AP 2 Chapter 20 Heart Part 2

Bradycardia

abnormally slow heart rate

Conduction Deficits

Damage to conducting pathways disturbs heart rhythim. AV node assumes command if -SA node or internodal pathways are damaged. -Resulting in slower heart rate Ventricular muscle cells can begin generating AP's at a high rate if there are abnormal conducting cells. -Ectopic pacemaker impulses can override the bodies SA or AV node disrupting ventricular contraction timing.

Stroke Volume

Amount of blood pumped out of each ventricle during a single heart beat. (generally SV refers to the left ventricle) Ejection fraction-Each Ventricle ejects 70-90mls of 140-144mL of blood. SV=55 to 70% of EDV

Pacemaker Cells

(cardiac Conductive cells) Make a small percentage of the total number of cardiac muscle cells. Undergo rhythmic spontaneous depolarizations that lead to action potentials. AP spread quickly through the heart by cardiac conduction system.

Cardiac Cycle begins when

- All chambers are relaxed - Ventricles are partially filled with blood.

ANS divisons innervation the heart via the cardiac plexus

- post ganglionic SYMP neurons of the cervical and upper thoracic ganglia to the cardiac plexus. - The Vagus nerve (CN X) caries PSYMP preganglionic fibers to the small ganglia with cardiac plexus both Ans divisions innervate the: -SA nodes -AV Nodes - Atrial muscle cells Ventricular muscle cells (SYMP out number PSYMP)

Contractile Muscle Cells

-Accounts for 99% of all muscle cells in the atrial and ventricle walls.

As Ventricular pressure falls below atrial pressure....

-Atrial pressure forces AV Valves to open - Blood Flows from atria to ventricles. - Both atria and ventricles are in diastole. Primary mechanisms of ventricular filling Ventricles become nearly 3/4 full before cardiac cycle ends

Cardiac Centers Monitor

-BP of the baroreceptors of carotid sinus and aortic arch. -Atrial concentration of O2 and CO2 (chemoreceptors of common carotid artery and aortic arch) -Proprioceptive info: Cerebral cortex/ Hypothalamus/ Limbic Cardiac centers adjust cardiac activity accordingly to maintain adequate circulation to vital organs.

Pacemaker potential

-Spontaneous depolarization -Prepotential

Cardiac muscle cell's gated ion channels in the sarcolemma

-Voltage gated sodium ion channels. -Calcium ion channels -Potassium ion channels Opening and closing action of these ion channels are responsible for contractile cardiac AP's

Phases of the Cardiac Cycle

1) Atrial Systole 2) Atrial Diastole 3) Ventricular Systole 4) Ventricular Diastole

Plateau Phase Benefits

1) Increases the strength of the hearts contractions -Prolonged AP make muscle twitch. lasting longer to develop more force. 2) Allows more calcium ions to enter cell, needed for contraction. (sliding filament mechanism) 3) Effectively prevents fatigue and tetany (sustained contraction) in heart muscle by lengthening refectory period (which is time which excitable cannot be stimulated to contract again) 4) Provides time required for heart to fill with blood and eject blood.

Skeletal and Cardiac Differ in terms of

1) Nature of the Action Potention 2) Source of the calcium 3) Duration of Resulting Contraction

Three steps once threshold is reached

1) Rapid Depolarization 2) The Plateau 3) Depolarization

Pacemaker potential Node Cycle

1) Slow Initial depolarization phase 2) Full depolarization phase 3) Repolarization phase 4) Minimum potential phase

Two Phases of Cardiac Cycle

1) Systole (contraction) 2) Diastole (relaxation)

End-Systolic Volume

Amount of blood remaining in each ventricle at the end of ventricular systole. (at the start of ventricular diastole)

SYMP & PYMP effects on SA Node

ANS alters heart rate by changing ion (K+ & Ca) permeability of conducting system cells. -the dramatic effect at the SA node. (changes rate which impulses are generated) Heart rate is altered by any factor that changes: -rate of spontaneous depolarization in the nodal cells -duration of repolarization in the nodal cells These alter heart rate by changing time required nodal cells need to reach threshold.

