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Questions and Answers
Which layer of the heart wall is also known as the visceral layer of the serous pericardium?
Which layer of the heart wall is also known as the visceral layer of the serous pericardium?
What is the space between the parietal and visceral layers of the serous pericardium called?
What is the space between the parietal and visceral layers of the serous pericardium called?
Which of the following is the outermost layer that surrounds the heart?
Which of the following is the outermost layer that surrounds the heart?
Which layer of the heart wall is responsible for the heart's pumping action?
Which layer of the heart wall is responsible for the heart's pumping action?
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Which layer of the heart is in direct contact with the blood in the heart chambers?
Which layer of the heart is in direct contact with the blood in the heart chambers?
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What is the primary cause of the pain experienced during angina pectoris?
What is the primary cause of the pain experienced during angina pectoris?
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In myocardial infarction, what type of tissue typically replaces the dead cardiac cells?
In myocardial infarction, what type of tissue typically replaces the dead cardiac cells?
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Which of the following is a unique structural characteristic of cardiac muscle cells?
Which of the following is a unique structural characteristic of cardiac muscle cells?
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What is the function of desmosomes within the intercalated discs of cardiac muscle?
What is the function of desmosomes within the intercalated discs of cardiac muscle?
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What is the primary function of the tricuspid valve?
What is the primary function of the tricuspid valve?
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Which vessels deliver oxygen-poor blood to the right atrium of the heart?
Which vessels deliver oxygen-poor blood to the right atrium of the heart?
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What is the primary role of gap junctions in cardiac muscle tissue?
What is the primary role of gap junctions in cardiac muscle tissue?
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Where does the pulmonary trunk transport blood to?
Where does the pulmonary trunk transport blood to?
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Why do cardiac muscle cells contain a large number of mitochondria?
Why do cardiac muscle cells contain a large number of mitochondria?
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The arrangement of cardiac muscle cells interconnected by intercalated discs allows the heart to function as a:
The arrangement of cardiac muscle cells interconnected by intercalated discs allows the heart to function as a:
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What is the purpose of the pulmonary semilunar valve?
What is the purpose of the pulmonary semilunar valve?
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How do the T tubules and sarcoplasmic reticulum (SR) in cardiac muscle compare to those in skeletal muscle?
How do the T tubules and sarcoplasmic reticulum (SR) in cardiac muscle compare to those in skeletal muscle?
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What is the key difference between blood in the pulmonary arteries versus blood in the pulmonary veins?
What is the key difference between blood in the pulmonary arteries versus blood in the pulmonary veins?
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A blockage in the superior vena cava (SVC) would directly impede blood flow from which region of the body?
A blockage in the superior vena cava (SVC) would directly impede blood flow from which region of the body?
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If the tricuspid valve were to fail, allowing significant backflow, what immediate effect would this have on the body?
If the tricuspid valve were to fail, allowing significant backflow, what immediate effect would this have on the body?
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Why is it essential for blood to pass through the pulmonary circuit?
Why is it essential for blood to pass through the pulmonary circuit?
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If the internodal pathways were damaged, disrupting normal signal transmission, which of the following is the most likely immediate consequence?
If the internodal pathways were damaged, disrupting normal signal transmission, which of the following is the most likely immediate consequence?
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What would be expected if the AV node failed to delay the impulse from the SA node?
What would be expected if the AV node failed to delay the impulse from the SA node?
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Which of the following correctly describes the role of the subendocardial conducting network (Purkinje fibers)?
Which of the following correctly describes the role of the subendocardial conducting network (Purkinje fibers)?
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A doctor discovers that a patient's sinoatrial (SA) node is firing at a slower than normal rate. What is the most likely effect of this condition?
A doctor discovers that a patient's sinoatrial (SA) node is firing at a slower than normal rate. What is the most likely effect of this condition?
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Why is the slight delay of the impulse at the atrioventricular (AV) node critical for effective heart function?
