute ventilation. In other words, doubling either of them produces the same increase in minute ventilation. When it comes to alveolar ventilation, though, increasing tidal volume is a more efficient way than increasing respiratory rate. As such, doubling tidal volume improves alveolar ventilation more than doubling the respiratory rate does. The concept proves relevant when it comes to patients with hypercapnia. Hypercapnia induces a breathing pattern characterized by a relatively larger increase in tidal volume than the respiratory rate to minimize dead space ventilation. In other terms, Hypercapnic patients compensate by taking slow, deep breaths to optimize CO2 elimination. The only way to minimize dead space ventilation is to increase the volume of air that reaches the respiratory zone, which can only be done by increasing tidal volume.[6]

Mechanism
Air moves in and out of the lungs through movements of the diaphragm and the chest wall. The diaphragm is the primary muscle of inspiration and is the one that contributes the most to tidal volumes. When the diaphragm contracts, the thoracic cavity expands vertically. As a result, intrapleural pressure decreases from -5 cm H2O to around -8 cm H2O. Since the lungs are connected to the chest wall via the pleura, the negative intrapleural pressure pulls the lungs towards the chest wall leading to an increase in lung volume. As lung volume increases, pressure decreases as per Boyle's law. The resulting sub-atmospheric intra-alveolar pressure then draws air into the alveoli based on the pressure difference. Once the pressure equalized, a tidal volume of approximately 500 mL is delivered.

In contrast, expiration is generally a passive process that occurs due to the lungs' elastic properties once the diaphragm relaxes. Relaxation of the diaphragm causes the rib cage to move closer to the lungs leading to an increase in intrapleural pressure back to -5 cm H2o. As a result, lung volume decreases, and pressure becomes higher than atmospheric pressure. This forces air out of the lungs as per pressure difference and the lungs get back to their resting state.

Tidal Volume During Sleep

Sleep alters respiratory physiology in various ways. REM sleep, in particular, is the sleep phase with the highest degree of breathing irregularity, both in frequency and respiratory rate. During REM, almost all body muscles, including respiratory muscles, become hypotonic, except for the diaphragm. Therefore, a person relies on the diaphragm to maintain an adequate tidal volume during REM. Additionally, respiratory response to hypoxic and hypercapnic stimuli decreases, not to mention the decreased central respiratory drive, which, along with accessory muscle paralysis, leads to a slight decrease in tidal volume and minute ventilation. The change is usually not prominent in healthy individuals but becomes prominent in patients with preexisting respiratory disease.[7]

Related Testing
Physiologically, lung volumes can be either dynamic or static. Dynamic lung volumes are, by definition, dependent on airflow rate. In contrast, static lung volumes are not affected by the flow velocity. A variety of lung pathologies induce changes in lung volumes. Therefore, pulmonary function testing provides valuable diagnostic information since it helps measure various lung volumes and capacities.

Spirometry is a crucial test used by pulmonologists to diagnose restrictive and obstructive pulmonary diseases. It measures how air flows in and out of the lungs and records several lung volumes and lung capacities. During spirometry, the patient takes a normal breath, followed by a full inhalation, a maximum forced exhalation, and then another normal tidal breath.

Tidal volume is a static lung volume that, along with other static and dynamic lung volumes, is important for the diagnosis of patients with obstructive and restrictive lung diseases. Spirometry records tidal volume while the patient breathes quietly. In healthy adults, it measures approximately 7 mL/kg of ideal body weight. In an average healthy adult, 500 mL enters the lung with each tidal breath, of which only 350 mL reaches the respiratory zone since dead space measures approximately 150 mL.[5]

Clinical Significance
Restrictive Lung Diseases

Restrictive lung diseases are a group of chronic pulmonary conditions characterized by the inability of the lungs to fully expand, owing to problems in the lungs themselves or the structures surrounding them. Interstitial lung diseases, such as idiopathic pulmonary fibrosis and asbestosis, cause progressive fibrosis of the lung tissue. As such, they represent an intrinsic lung pathology that leads to a restrive physiology due to increased stiffness and decreased compliance. Morbid obesity and sarcoidosis are examples of extrinsic problems that cause restriction by limiting chest wall expansion. In restrictive lung disease, the patient adapts a breathing pattern of rapid, shallow breaths to minimize the work of breathing.

Obstructive Lung Diseases

The hallmark of obstructive lung disease is difficulty expelling air out of the lungs due to progressive airway narrowing. Chronic obstructive pulmonary disease (COPD) and asthma are the two typical examples of obstructive lung disease. Asthma is a reversible condition characterized by airway hyperresponsiveness to various stimuli. It causes episodes of excessive mucous production, bronchoconstriction, and airway narrowing. On the other hand, COPD is an irreversible chronic inflammatory process that leads to a gradual reduction in the lumen of the conducting airways. As the condition progresses, air-trapping ensues, leading to lung hyperinflation. Since the problem in obstructive lung disease is expiratory, breathing with higher tidal volumes helps overcome airway resistance. Therefore, patients acquire a breathing pattern of deep, slow breaths to minimize the work of breathing.

