CH20: The Heart Flashcards
Describe the various coverings of the heart
The membrane surrounding and protecting the heart is pericardium. It confines the heart to its position in the mediastinum, while allowing sufficient freedom of movement for vigorous and rapid contraction. The pericardium consists of two main parts: the fibrous pericardium and the serous pericardium
The superficial fibrous pericardium is composed of tough, inelastic, dense irregular connective tissue. It resembles a bag that rests on and attaches to the diaphragm; its open end is fused to the connective tissues of blood vessels entering and leaving the heart. The fibrous pericardium prevents overstretching of the heart, provides protection and anchors the heart in the mediastinum
The deeper serous pericardium is a more delicate mesothelial membrane that forms a double layer around the heat. The outer parietal layer of the serous pericardium lines the inside of the fibrous pericardium. The inner visceral layer of the serous pericardium also called the epicardium is one of the layers of the heart wall and adheres tightly to the surface of the heart.
Between the parietal and visceral layers of the serous pericardium is a thin film of a few milliliters of lubricating serous fluid. This slippery secretion of the pericardial cells, known as pericardial fluid, reduces friction between the layers of the serous pericardium as the heart moves. The space that contains the few milliliters of pericardial fluid is called the pericardial cavity.
Describe the three layers of the heart wall
The wall of the heart consists of three layers: the epicardium (external layer), the myocardium (middle layer) and endocardium (inner layer). The outermost, as you just learned, is called the visceral layer of the serous pericardium
This thin, transparent outer layer of the heart wall is composed of mesothelium. Beneath the heart wall is a variable layer of delicate fibroelastic tissue and adipose tissue. The adipose tissue predominates and becomes thickest over ventricular surfaces, where it houses the major coronary and cardiac vessels of the heart. The amount of fat varies from person to person and with age
The epicardium imparts a smooth, slippery slippery layer to the outermost surface of the heart. The epicardium contains blood vessels, lymphatics, and nerves that supply the myocardium
The middle myocardium is responsible for the pumping action of the heart and is composed of muscle tissue. It makes up approximately 95% of the heart wall. The muscle fibers (cells), like those of striated skeletal muscle tissue, are wrapped and bundled with connective tissue sheaths composed of endomysium and perimysium. The cardiac muscle fibers are organized in bundles that swirl diagonally around the heart (see diagram above) and generate the strong pumping actions of the heart. Although it is striated like skeletal muscle, recall that cardiac muscle is involuntary like smooth muscle.
The innermost endocardium is a thin layer of endothelium overlying a thin layer of connective tissue. It provides a smooth lining for the chambers of the heart and covers the valves of the heart. The smooth endothelial lining minimizes surface friction as blood passes through the heart. The endocardium is continuous with the endothelial lining of the large blood vessels attached to the heart
Describe the flow of blood
Blood received in the right atrium via the inferior and superior vena cava goes to the right ventricle via gravity
Blood received in the left atrium via the four pulmonary veins goes to the left ventricle via gravity.
Blood is pumped from the right ventricle to the lungs and from the left ventricle to the rest of the body
Contraction of the chambers occurs simultaneously
Describe the function of the chordae tendineae and papillary muscles
The valves located between an atrium and a ventricle are termed atrioventricular (AV) valves. When an AV valve is open, the rounded end of the cusps project into the ventricle. When the ventricles are relaxed, the papillary muscles are relaxed, the chordae tendinae are slack, and blood moves from higher pressure in the atria to lower pressure in the ventricles through open AV valves.
When the ventricles contract, the pressure of the blood drives the cusps upward until their edges meet and close the opening.At the same time, the papillary muscles contract, which pulls on and tightens the chordae tendineae. This prevents the valve cusps from everting (opening into the atria) in response to the high ventricular pressure
Describe systemic and pulmonary circulation
In postnatal circulation, the heart pumps blood into two closed circuits with each beat, system circulation and pulmonary circulation
The two circuits are arranged in series: The output of one becomes the input of another, as would happen if you attached two garden hoses
The left side of the heart is the pump for systemic circulation; it receives bright red oxygenated (oxygen-rich) blood from the lungs thorugh pulmonary veins. The left ventricle ejects blood into the aorta, from where the blood will divide into separate streams, entering progressively smaller systemic arteries that carry blood to all organs except for air sacs of the lungs
In systemic tissues, arteries give rise to smaller-diameter arterioles, which finally lead into extensive beds of systemic capillaries. Exchange of nutrients and gasses occurs across the thin capillary walls. Blood unloads O2 (oxygen) and picks up CO2 (carbon dioxide). In most cases, blood flows through only one capillary and then enters a systemic venule. Venules carry deoxygenated (oxygen-poor) blood away from tissues and merge to form larger systemic veins. Ultimately the blood flows back to the right atrium.
