1. PATHOPHYSIOLOGY OF THE CONDUCTION SYSTEM


2. Cardiac arrhythmias = deviation from normal rate, rhythm

    

   1. Heart block (types) = conduction system damage
      1. Complete Heart Block = 3rd degree block
         1. idioventricular beat (35-45/min)
         2. Atria at normal sinus rhythm
         3. Periods of asystole (dizziness, fainting)
         4. Causes = myocardial infarction of ventricular septum, surgical correction of interseptal defects, drugs
      2. Incomplete Heart Block = 2nd degree block
         1. Not all atrial beats reach ventricle
         2. Ventricular beat every 2nd, 3rd, etc. atrial beat, (2:1 block, 3:1 block)
      3. Incomplete Heart Block = 1st degree block
         1. All atrial beats reach ventricle
         2. PR interval abnormally long = slower conduction
      4. Bundle branch blocks (right or left)
         1. Impulses travel down one side and cross over
         2. Ventricular rate normal, QRS prolonged or abnormal
   2. Fibrillation
      1. Asynchronous contractions = twitching movements
      2. Loss of synchrony = little to No output
      3. Atrial Fibrillation
         1. Irregular ventricular beat & depressed pumping efficiency
         2. Atrial beat = 125 - 150/min, pulse feeble = 60 - 70/min
         3. Treatment = Digitalis - reduces rate of ventricular contraction, reduces pulse deficit
      4. Ventricular Fibrillation
         1. Almost no blood pumped to systemic system
         2. ECG = extremely bizarre
         3. Several minutes = fatal
         4. Treatment = defibrillation, cardiac massage can maintain some cardiac output

Carbon Dioxide Transport

Carbon dioxide (CO₂) combines with water forming carbonic acid, which dissociates into a hydrogen ion (H⁺) and a bicarbonate ions:

CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻

95% of the CO₂ generated in the tissues is carried in the red blood cells:

• It probably enters (and leaves) the cell by diffusing through transmembrane channels in the plasma membrane. (One of the proteins that forms the channel is the D antigen that is the most important factor in the Rh system of blood groups.)
• Once inside, about one-half of the CO₂ is directly bound to hemoglobin (at a site different from the one that binds oxygen).
• The rest is converted — following the equation above — by the enzyme carbonic anhydrase into
  • bicarbonate ions that diffuse back out into the plasma and
  • hydrogen ions (H⁺) that bind to the protein portion of the hemoglobin (thus having no effect on pH).

Only about 5% of the CO₂ generated in the tissues dissolves directly in the plasma. (A good thing, too: if all the CO₂ we make were carried this way, the pH of the blood would drop from its normal 7.4 to an instantly-fatal 4.5!)

When the red cells reach the lungs, these reactions are reversed and CO₂ is released to the air of the alveoli.

Cystic Fibrosis
→ Thick mucus coagulates in ducts, produces obstruction, Too thick for cilia to move
 
→ Major Systems Affected: Respiratory System, G. I. Tract,Reproductive Tract

→ Inherited, autosomal recessive gene, most common fatal genetic disorder

→    Major characteristic, Altered electrolyte composition (Saliva & sweat Na+, K+, Cl-)

→    Family history of Cystic Fibrosis
→    Respiratory Infections & G.I.Tract malabsorption
→    Predisposes lung to Secondary infection (Staphylococcus, Pseudomonas)
→    Damages Respiratory Bronchioles and Alveolar ducts, Produces Fibrosis of Lungs, Large cystic dilations)

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.

Asthma = Reversible Bronchioconstruction 4%-5% of population
    Extrinsic / Atopic = Allergic, inherited (familia), chromosome 11
    IgE, Chemical Mediators of inflammation
    
a.    Intrinsic = Negative for Allergy, Normal IgE, Negative Allergic Tests

    Nucleotide Imbalance cAMP/cGMP: cAMP = Inhibits mediator release, cGMP = Facilitates mediator release
b.    Intolerance to Asprin (Triad Asthma)
c.    Nasal Polyps & Asthma

d.    Treatment cause, Symptoms in Acute Asthma
    1.    Bronchial dilators
    2.    steroids edema from Inflamation
    3.    Bronchiohygene to prevent Secondary Infection, (Remove Excess Mucus)
    4.    Education

Cardiac Control: The Cardiac Center in the medulla.

Outputs:

The cardioacceleratory center sends impulses through the sympathetic nervous system in the cardiac nerves. These fibers innervate the SA node and AV node and the ventricular myocardium. Effects on the SA and AV nodes are an increase in depolarization rate by reducing the resting membrane polarization. Effect on the myocardium is to increase contractility thus increasing force and therefore volume of contraction. Sympathetic stimulation increases both rate and volume of the heart.

The cardioinhibitory center sends impulses through the parasympathetic division, the vagus nerve, to the SA and AV nodes, but only sparingly to the atrial myocardium, and not at all to ventricular myocardium. Its effect is to slow the rate of depolarization by increasing the resting potential, i.e. hyperpolarization.

The parasympathetic division controls the heart at rest, keeping its rhythm slow and regular. This is referred to as normal vagal tone. Parasympathetic effects are inhibited and the sympathetic division exerts its effects during stress, i.e. exercise, emotions, "fight or flight" response, and temperature.

Inputs to the Cardiac Center:

Baroreceptors in the aortic and carotid sinuses. The baroreceptor reflex is responsible for the moment to moment maintenance of normal blood pressure.

Higher brain (hypothalamus): stimulates the center in response to exercise, emotions, "fight or flight", temperature.

Intrinsic Controls of the Heart:

Right Heart Reflex - Pressoreceptors (stretch receptors) in the right atrium respond to stretch due to increased venous return. The reflex acts through a short neural circuit to stimulate the sympathetic nervous system resulting in increased rate and force of contraction. This regulates output to input

The Frank-Starling Law - (Starling's Law of the Heart) - Like skeletal muscle the myocardium has a length tension curve which results in an optimum level of stretch producing the maximum force of contraction. A healthy heart normally operates at a stretch less than this optimum level and when exercise causes increased venous return and increased stretch of the myocardium, the result is increased force of contraction to automatically pump the increased volume out of the heart. I.e. the heart automatically compensates its output to its input.

An important relationship in cardiac output is this one:

Blood Flow =  D Pressure / Resistance to Blood Flow