Cardiovascular Physiology Flashcards
Cardiac Muscle Cell Contraction
Resting potential ventricular contractile cell ~ -90mV and atrial contractile cell ~ -80mV (we’ll use ventricle as example)
Action potential begins when the membrane of the muscle cell reaches -75mV (threshold).
Usually occurs next to an intercalated disc (why?)
Once threshold is reached the action potential proceeds in three steps (next slide)
As in skeletal muscle the action potential leads to the binding of Ca2+ to troponin and the sliding of thin filaments past thick filaments
Let’s do a quick review of sliding filaments
The nature of the action potential, the source of Ca2+ and the duration of the contraction differ from skeletal muscle however
Cardiac Muscle Cell Contraction
Rapid Depolarization
Sodium channels open and sodium (Na+) rushes into the cell
“Fast” channels b/c they open quickly and close w/in 3-5 ms
Results in rapid depolarization of sarcolemma
Plateau
Transmembrane potential approaches +30mV results in closing of Na+ channels
Ca2+ channels open and calcium ions enter the cell
“Slow” channels b/c they open slowly and remain open for a longer period of time (~175ms)
b/c Ca2+ entry balances out Na+ loss the membrane remains ~ 0mV from ~175ms
Plateau is the major difference b/t cardiac and skeletal muscle contractions
Repolarization
Ca2+ channels close and K+ channels open (also “slow” ~75 ms)
K+ leaves the cell and results in rapid repolarization restoring resting potential
Cardiac Cycle
The Cardiac Cycle is the period between the start of one heartbeat and the beginning of the next heartbeat (The start of one T-wave to the start of the next T-wave).
Systole is the contraction of a chamber when blood is pushed into the adjacent chamber or vessel.
Diastole is when the chamber relaxes this is when the chamber fills with blood.
Phases of the Cardiac Cycle
Atrial systole
Atria contract completely filling the ventricles with blood
Atrial diastole
Atria fill with blood arriving as the result of ventricular systole
Ventricular systole
Ventricles contract sending blood through systemic, pulmonary and cardiac circuits
Ventricular diastole
Ventricles relax and passively fill with blood until start of next cycle
Heart Sounds
Four different heart sounds (S1-S4, of which two are easily heard through a stethoscope.
“Lubb” is the first (S1) it is the closing of the AV valves and is the (start of ventricular systole).
“Dupp” (S2) is the second and is the closing of the semilunar valves (start of ventricular diastole).
What part of the ECG is the “lubb” and what is the “dupp”?
The other two heart sounds are the result of blood flowing into the ventricles (S3) and atrial contraction (S4)
Cardiac Output
Cardiac Output (ml/min) = Stroke Volume (ml/beat) x Heart Rate (beats/min)
CO = amount of blood pumped by each ventricle in 1 min. SV = amount of blood ejected by a ventricle during 1 beat.
Control of Cardiac Output
Sympathetic and parasympathetic stimulation
Sympathetic increases
Parasympathetic decreases
Hormones
E, NE, and T3 accelerate
Increased venous return
Atrial reflex
Available ventricular filling time
Strength of contractions
Arterial resistance
Cardiovascular Physiology
Under normal circumstances blood flow = cardiac output (CO)
High CO = High flow
Low CO = Low Flow
Capillary flow is determined by interplay between Pressure (P) and Resistance (R)
Flow is proportional to pressure gradient of vessel divided by vessel resistance
For blood to flow the vessel pressure must exceed the vessel resistance
Cardiovascular Pressures
Blood pressure (BP) Arterial pressure From 100 mm Hg to 35 mm Hg Systolic vs. Diastolic Capillary hydrostatic pressure (CHP) Pressure within capillaries From 35 mm Hg to 18 mm Hg Venous pressure (VP) Relatively low Blood flow results from skeletal muscle contraction and valve system
Cardiovascular Resistance
Total peripheral resistance due to a combo of vascular resistance, viscosity and turbulence
Vascular resistance
Resistance of the blood vessels
Due mainly to friction between blood and vessel walls
Depends on length and diameter of vessel
Vessel diameter has a more significant impact than length
Diameter can be changed, length can not
Cardiovascular Resistance
Viscosity
Resistance to flow caused by interactions among molecules
Low viscosity = low resistance
High viscosity = high resistance
Blood viscosity due to plasma proteins and blood cells
Anemia and other disorders can change blood viscosity
Turbulence
Caused by eddies and swirls created by changes in diameter, direction, surface irregularities and different flow rates
Increased turbulence = increased resistance
Usually only occurs in large vessels but can occur as a result of atherosclerotic plaques
Capillary Pressures and Exchange
How nutrients, waste etc… enter or leave tissues
3 factors; diffusion, filtration, reabsorption
At the arteriole end of the capillary filtration usually occurs and at the venule end of the capillary reabsorption tends to occur
Diffusion
When ions or molecules enter or leave tissue from an area of high concentration to lower concentration
Occurs rapidly when;
Distance is small
Concentration gradient is large
Ions or molecules crossing membranes are small
Filtration
Removal of solutes as a solution flows across a porous membrane
Solutes too large to pass are filtered out
Driving force is hydrostatic pressure
At the capillaries, water and small solutes are forced across the capillary wall, leaving large solutes and suspended proteins in the bloodstream
Reabsorption
Occurs due to osmosis
Water diffuses from an area of low to high solute concentration
Creates osmotic pressure