The right side of the heart is the pump for pulmonary circulation, in that it receives dark red deoxygenated blood returning from systemic circulation. Blood ejected from the right ventricle flows into the pulmonary trunk, which branches into pulmonary arteries that carry blood to the right and left lungs. In pulmonary capillaries, around pulmonary alveoli, blood unloads CO2, which is exhaled, and picks up O2 from inhaled air. The freshly oxygenated blood then flows into pulmonary veins and returns to the left atrium
Describe the right and left coronary arteries
The left coronary artery passes inferior to the left auricle and divides into three arteries.
The anterior inter-ventricular artery runs along the anterior inter-ventricular sulcus and supplies oxygenated blood to the walls of both ventricles
The circumflex artery lies in the coronary sulcus and distributes oxygenated blood to the walls of the left ventricle and atrium
There is also a left marginal branch running along the left margin of the heart and feeding the left ventricle
The right coronary artery divides into the posterior ventricular artery along the posterior inter-ventricular sulcus (kinda like the opposite of anterior inter-ventricular artery) and also supplies the two ventricles with oxygenated blood
The right marginal branch, like the other marginal branch rides along the right margin of the heart and feeds oxygenated blood to the wall of the right ventricle
Describe the sequence for action potential generation in the cardiac conductino system
Cardiac excitation normally begins in the sinoatrial (SA) node, located in the right atrial node. SA node cells do not have a stable resting potential, and instead continuously spontaneously depolarize to threshold. This repolarization is a pacemaker potential, and when it reaches threshold, triggers an action potential. Each action potential from the SA node propagates throughout both atria via gap junctions in the intercalated discs of atrial muscle fibers, so the two atria contract at the same time
The action potential then reaches the atrioventricular (AV) node, located in the interatrial septum. At the AV node, the action potential slows as a result of various differences in the cell structures of AV node cells, which provides a delay of time that allows the atria to empty their blood into the ventricles
From the AV node, the action potential enters the atrioventricular (AV) bundle, also known as the bundle of His. This is the only site where action potentials can conduct from atria to the ventricles, as elsewhere, fibrous skeleton of the heart electrically insulates the atria from the ventricles
After propagating through the AV bundle, the action potential enters both the right and left bundle branches. The bundle branches extend through the interventricular septum toward the apex of the heart
Finally, a large-diameter subendocardial conducting network or Purkinje fibers rapidly conducts the action potential beginning at the apex of the heart upward to the remainder of the ventricular myocardium. This causes upward movement of blood toward the semilunar valves
Describe how action potential occurs in a contractile fiber
Depolarization: The stable resting membrane potential is close to -90mV. When a contractile fiber is brought to threshold by an action potential from neighboring fibers, its voltage-gated fast Na+ channels open. These ion channels are so named because they open rapidly in response to a threshold-level depolarization, and opening of these channels causes inflow of Na+. Inflow of Na+ against its electrochemical gradient produces a rapid depolarization. The channels close very quickly
Plateau: The next phase of an action potential in a contractile fiber is the plateau, which is a period of maintained depolarization . It is due in part to opening of voltage-gated slow Ca2+ channels in the sarcolemma. When these channels open, calcium ions move from the interstitial fluid (which has a higher Ca2+ concentration) into the cytosol. This inflow of Ca2+ causes even more Ca2+ to pour out of the sarcoplasmic reticulum into the cytosol through additional Ca2+ channels in the sarcoplasmic reticulum membrane. The increased Ca2+ concentration in the cytosol ultimately triggers contraction.
Several different types of voltage-gated K+ channels are also found in the sarcolemma of a contractile fiber. Just before the plateau phase begins, some of these K+ channels open, allowing potassium ions to leave the contractile fiber. Therefore, depolarization is sustained during the plateau phase because Ca2+ inflow just balances K+ outflow. The plateau phase lasts for about 0.2 sec, and the membrane potential of the contractile fiber is close to 0 mV. By comparison, depolarization in a neuron or skeletal muscle fiber is much briefer, about 1 msec (0.001 sec), because it lacks a plateau phase
Repolarization: The recovery of the resting membrane potential during the repolarization phase of a cardiac action resembles that in other excitable cells. After a delay (which is particularly prolonged in cardiac muscle), additional voltage-gated K+ channels open. Outflow of K+ restores the negative resting membrane potential (−90 mV). At the same time, the calcium channels in the sarcolemma and the sarcoplasmic reticulum are closing, which also contributes to repolarization.