Autonomic tone of the HEart

ANS dual innervation makes fine adjustments in the CV functions to meet needs of other systems. Dual innervation maintains resting tone. -releases ACH (decreases heart rate) & NE (increases heart rate) at the nodes and myocardium -Cutting vagus nerves (increases heart rate): SYMP blocking agents (decrease heart rate Parasympathetic Innervation: (at SA Node) Dominates in a healthy resting individual -Typical adult heart rate is 70-80bpm

Cardiac Conduction system

AP are transmitted from the pacemaker cells to the contractile muscle cells via the intercalated disc and gap junctions. Allowing the heart to contract as a unit. Producing a coordinated heart beat. Cells of the heart are referred to as a "Functional Syncytium"

Heart Rate of Cardiac Cycle

AP's of pacemaker and conducting cell systems provide the timing required between atrial and ventricular systole. 75bpm the cardiac cycle lasts 800msec When heart rate increases all phases of cardiac phases shorten. Particularly diastole

Tachycardia

Abnormally fast heart rate

Ectopic pacemaker

Abnormally functioning cells generate high rate of AP's Bypass the conducting system Disrupt ventricular contractions

Similarities between Cardiac and Skeletal muscle Cells

Action potential leads to the spread of calcium among myofibrils Binding of calcium to troponin on thin filaments initiates contractions.

Three Populations of Pace Maker cells

All capable of spontaneously generating AP's there by setting pace of heart 1) SA Node 2) AV Node 3) Purkinje Bundle Collectively these make a group of interconnected 'pacemaker" cells known as the cardiac conduction system.

Isovolumetric relaxation

All heart valves are closed Ventricular myocardium is relaxing with pressure decreasing rapidly. Blood cannot flow into ventricles -because ventricular pressure is still higher than atrial pressure.

End-Diastolic Volume

Amount of blood in each ventricle at the end of ventricular diastole. (which is the start of ventricular systole)

Repolarization

As the Plateau continues slow calcium channels being to close. Slow potassium channels bein to open. -potassium rushes out of the cell resulting in rapid repolarization that restores resting membrane potential.

Rapid Depolarization

At threshold: -Voltage gated sodium channels (fast Na Channels) open for a few mili seconds -Membrane becomes permeable to Sodium -Massive influx of sodium depolarizes the sarcolemma. Resulting in rapid membrane depolarization

Drugs

Caffeine- increases heart rate by acting on the conducting system and increases rate of depolarization on the SA nodes. Nicotine: increase heart rate by stimulation activity of SYMP neurons.

Repolarization Phase

Calcium ion channels close Voltage gated potassium ion channels begin to open. resulting in potassium ions exiting cells. Membrane beings to repolarize.

Absolute Refractory Period

Cardiac Muscle cells cannot respond at all because sodium channels are in activated. Included plateau and period of rapid depolarization. Last 200msec in the ventricle muscle cell.

Refractory Period

Cardiac cells cannot maintain a sustained contraction. Membrane will not respond to second stimuli's for some time after an AP begins .

Factors affecting cardiac output

Cardiac output can be adjusted by changes in Heart Rate: adjusted by ANS or hormones Stoke Volume: Adjusted by changing one or both of the -EDV ex. how full the ventricles are at the start of ventricular contraction -ESV ex how much blood remains following ventricular contraction.

Sequence of Excitation

Cardiac pacemaker cells pass impulses in order 1) SA Node 2) AV Node 3) AV Bundle 4) Right and Left Bundle Branches 5) Purkinje Fibers

Purkinje Fibers

Conducts AP rapidly to the ventricle cells. -signals reaching ventricular cardiac cells begin to contract with 75m/sec. By this time atria has completed the contractions. The entire process from generation of impulse at SA Node to complete depolarization of the ventricular myocardium takes two 225m/sec -Ventricle contract in waves that begins at apex and spread to base of heart -pushing blood toward base of heart into aorta and pulmonary trunk

Systole

Contraction. Blood pushed into adjacent chamber or arterial trunks (pulmonary & aorta)

Body Temperature

Decreases temperature. Slows depolarization rate at the SA Node lowering HR and strength of contractions. Increases temperature accelerating heart rate and contractile forces

Bundle Branches

Delivers the impulses to the Purkinje fibers of the ventricles. Right bundle branch also delivers across to the moderator band and then the papillary muscle of the right ventricle directly.

Action Potential Physiology

Differs between the pacemaker cells and the contractile cardiac muscle cells. How ever sodium and potassium play essential roles in both of these cell types Calcium ions are critical for both of these cell types

Cardiac Conductive Cells

Do not have a stable resting potential like skeletal muscles and neurons. Contains a series of sodium ion channels that allow a normal but slow influx of sodium ions causing the membrane potential to rise slowly. Resulting in a spontaneous depolarization known as prepotential.

Prepotential

Drives the self generated rhythmic firing (automaticity) of pace maker cells. Example: The tendency for the AP of cardiac cell membranes to drift towards thresh hold following repolarization.

