Week 8 Cardiovascular System

- The Heart
- Features of Cardiac Muscle Tissue
- Excitability
- The ability of cardiac muscle to respond to electrical stimulus by contracting
- Cardiac Muscle Action Potential
- Stimulation opens both sodium and calcium gates, sodium and calcium enter cell and start
depolarization
- Calcium gates open slower and stay open longer than sodium gates
- Sodium gates then close, potassium gates open causing a slight drop in voltage to 0 MV
- Just after that calcium gates are fully open, resulting in calcium coming into the cell as
potassium is leaving it creating a balance
- The calcium gates then close causing the significant drop in voltage seen below
- The cell remains depolarized for 0.2-0.3 sec. (plateau phase) which is the decreased line after
that apex decent
- The plateau phase results in a much longer refractory period in cardiac muscle
- Total time for muscle is 2 msec total time for cardiac muscle is 200 msec
- Be sure to compare this to nerve action potential
- Cardia muscle cells contract and relax before the end of the refractory period
- To have a stronger reaction more nerve impulses are sent to the same muscle tissue
- Cardiac muscle’s long refractory stage prevents tetanic contraction of cardiac muscle
- Skeletal muscles can also recruit more muscle to increase muscle tension whereas cardiac
cannot
- tetanic contraction is a sustained muscle contraction evoked when the motor nerve that
innervates a skeletal muscle emits action potentials at a very high rate
- Tetanic contractions can lead to fatigue of muscles
- If this happened in the heart it would stop or be unable to pump leading to death
- Difference between skeletal and cardiac
- Cardiac has slow calcium gate, they open slowly and longer
- Cardiac has plateau phase
- Cardiac can not constantly contract
- Cardiac myocytes (muscle cells) have graded responses (calcium-inducted calcium release)
meaning calcium is able to stimulate more calcium release from intracellular fluid
- Automaticity
- The ability of some cardiac muscles to initiate its own stimulus
- Autorhythmic cells specialized cell that allow the heart to act and initiate its own stimuli
- Cardiac muscle cells have leaky membranes (more so than skeletal muscle or neurons)
- The potential of cardiac membrane reaches its threshold due to leaking ions (no stimulations
required)
- Pacemaker potential = -60mV
- Threshold potential = -40 mV

- Rhythmicity
- Regularity of beat
- Pace making activity
- Refractoriness
- Ability of cardiac muscles cells to recover from stimulus such as from ANS, or CNS
- Conductivity
- Cardiac muscles consist of branched cells, connected by intercalated discs
- Allows the muscles to act as a functional syncytium
- Syncytium is a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells
or by division of nuclei. Acting as a single cell
- Heart muscle functions as a unit
- Once an action potential is initialed in one cell is spreads throughout the entire myocardium
- Ions diffuse from one cardiac muscles cell to another via the discs (gap junctions)
- Fibro skeleton of the Heart
- Wall of connective tissue between atria and ventricles
- Supports the AV valves

- Has high electrical resistance (i.e.,

non-conductive)
- AV node is the only “window” from atria to ventricles
- This prevents SA impulses from passing through the walls of the atria into the ventricles making
sure the propagation of pumping is done in the correct order
- Causes a delay between atrial contraction and ventricular contraction allowing time for
ventricular filling
- Cardiac Conduction
- Cardiac conduction fibers are autorhythmic cells
- They behave like neurons but are automatic as well
- Controlled by pacemaker cells throughout conduction system
- Review Heart Conduction Notes from ANAT
- SA node has cells in it that depolarize 100 times a minute
- AV node depolarizes 40-60 times/min
- AV bundle. Bundle branches and purkinje fibers all have own intrinsic rates, depolarizing 20-35
times/min
- But the heart is a functional syncytium so the cells which depolarize most rapidly set the rate for
the entire heart making the SA node the master pacemaker
- Cardiac Cycle
- Sequence of events in a “heartbeat”
- This includes electrical and mechanical events
- Electrical events: depolarization, repolarization, recorded as the electrocardiogram (EKG) bloody
Germans
- EKG or ECG
- Leads (electrodes) are placed around the body to monitor heart activity
- Electrical current flowing toward a positive electrode result in a positive deflection
- Current flowing away from a positive electrode result in a negative deflection
- Electrocardiogram consists of five waves (deflections)
- Deflection upward means positive current going toward electrode
- Deflection downwards means current heading away from electrode
- The natural and healthy line on an EKG is called isoelectric
- Patient needs to stay as still as possible due to skeletal muscle impulses interfering with the EKG
- P wave is the electrical signature of initiation and eventual completion of atrial depolarization
- QRS complex indicates ventricular repolarization, electrical impulse travels though bundle of his
to bundle branches and starts spreading. Because everything is long and thick that is the reason
for large deflections
- Ventricular repolarization indicated by T wave
- Reason we don’t see atrial repolarization is because it’s hidden under QRS complex
- Space between P wave and QRS represents area of ISO line where atrial contraction as a
mechanical event is taking place
- From S to beginning of T wave is where mechanical ventricular contraction is located

