The Transport System

1. The Cardiac Cycle- one complete sequence of pumping and filling

A. Note: *Systole=contraction *Diastole=relaxation *Average cycle= 0.8 seconds (pulse of 65-75 bpm) *7/8ths of the time atria are relaxed and filling with blood from veins. 1. Pulse- pressure wave created by alternating expansion and recoiling of an artery that occurs with each beat of the left ventricle -Influenced by: 1. level of activity 2. emotions 3. changes in posture 2. Blood pressure- pressure blood exerts against the inner walls of the blood vessel -Influenced by: 1. chemicals 2. diet 3. temperature 4. neural factors (fear) 5. renal factors B. Steps 1. Atrial systole, Relaxation phase (diastole) -lasts 0.4 seconds -Blood returning from large veins flows into aria and ventricles. -ventricles 70% full 2. Ventricular systole, Atria contract (atrial systole) -lasts 0.1 seconds -blood forced into ventricles -ventricles now 100% full 3. Atrial Diastole, Ventricles contract (ventricular systole) -lasts 0.3 seconds -forcing blood forced into large arteries. C. Cardiac output =volume of blood per minute that flowed from ventricle pumps into the systemic circuit *Can increase 5x during heavy exercise *Depends on two factors: 1. Rate of contraction 2. Stroke volume =amount of blood pumped by left ventricle in each contraction -average is 75ml, with heart rate of 70 bpm and cardiac output of 5.25 L/minute -Equivalent to total volume of blood in human body

2. Pressure: Atria, Ventricles, and Aorta

A. Atria -Pressure greatest during contraction (atrial systole) -Immediately before ventricular contraction when semilunar valves are closed and AV valves open B. Ventricles -Pressure greatest during contraction (ventricular systole) *closes AV valves *opens aortic semilunar valve C. Aorta -Pressure greatest during VENTRICULAR contraction (ventricular systole)

3. Volume: Atria, Ventricles, and Aorta

A. Atria -Volume greatest immediately before contraction (atrial systole) B. Ventricles -Volume greatest during filling (relaxed, diastole) -AV valves open -Volume lowest during contraction (systole) *AV valves closed *Aortic valve open -At rest=70% -Atria contract=30% added C. Aorta -Volume greatest when ventricles contract (ventricular systole)

4. Electrocardiogram
-Graphs electrical conduction in the heart during: *the stimulus for ventricular contraction *repriming the ventricles

-P wave- caused by atrial systole -QRS wave- caused by ventricular systole -T wave coincides with ventricular diastole

5. Heart Sounds
=closing of the valves 1. First heart sound=recoil of blood against the closed AV valves (tricuspid/bicuspid). -The valves and heart walls vibrate -ventricular systole 2. Second heart sound=recoil of blood against the closed semilunar valves -atrial and ventricular diastole, everything is relaxed -Tools: A. Stethoscope B. Phonocardiogram -shows where the sounds are made during the cardiac cycle

6. Control of The Heartbeat and Conduction System of The Heart

*The ability of cardiac muscle to contract is intrinsic -its a property of the heart itself and doesnt depend on extrinsic nerve impulses(myogenic heart) *Activity depends on 2 factors: 1. The nerves of the involuntary nervous (autonomic) which can act as brakes or accelerators. 2. The intrinsic conduction system or nodal system that is built into the heart tissue.

Nodal System of Conduction

A. Consists of specialized muscle tissue but is noncontractile -Cardiac cells that initiate and distribute impulses throughout the heart so that the myocardium contracts in an orderly sequence. B. Nerves and hormones can transmit messages to the pacemaker -One nerve carries messages from the brain to the pacemaker to speed up beating -Second nerve carries messages from the brain to slow down contractions C. Adrenaline -tells the pacemaker to increase the beating of the heart -carried to the pacemaker in the blood

Nodes
1. Pacemaker or Sinoatrial (SA) Node -area that initiates each heartbeat -Generates electrical impulses. -Spread rapidly through walls of the atria, making them contract in unison because cardiac muscle cells are electrically coupled through gap junctions. 2. Atrioventricular (AV) Node *relay point *in the wall between the right atrium and right ventricle *signals delayed for about 0.1 second when atria empty into the ventricles

7. Specialized muscle fibers

*Bundle branches and Purkinje fibers -Conduct the signals to the apex of the heart and throughout the ventricular wall -signals trigger wave of powerful contractions of both ventricles from apex toward atria, driving blood into large arteries

