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Showing posts with label physiology. Show all posts
Showing posts with label physiology. Show all posts

Types of Cerebellar nucleus its connection and function

There are four main cerebellar nuclei, which are clusters of neurons located in the deep cerebellar white matter. The four nuclei are:

The dentate nucleus: The dentate nucleus is the largest and most lateral of the cerebellar nuclei. It receives input from the neocerebellum, which is involved in the planning and execution of voluntary movements. The dentate nucleus sends output to the thalamus and then to the cerebral cortex, where it modulates the activity of the corticospinal tract, which is responsible for controlling voluntary movements.

The interposed nuclei: The interposed nuclei consist of the emboliform and globose nuclei. They receive input from the spinocerebellum and the neocerebellum and send output to the red nucleus and the thalamus. The interposed nuclei are involved in the regulation of muscle tone, the control of movement accuracy, and the coordination of multi-joint movements.

The fastigial nucleus: The fastigial nucleus is located in the midline of the cerebellum and receives input from the vestibulocerebellum and the spinocerebellum. The fastigial nucleus sends output to the vestibular nuclei and the reticular formation, which are involved in the regulation of posture and balance.

The vestibular nucleus: The vestibular nucleus is located in the brainstem and receives input from the vestibulocerebellum. The vestibular nucleus is involved in the regulation of balance, posture, and eye movements.

The cerebellar nuclei are connected to the cerebellar cortex and receive input from the different regions of the cerebellum. They integrate this input and send output to other regions of the brain, including the thalamus, red nucleus, and brainstem nuclei, which are involved in the regulation of movement, posture, and balance.

Overall, the cerebellar nuclei play a critical role in the regulation of movement, posture, and balance, and dysfunction of these nuclei can lead to a variety of neurological disorders, including ataxia, tremors, and gait disturbances.

Electrical activity- the action potential of the heart explained

Cardiac cells can contract without Nervous Stimulation.
  • Cardiac muscle, like skeletal muscle & neurons, is an excitable tissue with the ability to generate action potential.
  • Most cardiac muscle is contractile (99%), but about 1% of the myocardial cells are specialized to generate action potentials spontaneously. These cells are responsible for a unique property of the heart: its ability to contract without any outside signal.
  • The heart can contract without an outside signal since the signal for contraction is myogenic, that is these signals originating within the heart itself.
  • The heart contracts, or beats, rhythmically as a result of action potentials that it generates by itself, this  property of heart is called auto rhythmicity -auto means “self”.
  • Most important thing to understand is that the signal for myocardial contraction NOT comes from the nervous system but occur from the specialized myocardial cells also called auto rhythmic cells.
  • These cells are also called pacemaker cells of the heart as they set the rate of the heart beat. 
The cells of myocardium
Two specialized types of cardiac muscle cells:
Each of these 2 types of cells has a distinctive action potential.
They are
Contractile cells /working cell that include 99% of the cell
Myocardial Auto rhythmic cells (1%)  include 1% of cardiac cell
Myocardial Contractile cells
  • These cell constitute  99% of the cardiac muscle cells,
  • They do the mechanical work of pumping.
  • These cells normally do not initiate their own action potentials.
  • These cells contract and are also known as the Working Myocardium
  • Contractile cells which include most of the heart muscle Atrial muscle and Ventricular muscle
Myocardial Auto rhythmic cells
  • The small but extremely important remainder of the cardiac cells,include (1%) of cardiac cell
  • They  are specialized for initiating and conducting the action potentials responsible for contraction of the contractile cells.
  • They  do not contract because the cells are smaller and contain few contractile fibers or organelles. as they do not have organized sarcomeres, they do not contribute to the contractile force of the heart.
Action Potential of the Autorrythmic cardiac cells
  • The auto rhythmic cells do not have a stable resting membrane potential like the nerve and the skeletal muscles.
  • But  they have an unstable membrane potential that starts at – 60mv and slowly drifts upwards towards threshold.
  • Because the membrane potential never rests at a constant value, this  is called a Pacemaker Potential rather than a resting membrane potential. 
 What causes the membrane potentials of these cells to be unstable?
  • Auto rhythmic cells have  channels different from other excitable cells.
  • When cell membrane potential is at -60mv, channels are permeable to both Na and K ions .
  • This leads to Na influx and K efflux.
  • The net influx of positive charges slowly depolarizes the auto rhythmic cells.It will leads to opening of Calcium channels.
  • This moves the cell more towards threshold. When threshold is reached, many Calcium channels open leading to the Depolarization phase. 
Action potential of a contractile myocardial cell:a typical ventricular cell
Unlike the membranes of the autorrythmic cells, the membrane of the contractile cells remain essentially at rest at about -90mv until it is excited by electrical activity propagated by the pacemaker cells.
Depolarization
  • Opening of fast voltage-gated Na+ channels.
  • Rapid Influx of Sodium ions leading to rapid depolarization.
Small Repolarization
Opening of a subclass of Potassium channels which are fast channels.
Rapid Potassium Efflux.
Plateau phase
  • 250 msec duration (while it is only 1msec in neuron)
  • Opening of the L-type voltage-gated slow Calcium channels & Closure of the Fast K+  channels.
Large Calcium influx
K+ Efflux is very small as K+ permeability decreases & only few K channels are open.
Repolarization
Opening of the typical, slow, voltage-gated Potassium channels.
Closure of the L-type, voltage-gated Calcium channels.
Calcium Influx STOPS
Potassium Efflux takes place.
 Summary of Action Potential of a Myocardial Contractile Cell
  •  Depolarization= Sodium Influx
  • Rapid Repolarization= Potassium Efflux
  • Plateau= Calcium Influx
  • Repolarization= Potassium Efflux 