- When analyzing EKGs there are things called 2 plus one 2 (+1) so three in total segments
- Within five waves what’s known as PR segment which represents an atrial contraction it occurs
due to passage of impulse through AV node.
- ST segment which is between S deflection and beginning of T wave which represents ventricular
contraction
- The plus one segments is known as TP segment, which represents space between T wave of one
heartbeat and beginning of next heartbeat represented by the P wave
- The T wave to P wave represents a single heartbeat and the TP segment is the gap in between
heartbeats
- There are 2 intervals
- First is known as P-R interval which represents onset of atrial depolarization at the SA node to
onset of ventricular depolarization which occurs when impulse passes though to ventricles via
AV node can last from .12 - .20 seconds

- QT interval is .32-.38 seconds represents onset of ventricle depolarization to end of ventricular

repolarization
- It is quite long because it has to penetrate and activate essentially all cells in ventricular walls,
therefore more distance to travel

- There is a portion of QT interval in which the QRS complex takes place only 0.6 to .10 seconds
and it represents onset of ventricular depolarization
- Despite being a repolarization
(which means it shouldn’t have a positive deflections) the T wave puts out a reading of positive
because the ions moving to restore the chemical equilibrium move from the outside in and
during depolarization the last cells to depolarized are the first ones to be repolarized
- Because of this, it looks like a positive deflection moving away when in reality its negative
particles being moves away, a type of double negative
- Common EKG Abnormalities
- Prolonged PR-segment is a heart block is when there is a lack of QRS complex, meaning there is
a lack of proper conduction because the AV node isn’t taking over passing the depolarization to
the ventricles all the time. Its possible the problem can also rest at the bundle branches or
purkinjie fibers
- ST-segmental elevation going from S to T there is a slope. This can represent an acute
myocardial infarction
- Ventricular Fibrillation: Rapid/large random voltage fluctuation. Extremely dangerous and
deadly.
- Mechanical Events
- Systole – contraction, can be ventricular or atrial
- Diastole – relaxation
- Valvular changes – opening and closing of valves
- Heart sounds – valves closing, they slam shut
- Blood flow – self-explanatory, blood moving through the heart
- Between Heartbeats
- All four heart chambers are relaxed
- Semi-lunar valves are closed
- AV valves are open
- Blood passively flowing though atria, 70% into ventricles, 30% remains in atria
- Cardiac Cycle
- Starts electrically in the SA node
- Depolarization spreads from SA node through atrial walls
- Mechanically this causes the atria contract causing atrial systole
- Atrial blood enters ventricles on both sides
- AV node receives impulse that has traveled through atria, fibro skeleton slows this down
- Depolarization then travels from AV node down to AB bundle or bundle of his then purkinje
fibers
- Atria then relaxes and start diastole and ventricles start systole
- Mechanically more intra-ventricular pressure closes AV valves (lub), and opens semilunar valves
- This forces the blood into the aorta and pulmonary trunk
- The ventricles then relax and begin diastole, where pressure drops
- Semi-lunar valves then close due to arterial BP and the AV valves open once again
- Rinse and repeat
- Cycle repeats 60-100 times/min
- Bradycardia is abnormally low heartrate
- Tachycardia is abnormally high heartrate
- May exceed 200 times a minute during intense exercise or below 60 BPM if in great shape
- The 200 BPM is achieved via contributions from ANS that cause nerves to innervate which cause
the SA and AV nodes to increase heart rate
- Cardiac Output
- Has two components: heart rate, and stroke volume
- Heart rate is the number of cardiac cycles (heartbeat) in one minute
- Measured in beats per minute (BPM)
- Average 60- 100 bpm at rest
- Infant is above 120 bpm, which falls gradually during aging
- Children and teenagers have nigher heartrates as well
- Obese people have higher resting heart rates
- Fit persons have lower resting heart rate
- Stroke Volume is the volume of blood pumped out of one ventricle in one contraction
- Some definitions are specific to the left ventricle
- Left and right ventricle stoke volumes are within a few millimeters
- Measured in mL (mL/beat)
- Average around 75 mL for healthy adult (relaxed ventricle holds 130 mL of blood)
- Cardiac Output- volume of blood pumped by one ventricle in one minute, measured in mL/min
- Determined by heart rate multiplied by stroke volume
- 80 bpm X 75 mL/beat = 6000 mL/min
- Factors that affect heart action
- Autonomic Nervous System Regulation
- Cardiac accelerator center
- Activated by emotional of physical stress (fright, anxiety, exercise)
- Stimulates sympathetic neurons which exit spinal cord at T1-T5 and innervate SA and AV nodes
- This increases rate and force of contraction
- Cardiac Inhibitory center
- Decreases heart activity when stressors removed
- Parasympathetic fibers pass via vagus nerve to SA and AV nodes
- Decreases rate and force of contraction
- Both are separate sections in the brain
- Under relaxed conditions both centers send impulses to SA and AV nodes
- Inhibitory impulses predominate vagal tone (decreases heart rate do to vagal inhibition)
- Under stressful conditions
- SNS predominates
- Vagal tone is overcome, increasing HR and force of contraction
- Temperature
- Increase in core temperature results in increased heart rate (get rid of excess heat)