8. Cardiovascular Disease: Disease of the Heart and Blood Vessels

1. Heart Attack (myocardial infarction) =death of cardiac muscle caused by prolonged blockage of one or more coronary arteries (supply oxygen-rich blood to the heart) -patches of dead cells, blood has to go around 2. Stroke =death of nervous tissue in the brain caused by rupture or blockage of arteries in the head 3. Thrombus =clot that can clog an artery *may form in : 1. a coronary artery (heart attack/myocardial infarction) 2. an artery in the brain (stroke) 3. somewhere else in the circulatory system and reach the heart, brain, or lungs via the blood stream *this transported clot = embolus -can become lodged in an artery too small for the clot to pass -blocks blood flow -can form anywhere -shouldnt sit in one place for two long, in danger of having blood pool and form deep-vein clots 4. Atherosclerosis =narrowing of the arteries -chronic cardiovascular disease of the arteries which leads to 3 previous diseases: heart attack, stoke, thrombus

*this lining should be smooth and can be damaged as a result of: a) untreated high blood pressure (hypertension) b) smoking- will irritate and damage the lining c) diet rich in animal fat d) abnormally high concentration of cholesterol in the blood *results in plaque =narrowed areas, buildup of lipids like cholesterol *phagocytes release growth factors at the damaged site of all connective tissues -stimulate the muscle and fibrous tissue in the artery wall to thicken and become infiltrated with circulating, low-density lipids (cholesterol) *calcium deposits can harden plaque, causing in arteriosclerosis (hardening of the arteries) -no longer as expansive -no recoiling, -no contracting -only cure is Ornish diet, almost all vegetarian, protein=condiment, high fiber *arteries become narrowed, embolus likely to become trapped *common sites of thrombus formation

Risk Factors
1. Increasing age: old age leads to less flexible blood vessels 2. Being male: estrogen is protective for women until menopause 3. Obesity: strains the heart 4. Physical inactivity: correlated with obesity 5. Diet *High salt-increases blood pressure *Excessive alcohol-stresses cardiovascular system *Increased levels of low density lipoproteins (LDL), increased levels of triglycerides (fats) in the blood -also could be from genetic factors *Trans. fat and sat. fat intake: positively correlated. -casual link substantiated with trans fat but not sat. fat. *cholesterol intake (check book) 6. Having a parent (or other close relative) who suffered a coronary at an early age (heredity/genetic factors) -hypercholesterolemia -dominant gene -cant avoid it, all you can do is minimize risks -untreatable, not even anticholesterol meds 7. Hypertension: damages blood vessels 8. Smoking: raises blood pressure because nicotine causes vasoconstriction -also damages blood vessels 9. Stress 10. Negative correlation-promotes heart health: cis-unsaturated fatty acid intake (olive oil, oily fish like salmon).

Ventilation: create negative pressure and draw air inside; everything diffuses passively
1. Partial Pressure
A. Atmospheric pressure =downward force exerted by air on the earths surface -at sea level, equivalent to force of a column of mercury at 760mmHg high B. Partial pressure of oxygen =0.21 x 760mm = 160 mmHg. -atmosphere is 21% oxygen by volume -portion of atmospheric pressure contributed by oxygen C. Partial pressure of CO2 -CO2 carried: 1.) dissolved in plasma (7%) 2.) bicarbonate ions (70%) 3.) as carbaminohemoglobin (25%) -at sea level, 0.23 mmHg -CO2 in blood is temporarily converted to carbonic acid -catalyzed by carbonic anhydrase =enzyme in red blood cells -dissociates (ionizes) into H+ ions and bicarbonate ions -as H ions increase, pH decreases -many of the H+ combine with hb or other plasma protein buffers -pH buffering system to keep you from dropping dead when exercising -as bicarbonate ions accumulate inside the RBC, some of them diffuse into the plasma, down their concentration gradient (facilitative diffusion)

2. Dissolved Gasses
-proportional to: -their partial pressure in the air -their solubility in water -Diffusion -from region of higher partial pressure to low partial pressure ex. Blood arriving at lungs has lower PO2 and higher PCO2 than air in alveoli -diffusion of gases in tissues works the same way -oxygen transport -at normal body temperature (98.6 degrees F, 37 degrees C) and air pressure, only 4.5 ml of oxygen can dissolve into a liter of blood -during exercise, a person can consume almost 2L oxygen per minute leading to a need for 500 L of blood to be pumped per minute, unrealistic (you only have 6-8 L in you) -respiratory pigments -special proteins bound to transported oxygen in most animals, instead of dissolved in solution -2 types 1) hemoglobin (4 polypeptide chains) -4 subunits, each with cofactor called heme group -each heme group has an iron atom at its center -each hemoglobin can carry 4 molucules of O2. -must bind oxygen reversibly, loading oxygen in lungs and unloading in other parts of the body -most oxygen in your body attached to hemoglobin 2) myoglobin (1 polypeptide chain) -Peer pressure among O2 molecules -cooperativity in subunits =binding of oxygen to one subunit so that their affinity for oxygen increases -when one subunit unloads its oxygen, the other three follow quickly because of a conformation change that lowers their affinity for oxygen