Ionic basis of action potential of autorrythmic cells

Phase 1: Pacemaker Potential:
Opening of voltage-gated Sodium channels called Funny channels  (If or f channels ).
Closure of voltage-gated Potassium channels.
Opening of Voltage-gated Transient-type Calcium (T-type Ca2+ channels) channels .
Phase 2: The Rising Phase or Depolarization:
Opening of Long-lasting voltage-gated Calcium channels (L-type Ca2+ channels).
Large influx of Calcium.
Phase 3: The Falling Phase or Repolarization:
Opening of voltage-gated Potassium channels
Closing of L-type Ca channels.
Potassium Efflux.

Physiology and autoregulation of cerebral circulation

Cerebral circulation  is very important and essential circulation
Why because if there is arrest of cerebral circulation
for more than 5 seconds it  causes loss of consciousness
Arrest for more than 3 min causes irreversible damage of the grey mater of the cortex of brain
 Cerebral Blood Vessels
2 internal carotid arteries (major source)
2 vertebral arteries join to form basilar artery
These arteries unit together forming the circle of Willis from which 6 cerebral arteries arise to supply the brain
There is no crossing of circulation from one side to the other as pressure is equal on both sides
functionally  these vessels are called end arteries .The cerebral arteries are connected together by pre-capillary anastomosis, but can't prevent cerebral infarction
Normal values
In normal adult the brain weights 1400 gm.
It receives 750 ml blood/min (14%of COP).             
In children CBF is double the adult value and it falls to the adult level at puberty.
Factors involved in regulation of CBF
Intrinsic and  extrinsic mechanism is involvedin  cerebral autoregulation
Intrinsic mechanisms 
Change in arterial blood pressure  ( Autoregulation of CBF)
Extrinsic mechanisms are the following
  • Nervous regulation
  • Chemical regulation
  • Mechanical regulation
Autoregulation of CBF
This  is the ability of brain to maintain its flow constant despite of changes in ABP.
Range of cerebral blood flow
Range of cerebral blood flow varies  from 70 to 150 mmHg.
In hypertensive patient this mechanism operates up to a blood pressure level of 180 mmHg
 Time :
It operates and restores the CBF to its normal basal level within 1-2 minutes of derangement
Mechanism of autoregulation of cerebral blood flow
1.Myogenic response
It is produced by the smooth musles response to stretch by contraction
Myogenic Mechanism
  • With increased ABP  stretch of the vascular wall  result in smooth musles contraction  vasoconstriction and decrease of  CBF  back to its normal  level.
  • With reduction in ABP the opposite occurs.
2. Metabolic response is the local changes in brain metabolites
  •  Increased ABP leads to:Local   increase in O2 tension  and  reduction of CO2 and  H+(hydrogen ion) will lead to cerebral vasoconstriction   and CBF back to its normal level.
  • On the other hand decreased ABP leads to: Local  decrease in O2 tension  and  increase in CO2 and  H+ (hydrogen) will result in  vasodilatation   of  cerebral vessels and  bring the CBF back to its normal level
3. Nervous Regulation of cerebral blood
It include both sympathetic and parasympathetic regulation
a) Sympathetic regulation:
The cerebral blood vessels receive sympathetic supply from the superior cervical ganglia
 i) Mild to moderate sympathetic stimulation results in cerebral vasoconstriction and  has little effect on the CBF as it is overcomed by the autoregulation mechanism
ii) In severe sympathetic stimulation (as in moderat to severe  exercise) there is strong vasoconstriction of large and medium sized arteries and  is very important to prevent the high pressure to reach the small cerebral vessels and  protect them from rupture (cerebral hemorrhage)
 b. Parasympathetic stimulation 
It has  no role in regulation of CBF
 4.Chemical Factors for cerebral autoregulation
Hypercapnia (↑CO2) and acidosis (↑H)  result in marked vasodilatation of the cerebral vessels and ↑ the CBF.
When the CO2 tension increase in the blood, it crosses the blood-brain barrier and combines with H2O to form H2CO3 which dissociates to HCO3 & H → H causes dilatation of the cerebral vessels (CO2 has no direct VD effect).
 5.Mechanical Factors of cerebral autoregulation
Blood viscosity-  when there is a reduction in  blood viscosity it increase  the CBF and vice versa.
The mean cerebral arterial and venous blood pressures:The CBF depends mainly on the difference between the arterial and venous pressures at the brain level, which is called the effective perfusion pressure.This means that, the CBF increaseses when the arterial pressure is ↑ed or venous pressures ↓ed, and vice versa. 
The intracranial pressure (ICT):The ICT is produced mainly by the cerebrospinal fluid (CSF) and normally this is about 11 mmHg.The effect starts to occur when the ICT rises to about 33 mmHg.Slight rise of ICT results in compression of cerebral  vessels slightly with slight reduction  of CBF.Marked rise of ICT (more than 33 mmHg), compresses the cerebral vessels with marked reduction of CBF
The intracranial pressure (ICT):In forced expiration with straining as in cough, defecation and labour, the mean venous pressure increases which increased ICT and the CBF  is decreased markedly  by,decrease in effective perfusion pressure.Compression on vesselsThis  protect the cerebral vessels from rupture (cerebral haemorrhage).
 (The cerebrospinal fluid (CSF) is the fluid which fills the ventricles of the brain and the subarachnoid space. Its volume is about 150 ml. CSF has almost the same constituents as the brain interstitial fluid)
Cushing Reflex
Cushing reflex is a physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia
Acceleration forces:
During acceleration of the body upwards against  gravity blood moves towards the feet and the ABP at the level of the head falls.  The venous pressure also decreases, consequently the ICT drops to maintain the CBF.
During acceleration downwards (-ve gravity)  Opposite occurs  