- A decreased core temperature results in a decreased heart rate
- Hormones
- These are main physiologically regulated levels of hormones that we would have to control
heart rate
- Epinephrine mimics SNS increasing contraction, its complementary to CNS
- Thyroxine increases heart rate, increases effects of norepinephrine and epinephrine
- Slower, longer lasting than epinephrine
- Ions
- Calcium
- Hypercalcemia causes prolonged contraction (strength) but decreased rate
- Hypocalcemia causes a decrease in strength, and can weaken the overall pumping strength of
the heart over time
- Sodium
- Hypernatremia can result in tachycardia
- Hyponatremia can result in congestive heart failure
- Potassium
- Hyperkalemia heart black, bradycardia, cardiac arrest
- Hypokalemia: arrythmias (fibrillation)
- Drugs
- Antiarrhythmics
- Beta blockers (decrease heart rate and force of contraction)
- Channel blockers (flecainide which blocks sodium, or sotalol which blocks potassium channels)
- Cardiac Glycosides
- Many are natural toxins with cardiac effects can be used as drugs (digitoxin from digitalis blocks
sodium and potassium pump to increase sodium and calcium levels)
- Heart Rate
- Remember heart rate is the number of times the left ventricle pumps in one minute
- Excessively high or low heart rate can result in low cardiac output
- Bradycardia is reduced cardiac output due to fewer contractions a min (lower heartrate)
- Usually, bradycardia is below 40 bpm
- Tachycardia is reduced cardiac output due to insufficient filling time (lower stroke volume)
- Starlings law of the heart
- Within limits, force of contraction of cardiac muscles increases with degrees of cardiac muscle
cell stretch
- Amount of blood heart gets is what determines muscles cell stretch
- Stretch is caused by blood (volume) entering the heart, more stretch more force and vice versa
- Increased end diastolic volume results in increased force of contraction resulting in increased
cardiac output
- End Diastolic Volume (EDV and preload)
- Volume of blood in ventricles at the end of diastole
- Represents stretch o f myocardial fibers
- Determined by venous return
- Venous Return
- Volume of blood returning to the heart from the venous system
- Influenced by
o sympathetic nervous system
o skeletal muscle pump which works by alternative contractions occurring in lower limbs
which help return blood to the heart from the limbs, venous values prevent backflow
and the muscles themselves force blood along by “milking” the blood along veins
muscles by putting pressure on veins whenever they contract
 o respiratory pump AKA the diaphragm (pressure difference between thoracic and
abdominal) there are changes in thoracic pressures due to inspiration and expiration.
Expiration increases pressure forcing old air out and the veins in the thoracic region are
pressured as well, on inspiration pressure is released allowing for intake and milking of
the veins as well
- Contractility
- The ability of cardiac muscle fibers to shorten
- Increased by action of calcium, epinephrine, and sympathetic nervous system
- Afterload (systemic vascular resistance)
- The load or resistance against which left ventricles must pump its blood during contraction
(resistance due to arterial BP)
- Circulation
- Blood Vessels
- Arteries carry blood away from the heart, they empty into capillaries where gas, nutrient and
waste exchange take place, veins then take the blood back to the heart via the liver to drop off
the waste products
- Artery has thick walls with smaller diameters with blood under higher pressure, vein has thin
walls larger diameters, but they also have valves
- Capillaries have very thing walls to allow effective transfer of nutrients and gasses by way of
diffusion. Operate under much lower pressure
- Veins are also capacitance or reservoir vessels because at any one time they contain 75% of the
bodies blood
- Veins have a minor degree of elasticity but not much
- Elasticity of Arteries causes blood flow to be continuous
- During ventricular systole
o Blood enters arteries under high pressure
o Pressure of blood stretches walls of elastic arteries
- Elastic arteries
- Large arteries near the heart
- Large diameter lumen and elastic walls
- During Ventricular Diastole
- Stretched arteries recoil,
- Drive blood through the arteries and capillaries maintaining a continuous flow (preventing
pulsatile flow)
- Blood Pressure
- Force of blood pressing against the inner walls of blood vessels
- Types of blood pressure
o Arterial blood pressure (ABP)
o Capillary pressure (hydrostatic pressure)
o Venous blood pressure
- Arterial blood pressure
- Pressure of blood against the walls of an artery
- Typically, 120/80
- Determined by cardiac output, peripheral resistance, and blood volume
- Pulse pressure
- Systolic pressure – diastolic pressure
- = 40 mm Hg (120 – 80)
- It tells us how well the heart is pumping as pulse pressure tells us how much the heart is
pumping in a single pulse
- Mean Arterial Pressure
- Is 1/3 pulse pressure + diastolic pressure.
- the average arterial pressure throughout one cardiac cycle, systole, and diastole.
- Reason for 1/3 is because it is considering the amount of time heart actually spends in systole as
opposed to diastole, heart spends 1/3 of time actively contracting
- Average = 95 mm Hg (40/3 + 80)
- Represents perfusion to organs of tissues of body
- Capillary Pressure
- Pressure of the blood in the capillaries, largely represented by hydrostatic pressure
- = 30 mm Hg (arterial end) to 15 mm Hg (venous end)
- Venous Blood Pressure
- Pressure of the blood in the veins
- = 2 mm Hg in vena cava