Why is the slight delay of the impulse at the atrioventricular (AV) node critical for effective heart function?
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What is the primary reason for the AV node delay?
What is the primary reason for the AV node delay?
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If the SA node fails, what happens to the heart rate and why?
If the SA node fails, what happens to the heart rate and why?
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Why is the subendocardial conducting network more elaborate on the left side of the heart?
Why is the subendocardial conducting network more elaborate on the left side of the heart?
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Which of the following describes the function of the bundle branches?
Which of the following describes the function of the bundle branches?
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What property of the SA node makes it the heart's primary pacemaker?
What property of the SA node makes it the heart's primary pacemaker?
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Why is the AV bundle the only electrical connection between the atria and ventricles?
Why is the AV bundle the only electrical connection between the atria and ventricles?
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Following damage to the AV node, what inherent rate of depolarization would you expect to see in the subendocardial conducting network?
Following damage to the AV node, what inherent rate of depolarization would you expect to see in the subendocardial conducting network?
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Ventricular contraction starts at the apex of the heart due to the subendocardial conducting network. Why is this contraction pattern important?
Ventricular contraction starts at the apex of the heart due to the subendocardial conducting network. Why is this contraction pattern important?
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If the sinoatrial (SA) node were damaged, what would be the most likely consequence?
If the sinoatrial (SA) node were damaged, what would be the most likely consequence?
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What is the functional significance of the 0.1 s pause at the atrioventricular (AV) node?
What is the functional significance of the 0.1 s pause at the atrioventricular (AV) node?
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Which of the following is the correct sequence of excitation waves in the heart?
Which of the following is the correct sequence of excitation waves in the heart?
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What would be the effect of a drug that slows conduction through the atrioventricular (AV) node?
What would be the effect of a drug that slows conduction through the atrioventricular (AV) node?
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Why is the intrinsic conduction system of the heart crucial for proper heart function?
Why is the intrinsic conduction system of the heart crucial for proper heart function?
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Which component of the intrinsic conduction system is located within the interventricular septum?
Which component of the intrinsic conduction system is located within the interventricular septum?
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If the internodal pathways are damaged, but the SA and AV nodes are still functional, what effect might be observed?
If the internodal pathways are damaged, but the SA and AV nodes are still functional, what effect might be observed?
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A cardiologist observes that a patient's ECG shows a prolonged PR interval (time between atrial and ventricular depolarization). Which component of the intrinsic conduction system is most likely affected?
A cardiologist observes that a patient's ECG shows a prolonged PR interval (time between atrial and ventricular depolarization). Which component of the intrinsic conduction system is most likely affected?
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Flashcards
Pulmonary Trunk
Pulmonary Trunk
The major vessel that carries deoxygenated blood from the right ventricle to the lungs.
Fibrous Pericardium
Fibrous Pericardium
The tough outer layer of the pericardium that protects the heart.
Serous Pericardium
Serous Pericardium
The inner layer of the pericardium, which includes parietal and visceral layers.
Myocardium
Myocardium
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Endocardium
Endocardium
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Oxygen-rich blood
Oxygen-rich blood
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Pulmonary circuit
Pulmonary circuit
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Superior vena cava (SVC)
Superior vena cava (SVC)
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Right atrium
Right atrium
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Tricuspid valve
Tricuspid valve
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Right ventricle
Right ventricle
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Pulmonary arteries
Pulmonary arteries
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Oxygenation
Oxygenation
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Angina pectoris
Angina pectoris
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Myocardial infarction
Myocardial infarction
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Cardiac muscle structure
Cardiac muscle structure
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Intercalated discs
Intercalated discs
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Desmosomes
Desmosomes
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Gap junctions
Gap junctions
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Functional syncytium
Functional syncytium
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Mitochondria in cardiac muscle
Mitochondria in cardiac muscle
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Internodal pathway
Internodal pathway
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Sinoatrial (SA) node
Sinoatrial (SA) node
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Atrioventricular (AV) node
Atrioventricular (AV) node
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Purkinje fibers
Purkinje fibers
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Electrical impulse pause
Electrical impulse pause
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Sequence of Excitation
Sequence of Excitation
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Atrioventricular (AV) bundle
Atrioventricular (AV) bundle
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Right and left bundle branches
Right and left bundle branches
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Subendocardial conducting network
Subendocardial conducting network
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Ventricular contraction
Ventricular contraction
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Impulses per minute
Impulses per minute
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Bundle Branches
Bundle Branches
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Interventricular Septum
Interventricular Septum
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Electrical Excitation
Electrical Excitation
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Study Notes
Chapter 18: The Cardiovascular System: The Heart
- The heart is a transport system, functioning as two side-by-side pumps.