The key characteristics of cerebral circulation
  • Cerebral circulation is enclosed in a solid skull, so the brain tissue, blood and CSF volumes are kept constant at any time.
  • Brain tissue and CSF are incompressible while the blood vessels are compressible.So ↑ ICT affects mainly blood vessels and ↓CBF
  • Glucose is the major source of energy in the brain and sometimes amino acids during starvation.
  • Brain is very sensitive to hypoxia and hypoglycemia however, hypoxia is more serious:
  • Loss of consciousness if hypoxia is more than 5 sec.
  • Irreversible tissue damage if hypoxia is more than 3 min.



Characteristics of coronary circulation -explained

Key characteristics of  coronary circulation
  • Coronary circulation is very short , rapid, and  phasic .
  • Blood flow mainly occur during cardiac diastole
  • No efficient anastomoses between the coronary vessels.
  • It is a rich circulation (5% of the CO ,as heart wt is 300gm)
  • Regulation of coronary circulation is mainly by metabolites and not neural
  • Capillary permeability is high (the cardiac lymph is rich in protein)
  • Vessels are susceptible to degeneration and atherosclerosis.
  • Evident regional distribution of blood flow is noticed (subendocardial layer in LV receives < blood, due to compression (but normally compensated during diastoles by V.D).Hence it more prone to IHD+MI.
  • Eddy current keep the valves away from the orifices of arteries it keeps the orifices patent throughout the cardiac cycle.
  • As having highest O2 uptake achieved by a dense network of capillaries, all is perfused at rest (no capillary reserve)
The Coronary artery
  • Coronary artery represent the enlarged vasavasorum of larger vessels in the heart.
  • They are about the width of a drinking straw tht is 1/8 inch (4mm) .
  • The term Coronary comes from the latin word ”Coronarius= “Crown”. 
  • Coronary artery arises from the coronary sinuses just superior to the aortic valve behind the cusps
It has 3 cusps
  • Left coronary (LC), 
  • Right coronary (RC)
  • Posterior non-coronary(NC) cusps.  
The left coronary artery
Left coronary artery is about 10-15mm long
It arises from left coronary cusps
Left coronary artery almost immediately bifurcate into
1. left anterior descending
  • Diagonal Branch supply most of Anterior Left ventricular wall, A small part of  rightventricle
  • Septal perforating Branch supply anterior 2/3rd to interventricular septum
  • A part of the left branch of the AV bundle
  • Terminal branch supply the cardiac apex
2. Left circumflex artery.
The right coronary artery
Origin R anterior coronary sinus origin of Valsalva
It courses through the right AV groove
Branches ;
1. Conus branch
1st branch supplies the RVOT• Sinus node artery
2nd branch - SA node.(in 40% they originate from LCA)        
2.Acute marginal arteries-Arise at acute angle and runs along the margin of RV above the diaphragm. 3, Whole of the conducting system of the heart, except part of the left br of AV node
4. Posterior descending artery : Supply lower part of the ventricular septum & adjacent ventricular walls. Arises from RCA in 85% of case.
Branches of first and second segment of RCA
Branches of 1st Segment: 
  • Anterior Atrial Branch
  • Artery to SA node
  • Anterior Ventricular Brs
  • Right Marginal Artery
Branches of 2nd Segment
  • Posterior Ventricular branch
  • Posterior Interventricular branch
