CVS Flashcards
What is the primary difference in the formation of muscle fibres between skeletal and cardiac muscle?
In skeletal muscle, a true syncytium forms where multiple muscle cells fuse to form a long multinucleated muscle fibre. In cardiac muscle, a functional syncytium is formed where cells are joined electrically by gap junctions and physically by desmosomes.
What is the role of intercalated discs in cardiac muscle?
Intercalated discs in cardiac muscle are composed of gap junctions followed by desmosomes, repeated in sequence, facilitating both electrical and physical connectivity between cells.
Compare the duration of action potentials in skeletal and cardiac muscle.
In skeletal muscle, action potentials last 1-2 ms, whereas in cardiac muscle, they last 200-250 ms due to a prolonged plateau phase mediated by voltage-gated calcium channels in addition to sodium channels.
How does the regulation of calcium affect the contraction strength in cardiac muscle?
In cardiac muscle, the modulation of calcium influx, which saturates troponin, varies the number of crossbridges formed, thereby changing the strength of contraction.
Why can’t cardiac muscle undergo tetanic contractions like skeletal muscle?
Cardiac muscle has a longer refractory period to prevent the summation of contractions, which makes tetanic contractions useless and prevents them in the heart.
Describe the stability of resting membrane potentials in skeletal muscle, cardiac muscle, and pacemaker cells.
Both skeletal muscle and most cardiac muscle cells have very stable resting membrane potentials. However, about 1% of cardiac cells, known as pacemaker cells, have unstable resting potentials that spontaneously depolarise.
What triggers depolarisation in non-pacemaker cardiac cells?
Depolarisation in non-pacemaker cardiac cells is triggered by a neighbouring cell and involves the rapid opening of voltage-gated sodium channels allowing sodium influx.
How do non-pacemaker action potentials in cardiac muscle reach a plateau phase?
The plateau phase in non-pacemaker cardiac action potentials occurs as leaky potassium channels close and voltage-gated calcium channels (particularly L-type) fully open, maintaining a prolonged depolarisation.
What happens when L-type calcium channels close during a cardiac action potential?
When L-type calcium channels close, the cell begins to repolarise as potassium channels reopen, eventually restoring the resting membrane potential.
Describe the stages involved in a pacemaker action potential.
The pacemaker potential starts with the closure of potassium channels and the movement of sodium ions through ‘funny’ channels, followed by the opening of T-type calcium channels causing rapid depolarisation. The action potential peaks with the opening of L-type calcium channels, facilitating calcium influx.
Explain the pathway of cardiac depolarisation in the special conducting system.
Depolarisation originates at the sinoatrial node (SAN), passes through the atria, and is delayed by the atrioventricular node (AVN) to allow ventricular filling. It then travels down the bundle of His, and rapidly through the Purkinje fibres to facilitate coordinated ventricular contraction.
What does an ECG show and how is it useful?
An ECG records the electrical activity of the heart, showing waves like the P wave (atrial depolarisation), the QRS complex (ventricular depolarisation), and the T wave (ventricular repolarisation). It is non-invasive, quick, and reveals the heart’s rhythm and the state of its conducting system.
Describe the types of heart block and their ECG characteristics.
In 1st degree heart block, the PR interval is prolonged; in 2nd degree (Mobitz type 1), the PR interval lengthens progressively until a QRS complex is skipped. In 3rd degree heart block, the atria and ventricles beat independently of each other, often requiring a pacemaker implant.
How does atrial flutter differ from atrial fibrillation on an ECG?
Atrial flutter shows rapid, regular atrial contractions visible as multiple P waves between QRS complexes, whereas atrial fibrillation displays irregular rhythms with no distinct P waves, and random QRS timings.
What is ventricular fibrillation and why is it critical?
Ventricular fibrillation is an uncoordinated contraction of the ventricles, shown as irregular, undefined ECG waves. It is life-threatening as it severely disrupts blood flow, requiring immediate defibrillation to restore normal heart rhythm.
Explain the role of the annulus fibrosus in the heart’s electrical activity.
The annulus fibrosus acts as a barrier that prevents the immediate spread of electrical impulses from the atria to the ventricles.
How do Purkinje fibres influence cardiac contraction?
Purkinje fibres facilitate the rapid conduction of electrical impulses through the ventricle walls, enabling a powerful and synchronized ventricular contraction.
What are the implications of atrial repolarisation occurring within the QRS complex on an ECG?
Atrial repolarisation occurs during the QRS complex but is overshadowed by the larger electrical activity of ventricular depolarisation.
