CV-2

The heart is positioned with the apex of the heart, projecting anteriorly and inferiorly towards the left fifth intercostal space at the midclavicular line.

The heart is surrounded by a fibrous double walled sac called the pericardium, which envelops the heart and the roots of the great vessels.

The pericardium protects the heart and holds it in place.

The pericardium is pierced, meaning something's going through it superiorly by the aorta, the pulmonary trunk, and the superior vena cava.

The space in the pericardial cavity normally contains about ten to 25 mLs of a serous fluid, which provides lubrication so that the heart can move freely within the mediastinum.

​The tricuspid valve has three leaflets, papillary muscles and chordae tendineae attached to the leaflets to prevent it from eroding during systole and therefore prevents back flow of blood from the ventricles to the atria during ventricular systole.

The chordae tendineae, along with papillary muscle hold the flaps, or cusps, of each valve in place.

When the ventricles contract, pressure gradients across the valves pull the cusps of the mitral and tricuspid valves shut.

The configuration of the pulmonary and aortic valves is similar, each valve is composed of three cusps, not leaflets.

The cusps of the aortic and pulmonary valve are flaps of endocardium and connective tissue reinforced by fibers that prevent the valves from turning inside out.

The cusps of the aortic valve are slightly thicker than pulmonary valve because it is subjected to greater pressures, which is created by that left ventricular ejection.

The semilunar valves are the aortic valve and pulmonary valve.

Above the aortic valve is a dilation known as the sinus of Valsalva, which will allow the valve to open efficiently without occluding the coronary ostia.

The coronary ostia is the openings above the aortic valve that communicate with the coronary arteries​.

Normal coronary blood flow is 225ml/min.

Normal coronary blood flow is 4-5% of the cardiac output.

Myocardial oxygen consumption is 65-70%.

To increase coronary blood flow and increase myocardial oxygen supply you must increase CPP or induce coronary vasodilation.

Coronary autoregulation is under the control of neurohormonal, endocrine, metabolic and endothelial derived systems which induce either coronary vasoconstriction or vasodilation.

CPP is the pressure that drives coronary perfusion.

CPP is autoregulated between MAP of 60-140.

CPP = (aortic) DBP minus LVEDP.

The major determinant of CPP is DBP.

CPP is inversely related to HR and coronary vascular resistance.

CPP is inversely related to increased vascular resistance with CAD, increased sympathetic tone and increased blood viscosity.

The a wave represents the end of atrial systole just before the mitral valve closes.

The c wave represents ventricular contraction and it's produced by bulging of the mitral valve caused by increased left ventricular pressure.

The V wave represents increased pressure in the left atrium, caused by blood return from the pulmonary veins before the mitral valve opens.

The QRS wave is the electrical depolarization of the ventricles, which initiates contraction of the ventricles. The T wave is the ventricular repolarization when the ventricular muscle fibers begin to relax.

S1 is the first sound being the mitral and tricuspid valves closing.

The second sound, S2, being the closure of the aortic and pulmonary valves.

The third sound is made during passive left ventricular filling and of the blood striking the left ventricle.

This period of this period of rapid filling last for about the first third of diastole.

Approximately 60 percent of the blood in the ventricles at the end of diastole is ejected during systole. And about 70 percent of this portion flows out during the first third of the ejection period with the remaining 30 percent emptying in the next two thirds of that cycle. And so therefore, the first third is called a period of rapid ejection, where the last third is called a period of slow ejection.

During diastole, normal filling of the ventricles increases the volume of each ventricle to about a 110 to a 120 mLs, this volume is called end-diastolic volume.

Stroke volume is the volume emptied by the ventricle or pumper out.

Normal stroke volume is 70ml.

End systolic volume is the volume of blood in the ventricle at the end of systole which is approximately 40-50.

At rest the heart pumps 4 to 6 liters of blood per minute.

Pumping of the heart is regulated by intrinsic response to changes in volume of blood flowing into the heart which is Frank starling.

Under most conditions, the amount of blood pumped out by the heart each minute is normally determined by the rate of blood flow into the heart from the venous system, the venous return into the heart.

The heart has an intrinsic ability to adapt to increasing or decreasing volumes of inflowing blood which is called the Frank Starling mechanism of the heart.

The frank starling mechanism explains that the more the heart muscle stretches during diastole the more forcefully they contract during systole, up to a point.

If the muscles are stretched too much those actin and myosin filaments are stretched too far and contraction is no longer effective.

For a given levels of atrial pressure, the amount of blood pumped out each minute, the cardiac output can increase more than a 100 percent.

By increasing sympathetic stimulation, CO can be decreased to almost 0 output by vagal stimulation, which is also very powerful.

SNS innervates both atria, ventricles and SA and AV node conduction to increase HR and contractility.

The sympathetic nerves fibers originate from the thoracic vertebrae one through four.

T1-T4 part of the thoracic or spinal cord segments are known as the cardiac accelerator fibers which innervate the entire myocardium of ventricles.

There is a greater SNS innervation to the ventricles.

NE and Epi primarily bind to beta 1 receptors on the heart that increase its contractility.

Strong stimulation of the parasympathetic nerve fibers can actually stop the heartbeat for a few seconds, but then the heart usually has some escape beats and is able to continue beating.

Strong vagal stimulation can decrease the strength of heart muscle contraction.

So the vagal fibers are actually mainly distributed to the atria and not so much the ventricles where the power of contraction is.

Vagal stimulation mainly decreases heart rate rather than decreasing the strength of contraction.

PNS innervates SA and AV nodes and atria, no major input to ventricles.