  • Posterior Interventricular (descending) Artery
  • Septal branch
  • AV nodal Artery
Venous drainage of heart
There are 2 systems:
There is superficial and deep venous system
Superficial system: which drains the left ventricle. It is formed of coronary sinus and anterior cardiac veins  which opens into the right atrium.
Deep system: It drains the rest of the heart. It is formed of the basian veins and arterio-sinusoidal vessels that open directly into the heart chamber.
Anastomotic channels
Between coronary arteries & extracardiac arteries there is intercoronary anastomosis
IN NORMAL HEART THERE ARE NO COMMUNICATIONS BETWEEN THE LARGE CORONARIES.
ANASTOMOSES DO EXIST AMONG THE SMALLER ARTERIES SIZED 20 TO 250 ยต m.
There is three common areas of anastomoses.
    1. Between branches of LAD & PIV OF RCA in iv groove
    2. Between LCX & RCA IN AV groove.
    3. Septal branches of 2 coronary arteries in the IVS
What is the Lifesaving value of collaterals in heart?
It there is occlusion in one of the larger coronary within seconds;
Dilatation n of small anastomoses( blood flow < ½)-normal or almost normal coronary (within 1 month).
Small branches of the LAD (left anterior descending/anterior interventricular) branch of the left coronary join with branches of the posterior interventricular branch of the right coronary in the interventricular groove. More superiorly, there is an anastomosis between the circumflex artery (a branch of the left coronary artery) and the right coronary artery in the atrioventricular groove. There is also an anastomosis between the septal branches of the two coronary arteries in the interventricular septum. The photograph shows area of heart supplied by the right and the left coronary arteries.


Features of pulmonary and systemic circulation

Features of pulmonary circulation
It is a low pressure system
Because it only needs to pump  blood to the top of the lungs.
If it is high pressure, then  following Starling forces, the fluid  would flood  the lungs.
Advantages of Pulmonary Circulation being a Low Resistance system
  • Accommodates more blood as a person shifts from the standing to the lying position.
  • High compliance allows the vessel to dilate in response to modest increase in Pulmonary arterial pressure.
  • Pulse pressure in the pulmonary circulation is rather low
Pressures in the pulmonary system
Right Ventricle:
Systolic= 25 mmHg
Diastolic= 0-1 mmHg,
Pulmonary artery:
Systolic= 25 mmHg
Diastolic= 8 mmHg
Mean Pulmonary arterial pressure= 15 mmHg.
Pulmonary Vein:
Averages about 5 mmHg
Pulmonary capillaries:
7 mm Hg
Left atrium:
Averages 2 mmHg
It is a low resistance system
  • Only 1/10th of the resistance of the systemic circulation
  • Arterioles have less smooth muscle, veins are wider & shorter& pulmonary vessel walls are thinner. 
Pulmonary vasculature has High compliance
  • Accommodates 5 L of blood  (same as the systemic circulation)
  • Accommodates shifts of blood more  quickly e.g. when a person shifts from  a standing to a lying position
Features of systemic circulation
Systemic circulation is a High pressure system
Because it needs to send blood to the brain even when standing & to the tip of en elevated fingertip.
Systemic circulation has High resistance
Because of increased smooth muscle in the  arterioles & the  metarterioles. 
Systemic circulation has Low compliance
Because of resistance  offered by the arterioles  and the metarterioles