Explain how heart rate is calculated using an ECG.
Heart rate can be calculated manually by measuring the RR interval on an ECG, where a large square represents 0.2 seconds.
Describe Mobitz type 2 and 2:1 AV block.
Mobitz type 2 heart block involves consistent PR intervals with occasional skipped QRS complexes. A 2:1 AV block indicates intermittent failure in AV conduction.
How does defibrillation work in treating ventricular fibrillation?
Defibrillation works by delivering a strong electrical shock to depolarise all heart cells simultaneously, allowing the sinoatrial node a chance to re-establish a normal sinus rhythm.
What is the significance of the plateau phase in cardiac muscle action potentials?
The plateau phase is crucial for preventing tetanus by prolonging the refractory period, mediated by the slow closing of L-type calcium channels.
Why is tetanic contraction undesirable in cardiac muscle?
Tetanic contraction would prevent the chambers from properly filling with blood between contractions, crucial for maintaining efficient blood flow.
What role do gap junctions and desmosomes play in cardiac muscle cells?
Gap junctions allow for electrical coupling of adjacent cells, facilitating synchronous contraction, while desmosomes provide structural integrity.
Explain the importance of Purkinje fibers in the timing of cardiac muscle contraction
Purkinje fibers facilitate the rapid and coordinated spread of electrical impulses to the ventricular myocardium, ensuring that ventricular contraction occurs immediately following atrial contraction. This rapid conduction allows for efficient pumping of blood from the ventricles to the body and lungs
Describe how atrial fibrillation affects heart function and its appearance on an ECG
Atrial fibrillation is characterized by rapid, irregular electrical impulses in the atria, leading to a disorganized and dysfunctional atrial contraction. On an ECG, it appears as irregularly irregular rhythm without distinct P waves before each QRS complex, reflecting the erratic atrial activity.
What is the clinical significance of the QRS complex on an ECG?
The QRS complex on an ECG represents ventricular depolarization and is crucial for diagnosing the timing, sequence, and health of ventricular contractions. Abnormalities in the QRS complex can indicate ventricular hypertrophy, conduction delays, or other cardiac pathologies.
Describe the clinical significance of atrial fibrillation and its management.
Atrial fibrillation involves chaotic atrial electrical activity leading to ineffective atrial contractions and potentially compromised ventricular filling and cardiac output. It increases the risk of stroke and heart failure. Management typically involves rate control, rhythm control, and anticoagulation to prevent thromboembolic events.
What are the specific ion movements during the cardiac action potential phases?
During cardiac action potential, initial rapid depolarization is due to Na+ influx through fast channels. The plateau phase is maintained by Ca2+ influx through L-type channels, and repolarization occurs due to K+ efflux through delayed rectifier channels.
distinguish between Mobitz type 1 and Mobitz type 2 heart block
Mobitz type 1 (Wenckebach) heart block shows progressively lengthening PR intervals until a beat is dropped, indicating a weakening atrioventricular node conduction. Mobitz type 2 involves dropped beats without prior change in the PR interval, suggesting a more severe and localized block in conduction below the AV node.
What happens during late diastole in the cardiac cycle?
During late diastole, all chambers of the heart are relaxed and filling passively.
What triggers atrial systole?
Atrial systole is triggered when the sinoatrial node (SAN) reaches threshold potential, causing depolarization and atrial contraction.
Describe isovolumic ventricular contraction.
During isovolumic ventricular contraction, the ventricles depolarize and contract, increasing pressure inside, which closes the mitral and tricuspid valves but isn’t yet enough to open the aortic and pulmonary valves.
What occurs during ventricular ejection?
As ventricular contraction continues and pressure increases, it causes the pulmonary and aortic valves to open, allowing blood to be forced out of the ventricles.
Explain isovolumic ventricular relaxation.
In isovolumic ventricular relaxation, the ventricles relax, causing pressure to fall, leading to blood flow back towards the pulmonary and aortic valves, which forces them shut. The atria start to fill passively, increasing pressure to open the mitral and tricuspid valves.
What are the phases of systole and diastole in the cardiac cycle?
Diastole is the filling phase, and systole is the ejection phase. Systole comprises about ⅓ of the cardiac cycle, while diastole takes up the remaining ⅔. The total duration of the cardiac cycle is approximately 0.8 seconds.
How do systole and diastole durations change with heart rate?
At higher heart rates, the duration of diastole decreases and the duration of systole increases.
Describe the changes in pressure and volume in the left ventricle at the start of contraction.