PNS fibers originate in the dorsal motor nucleus of the vagus nerve in the medulla.

Ach is the transmitter of PNS.

Catecholamines released during SNS stimulation activate beta 1 on the heart.

Lusitropy is effecting rate of myocardial relaxation and diastolic function.

Lusitropy is related to the removal of calcium back into the sarcoplasmic reticulum.

Dromotropy is effecting the conduction speed in the AV node.

Ionotropy has to do with systolic function.

Preload is the amount of passive stretching of muscle fibers in ventricle at the end of diastole, influenced by volume of blood in ventricles at end of diastole.

Preload is measured by pressure in the ventricle at the end of diastole (LVEDP, PCWP, CVP).

Afterload is amount of resistance or pressure the ventricular muscles must generate to overcome higher pressure in the aorta to eject the blood (preload) out of the heart.

Afterload is pressure on the ventricular wall during contraction/systole and influenced by pulmonary vascular resistance for the right ventricle and the systemic vascular resistance for the left.

Barorecptor reflex is responsible for the maintenance of arterial blood pressure to a preset value through a negative feedback loop where high blood pressure (stretch) causes decrease in HR.

Baroreceptors stretch receptors in carotid sinus and aortic arch (afferent fibers of glossopharyngeal and vagus nerves) depressor system effect of decreasing cardiac contractility, decreasing heart rate, and decreasing vascular tone.

Chemoreceptor reflex is chemosensitive cells in carotid bodies and aortic arch that responds to pH and oxygen tension.

Bainbridge reflex has stretch receptors in RA wall and cavoatrial junction which inhibit PNS with stretch of RA, increasing HR.

Bainbridge stretch of SA node will cause inhibition of PNS increases HR.

In chemoreceptor when you have low periods of oxygen tensions, so you're hypoxic or in conditions of acidosis the chemo receptors respond by going to the respiratory center and increasing your ventilatory drive to decrease your CO2.

With chemoreceptor reflex you get activation of the parasympathetic system and that leads to a reduction in heart rate and myocardial contractility.

So in cases of persistent hypoxia, the CNS will be directly stimulated, which will result in increased sympathetic activity with chemoreceptor reflex.

Bezold Jacob reflex response to pain and increases PNS tone leading to a decreased HR.

Bezold jacob sensed by chemo and mechano receptors in ventricles to noxious stimuli which is sensed during hypotension or bradycardia.

Bezold jacob activated by C fibers which increase PNS tone to decrease HR.

Bezold jacob reflex causes vasodilation, bradycardia and hypotension.

Baroreceptor reflex is lost when arterial pressure is below 50.

Barorecptor range can be adjusted with conditions like chronic hypertension.

Valsalva is forced expiration through a closed glottis which produces increased intrathoracic pressure, increased central venous pressure and decreased venous return which will decrease CO and BP. The decrease in venous return will be sensed by baroreceptors which will then cause reflexive increase in HR and contractility.

Cushing reflex is caused by cerebral ischemia due to ICP and results in activation of SNS to increase HR, contractility and BP to increase cerebral perfusion. Reflexive bradycardia mediated via baroreceptors can result due to the really high vascular tone.

The ocular cardiac reflex is provoked by pressure applied to the globe of the eye or traction on the muscle surrounding the structures of the eye.

Stretch receptors are located in these extra ocular muscles of the eye.

Ocular stretch receptors once activated, these stretch receptors will send signals and which result in increase parasympathetic tone and subsequent bradycardia.

The primary control of cardiac output is venous return because of the frank starling mechanism.

Stretching of SA node increases HR and stretched RA increases HR via bainbridge.

The main reason why peripheral factors are so important in controlling cardiac output is that the heart has a built-in mechanism that normally allows it to pump automatically the amount of blood that flows from the veins into the right atrium and then out. And this mechanism, as you roll call is called the Frank Starling law of the heart or the Frank Starling mechanism. This law states that when increased quantities of blood flow into the heart, the increased volume of blood stretches the walls of the heart chambers. And as a result of that stretch, the heart muscle contracts with increased force

Cardiac output level varies inversely with changes in total peripheral vascular resistance. As long as the arterial blood pressure is unchanged.

So when the total peripheral resistance is normal, the cardiac output is also normal. When the total peripheral resistance increases, cardiac output falls.

Factors affecting HR include atrial reflex which effects ANS and hormones.

Factors affecting stroke volume include venous return, filling time, ANS innervation, hormones and vasodilation or constriction.

Afterload is impacted by vasodilation and vasoconstriction.

Contractility is affected by ANS and hormones.

Preload is affected by venous return and filling time.

Things that cause hypereffective CO is nervous system stimulation and hypertrophy of heart muscle.

The normal intrapleural pressure, the pressure in the chest cavity for everyone is usually about negative four. This negative intrapleural pressure allows the lungs to expand and stay expanded during exhalation. Otherwise, they would collapse during exhalation. However, this negative intrapleural pressure causes external pressure on the heart.

If intrapleural pressure rises to negative two, this shifts the entire cardiac output curve to the right by the same amount. This shift occurs because filling of the cardiac chambers with blood requires an extra two millimeters of pressure.

Factors that alter the external pressure on the heart and shift curve to the right include cyclical changes of intrapleural pressure during normal inspiration, strenuous exercise, breathing against negative pressure, positive pressure breathing with ventilator.

Principle factors that affect venous return to the heart include right atrial pressure, degree of filling of the systemic circulation and resistance to blood flow between the peripheral vessels and the right atrium.

right atrial pressure, which exerts a backward force on the veins to keep blood from coming from the veins into the right atrium.