- The right side receives oxygen-poor blood from tissues and pumps it to the lungs for CO2 removal and O2 acquisition.
- The left side receives oxygenated blood from the lungs and pumps it to body tissues via the systemic circuit.
- The heart has receiving chambers: the right atrium receives blood returning from the systemic circuit and the left atrium receives blood returning from the pulmonary circuit.
- The heart has pumping chambers: the right ventricle pumps blood through the pulmonary circuit and the left ventricle pumps blood through the systemic circuit.
- The heart wall is composed of three layers: the epicardium (visceral layer of the serous pericardium), the myocardium (contractile cardiac muscle cells), and the endocardium (lining the chambers & valves). The cardiac skeleton is a layer of connective tissue within the myocardium.
Heart Anatomy
- Approximately the size of a fist.
- Located in the mediastinum between the second rib and fifth intercostal space.
- Rests on the superior surface of the diaphragm.
- Two-thirds of the heart is to the left of the midsternal line.
- Anterior to the vertebral column, posterior to the sternum.
- The base leans toward the right shoulder.
- The apex points toward the left hip.
- The apical impulse is palpable between the fifth and sixth ribs, just below the left nipple.
Coverings of the Heart: Pericardium
- A double-walled sac.
- The superficial fibrous pericardium protects and anchors the heart to surrounding structures. Prevents overfilling.
- The deep two-layered serous pericardium consists of a parietal layer lining the internal surface of the fibrous pericardium and a visceral layer (epicardium) on the external heart surface. The pericardial cavity between the layers contains fluid, reducing friction.
Homeostatic Imbalance
- Pericarditis: Inflammation of the pericardium, causing a friction rub (creaking sound) that may be detected with a stethoscope. A severe form is cardiac tamponade, characterised by excess fluid compressing the heart and limiting its pumping ability.
Layers of the Heart Wall
- The heart wall is composed of three layers: the epicardium (visceral layer of the serous pericardium), the myocardium (contractile cardiac muscle cells), and the endocardium (lining the chambers & valves). The cardiac skeleton is a layer of connective tissue within the myocardium.
Chambers
- Four chambers: two superior atria and two inferior ventricles.
- The interatrial septum separates the atria. The fossa ovalis is a remnant of the foramen ovale of the fetal heart.
- The interventricular septum separates the ventricles.
Chambers and Associated Great Vessels
- Coronary sulcus (atrioventricular groove): Encircles the junction of the atria and ventricles.
- Anterior interventricular sulcus: Anterior position of the interventricular septum.
- Posterior interventricular sulcus: Landmark on the posteroinferior surface.
Atria: The Receiving Chambers
- Auricles: Appendages that increase atrial volume.
- Right atrium: Pectinate muscles; separated by the crista terminalis (posterior and anterior regions).
- Left atrium: Pectinate muscles only in auricles.
- The right atrium receives blood from the superior vena cava, inferior vena cava, and coronary sinus.
- The left atrium receives blood from the four pulmonary veins.
Ventricles: The Discharging Chambers
- Most of the heart's volume. The shape varies.
- The right ventricle lies mostly on the anterior surface.
- The left ventricle is located on the inferior surface.
- Trabeculae carneae: Irregular ridges of muscle on the ventricular walls.