2. Oxygen Transport 3. Oxygen Dissociation Curve

-show relationship between % saturation of hemoglobin and partial pressure of oxygen 1. Normal conditions: a) when pO2 is high, hemoglobin binds with large amounts of oxygen and is almost fully saturated b) when pO2 is low, hemoglobin is only partially saturated and oxygen is released from hemoglobin c) therefore in pulmonary capillaries a lot of oxygen binds with hb but in tissue capillaries where the p02 is lower, hb does not hold as much oxygen and the oxygen is released for diffusion into tissue cells. d) note that at a pO2 of 40 mmHg, the average p02 of tissue cells at rest only 25% of the available oxygen splits from hb and is used (big reserve of oxygen) e)several other factors influence the affinity of hb for oxygen, the strength of the hb-02 binding. Keep in mind that metabolically active cells need oxygen and produce: 1) acids 2) CO2

3) heat 2. Effects of Acidity -Bohr Effect -in an acid environment, hemoglobins affinity for oxygen is lower and oxygen splits more readily from hemoglobin -when H+ ions bind to certain amino acids in Hb, they alter its structure and decrease its oxygen-carrying capacity this makes more O2 available for tissue cells 3. Temperature -as temperature increases, so does the amount of ocygen released from hemoglobin. -temperature rises as a result of activity and infection 4. Fetal hemoglobin -fetal hemoglobin differs from adult hemoglobin in structure and in affinity for oxygen -so when pO2 is low, fetal Hb can carry up to 30% more oxygen -as maternal blood enters the placenta, ocygen is readily transferred to fetal blood. -this is good because oxygen saturation in maternal blood in the placenta is low

5. Chloride Shift
-in exchange, chloride ions (Cl-) diffuse from plasma into the RBCs. This exchange of negative ions maintains the ionic balance between plasma and RBCs and is known as the chloride shift. -the net effect of these reactions is that CO2 is carried from tissue cells as bicarbonate ions in plasma. Low pH can also result from lactic acid, a by-product of anaerobic metabolism within muscles. Acclimatization -red blood cell production is stimulated by the hormone, erythropoietin -ventilation rate increases -muscles produce more myoglobin -people living permanently at high altitudes have greater lung surface area and larger lung capacity than those living at sea level -might even have variant hemoglobin

6. Acute Mountain Sickness (High altitude sickness)

a) as a person ascends in altitude, the atmospheric pO2 decreases, the alveolar pO2 decreases correspondingly, and less oxygen diffuses into the blood. -ex. At sea level, pO2 is 160mmHg -at 10,000 ft, it decreases to 110mmHg -at 20,000 ft to 73 mmHg -at 50,000 ft to 18mmHg b)symptoms of altitude sickness -shortness of breath -headache -fatigue -insomnia -nausea -dizziness Exercise -leads to increased metabolic activity and therefore an increase in carbon dioxide output which lowers blood pH -this change in pH is detected by chemosensors in the carotid arteries and aorta that send impulses to the breathing center of the brain. -nerve impulses are then sent to the diaphragm and the intercostal muscles to increase contraction or relaxation rates Myoglobin -consists of 1 heme group attached to a globin -used to store oxygen in muscle -myoglobin has higher affinity for oxygen than hemoglobin -at moderate pO2, hb releases oxygen and myoglobin binds it -myoglobin does not release oxygen to tissue until the pO2 is very low in tissues -delays the shift to anaerobic cell respiration asthma -chronic, inflammatory disorder that produces sporadic narrowing of airways -attacks are brought on by spasms of the smooth muscle in the walls of the smaller bronchi and bronchioles, causing the passageways to close partially or completely (bronchoconstriction) -symptoms include periods of coughing, difficulty breathing, and wheezing -the patient has trouble exhaling and air may be trapped in the alveoli during expiration -during the early phase of an acute response, there is excessive secretion of mucus that may clog bronchi and bronchioles and worsen the attack. -in the alte phase (chronic response), inflammation continues, accompanied by fibrosis, edema, and necrosis (death) of bronchial epithelial cells -causes of asthma attack -airways of people with asthma are hyperactive to a variety of stimuli that normally do not trigger bronchoconstriction: allergens such as pollen, house dust mites, mold, or particular food -other common triggers: emotionally upset, aspirin, sulfating agents (used in wine and beer and to keep greens fresh at salad bars), exercise, and breathing cold air or cigarette smoke

-effect on ventilation: breathing problems, coughing, and shortness of breath The Bohr effect is the change in an environment that allows for H+ ions to bind to certain amino acids in hemoglobin, altering its structure and decreasing its oxygen-carrying capacity, making more O2 available for tissue cells.