Mechanical Ventilation

Acute respiratory distress syndrome, or ARDS, is a condition characterized by widespread inflammation of the lungs following an inciting pulmonary or extrapulmonary event. ARDS usually causes hypoxemic respiratory failure or critically low arterial oxygen tension necessitating mechanical ventilation. Patients with ARDS already have injured lungs, and mechanical ventilation should follow a lung-protective strategy. In other terms, tidal volumes should be kept as low as possible to prevent volutrauma and barotrauma. The problem in ARDS is that pulmonary edema and distal airway collapse decrease the surface area of the aerated lungs. Therefore, ventilation with large or even regular tidal volumes may cause hyperinflation of the healthy aerated portion of the lungs since air does not reach the already collapsed airways. As a result, alveolar overdistension and lung injury might occur. Generally, lung-protective strategies in patients with ARDS involve administering tidal volumes of approximately 6-8 mL/Kg of ideal body weight.[8][9]

Neuromuscular Disease

Neuromuscular diseases refer to a group of disorders characterized by progressive muscle weakness due to problems in the muscles themselves or the nerves that supply them. Patients with neuromuscular diseases (NMDs) eventually develop respiratory muscle weakness. The diaphragm is the primary muscle of inspiration and is the one most commonly affected in NMDs. Patients with a weak diaphragm rely on other muscles of inspiration, such as the external intercostals, to maintain adequate tidal volume. During REM sleep, there is generalized hypotonia of all respiratory muscles, except for the diaphragm, and a healthy person becomes diaphragm dependent. In patients with NMDs, dyspnea becomes prominent at night due to diaphragmatic weakness. Nocturnal REM-related hypoventilation is one of the earliest signs of respiratory muscle involvement in neuromuscular disease. As the disease progresses, daytime symptoms become prominent, and patients rely on a breathing pattern similar to the one seen in other restrictive lung diseases, i.e., shallow, rapid breathing.

Neural Tube Defect
Neural tube defects are birth defects of the brain, spine, or spinal cord. They happen in the first month of pregnancy, often before a woman even knows that she is pregnant. The two most common neural tube defects are spina bifida and anencephaly. In spina bifida, the fetal spinal column doesn't close completely. There is usually nerve damage that causes at least some paralysis of the legs. In anencephaly, most of the brain and skull do not develop. Babies with anencephaly are usually either stillborn or die shortly after birth. Another type of defect, Chiari malformation, causes the brain tissue to extend into the spinal canal.

The exact causes of neural tube defects aren't known. You're at greater risk of having an infant with a neural tube defect if you

Have obesity
Have poorly controlled diabetes
Take certain antiseizure medicines
Getting enough folic acid, a type of B vitamin, before and during pregnancy prevents most neural tube defects.

Neural tube defects are usually diagnosed before the infant is born, through lab or imaging tests. There is no cure for neural tube defects. The nerve damage and loss of function that are present at birth are usually permanent. However, a variety of treatments can sometimes prevent further damage and help with complications.

Brachial plexus lesions
1.Erb palsy
2.claw hand
3.wrist drop
4.winged scapula
5.deltoid paralysis
6.saturday night palsy
7.difficulty flexing elbow, variable sensory loss
8.decreased thumb function, Pope's blessing
9.intrinsic muscles of hand, claw hand
# El husseiny's

EFfect of exercise on cardiac output
-during the early stage of exercise ,cardiac output is maintained by increase Heart rate and stroke vokume
-during the late stage of exercise ,cardiac output is maintaned by increase Heart rate only
-diastole is preferentially shortened with increase Heart rate
mohamed

.Aging and atherosclerosis reduce aortic
compliance and the reduced stretch durind ejection means an increasedsystolic blood pressurethe most important factor determining diastolic blood pressure is the resistence of the arterioles

Atrial left to right shunts cause wide and fixed splitting of S2 and facilitate paradoxical embolism due to periods of transient shunt reversal (during straining or coughing )

# Delayed transfusion reaction occur 5_10 days post transfusion due to the development of red cell alloantibodies Clinical features :
Include unexplained pyrexia ,jaundice or unexplained drop in hemoglobin diagnosis:
Urinalysis shows urobilinogenuria and blood shows fragile ballooned spherocytes,diagnosis is confirmed by coombs test which is done by adding antihuman globulin (AHG)(anti-IgG and anticomplement )to the patient's washed RBCs.apositive test result in red cell agglutination.

.IgG antibodies cause delayed extravascular hemolytic transfusion reactions much more commonly than acute intravascular reaction .ABO antigens are present from birth ,whereas ABO antibodies are usually acquired in the first 6 months of life.