Cardiac electrical activity –salient features

Cardiac cells can contract without Nervous Stimulation
  • Cardiac muscle, like skeletal muscle & neurons, is an excitable tissue with the ability to generate action potential.
  • Most cardiac muscle is contractile (99%), but about 1% of the myocardial cells are specialized to generate action potentials spontaneously. These cells are responsible for a unique property of the heart: its ability to contract without any outside signal.
  • The heart can contract without an outside signal because the signal for contraction is myogenic, originating within the heart muscle itself.
  • The heart contracts, or beats, rhythmically as a result of action potentials that it generates by itself, a property which is called auto rhythmicity (auto means “self”).
  • The signal for myocardial contraction comes NOT from the nervous system but it is from specialized myocardial cells also called auto rhythmic cells.
  • These specialised cells are also called pacemaker cells of heart because they set the rate of the heart beat. 
The myocardium
Two specialized types of cardiac muscle cells exist
Each of these 2 types of cells has a distinctive action potential.
Electrical Activity of the Heart
Myocardial Auto rhythmic cells (1%)
These cells are smaller and  they contain few contractile fibers or organelles. Because these cell do not have organized sarcomeres, they do not contribute to the contractile force of the heart.
Myocardial Contractile cells (99%) -Contractile cells include most of the heart muscle
  • Atrial muscle
  • Ventricular muscle
These cells contract and are also called as the working myocardium
Action Potential of the Autorrythmic cardiac cells
  • The auto rhythmic cells do not have a stable resting membrane potential like the nerve and the skeletal muscles.
  • Instead they have an unstable membrane potential that starts at – 60mv and slowly drifts upwards towards threshold.
  • Because the membrane potential never rests at a constant value, it is called a Pacemaker Potential rather than a resting membrane potential.
What causes the membrane potentials of these cells to be unstable?
  • Auto rhythmic cells contain channels different from other excitable cells.
  • When cell membrane potential is at -60mv, channels are permeable to both Na and K.
  • This will leads to Na influx and K efflux.
  • The net influx of positive charges slowly depolarizes the auto rhythmic cells. It will leads to opening of Calcium channels.
  • This moves the cell more towards threshold. When threshold is reached, many Calcium channels open leading to the Depolarization phase. 
Ionic basis of action potential of autorrythmic cells
Phase 1: Pacemaker Potential:
Opening of voltage-gated Sodium channels called Funny channels  (If or f channels ).
Closure of voltage-gated Potassium channels.
Opening of Voltage-gated Transient-type Calcium (T-type Ca2+ channels) channels .
Phase 2: The Rising Phase or Depolarization:
Opening of Long-lasting voltage-gated Calcium channels (L-type Ca2+ channels).
Large influx of Calcium.
Phase 3: The Falling Phase or Repolarization:
Opening of voltage-gated Potassium channels
Closing of L-type Ca channels.
Potassium Efflux.
Action potential of a contractile myocardial cell:a typical ventricular cell
Unlike the membranes of the autorrythmic cells, the membrane of the contractile cells remain essentially at rest at about -90mv until excited by electrical activity propagated by the pacemaker cells
Action potential of a contractile myocardial cell:a typical ventricular cell
Depolarization
  •   Opening of fast voltage-gated Na+ channels.
  •    Rapid Influx of Sodium ions leading to rapid depolarization.
Small Repolarization
  • Opening of a subclass of Potassium channels which are fast channels.
  • Rapid Potassium Efflux.
Plateau phase
  •  250 msec duration (while it is only 1msec in neuron)
  • Opening of the L-type voltage-gated slow Calcium channels & Closure of the Fast K+   channels.
  • Large Calcium influx
  • K+ Efflux is very small as K+ permeability decreases & only few K channels are open.
Repolarization
  • Opening of the typical, slow, voltage-gated Potassium channels.
  • Closure of the L-type, voltage-gated Calcium channels.
  • Calcium Influx STOPS
  • Potassium Efflux takes place.
Summary of Action Potential of a Myocardial Contractile Cell
  • Depolarization= Sodium Influx
  • Rapid Repolarization= Potassium Efflux
  • Plateau= Calcium Influx
  • Repolarization= Potassium Efflux


Conduction system of the heart Explained

The heart has a special conduction system for the following purpose
  • Generating  rhythmical electrical impulses to cause rhythmical contraction of the heart muscle.
  • Conducting these impulses rapidly through the heart.                      
What is Automaticity/Rhythmicity?
Automaticity means the ability of the cell to undergo depolarization spontaneously causing the production of electrical impulses.
Rhythmicity means that spontaneous depolarization occurs at regular intervals that is  in a rhythmic manner.
What is a Cardiac Impulse?
The action potential in the heart is called the cardiac impulse and like action potential in the nerve fibers it can travels.
What are the components of the Conductive System
  • SA node
  • Internodal pathways
  • A-V node
  • A-V bundle
  • Right and Left bundle  branches
SA node
SA node is called the pacemaker of the heart. Normally SA node is responsible for generating the cardiac electrical impulses that bring about the mechanical activity that is  contraction of the heart. 
SA node has the fastest rate of autorhythmicity.
Where is the location of the SA node?
  • SA node is a small, ellipsoid strip of specialized cardiac muscle about 3mm wide, 15 mm long, and 1mm thick. This is located in the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior venacava in to the right atrium.
  • SA nodal fibers are connected  directly with the atrial muscle fibers.
How the cardiac Impulse spread from SA node to Atrial muscle?
The cardiac impulse after it’s origin in the SA node spreads through out the atrial muscle through two routes
1.Ordinary Atrial muscle fibers
2. Specialized anterior, middle and posterior conducting bundles