Atrial Systole (at the end)

Each ventricle contains max amount of blood known as end-diastolic volume. (4.4oz in adults standing at rest.)

Aerobic Energy of Heart

From Mitochondrial breakdown of fatty acids and glucose in the presence of O2 O2 is necessary for aerobic reaction is derived from the -1) Coronary circulation 2) Cardiac muscle cells that maintain O2 reserves from Coronary circulation O2 is bound to heme myoglobin molecules.

Spontaneous Depolarization

Generates a pacemaker potential or prepotential due to -Decreasing potassium -increasing sodium and calcium permeability in conductive cell membrane Slow influx of sodium through voltage gated sodium ion channels

Damage to SA node or Atrial internodal pathways

Heart will beat slower at 40-60bpm. This is dictated by AV Node If there is damage to conducting system. -Purkinje fiber network can stimulate the heart at 20-40bpm. Under normal conditions the cells of the AV Bundle, Bundle branches, and Purkinje fibers do not all depolarize at same time. Resulting in the heart no longer pumping effectively.

Plateau Phase

If cardiac AP last 1 to 5 milisec resting heart rate would be 15x faster than it should be at rest. This lengthens cardiac AP;s 200-300msec Resulting in a slower heart rate providing time required for hear to fill and eject blood.

Blood pressure of cardiac cycle

In any chamber -Rises during systole -Falls during diastole Blood flows from high pressure to low pressure example: Blood flows from one chamber to another only if pressure in first chamber exceeds that of the second chamber. Correct pressure relationships are controlled by the 1) Timing of contractions between atrial and ventricles. 2) Direction of one way valves

Role of Calcium Ions

In cardiac contractions. Appearance of an AP in cardiac muccle membrane produces a contraction by causing an increase in calcium ion concentration around the myofibrils in two ways 1) Extracelluar calcium ions crossing the membrane during action potential phase provide 20% of calcium required for contraction 2) The arrival of extra cellular calcium triggers release of additional calcium SR reserves. Cardiac tissue is very sensitive to changes in ECF calcium concentration

Cardiac reflexes (in medulla oblongata)

Information about status of CV system arrive by the -Visceral sensory fibers that accompany the Vagus nerve -SYMP nerves of the cardiac plexus.

Reversal of contractile cardiac muscle cell

Is inside a plasma membrane. Swings from negative (-80mv) to Positive for a moment (ranging for 0 to +30mv) These changes occur in the voltage gated ion channels of the sarcolemma. -Due to unequal concentrations of sodium and potassium on either side of the membrane drives ions in or out of the cell through channels.

Timing of Refractory Period

Length of Cardiac AP in the Ventricular cell. Lasts 250-300msec. 30x Longer than skeletal muscle fiber. Long refractory period (absolute and Relative) Prevents summation, tetany, and fatigue that occurs in skeletal muscles.

AV node cells impulses

Max rate of 230/min Each impulse results in ventricular contraction This value is the max normal heart rate even if the SA node generates faster impulses. -Mechanical factors decrease the pumping efficiency of the heart with rates above 180bpm. - Rates above 230bpm occurs with the heart of conducting system because of damage or drugs

Slow Initial Depolarization Phase

Pacemaker potential starts with plasma membrane in a *hyperpolarized* state. Example: minimum membrane potential. -opens nonspecific cation channels in membrane. allowing sodium ions to leak into cell & potassium ions to leak out of cell results in an overall *slow* depolarization to *threshold*

Cardiac Cycle

Period between the start of one heart beat and the beginning of the next heart beat. Alternating periods of contraction and relaxation.

Minimum potential phase

Potassium ion channels remain open until membrane reaches it minimum potential results in membrane being hyperpolarized. opening non-specific cation sodium channels and cycle beings again.

Cardiodynamics

Refers to the movement and force generate by cardiac contractions.

Diastole

Relaxation Chamber fill with blood

Atrial Systole (as atria contracts)

Rising atrial pressure push blood into the ventricle through the open right and left AV valves

Rate of spontaneous depolarization differs

SA Node= Depolarizes first. establishing the heart rate. Generates 80-100 AP's a min without neural or hormonal stimulation. AV Node= Generates 40-60 AP's a min. Normal Resting Heart rate= Generally slower than 80-100 bpm, due to the affects of PSYMP innervation.

