Chapter 14 – Cardiovascular Physiology

I – Cardiovascular System

Heart, blood vessels and blood
Function - transport materials throughout body

Nutrients, water, gases from exterior to interior
Move materials from cell to cell within body
Move wastes from cells to exterior

Arteries move blood away from heart, veins return blood to heart
Backflow prevented by one-way valves
Circulation

Right atrium -> right ventricle -> pulmonary arteries -> lungs -> pulmonary veins -> left atrium -> left ventricle -> aorta -> systemic circulation -> superior vena cava & inferior vena cava -> right atrium

Coronary circulation-separate system serves heart

Hepatic portal system – blood from digestive tract goes directly to liver via hepatic portal vein

II - Pressure, Volume, Flow, and Resistance

Blood flows due to pressure gradient

Pressure

Hydrostatic, if fluid not moving
Pressure lost via friction in cardiovascular system

Pressure increases if pressure put on container (heart or blood vessels) and volume does not change

Flow proportional to change in pressure

Cardiovascular system presents resistance to flow

flow inversely proportional to resistance 
resistance increases with length of tube and viscosity of fluid, and decrease in radius of tube
Important factors in cardiovascular flow - pressure/resistance

Vasoconstriction = smaller diameter of blood vessel
Vasodilation = larger diameter of blood vessel

Velocity

Flow rate = amount of fluid past a point in given time (L/min)
Velocity of flow = distance a fixed volume of blood travels in given time
Smaller cross-sectional area -> faster velocity of flow
Larger cross-sectional area -> slower velocity of flow

III - Cardiac Muscle and the Heart

Anatomy

Myocardium - muscle
Pericardium – sac surrounding heart
Coronary arteries & coronary veins supply blood to heart muscle
A(trio)V(entricular) valves separate atria from ventricles, prevent backflow from ventricles to atria
Tricuspid valve from right atrium to right ventricle
Mitral valve (bicuspid) from left atrium to left ventricle
Chordae tendinae keep valves from blowing back into atria

Semilunar valves prevent backflow from ventricles to arteries
Pulmonary valve between right ventricle and pulmonary trunk
Aortic valve between left ventricle & aorta

Septum separates left from right chambers

Muscle structure

relatively small, branched, uninuclear cells

cells connected via intercalated disks – strongly bonded together via desmosomes with gap junctions which electrically connect cardiac muscle cells to each other

Excitation-contraction coupling

Action potential originates spontaneously in pacemaker cells, spreads through contractile cells through gap junctions
Action potential moves across sarcolemma and into t-tubules
Ca++ enters cells
Ca++ binds to troponin, initiates cycle of crossbridge formation & movement via sliding filament movement

Muscle fiber can have graded contraction

Force proportional to number of crossbridges, determined by how much Ca++ bound to troponin

Relaxation

Ca++ transported back into sarcoplasmic reticulum
Lower Ca++ concentration in cytoplasm -> Ca++ unbinds from troponin
Myosin releases actin
Contractile filaments slide back to relaxed position

More stretch of cardiac muscle -> more forceful contraction

Action potential in cardiac muscle

Depolarization – Na+ channels open, ->Na+ in
Na+ channels close
Initial repolarization - K+ channels open-> K+ out
Plateau – decrease in K+ efflux, Ca++ enters -> little change in membrane potential
Rapid repolarization – Ca++ channels close, K+ goes out again
Influx of Ca++ lengthens duration of myocardial action potential & refractory period, prevents sustained contraction (tetanus)

Pacemaker cells

Autorhythmic
Slow influx of positive ions slowly depolarizes cell
At threshold, many Ca++ channels open, -> steep depolarization

Autonomic neurotransmitters

Sympathetic –norepinephrine, epinephrine -> faster heart rate
Parasympathetic – Ach, -> slower heart rate
Work by influencing ion flow rates

IV - The Heart as a Pump

Electrical Conduction in whole heart

1. Action potential in autorhythmic cell

2. Depolarization spreads through contractile cells through gap junctions in intercalated disks

3. Contraction

Structures

• S(ino)A(trial) node in right atrium sends depolarization to
• Internodal pathway to
• A(trio)V(entricular) node in bottom of right atrium to
• Purkinje fibers in septum to
• Left and right bundle branches

Contraction

SA node causes atria to contract
Slower conduction through atria and slight AV node delay prevents ventricular contraction before atria finish filling ventricles
Action potential reaches apex of heart before upper part of ventricles
Ventricles contract from bottom upwards to eject blood from pulmonary arteries and aorta

SA node is heart’s pacemaker (has faster intrinsic rate than AV node)

ECG

Extracellular recording that represents the sum of multiple action potentials in many heart muscle cells
Provides information on heart rate, rhythm, conduction velocity and condition of tissues

Cardiac Cycle

Diastole-cardiac muscle relaxes, Systole-cardiac muscle contracts
1.  Atrial and Ventricular diastole. Atria & ventricles filling. AV valves open
2. Atrial systole -> complete ventricular filling.
3. Early ventricular contraction -> slight backflow towards atria, causing AV vales closed -> “lub” (1st) of “lub-dup” heart sounds.
Semilunar valves still closed, pressure increases = isovolumic ventricular contraction.
Atria relax and begin to fill.
4. Ventricular ejection. Ventricular contraction -> enough pressure to open semilunar valves, blood goes into arteries.
5. Ventricles relax. Backflow towards ventricles closes semilunar valves, -> “dup” (2nd) of “lub-dup” heart sounds.
When ventricular relaxation causes ventricular pressure to becomes less than atrial pressure, the AV vales open and blood from atria enters.

Cardiac Output

Cardiac output = heart rate X stroke volume

Regulated by autonomic neurons & catecholamines
Both branches alter rate of conduction through AV node
Increase heart rate by:

• decrease parasympathetic activity
• increase sympathetic input

Stroke volume

Amount of blood pumped by one ventricle during a contraction
Directly related to force generated by cardiac muscle during contraction
Determined by:

1. Ventricular volume -> stretch of muscle fibers
Starling curve – plots relationship between stretch and stroke volume.  Increased stretch increases stroke volume until upper limit.

2. Contractility = intrinsic ability of a cardiac muscle fiber to contract and is a function of Ca++ interaction with contractile filaments

Venous return = stroke volume, in normal health. Venous return determined by:

• Skeletal muscle contraction squeezes veins, pushing blood towards heart (1 way valves) (skeletal muscle pump)
• Respiratory pump = compression or relaxation of veins in abdomen and chest. Inhalation -> squeeze veins in abdomen, pushes blood toward heart (1 way valves) & decrease pressure in thoracic cavity and veins in it
• Sympathetic activity constricts veins -> more blood into heart

Contractility

Inotropic agent = any chemical that affects contractility
Inotropic effect = influence of inotropic agent
Catecholamines, epinephrine & norepinephrine, some drugs have positive inotropic effect. Work by:

• increase Ca++ release into cytosol -> more active crossbridges
• Ca++ removed from cytosol faster -> shorter contraction

Afterload = load of end diastolic volume plus arterial resistance during ventricular contraction

Arterial resistance can be from elevated arterial blood pressure and/or loss of stretchability in the aorta.
Increased afterload -> more work for ventricles, can -> myocardial hypertrophy