  • Anterior internodal bundle of Bachman
  •  Middle internodal bundle of Wenkebach
  •  Posterior internodal bundle of Thoral    
                                                                
The inter nodal pathways
Specialized anterior, middle and posterior conducting bundles are called the internodal pathway that is given above.
  • These inter nodal pathways conduct the impulses at a faster rate than the ordinary atrial muscle fibers.
  • The cause of rapid conduction in these bundles is the presence of specialized conduction fibers.
  • These inter nodal pathways conduct the impulses at a faster rate than the ordinary atrial muscle fibers.
  • The cause of rapid conduction in these bundles is due to  the presence of specialized conduction fibers.
  • The velocity of conduction in most atrial muscle is about 0.3m/sec.
  • In the specialized internodal pathways the conduction velocity may reach upto 1m/sec.
  • The impulse after leaving SA node takes 0.03 sec to reach the AV node
The AV node
The AV node is located in the posterior wall of the right atrium immediately behind the tricuspid valve.
Cause of Slow Conduction in the A-V Node
The cause of slow conduction is mainly due to reduced  number of gap junctions between the successive cells in the conducting pathways. Becauses of this  there is great resistance to conduction of excitatory ions from one conducting fiber to the next.
What is the significance of AV nodal delay?
The cardiac impulse does not travel from the atria to the ventricles too rapidly.
This delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. This increases the efficiency of the pumping action of the heart.
It is primarily the AV node and it’s adjacent fibers that delay this transmission into the ventricles    
AV Bundle or Bundle of His
  • From the AV node arises a special conducting pathway named the bundle of His. Except for the very small part which penetrates through the AV fibrous tissue and has low conduction velocity, the bundle of His is made up of purkinje fibers which possess maximum conduction velocity in the heart
  • Purkinje fibers are very large fibers and they transmit action potentials at a velocity of 1.5 to 4.0 m/sec.
  • The rapid transmission of action potentials through the Purkinje fibers is believed to be caused by a very high level of permeability of gap junctions at the intercalated discs between the successive cells of Purkinje fibers.   
  • The rapid conduction through the purkinje fibers ensures that different parts of ventricles are excited almost simultaneously; this greatly increases the efficiency of heart as a pump
  • Normally the Bundle of His is the only conducting mass between the atrial and ventricular musculature and it transmits the cardiac impulses from the AV node to the ventricles.
Right and Left Bundle Branches
  • After penetrating the fibrous tissue between the atrial and ventricular muscle, the distal portion of the A-V bundle passes downward in the ventricular septum for 5 to 15 mm toward the apex of the heart.
  • Then the bundle of His splits into two branches which are called right and left bundle branches that lie on the respective sides of the ventricular septum
  • Each branch spreads downward toward the apex of the ventricle, progressively dividing into smaller branches.
  • These branches inturn course sidewise around each ventricular chamber and back toward the base of heart.
  • The ends of Purkinje fibers penetrate about one third of the way into muscle mass and finally become continuous with cardiac muscle fibers
  • From the time the cardiac impulse enters the bundle branches until it reaches the terminations of Purkinje fibers , the total elapsed time averages only 0.03 sec.
One- way Conduction through AV bundle
  • A special characteristic of the A-V bundle is it’s inability, except in the abnormal states , of action potentials to travel backward from the ventricles to the atria.
  • It will prevents re-entry of cardiac impulse by this route from the ventricles to the atria.
  • The atrial muscle is separated from the ventricular muscle by a continuous fibrous barrier that  acts as an insulator to prevent the passage of cardiac impulse between the atrial and ventricular muscle through any other route besides forward conduction through A-V bundle itself.  
Conduction in the Cardiac Muscle
  • Once the impulse reaches the ends of the Purkinje fibers it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. 
  • For transmission of the cardiac impulse from the endocardial surface to the epicardial surface recquires another 0.03 sec.
  • Thus the total time for transmission of cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about 0.06 sec
Conduction speed in Cardiac tissues

Hormones secreted by the pituitary gland

This include hormone secreted by adenohypophysis (anterior pituitary)and neurohypophysis (posterior pituitary)
Hormone secreted by the adenohypophysis (anterior pituitary)
1.Thyroid stimulating hormone (TSH)
Triggers the release of thyroid hormones
Thyrotropin releasing hormone promotes the release of TSH
2.Adrenocorticotropic hormone (ACTH)