At time 0 of ventricular contraction, left ventricular pressure rapidly increases. When it surpasses 5 mmHg (the pressure in the left atrium), the mitral valve closes. The left ventricle’s volume then plateaus at 140 ml.
What occurs when the pressure in the left ventricle exceeds aortic pressure during contraction?
When left ventricular pressure exceeds the aortic pressure (80 mmHg), the aortic valve opens, allowing blood to be ejected until the pressure peaks at about 120 mmHg.
What happens when the contraction ends in the left ventricle?
As contraction ends, the pressure in the left ventricle drops below the aortic pressure (95 mmHg), causing the aortic valve to shut. Pressure continues to drop below the left atrial pressure (10 mmHg), allowing the mitral valve to reopen.
Define Pulse Pressure and provide its typical value.
Pulse pressure is the difference between systolic and diastolic pressures, typically around 40 mmHg.
How is Mean Arterial Pressure (MAP) calculated and what is its approximate value?
Mean Arterial Pressure (MAP) is calculated as the diastolic pressure plus one-third of the pulse pressure, approximately 90 mmHg.
What are End Diastolic Volume (EDV) and End Systolic Volume (ESV)?
End Diastolic Volume (EDV) is the maximum volume at the end of diastole (140ml), and End Systolic Volume (ESV) is the minimum volume at the end of systole (60ml).
Define Stroke Volume and Ejection Fraction.
Stroke Volume (SV) is the volume of blood pumped out of the ventricle with each beat, calculated as EDV minus ESV. Ejection Fraction is the percentage of EDV pumped out with each contraction, typically 60%.
Explain the relationship between preload, venous return, and stroke volume.
Preload, influenced by venous return and represented by EDV, affects the stroke volume. Increased venous return raises EDV and stroke volume by stretching cardiac muscles more, enhancing their contraction. Conversely, decreased venous return lowers EDV and stroke volume.
Describe the concept of afterload and its impact on the heart.
Afterload is the resistance the heart must overcome to eject blood during systole. High total peripheral resistance increases afterload, prolonging the isometric contraction phase, which can decrease stroke volume.
What is contractility and how is it influenced?
Contractility refers to the heart muscle’s ability to contract forcefully. It increases with activation of B1 receptors by noradrenaline, enhancing calcium release and crossbridge formation in cardiomyocytes, leading to a stronger and shorter contraction.
How do the mechanisms of heart rate, stroke volume, and contractility interact to control cardiac output?
Heart rate, stroke volume, and contractility interact to determine cardiac output, which is the product of heart rate and stroke volume. Changes in these parameters affect how much blood is pumped to the tissues. During exercise, for example, increases in heart rate and contractility, along with adjustments in stroke volume, significantly raise cardiac output.
What is the effect of exercise on cardiac output?
During exercise, increased heart rate, enhanced contractility, and higher venous return work together to significantly increase cardiac output, up to 4-6 times normal levels, by improving filling time and reducing afterload through arteriolar dilation.
Explain the relationship between murmurs, heart sounds, and cardiac function.
Murmurs are additional heart sounds that may indicate physiological conditions or pathological issues. The first two heart sounds (closure of AV valves and semilunar valves, respectively) are normal, but additional sounds may indicate anomalies in blood flow or valve function. Murmurs can be due to valve stenosis or regurgitation, or from a patent ductus arteriosus.
What causes the dicrotic notch in the aortic pressure curve?
The dicrotic notch appears when the aortic valve closes, resulting from the elastic recoil of the aorta.
Describe the a, c, and v waves in atrial pressure.
The ‘a wave’ represents an increase in atrial pressure due to atrial contraction. The ‘c wave’ occurs when the mitral valve bulges into the left atrium during ventricular contraction. The ‘v wave’ is a slow increase in atrial pressure as the atrium refills passively.
What is the relationship between the phonocardiogram and heart sounds?
Heart sounds on a phonocardiogram are due to turbulence in blood flow: the first sound from AV valve closure, the second from semilunar valve closure, the third from rapid passive filling, and the fourth from active filling. The first two sounds are typical, but the latter two might not always be heard.
Differentiate between physiological and pathological murmurs.
Physiological murmurs are innocent and common in infants, children, and pregnant women, caused by normal blood flow. Pathological murmurs usually indicate a stenosed (narrowed) valve that should be open or a leaky valve that should be closed, allowing blood regurgitation.
What triggers systolic and diastolic murmurs?
A systolic murmur occurs during systole, typically due to stenosis of semilunar valves or regurgitation through AV valves. Diastolic murmurs occur during diastole, usually caused by stenosis of AV valves or regurgitation through semilunar valves.