- Papillary muscles: Anchor chordae tendineae.
- The right ventricle pumps blood into the pulmonary trunk.
- The left ventricle pumps blood into the aorta.
Heart Valves
- Ensure unidirectional blood flow.
- Two atrioventricular (AV) valves (tricuspid and mitral) prevent backflow into atria when ventricles contract.
- Two semilunar (SL) valves (pulmonary and aortic) prevent backflow into ventricles when ventricles relax.
Pathway of Blood Through the Heart
- Pulmonary circuit: Right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs → pulmonary veins → left atrium.
- Systemic circuit: Left atrium → mitral valve → left ventricle → aortic semilunar valve → aorta → systemic circulation.
Coronary Circulation
- Functional blood supply to heart muscle itself, delivered when the heart is relaxed.
- The left ventricle receives most of the blood supply, while the arterial blood supply varies by individuals, containing many anastomoses or junctions.
- The coronary arteries arise from the base of the aorta. Branches include the left coronary artery (with anterior interventricular artery and circumflex artery) and the right coronary artery (with right marginal artery and posterior interventricular artery).
- Cardiac veins collect blood from capillary beds, merging to form the coronary sinus which empties into the right atrium.
Cardiac Muscle
- Striated, short, branched cells with one (or perhaps two) central nuclei.
- Connective tissue matrix (endomysium) connects to the cardiac skeleton.
- Contains numerous capillaries.
- T tubules are wider, and less numerous, and SR is simpler than in skeletal muscle.
- Large number of mitochondria (25-35% of cell volume).
- Intercalated discs: Junctions between cells that anchor cardiac cells and prevent separation during contraction. Desmosomes strengthen the connection, while gap junctions allow ions to pass, allowing the heart to function as one coordinated unit (functional syncytium).
Cardiac Muscle Contraction
- Three differences from skeletal muscle:
- Autorhythmicity: ~1% of cells can spontaneously depolarize and initiate the action potential.
- Functional syncytium: All cardiomyocytes contract as one unit, either all or none.
- Refractory period: A long absolute refractory period prevents tetanic contractions.
- Three ways the contraction of cardiac muscle is similar to skeletal muscle:
- Fast Na+ channels
- Depolarization wave down T tubules
- Excitation-contraction coupling
Energy Requirements
- Cardiac muscle relies heavily on aerobic respiration due to a high number of mitochondria.
- It readily switches fuel sources and even utilizes lactic acid from skeletal muscles.
Homeostatic Imbalances
- Ischemic cells: Anaerobic respiration results in high lactic acid and Ca2+ concentration, leading to mitochondrial damage, reduced ATP production, and eventual gap junction closure, which leads to fatal arrhythmias.
- Angina pectoris: Thoracic pain caused by a fleeting deficiency of oxygen supply to the myocardium.
- Myocardial infarction (heart attack): Prolonged blockage of a coronary artery leads to areas of cell death, replaced by non-contractile scar tissue.
- Other imbalances include conditions affecting intrinsic conduction, such as arrhythmias, fibrillation and heart block. Defects in the intrinsic conduction system can also lead to ectopic foci, premature contractions (extrasystoles), or abnormal pacemaker activity.
Heart Physiology: Electrical Events
- The heart depolarizes and contracts without nervous system stimulation because cardiac cells exhibit autorhythmicity.
- The pacemaker potential allows certain cells to repeatedly reach threshold potential.
- Specific cells (SA node) depolarize faster than other cells, with the action potential conducted throughout the heart in 220ms.
Heart Physiology: Setting the Basic Rhythm
- The coordinated heartbeat is aided by gap junctions connecting all cardiac cells and an intrinsic conduction system (network of noncontractile cells).
- The intrinsic conduction system initiates and conducts the impulses that control heart contraction (depolarization and contraction of the heart).
Pacemaker (Autorhythmic) Cells
- These cells possess unstable resting membrane potentials (pacemaker potentials) which continuously depolarize and reach threshold, generating the action potential. This continuous depolarization results from the opening and closing of specific ion channels.