- (Physical) Determinants of Arterial Blood Pressure

- Peripheral Resistance
- Opposition to flow
- Due to friction encountered as blood flows through vessels
- Determined by
o Vessel diameter
o Vessel length
o Blood viscosity
- Increased peripheral resistance results from
o Decreased arteriole diameter
o Increased blood vessel length
o Increased blood viscosity (more formed elements, and the like)
- Arterial Blood Pressure
- Formula: cardiac output X peripheral resistance (BP = CO X PR)
- Control of Arterial BP
- Carotid and aortic baroreceptors
- Cardiac and vasomotor centers
- Baroreceptors (press receptors)
- Located in carotid sinuses and aortic arch
- Respond to pressure by stretching
- Send impulses to medulla oblongata
- Cardiac Center
- Located in the medulla oblongata
- Receives impulses from baroreceptors (press receptors), hypothalamus, and cerebral cortex
- Controls cardiac rate via SNS and PNS
- Vasomotor Center
- Located in medulla oblongata
- Receives impulses from baroreceptors, hypothalamus, and cerebral cortex
- Controls diameter of blood vessels (peripheral resistance) via SNS (only)
- Smooth muscles relax on its own without innervation
- Decreased BP results in
- Fewer afferent impulses (decreased Rate of AP) to the vasomotor center
- Vasoconstriction and vasodilation (vasomotor center)
- Increased heart rate and force of contraction (cardiac center)
- Increased BP
- Cardiac Center
- Affects heart rate/force
- Vasomotor Center
- Constricts blood vessels
- Renin-angiotensin Mechanism
- Activated by decreased BP
- Decreased blood pressure releases renin (enzyme secreted by kidneys)
- See renin-angiotensin cycle in prior notes
- Angiotensin 2
- Elevates BP in two ways
o Potent vasoconstrictor (increases peripheral resistance)
o Stimulates hormone (aldosterone and ADH) secretion
o Increases blood volume and sodium reabsorption
o Increases BP
- Vasoconstriction and hormone interventions increase blood pressure
- ACE Inhibitors
- Vasotec (enalapril), Zestril (lisinopril), Lotensin
- Inhibit the conversion of angiotensin 1 to angiotensin 2
- This decreases ABP