Explain the significance of a continuous murmur.
A continuous murmur, heard throughout systole and diastole, can be due to a patent ductus arteriosus, where a vessel that should close after birth remains open, causing blood to flow from the aorta to the pulmonary trunk.
How does the autonomic nervous system regulate heart rate?
The sympathetic nervous system increases heart rate by releasing noradrenaline, which acts on B1 receptors, increasing ion flow through sodium and calcium channels. The parasympathetic system decreases heart rate via the vagus nerve releasing acetylcholine, which hyperpolarizes pacemaker cells, slowing down their depolarization.
Describe Starling’s law of the heart.
Starling’s law states that the force of heart muscle contraction is proportional to its initial length. Preload, which reflects the initial stretching of cardiac muscle fibers due to venous return (EDV), directly affects this force, allowing the heart to adjust stroke volume based on venous return to maintain efficient pumping.
What are the implications of changes in total peripheral resistance on cardiac function?
An increase in total peripheral resistance (due to arteriole constriction) raises aortic pressure and afterload, making it harder for the ventricle to eject blood, potentially reducing stroke volume. Conversely, arteriolar dilation decreases resistance and afterload, aiding blood ejection during systole.
How does the control of cardiac output vary during exercise?
During exercise, cardiac output increases due to a combination of increased heart rate, enhanced contractility, and greater venous return. This is further supported by decreased total peripheral resistance due to arteriolar dilation in active areas, optimizing blood flow to meet metabolic demands.
What happens to diastolic pressure during ventricular diastole?
During diastole, the diastolic pressure in the aorta is maintained at about 80 mmHg due to the elastic walls of the aorta, which slowly decrease pressure.
How does stroke volume relate to larger heart sizes in different individuals?
Larger individuals typically have larger hearts, which results in a larger stroke volume due to a greater end-diastolic volume.
What is the inotropic effect and how is it influenced?
The inotropic effect refers to the change in strength of heart muscle contraction, influenced by neural factors such as the activation of B1 receptors by noradrenaline, which increases calcium release in cardiomyocytes and results in a stronger and shorter contraction.
How does the regulation of heart rate and stroke volume affect cardiac output during vigorous activity like exercise?
During vigorous exercise, cardiac output increases more significantly than by heart rate alone due to increased stroke volume and heart rate, supported by increased contractility, higher venous return, and reduced total peripheral resistance, all of which help maintain efficient cardiac function even under stress.
What is the effect of the autonomic nervous system on the pacemaker potential of SAN cells?
The sympathetic nervous system increases the slope of the pacemaker potential, causing SAN cells to reach threshold sooner, thus increasing heart rate (tachycardia). The parasympathetic nervous system decreases this slope, making SAN cells reach threshold later, thus decreasing heart rate (bradycardia).
What is an arterial line and where is it typically placed for measuring arterial pressure?
An arterial line is a thin catheter used to measure arterial pressure directly from within an artery, typically placed in the radial artery at the wrist or the brachial artery at the elbow. This method is invasive and generally reserved for critically ill patients in ICU or A&E.
How does the use of a sphygmomanometer and stethoscope function in measuring arterial pressure?
A sphygmomanometer is used alongside a stethoscope to measure arterial pressure by inflating a cuff to occlude the artery and then gradually releasing it. The first Korotkoff sound represents the systolic pressure, and the disappearance of the sound indicates diastolic pressure.
Explain the Korotkoff sounds method in measuring blood pressure.
Korotkoff sounds are produced by turbulent blood flow resuming in the artery as the cuff pressure of a sphygmomanometer is lowered below the systolic pressure. These sounds continue until the cuff pressure falls below diastolic pressure, at which point blood flow normalizes and the sounds cease.
What are the advantages and disadvantages of using a manual sphygmomanometer?
The advantage of a manual sphygmomanometer is that it is non-invasive and cost-effective. However, it provides discontinuous, potentially inaccurate measurements and requires significant skill and care to use properly.
How do automatic sphygmomanometers measure blood pressure compared to manual devices?
Automatic sphygmomanometers detect oscillations in the artery due to blood flow, calculate the mean arterial pressure where oscillations are maximized, and use an algorithm to estimate systolic and diastolic pressures. This method requires less skill and is faster than manual measurement.
Describe the role of elastic arteries in the circulatory system.
Elastic arteries, like the aorta, serve as a pressure reservoir that dampens pressure variations. They expand during ventricular contraction to store pressure and recoil when the ventricles relax, helping to propel blood through the circulatory system continuously.
What factors influence arterial blood pressure variations?