- Depolarization is caused by calcium influx through slow channels, causing excitation.
- Repolarization occurs with calcium channel inactivation and potassium channel opening.
Action Potential Initiation by Pacemaker Cells
- The action potential has three stages:
- Pacemaker potential: Repolarization closes K+ channels allowing Na+ channels to open and thus, continuously depolarize, reaching threshold and initiating the next potential.
- Depolarization: Calcium channels open; huge influx of calcium ions leads to the rising phase of the action potential.
- Repolarization: Calcium channels close and K+ channels open; efflux of potassium ions brings the potential back to its resting voltage.
Sequence of Excitation
- Impulses pass across the heart in order, ~220ms. The sequence begins at the SA node, through intermodal pathways to the AV node, then to the AV bundle, the right and left bundle branches and finally the subendocardial network (Purkinje fibers).
- The SA node, located in the right atrium, is the heart's pacemaker, depolarizing faster than other myocardial cells. The inherent rate of this node is 100/minute but tempered by extrinsic factors. Atrial contraction precedes ventricular contraction due to a brief pause of 0.1s at the AV node.
Heart Physiology: Sequence of Excitation
- SA node (right atrial wall) is the pacemaker, depolarizing faster than rest of myocardium; generates 75X/min impulses (sinus rhythm), with an inherent rate of 100/min that is tempered by extrinsic factors.
- Impulses then travel across the atria, and to the AV node.
- The AV node is located in the inferior interatrial septum, providing a delay of ~0.1 second. This delay allows the atria to contract before the ventricles, ensuring proper blood flow. Its inherent rate is 50x/minute in the absence of SA node stimulation.
- The signal then passes to the AV bundle (bundle of His), found in the superior interventricular septum, the only electrical connection between the atria and ventricles. Atria and ventricles are not connected via gap junctions.
- The AV bundle branches provide two pathways in the interventricular septum and carry the signal toward the apex of the heart.
- The cardiac impulse then passes through the subendocardial conducting network (Purkinje fibres), depolarizing the contractile cells of both ventricles. Ventricular contraction begins at the apex, moving upward towards the atria.
Homeostatic Imbalances
- Heart Block: Defective AV node may cause few (partial) or no (complete) impulses to reach ventricles. This results in ventricles beating at much too slow intrinsic rate (below 50bpm), resulting in inadequate circulation in most people. Artificial pacemakers can treat this condition.
- Arrhythmias: Defects in intrinsic conducting system, generating irregular heart rhythms (uncoordinated atrial and ventricular contractions).
- Fibrillation: Rapid, irregular contractions are useless for pumping blood; circulation ceases, leading to brain death. Defibrillation can help treat this condition.
- Ectopic Foci: Abnormal pacemaker cells initiate the impulse; these cells may be in the AV node (junctional rhythm — 40–60 beats/minute). Irregular rhythms can also arise from ectopic foci, often triggered by excessive caffeine or nicotine.
Extrinsic Innervation of the Heart
- The heartbeat is modified by the autonomic nervous system via cardiac centers in the medulla oblongata.
- The cardioacceleratory center (sympathetic) increases the heart rate and force of contraction. This is mediated by the sympathetic cardiac nerves that stimulate the SA and AV nodes, the atria, ventricles, and coronary arteries to increase the heart's rate and force.
- The cardioinhibitory center (parasympathetic) slows the heart rate through the vagus nerves. These parasympathetic nerves primarily affect the SA and AV nodes (and only slightly heart muscle and coronary arteries).
- Atrial (Bainbridge) Reflex: Increased venous return stretches the atrial walls stimulating the sympathetic cardiac nerves to increase the heart rate, hence overall cardiac output.
Electrocardiography
- An electrocardiogram (ECG or EKG) is a composite of all action potentials created by nodal and contracting cells at a given time.
- Three specific waves are analyzed:
- P wave—SA node depolarization of the atria.