What is a cardiac cycle and the consequences of it
A single cardiac cycle includes all of the events associated with one heartbeat. Thus, a cardiac cycle consists of systole and diastole of the atria plus systole and diastole of the ventricles.
In each cardiac cycle, the atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure. As a chamber of the heart contracts, blood pressure within it increases
Describe the events and any significant pressure/volume changes in a cardiac cycle during a cardiac cycle
During atrial systole, which lasts about 0.1 seconds, the atria are contracting, and the ventricles are relaxed.
1. Depolarization of the SA node causes atrial depolarization, marked by the P wave in the ECG
2. Atrial depolarization causes atrial systole, which causes the atria to contract, exerting pressure in the blood within, forcing blood through the open AV valves into the ventricles
3. Atrial systole contributes a final 25 mL of blood to the 105 mL of blood already in each ventricle. The end of each atrial systole is also the end of ventricle diastole (relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation period. This blood volume is called the end-diastolic volume (EDV)
4. The QRS complex in the ECG marks the onset of vascular depolarization
Ventricular Systole
During ventricular systole, which lasts about 0.3 sec, the ventricles are contracting. At the same time, the atria are in atrial diastole, relaxation baby.
- Ventricular depolarization causes ventricular systole. As the ventricular systole begins, pressure rises inside the ventricles and pushes blood up against the AV valves, forcing them shut. For about 0.05 seconds, the SL and AV valves are shut, a period known as isovolumetric contraction, as ventricular volume and muscle length remain constant.
- When left ventricular pressure surpasses aortic pressure at about 80 millimeters of mercury (mmHg) and right ventricular pressure rises above the pressure in the pulmonary trunk (about 20 mmHg), both SL valves open. At this point, ejection of blood from the heart begins. The period when the SL valves are open is ventricular ejection and lasts for about 0.25 sec. The pressure in the left ventricle continues to rise to about 120 mmHg, and the pressure in the right ventricle climbs to about 25–30 mmHg.
- The left ventricle ejects about 70 mL of blood into the aorta and the right ejects the same amount of blood into the pulmonary trunk. The volume remaining in each ventricle at the end of systole is about 60 mL, and is called end-systolic volume (ESV).
Stroke volume, the volume ejected per beat from each ventricle, equals end-diastolic volume minus end-systolic volume: SV = EDV − ESV. At rest, the stroke volume is about 130 mL − 60 mL = 70 mL (a little more than 2 oz). - The T wave in the ECG marks the onset of ventricular repolarization
Relaxation
During the relaxation period, which lasts about 0.4 seconds, the atria and the ventricles are both relaxed. As the heart beats faster and faster, the relaxation period becomes shorter and shorter, whereas the durations of atrial systole and ventricular systole shorten only slightly.
9. Ventricular repolarization causes ventricular diastole. As the ventricles relax, pressure within the chambers falls, and blood in the aorta and pulmonary trunk begins to flow backward toward the regions of lower pressure in the ventricles. Backflowing blood catches in the valve cusps and closes the SL valves. The aortic valve closes at a pressure of about 100 mmHg. Rebound of blood off the closed cusps of the aortic valve produces the dicrotic wave on the aortic pressure curve. After the SL valves close, there is a brief interval when ventricular blood volume does not change because all four valves are closed. This is the period of isovolumetric relaxation.
10. As the ventricles continue to relax, the pressure falls quickly. When ventricular pressure drops below atrial pressure, the AV valves open, and ventricular filling begins. The major part of ventricular filling occurs just after the AV valves open. Blood that has been flowing into and building up in the atria during ventricular systole then rushes rapidly into the ventricles. At the end of the relaxation period, the ventricles are about three-quarters full. The P wave appears in the ECG, signaling the start of another cardiac cycle.
What are the 3 factors controlling the stroke volume
(1) Preload: Preload is correlated to the amount of blood entering during diastole, which is the end-diastolic volume (EDV). Preload itself is the degree of stretching of the cardiac muscle fibers (myocytes) in the ventricles just before they contract. This causes a phenomenon known as the Frank-Starling mechanism, where a greater preload results in a more forceful contraction, leading to increased ejection of blood
(2) Afterload: Afterload is the resistance ventricles must overcome to circulate blood. An increased afterload can reduce stroke volume, as the heart has to work harder in order to overcome the resistance in the arteries, which can decrease the amount of blood ejected per contraction
(3): Contractility: Contractility refers to the force generated by the myocardium in response to a given level of stretch, and is often influenced by factors such as ion concentrations, sympathetic nervous system activity and certain medications. An increase in contractility generally leads to an increase in stroke volume, meaning the heart can eject more blood with each contraction