Arterial pressure variations are influenced by stroke volume, velocity of ejection, arterial elasticity, and total peripheral resistance. Increases in stroke volume and ejection velocity raise systolic pressure, while increased arterial elasticity and peripheral resistance affect both systolic and diastolic pressures differently.
How does pressure change across the vascular system from arteries to veins?
Pressure decreases progressively from arteries through arterioles to capillaries, then to veins and venules. Arterioles, being resistance vessels, contribute to a significant drop in pressure due to their narrow lumens and thick muscle walls.
Explain how the pressure in the pulmonary circulation compares to the systemic circulation.
Pressures in the pulmonary circulation are generally about one-fifth of those in the systemic circulation due to lower resistance and less muscle in the pulmonary arterial walls, reflecting the need for less force to pump blood through the lungs.
How does gravity affect venous blood flow and pressure?
Gravity affects venous blood flow by causing pooling in the legs when standing, which reduces the venous return to the heart and can lead to orthostatic hypotension. In the upper body, gravity can cause venous and venular collapse, especially noticeable in conditions like raised jugular venous pressure.
What is the impact of skeletal muscle contraction on venous return?
Skeletal muscle contraction in the legs compresses veins, enhancing venous return to the heart. Valves within the veins prevent the backflow of blood, ensuring that the contraction effectively pushes blood towards the heart.
How does the respiratory pump enhance venous return?
During inspiration, the diaphragm descends, creating a negative pressure in the thorax relative to the abdomen. This pressure differential drives blood from the lower body veins into the thoracic veins and right atrium, enhancing venous return.
What is venomotor tone and how does it affect venous capacity and return?
Venomotor tone is the state of contraction of venous smooth muscle, regulated by the sympathetic nervous system and hormones like adrenaline. Contraction reduces the capacitance of veins, pushing more blood back to the heart and increasing venous return.
Discuss the concept of systemic filling pressure and its change during exercise.
Systemic filling pressure is a measure of the venous pressure when the heart is stopped and reflects venous return. It increases during exercise due to heightened sympathetic activity that enhances heart contractility and decreases total arterial resistance, facilitating greater venous return and cardiac output.
How does venous return influence cardiac output?
Venous return affects the end-diastolic volume, which determines the preload on the heart. An increase in preload leads to an increase in stroke volume according to the Frank-Starling law, thereby enhancing cardiac output.
What physiological changes occur in the veins and venules in response to external influences?
Veins and venules are distensible and collapsible, meaning external influences such as gravity, mechanical compression, or venous tone can significantly affect blood flow and pressure within them.
How does gravity specifically impact venous distension and blood pooling in the legs?
Gravity causes venous distension in the legs, leading to blood pooling when upright. This reduces venous return to the heart, subsequently lowering end-diastolic volume, stroke volume, cardiac output, and mean arterial pressure, potentially causing orthostatic hypotension.
What is the clinical significance of raised jugular venous pressure?
A raised jugular venous pressure is often visible when the internal jugular vein becomes distended and is a clinical sign of several conditions, including right-sided heart failure. It indicates elevated central venous pressure, which can be due to heart conditions that impair the heart’s ability to move blood efficiently through the circulatory system.
Describe the role of flight socks in preventing deep vein thrombosis.
Flight socks are designed to compress the legs, mimicking the mechanism of the skeletal muscle pump. This compression helps maintain blood flow and prevent stasis, reducing the risk of deep vein thrombosis, particularly during prolonged periods of inactivity such as long flights or hospital stays.
Explain how the respiratory pump is particularly effective during exercise.
During exercise, faster and deeper breathing associated with the respiratory pump lowers thoracic pressure and raises abdominal pressure more significantly. This enhances the pressure gradient that drives venous blood back to the heart, compensating for the decreased end-diastolic volume caused by higher heart rates.
How does increased sympathetic tone during exercise affect the heart and blood vessels?
Increased sympathetic tone during exercise enhances cardiac contractility and decreases total arterial resistance. This results in dilation of arteries and an increase in both cardiac output and mean arterial pressure, facilitating improved blood flow to meet the metabolic demands of active tissues.
What is the overall impact of venous return on the heart’s pumping ability?
Venous return directly impacts the heart’s ability to pump blood efficiently. An adequate venous return ensures a sufficient preload, which is necessary for optimal cardiac muscle fiber stretch and contraction strength, thereby influencing the overall stroke volume and cardiac output.
How does the pressure change as blood travels from the arterioles to the capillaries?