Stimulates the release of glucocorticoids by the adrenal gland
Corticotrophin releasing hormone causes the secretion of ACTH
3.Follicle stimulating hormone (FSH)
Stimulates follicle development and estrogen secretion in females and sperm production in males
4.Leutinizing hormone (LH)
Causes ovulation and progestin production in females and androgen production in males
Gonadotropin releasing hormone (GNRH) promotes the secretion of FSH and LH
5.Prolactin (PH)
Stimulates the development of mammary glands and milk production
6.Growth hormone (GH or somatotropin)
Stimulates cell growth and replication through release of somatomedins or IGF
Secretion is controlled by Growth-hormone releasing hormone  (GH-RH) and Growth-hormone inhibiting hormone  (GH-IH)
7.Melanocyte stimulating hormone (MSH)
May be secreted by the pars intermedia during fetal development, early childhood, pregnancy or certain diseases
Stimulates melanocytes to produce melanin
The hormones secreted by posterior lobe of the pituitary gland (neurohypophysis)
Posterior pituitary contains axons of hypothalamic nerves
8.ADH
Neurons of the supraoptic nucleus manufacture antidiuretic hormone (ADH) 
Decreases the amount of water lost at the kidneys
Elevates blood pressure
9.Oxytocin
Neurons of the paraventricular nucleus manufacture oxytocin
Stimulates contractile cells in mammary glands
Stimulates smooth muscle cells in uterus

Mechanical events of the cardiac cycle

The cardiac cycle
The cardiac events occur from the beginning of one heart beat to the beginning of next heart beat.
It is initiated by spontaneous generation of action potential in SA (sinoatrial ) node.
Duration of one cardiac cycle is O.8 seconds.
Ventricular filling occur during  diastole.


Mechanical events of the  cardiac cycle
1.Atrial systole
2.Atrial diastole
3.Ventricular systole .
Isovolumetric contraction
Rapid ejection
Reduced ejection
4.Ventricular diastole
Proto diastole
Isovolumetric ventricular relaxation
Earlier rapid filling
Reduced filling
Last rapid filling due to atrial systole

Atrial systole
It follows the impulse generation in SA node and atrial depolarisation.
When the atrial muscle contracts, pressure in atria increases.
30% of blood is propelled into ventricle.
Narrowing of opening of SVC and IVC and pulmonary veins occur

Ventricular systole
Isovolumetric  contraction
In isovolumetric  contraction ventricular pressure  exceed  atrial pressure closure of AV valves occur producing first heart sound.
Opening of aortic valve occur when leftventricular pressure is > 8OmmHg.
Opening of pulmonary valve is seen when right ventricular pressure > 10 mmHg.
This will result in small rise in atrial pressure.
Rapid ejection
After opening of the aortic and pulmonary valves, ventricular ejection begins.
Intraventricular pressure rises to a maximum of 120 mmHg in left ventricle and 25mmHg in right ventricle.
2/3rd stroke volume is ejected during this phase.
Reduced ejection phase
Ventricular pressure decreases during this phase.
Arterial pressure increases.

Ventricular diastole
1.Protodiastole 
At the end of ventricular systole, ventricular pressure falls, arterial pressure is more than  pressure inside the ventricle resulting in closure of semilunar valves which produce second heart sound.
2.Isovolumetric ventricular relaxation
Ventricular pressure drop rapidly in this phase ,the ventricular muscle relax without change in ventricular volume.
This phase ends when ventricular pressure drops below atrial pressure resulting in opening of AV valves.
3.Phase of earlier rapid filling
Rapid filling of ventricles occur.
Pressure inside the ventricles remains low.
4.Phase of reduced filling
Filling of ventricles is due to continous venous return filling  both atria and ventricle.
70% ventricular filling.
5.Last rapid filling
Corresponds to atrial systole.
30% filling occur in this phase.

Atrial diastole
Atrial muscle relax and atrial pressure increase gradualy due to continous venous return.
After the opening of atrioventricular valves pressure drops to zero and again slowly rises until the next atrial systole.

Functions of liver and different liver function tests

Major functions of Liver are the following

  1. Blood glucose regulation
  2. Synthesis of glycogen
  3. Synthesis of triacyl glycerol
  4. Synthesis of plasma proteins
  5. Detoxification
  6. Bile production, helps in digestion
  7. Bilirubin metabolism

Biochemical test are done to assess the following
The hepatic function 
To detect hepatic injury
Patterns of abnormalities are more important than single test
May be normal in proven liver disease
Normal value never rules out liver Disease

Classification of liver function test based on laboratory findings
Hepatic excretory function is assessed with following tests
Serum Bilirubin
Urine: Bile Pigments, bile salt, urobilinogen
Liver enzymes
ALT,AST,ALP,GGT,5’ nucleotidase

