Heart Study Guide

• Pericardial sac ( parietal pericardium ) - Fibrous outer layer. ( superficial )
• Pericardial cavity - cavity between these two layers that contain pericardial fluid
• Visceral pericardium - inner deep layer of the pericardium

• Epicardium- Outer layer of the heart.
• Myocardium- middle layer of cardiac muscle as it is the thickest layer. Performs the work of the heart.
• Endocardium - Inner layer of the heart and lines the inner heart chambers

When vintricles of the heart contract and they exhibit a twisting or wringing motion that improves ejection of the heart.

• Framework of collagnenous elastic fibers in the heart found heavily in the walls between heart chambers.
• - Provide structure for the heart so that it prevents the valves and opening of the great vessels from overstretching.
• - Anchors cardiocytes so they have something to pull on
• - Prevents the atria from stimulating the ventricles directly by being an electrical insulator.
• - Aid in refilling the heart with blood.

• Intercalated discs join cardiocytes from end to end.
• They contain:
• - interdigitating folds that are plasma membranes in the end of cells that join with other cells and expand the surface area.
• - joined by mechanical junctions ( fascia adherens and desmosomes ) that anchors each plasma membrane and also prevents cardiocytes from pulling apart when contracting
• - electrical junctions that form channels to allow ions to flow from one cardiocyte to the next.

• 60 percent from fatty acids
• 35 percent from glucose
• 5 percent from other fuels like ketone, lactic acid, etc.

Makes little use of anaerobic fermentation and doesn't have oxygen debt mechanism unlike our skeletal muscle.

• 1. SA nodes fire.
• 2. Excitation spreads through the myocardium
• 3. AV nodes fire
• 4. Excitation spreads down the AV bundles
• 5. Purkinje fibers distribute excitation through ventricular myocardium

• Sympathetic - increases heart rate, contraction strength, and dilates coronary arteries thus increasing blood flow.
• Parasympathetic - reduces heart rate,

Normal heart beat triggered by SA node at 70-80 beats per minute. 60-100 though is not unusual

• Any spontaneous firing of the ventricles ( spontaneous heart beats ) other than from the sinoattrial node.
• Stimuli such as hypoxia, electrolyte imbalance, caffeine, and nicotine can cause this.

• When ectopic focus takes over for controlling heart rhythm when SA or AV node is damaged.
• Slow 40-50 BPM.

When SA and AV nodes are damaged and BPM drops to 20-40. This doesn't provide enough flow to the brain hence this is needed.

Abnormal cardiac rhythm caused by a heart block ( failure of any part of the cardiac conduction system to transmit signals )

• Disease and degeneration of conduction system fibers.
• Bundle branch block - damage to bundle of his branches.
• Total heart block - damage to AV node where ventricles don't receive signals.

• The membrane potential is at -60 MV and drifts upwards at depolarization.
• This is known as pacemaker potential

When membrane potential reaches -40 mV thus producing the rising phase of action potential until it slightly passes 0.

When membrane potential reaches 0 mV and starts repolization of the cell.

• 1. At -60 mV, Na+ slowly flows into the cell. ( Rising slowly and depolarizing )
• 2. At -40 mV, pacemaker potential reaches its threshold. Voltage gated channels of calcium open and Ca2 flows in from extracellular fluid. Depolarization is occuring.
• 3. Depolarization occurs until peaking at 0 mV. K+ channels open and K+ leaves the cell starting repolization bringing it back down to 60 mV.

• Cardiocyte resting potential = -90 mV
• Theyre different from SA nodes because they only deplarize when stimulated.

• 1. From resting ( - 90 mV ) It is stimulated and action potential occurs. Voltage-gated sodium channels allows sodium to flow in thus depolarizing the cells. As it depolarizes, it opens more voltage-gated sodium channels.
• 2. As the cell depolarizes and peaks at +30 mV, the channels close quickly
• 3. At +30 mV slow calcium channels open allowing Ca2+ to come in the cell.
• 4. As Ca2+ flows into the cell depolarization is prolonged ( plateau ) and falls slightly because of K+ leakage.
• 5. At hhe end of pleateu, Calcium Channel close and Ca2+ is transported out of the cell. Potassium channels open and rapid Potassium outflow retruns the membrane down to -90 mV.