Pressure drops significantly from about 90 mmHg in the arterioles to around 40 mmHg in the capillaries, reflecting the role of arterioles as resistance vessels with narrow lumens and thick muscular walls that regulate blood flow and pressure before it enters the delicate capillary networks.
What are the implications of low capillary pressure for capillary function?
Low pressure in the capillaries is crucial as it ensures the thin-walled capillaries can manage blood flow without damage and facilitates efficient nutrient and gas exchange between blood and tissues, due to slower blood flow and increased surface area contact.
How does velocity of blood flow relate to the total cross-sectional area of the blood vessels?
Blood velocity decreases as the total cross-sectional area of the vessels increases. The velocity is highest in the aorta and decreases in the capillaries, which have the largest total cross-sectional area due to their vast number and then increases again in the veins, culminating in the vena cava.
Explain the systemic filling pressure’s role in maintaining venous return during exercise.
Systemic filling pressure, which increases during exercise due to elevated sympathetic activity and decreased arterial resistance, helps maintain or enhance venous return. This is crucial during physical activity when the body requires increased blood flow to supply muscles with oxygen and nutrients.
How does the velocity of blood flow change from capillaries to vena cava?
The velocity of blood flow is slowest in the capillaries, where the total cross-sectional area is greatest and speeds up as the blood moves into the converging venous system, culminating in the vena cava where the velocity is maximized due to the narrower total cross-sectional area compared to the capillaries.
What are the physiological consequences of low venous pressure in the legs due to gravity?
Low venous pressure in the legs due to gravity can lead to reduced venous return to the heart. This reduction decreases the end-diastolic volume and subsequently lowers stroke volume, cardiac output, and mean arterial pressure, potentially leading to symptoms like light-headedness and fainting.
How do automatic sphygmomanometers estimate systolic and diastolic pressures from mean arterial pressure?
Automatic sphygmomanometers calculate the mean arterial pressure during cuff deflation by detecting the point of maximum oscillation amplitude. They then use a built-in algorithm to derive systolic and diastolic pressures from this value, providing an automated, quick, and less skill-dependent measurement.
What is the impact of changes in arterial elasticity on blood pressure as individuals age?
As individuals age, arterial elasticity typically decreases, leading to higher systolic pressure and potentially higher diastolic pressure. This loss of elasticity means the arteries are less able to expand and absorb the force of the blood ejected from the heart, leading to increased arterial pressure.
Describe the significance of vein distensibility and collapsibility in terms of venous pressure and flow.
The distensibility and collapsibility of veins allow these vessels to adapt to varying volumes of blood and external pressures. These properties help maintain venous return under different physiological conditions, but also make veins susceptible to external compression, which can affect blood flow and pressure regulation.
How does the positive pressure below the diaphragm during inspiration affect venous return?
During inspiration, the diaphragm moves downward, increasing abdominal pressure. This positive pressure helps propel blood towards the low-pressure environment of the thorax, enhancing venous return to the right atrium and improving cardiac filling and output during the respiratory cycle.
What physiological role does the negative pressure in the thorax play during inspiration?
During inspiration, the downward movement of the diaphragm enlarges the thoracic cavity, creating a negative pressure that aids in drawing blood into the central thoracic veins from the systemic circulation, enhancing overall venous return to the heart.
How does a change in total peripheral resistance impact diastolic blood pressure?
An increase in total peripheral resistance typically raises diastolic blood pressure because it maintains higher resistance in the arterial system during the relaxation phase of the heart, thus sustaining higher pressure throughout diastole.
What are the clinical implications of a visible point of collapse in veins in the neck?
A visible point of collapse in neck veins, especially noticeable above the collarbone, can indicate abnormal central venous pressure. It often points to complications such as right-sided heart failure or other conditions that impair venous return to the heart.
Explain how arterial blood pressure is maintained during the relaxation phase of the ventricles.
During the ventricles’ relaxation phase, the elastic recoil of the aorta and other large arteries maintains pressure, allowing continuous blood flow to the body. This elasticity helps dampen pressure fluctuations and ensures a steady flow during diastole.
How do vein valves function in response to skeletal muscle contraction in the legs?
Vein valves prevent the backflow of blood as skeletal muscles in the legs contract. This mechanism ensures that the blood pushed by muscle contractions moves towards the heart, aiding in efficient venous return and reducing the risk of venous stasis and potential thrombosis.
How is mean arterial pressure (MAP) calculated and what does it indicate?
Mean arterial pressure (MAP) is calculated by multiplying cardiac output (CO) by total peripheral resistance (TPR). It represents the driving force that pushes blood through the circulation, essential for delivering nutrients and oxygen to tissues.