- QRS complex—ventricular depolarization (and atrial repolarization).
- T wave—ventricular repolarization.
Heart Sounds
- Two characteristic sounds, "lub-dup," are related to the closing of heart valves (lub - AV closing, beginning systole; dup - SL closing, beginning diastole). A pause between the sounds signifies heart relaxation.
- Abnormal heart sounds (murmurs) often indicate incompetent or stenotic valves.
- Sounds are best heard in specific areas related to individual valves over the heart's surface.
Cardiac Cycle
- The cardiac cycle involves the pressure and blood volume changes associated with one heartbeat. It consists of:
- Ventricular filling: Blood enters the relaxing ventricles via open AV valves; the atria contract (systole) causing about 20% of the end-diastolic volume (EDV) contribution
- Isovolumetric contraction: Ventricles contract, but no blood leaves (all valves closed); ventricular pressure rises.
- Ventricular ejection phase: Ventricular pressure exceeds pressure in the large arteries, driving blood flow through the open semilunar valves.
- Isovolumetric relaxation: Ventricles relax, and the pressure falls below that of the systemic arteries. Backflow of blood from arteries closes semilunar valves.
Cardiac Output
- Cardiac Output (CO) refers to the volume of blood pumped by each ventricle in one minute.
- CO = HR (heart rate) x SV (stroke volume). Normal resting CO is approx 5.25 L/min.
- Factors that regulate stroke volume are the end-diastolic volume (EDV), the end-systolic volume (ESV), preload, contractility, and afterload.
Regulation of Stroke Volume
- Preload: Degree of stretch on cardiac muscle cells before they contract. Venous return (the volume of blood returning to the heart) is the major factor determining preload. Increased preload increases contractility.
- Contractility: Strength of cardiac contraction at any given muscle length, independent of preload (and thus stretch). Positive inotropic agents (e.g., thyroid hormone, sympathetic stimulation) increase contractility and negative inotropic agents (e.g., some drugs, acidosis, hyperkalemia) decrease contractility.
- Afterload: Pressure ventricles must overcome to eject blood. Increased afterload increases end-systolic volume (ESV) and reduces stroke volume.
Regulation of Heart Rate
- Positive chronotropic factors: Factors that increase heart rate include sympathetic stimulation (norepinephrine, epinephrine), increased body temperature, high blood Ca2+, and moderate thyroid hormone.
- Negative chronotropic factors: Factors that decrease heart rate include parasympathetic stimulation (acetylcholine) and moderate hypothermia.
Chemical Regulation of Heart Rate
- Hormones: Epinephrine and norepinephrine from the adrenal medulla increase heart rate and contractility. Thyroid hormone enhances these effects.
- Ions: Intra- and extracellular ion concentrations (especially Ca2+ and K+) must be maintained for proper heart function.
Other Factors that Influence Heart Rate
- Age: Fetus has fastest HR, and HR naturally slows with age.
- Gender: Females have faster heart rates than males.
- Exercise: Increases heart rate.
- Body temperature: Increased body temperature increases heart rate.
Homeostatic Imbalances
- Tachycardia: Abnormally fast heart rate, typically above 100 beats per minute. Persistence can lead to fibrillation.
- Bradycardia: Heart rate slower than 60 beats per minute; may be a desirable result from endurance training, but can cause inadequate circulation in most people.
- Congestive heart failure (CHF): Progressive condition where cardiac output (CO) is too low to meet the body's tissue needs, resulting from various causes including coronary atherosclerosis, persistent hypertension, or multiple myocardial infarctions (heart attacks).
- Various other complications from cardiac dysrhythmia, conduction issues, or valve problems in either atrial or ventricular chambers can occur, including pulmonary congestion, peripheral congestion, and tissue edema.
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Test your knowledge on the anatomy of the heart with this comprehensive quiz. Explore the function and structure of various heart layers, valves, and muscle tissues. Ideal for students studying human anatomy and physiology.