Synthetic Function
Total Proteins
Serum albumin, globulins
Prothrombin time

Special Test
Ceruloplasmin
Ferritin
Alpha1 antitrypsin
Alpha fetoProteins
Classification of liver function  based on clinical aspects
Markers of liver dysfunction
Serum Bilirubin
Urine: Bile pigments, bile salt, urobilinogen
Total proteins, albumin
Prothrombin time
Blood ammonia

Markers of hepato cellular Injury
ALT,AST
Markers of cholestasis
ALP
GGT
5’ Nucleotidase 

How to measure Jugular venous pulse (JVP)

Objectives of examination of JVP 
Estimation of jugular venous pressure.
Assessment of wave forms.
Most important bedside test for assessment of volume status.
Assessment of waves give important clues regarding certain conditions.

Internal jugular vein  is preferred because 
It has no valves.
It is in direct line with S uperior vena cava  and right atrium.
Not passing through facial planes, unlikely to be compressed by other structures.
Usually best felt when patient’s trunk is inclined by less than 30.
If pressure is very high, better in sitting position.
If volume depleted, supine is better.

If increased pressure is suspected and pulsations not obtained, make the patient to sit up by the legs dangling over the side of bed. 
Surrogate marker of right sided pressure.
Distance between centre of right atrium and sternal ankle varies in many individuals.
At 40 degree, varies between 6-15cm.
Pulsation above clavicle at sitting position is usually abnormal.
Distance between right atrium  to clavicle is at least 10cm.
Estimation of an elevated pressure is important rather than the exact value.

Origin and spread of cardiac Impulse

Cardiac impulse originate in SAnode then reach the AV node there is AV nodal delay SAN - AVN -Delay Conduction in the ventricle Depolarization - Start - Left side of interventricular Septum Moves to the right Spreads down to the apex Returns along the ventricular wall to the AV groove Last part of Depolarization: Posterobasal portion of the Lt.Ventricle, Pulmonary Conus, Upper most portion of the Septum.
Different cardiac rhythms Sinus rhythm is normal Nodal rhythm Idio ventricular rhythm Normal pacemaker SAnode Abnormal pacemaker (ectopic pacemaker) A pacemaker elsewhere than the sinus node. They produce arrhythmia Common abnormal pacemaker: AV node or Purkinje fibers Atrial or ventricular muscle.

Blood flow to heart during systole & diastole

During systole the heart muscle contracts, it compresses the coronary arteries so blood flow is less to the left ventricle during systole and more during diastole.
Blood flow to the subendocardial portion of Left ventricle occurs only during diastole
Due to lack of blood flow to subendocardial surface of left ventricle during systole this region is prone to ischemic damage and it is the most common site of Myocardial infarction.
Coronary blood flow to the right side of heart is not much affected during systole.
Reason-The Pressure difference between aorta and right ventricle is greater during systole than during diastole so more blood flow to right ventricle occurs during systole.

Effect of Tachycardia on coronary blood flow
When heart rate increases,the period of diastole is shortened therefore coronary blood flow is reduced to heart during tachycardia
Other causes of decreased blood flow to left ventricle
   1-Aortic stenosis
Reason-In aortic stenosis the left ventricle pressure is very high during systole thus, it compresses the coronary arteries more.
  2-When aortic diastolic pressure is low,the coronary blood flow is decreased

The accommodation or near reflex


Accomodation reflex involve a triad of changes when a person looks at a nearby object.
1. Convergence of eye due to contraction of medial and lateral rectus muscle
2. Miosis -constriction of pupils due to constrictor pupillae  muscle contraction.
3. Accomodation is associated with increased refractive power of the lens.This is due to the contraction of ciliaris muscle.

Pathway of accommodation
1. Afferent impulses from retina pass along the normal visual pathway to reach the visual areas in the occipital lobe
2. From the visual areas fibers descend to the oculomotor (3rd cranial nerve) nucleus of both side in the midbrain.
3. Efferent fibers pass along the 3 rd cranial nerve to the eye to supply the following muscle
  Medial rectus muscle
  Constrictor pupillae muscle 
  Ciliaris musle
In accommodation reflex the fibers reach the lateral geniculate body and the occipital cortex but they donot pass through the pretectal nucleus situated in midbrain.

Method of testing accommodation reflex
The patient is asked to look at a distant object and then at the examiners finger which is gradually brought within 5cm of the eyes.When the gaze is directed from a distant object to near one contraction of medial rectus brings about a convergence of of the ocular axis and along with this accommodation occurs by the contraction of ciliaris muscle and pupil constrict  as a part of associated movement .

Significance  of accommodation reflex
Accomodation reflex is absent in 
      Diphtheria
      Encephalitis
      Reverse Argyll Robertsons pupil
      Parkinsonism