What are the consequences of abnormally high or low MAP?
If MAP is too low, it can lead to fainting due to insufficient blood flow to the brain. If MAP is too high, it can cause hypertension, increasing the risk of stroke, heart disease, and other cardiovascular disorders.
What is the arterial baroreflex and where are its sensors located?
The arterial baroreflex is a mechanism for short-term control of MAP, essential for quickly correcting blood pressure deviations. It has sensors in the aortic arch and the carotid sinus, which detect changes in pressure by measuring how much the blood vessels are stretched.
How do baroreceptors respond to changes in MAP during systole and diastole?
During systole, as MAP increases and vessels stretch more, baroreceptors increase their firing rate. During diastole, as MAP decreases, the firing rate of baroreceptors decreases.
What pathways do baroreceptor signals travel to reach the brain?
Signals from aortic arch baroreceptors travel via the vagus nerve, and signals from carotid sinus baroreceptors travel via the glossopharyngeal nerve to the medullary cardiovascular centers in the medulla oblongata.
How do the medullary cardiovascular centers regulate heart rate and vascular tone in response to baroreceptor signals?
Upon receiving signals, the parasympathetic system may reduce heart rate and contractility via acetylcholine on muscarinic receptors. Conversely, the sympathetic system can cause vasoconstriction and venoconstriction through adrenaline and noradrenaline acting on adrenergic receptors.
What additional sensors contribute to the medullary cardiovascular centers’ regulatory functions?
Other sensors include cardiopulmonary baroreceptors, which sense central blood volume; chemoreceptors, which detect changes in CO2 and O2 levels; and joint receptors, which sense movement to adjust blood flow accordingly.
What physiological responses are triggered by the Valsalva Maneuver?
The Valsalva Maneuver causes initial increased thoracic pressure, reducing venous return, stroke volume, and cardiac output, which lowers MAP. This triggers a reflex to increase cardiac output and peripheral resistance, temporarily increasing blood pressure until it normalizes after the maneuver.
How does the Valsalva Maneuver affect cardiovascular function in different populations?
In older adults or those with arterial stiffness, the baroreflex sensitivity is reduced, altering the expected blood pressure response. Additionally, individuals with autonomic neuropathy may exhibit impaired reflex responses, affecting the maneuver’s efficacy.
What are the clinical uses and risks associated with the Valsalva Maneuver?
Clinically, the Valsalva Maneuver is used to test heart function and can help control supraventricular tachycardia. However, it can increase the risk of myocardial infarction by straining the heart due to reduced venous return during the maneuver.
How do the cardiovascular centers in the medulla oblongata adjust blood flow in response to external stimuli?
The cardiovascular centers adjust blood flow by integrating sensory input from higher brain centers, such as the hypothalamus and cerebral cortex, which respond to changes in external factors like temperature or emotional stress (fight or flight response).
What is the role of A1 receptors in the regulation of venous tone during cardiovascular adjustments?
A1 receptors are activated by the sympathetic nervous system to trigger venoconstriction, which helps increase venous return to the heart, enhancing end-diastolic volume and ultimately supporting increased cardiac output.
Describe the changes in thoracic pressure during the Valsalva Maneuver and their direct effects on cardiac dynamics.
During the Valsalva Maneuver, an increase in thoracic pressure directly transmits through the aorta, causing an immediate jump in blood pressure. This increased pressure reduces the filling pressure from the veins, subsequently decreasing venous return, stroke volume, and cardiac output.
What reflexive cardiovascular adjustments occur in response to the reduced MAP detected during the Valsalva Maneuver?
In response to reduced MAP detected during the Valsalva Maneuver, there is a reflexive increase in heart rate and total peripheral resistance initiated by the baroreceptors. This helps mitigate the initial drop in blood pressure by increasing cardiac output and arterial pressure.
What are the phases of blood pressure change during the Valsalva Maneuver?
The Valsalva Maneuver comprises four phases: 1) Initial pressure increase due to increased thoracic pressure, 2) Reduction in venous return and MAP, 3) Release of thoracic pressure leading to a temporary drop in pressure, and 4) Rapid restoration of venous return and subsequent normalization of blood pressure.
How do central chemoreceptors contribute to cardiovascular regulation during changes in arterial gas concentrations?
Central chemoreceptors in the medulla oblongata respond to increases in arterial partial pressure of carbon dioxide (PCO2) and decreases in partial pressure of oxygen (PO2). This sensory input prompts adjustments in cardiovascular function to enhance oxygen delivery and CO2 removal.