When a a signal from the SA node spreads through DEPOLARIZING the atria.

As the atrium depolarizes, atrial systole begins  known as the PQ segment.

• Q = A downward dip
• R = A tall sharp peak
• S= Final downward deflection.

Producerd when Signals from the AV node its the myocardium of ventricle and depolarizes the muscles.

• 1. Ventricular systole begins. 
• 2. Represents thetime durign whcih the ventricles contract and eject blood.

Occurs during the QRS complex.

Repolarization of ventriclles before diastole.

• Lupp: Closing of the AV valve within the heart.
• Dupp: Shutting of the aortic and pulmonary valve semilunar valves.

Indicates an enlarged failing heart.

• 1. Ventricular Filling
• 2. Isovulumetric Contraction
• 3. Ventricular Ejection
• 4. Isovulumetrix Relxation

Ventricles expand and pressure drops below that of atria.  AV valves open and blood flows into ventricles. This marks the P wave. This is where the amount of blood in the ventricle s at its highest ( End-diastolic volume )

Atria repolarizes remaining in diastole for the rest of the cardiac cycle after pushing the blood into the ventricles. At this time, the ventricles depolarize and contract but do nto eject blood yet because pressure in the ventricles is still not higher than that of the aorta.

When ventricular pressure exceeds that of the aorta, semilunar valves open pushing blood out of each ventricle rapidly.

Ventricular diastole occurs when the T wave ends and ventricles begin to expand.

The amount of blood ejected by each ventricle in 1 minute.

CO = Heart Rate x Stroke Volume.

• Heart Rate: 75 bpm
• Stroke Volume: 70 mL/beat

Heart rate above 100 bpm caused by stress, anxiety, drugs, heart disease etc.

Slow heart rate below 60 bpm.

Sympathetic and parasympathetic systems

Increases heart rate by promoting release of noepinephrine causing a second-messenger system in the cardiocytes and nodal cells.

Increase it via activating enzyme that opens Ca2 channels in the plasma membrane which accelerates the depolarization of the SA node ( hence speeding up the heart contraction )

It slows down heart rate by promoting acetycholine to bind with receptors in the cells thus opening Potassium Gates and removing potassium form the cells hence repolarization happens slowing down the heart rate.

They sense pressure in the aorta and internaal carotid arteries. When heart rate rises and raises blood pressure, the baro receptors find sense this and send signals to the medulla to lower the heart rate.

They can also sense drop in blood pressure hence the medulla tells the sympathetic center to increase heart rate.

Mostly important in respiratory control but can also slow down the heart so that the heart does not compete with the brain for limited oxygen supply.

Increases heart rate.

Increases heart rate by stimulating catecholamine secretion.

Increases heart rate.

Accelerates heart beat by inhibiting cAMp break down.

• Hyperkalemia = heart rate slows down because it inhibits caridocyte repolarization. 
• Hypokalemia = slows down because it makes membrane potential harder to stimualte because not enough potassium means the mebmrane potential is lower than normal.

• Hypercalcemia = causes slow heart rate
• Hypocalcemia = increases heart rate.

Amount of tension in the myocardium immediate before it begins to contract.

Increased preload increases stroke volume.

How the myocadrium conntracts for the given preload.

Increase in contractiltiy increases Stroke Volume

• Factors that increase contractility.
• Negative inotropic agents oppose this.

• Chromnotropic influences heart rate.
• Inotropic influences contraction strength.

The sum of all forces ventricle must overcome before it can eject blood specifically the pressure in the aorta and pulmonary trunk.

The ventricels must have higher blood pressure to eject this.

Increases it because it increase the heart rate to supply muscles with enough oxygen and blood.

Exercise causes hypertrophy of the ventricles which increaes their stroke volume.