Effects on the SA node

SYMP & PYMP has the greats effect at the SA node (heart rate) ACH (PYSMP Stimulation) Slows the heart rate by: Opening chemically gated potassium channels in the plasm membrane (potassium leaves the nodal cell)

Ventricular Ejection

Semilunar valves open once ventricular pressure exceeds pressure in atrial chambers and trunks. -blood flows into pulmonary and aortic trunks. Ventricle muscle cells contract isotonic (shorten)

Relative Refractory Period

Short lasts 50msec Volatage gated sodium channels are closed but could open. Membrane can respond to a stronger than normal stimulus and iniate another AP

Cardiac Centers of the Medulla Oblongata

The Cardioacceleratory center -controls SYMP Neurons (increase heart rate) Cardio inhibitory center -Controls PSYMP neurons (decreases heart rate) Cardiac centers also receive input from higher brain centers. -epically from the PSYMP and SYPMP in the hypothalamus

Population of pacemaker cells pace the heart

The cell that depolarizes the fastest sets the heart rate. -other cells will pace heart only if the fastest pacemaker stops functioning. SA Node is the Normal pacemaker of entire heart -Electrical beats generated and maintained by this node are sinus rhythms Occasially another group of cells will attempt to pace the heart at the same time as the SA node. -known as ectopic pacemaker results in irregular sinus rhythm.

AV Bundle (bundle of his)

The only electrical connection between the atria and ventricles example pathway between the AV node and AV bundle impulse enters the AV bundle in the interventricular septum and then enters the right and left bundle branches. - both branch extend toward heart apex and fan out deep into the endocardial surface - left branch is larger than the right.

Prepotential (spontaneous depolarization)

This is the slow positive increase in voltage across the cell membrane. (the membrane potential) that occurs between the end of one AP and the beginning of the next AP. The increase in membrane potential is what causes the cell membrane to reach the thresh hold potential and fire the next AP.

Resting Membrane Potential

Ventricle contractile cell= -90mv Atrial contractile cells = -80mv Action potential begins when ventricle muscle cell membrane reaches threshold at -75mv -Thresh hold is reached in a portion of the membrane next to intercalated disc

Atrial Systole (at the start)

Ventricles are already filled to 70% compacity -due to passive blood flow during the end of previous cardiac cycle. As Atrial contraction ensures pressure raises providing the remain 30% by pushing thru the open AV Valve

Ventricular Systole (early stage)

Ventricles are contracting isometrically. (generate tension with pressure raising inside) -No blood flow has occurred -Pressure not high enough to force open the semilunar valves and blood into pulmonary or arotic trunk. Ventricles are in isovolumetric contraction -All heart valves are closed -No change in blood volume -Ventricular pressure is raising

Approaching the end of Ventricular Systole

Ventricular pressure falls rapidly. Semilunar valves close to back flow of blood in the aorta and pulmonary trunk. - Pressure decreases in the aorta as blood backflow begins - When semilunar valves close pressure temporarily raises again in the aorta as the elastic atrial walls recoil. Aortic Valve closure produces a diacritic notch Amount of blood remaining in ventricle is the ESV which is 50mL

The Plateau

Voltage gated sodium channels close as transmembrane potential reaches +30mv. -Na+ channels will remain closed and inactivated until transmembrane potential drops back to -60mv. -Voltage gated calcium remain open (slow Ca Channels) with calcium entering sarcoplasm to balance sodium lost Results in transmembrane potential remains near 0mv for an extended period (known as plateau).

Cardiac Output

Volume of blood pumped by left ventricle in one minute. Gives an indication of blood flow through peripheral tissues. Indicates ventricular efficiency over time.

Full Depolarization Phase

When membrane reaches thresh hold voltage gated calcium ion channels open allowing calcium ions to enter Resulting in membrane to fully depolarize.

Disorders of ion concentrations (Potassium/ Calcium)

affects strength of contractions which then affect stroke volume. -also affects SA Nodal cells

Ventricular Systole begins

as Atrial Systole Ends. AV Valves are pushed closed as ventricular pressure rises above atrial pressure.

Ejection fraction

the fraction of outbound of diastolic blood pumped from a filled ventricle with each ventricular contraction. General measure of cardiac function When heart contracts it ejects blood from the two pumping ventricle chambers. When heart relaxes the ventricles refill with blood. No matter how forceful the contraction it does not empty all of the blood out of the ventricle.

Ejection fraction decreases

with -Weakness of heart muscle -Damage of heart from heartattack -Heart valve problems -Long standing uncontrolled high blood pressure - More than 40% confirmed diagnosis of heart failure. Measured by -EKG -Cardiac Catheterization -MRI or Cat Scan or Nuclear Medicine scan.