How do muscle chemoreceptors influence blood flow during physical activity?
Muscle chemoreceptors detect increases in metabolite concentrations (such as lactic acid) during physical activity. This detection triggers reflexive cardiovascular adjustments that increase blood flow to active muscles, ensuring adequate nutrient delivery and waste removal.
What is the function of the higher brain centers in cardiovascular regulation during physical or emotional stress?
Higher brain centers like the hypothalamus and cerebral cortex can modulate cardiovascular responses during stress by directly influencing the medullary cardiovascular centers. This integration allows for the adjustment of heart rate, blood pressure, and vascular tone in response to changes in temperature, stress, or threat perception.
What specific role does the parasympathetic nervous system play during the arterial baroreflex response to increased blood pressure?
During the arterial baroreflex response to an increase in blood pressure, the parasympathetic nervous system reduces heart rate and contractility by releasing acetylcholine, which acts on muscarinic receptors in the heart, helping to decrease blood pressure back to normal levels.
How does the sympathetic nervous system enhance cardiac output during decreased blood pressure detected by baroreceptors?
When baroreceptors detect a decrease in blood pressure, the sympathetic nervous system increases heart rate and contractility, and causes peripheral vasoconstriction by releasing noradrenaline, which acts on beta-1 adrenergic receptors in the heart and alpha-1 adrenergic receptors in vascular smooth muscle.
Explain how joint receptors contribute to cardiovascular adjustments during movement.
Joint receptors, sensitive to physical activity involving joint movements, send signals to the cardiovascular centers to increase blood flow to active areas. This ensures that muscles and joints receive sufficient oxygen and nutrients during movement.
Describe how the Valsalva Maneuver’s phases affect venous return and arterial pressure.
In the Valsalva Maneuver, initially increased thoracic pressure decreases venous return, reducing stroke volume and cardiac output, which lowers arterial pressure. Upon release, venous return is rapidly restored, which temporarily overshoots arterial pressure until homeostasis is regained.
How does the response to the Valsalva Maneuver differ in individuals with autonomic neuropathy?
Individuals with autonomic neuropathy may show an impaired reflex response during the Valsalva Maneuver, characterized by less pronounced or delayed adjustments in heart rate and peripheral resistance, which can affect the overall effectiveness in modulating blood pressure.
What clinical indicators suggest effectiveness or limitations of the Valsalva Maneuver in assessing cardiovascular function?
The effectiveness of the Valsalva Maneuver in assessing cardiovascular function can be indicated by the responsiveness of blood pressure changes and heart rate adjustments. Limitations occur in individuals with reduced elasticity of arteries or impaired autonomic function, where expected reflexes may be diminished or absent.
How does the medullary cardiovascular center integrate signals from cardiopulmonary baroreceptors?
The medullary cardiovascular center integrates signals from cardiopulmonary baroreceptors, which detect changes in blood volume within the heart and lungs, to regulate cardiovascular responses that balance blood flow and pressure according to the body’s needs.
What is the impact of increased sympathetic activity on venoconstriction during cardiovascular adjustments?
Increased sympathetic activity stimulates venoconstriction through the activation of alpha-1 adrenergic receptors on venous smooth muscle. This reduces the capacitance of veins, effectively pushing more blood toward the heart to increase cardiac output.
Explain the role of arterial chemoreceptors in cardiovascular response to hypoxia.
Arterial chemoreceptors, located primarily in the carotid and aortic bodies, are sensitive to decreases in oxygen levels (hypoxia). They trigger reflexive increases in heart rate and vasoconstriction to boost blood circulation and oxygen delivery to vital organs.
How do higher brain centers affect cardiovascular function during environmental changes?
Higher brain centers, such as the hypothalamus, can trigger adjustments in cardiovascular function in response to environmental changes like extreme temperatures. These centers initiate signals that adjust heart rate, blood flow, and vasoconstriction or vasodilation to maintain homeostasis.
What physiological changes occur during the first phase of the Valsalva Maneuver that affect cardiac output?
In the first phase of the Valsalva Maneuver, increased intrathoracic pressure directly compresses the heart and great vessels, which reduces the preload (venous return) and momentarily decreases cardiac output and arterial pressure.
Describe the cardiovascular adaptations during phase four of the Valsalva Maneuver.
In phase four of the Valsalva Maneuver, after releasing the breath and reducing intrathoracic pressure, there is a rapid influx of venous blood back to the heart, temporarily elevating stroke volume and blood pressure. The cardiovascular system then stabilizes as reflex responses taper off, returning blood pressure to baseline levels.
