File Name: human cardiovascular physiology blood pressure and pulse determinations .zip
Pulsatile pressure has been recorded routinely in human cardiovascular diagnostic laboratories, operating rooms and critical care units since the present generation started work, and pulsatile flow patterns are now used increasingly both invasively and noninvasively for the quantification of a number of cardiovascular parameters.
- Cardiac and vascular pathophysiology in hypertension
- Deciphering the neural signature of human cardiovascular regulation
- Arterial waveform analysis to determine cardiovascular parameters
ECG J. I am glad I could help you out cause I wish I had someone to help me out when I took this course. I know Anatomy is super hard.
Pulse pressure is the difference between systolic and diastolic blood pressure. It is measured in millimeters of mercury mmHg. It represents the force that the heart generates each time it contracts. Pulse pressure is the higher systolic blood pressure minus the lower diastolic blood pressure.
Cardiac and vascular pathophysiology in hypertension
Hypertension is one the earliest recorded medical conditions Nei Jin by Huang Ti around BC ; it has shaped the course of modern history 1 and the consequences of hypertension myocardial infarction, strokes, and heart failure will soon be the leading global cause of death. The role of the circulation is to deliver blood to the tissues and flow occurs because of the pressure difference established by the pumping action of the heart.
This relation can be restated for the whole circulation in terms of mean arterial pressure, cardiac output, and peripheral resistance box 2. Although a simplification, this emphasises that an elevation of mean blood pressure can only come about as a result of an increase in cardiac output CO , an increase in total peripheral vascular resistance PVR , or a combination of both. Mechanisms regulating mean arterial blood pressure. So small changes in arterial diameter or radius have a profound effect on flow or resistance.
In the short term, the diameter of small arteries and arterioles is controlled by the contractile state of their smooth muscle. The discussion above assumes that pressure and flow in the circulation are steady. This is clearly not the case. Cardiac output depends on the dynamic interaction between the mechanics of ejection and the properties of the vasculature.
Pressure and flow show cyclical changes at all sites in the circulation, although the changes are considerably damped in capillaries. Once the heart ceases ejection and pressure falls, the walls of these arteries recoil and the elastic energy is reconverted into pressure. This reduces the magnitude of pressure change and accounts to a large extent for the diastolic component of arterial pressure.
The Windkessel model of the circulation. The circulation can be approximated by a pump connected to a compliant chamber elastic arteries and a flow resistance resistance vasculature. Although this model is an oversimplification, it emphasises that arterial compliance stiffness or elastance is the reciprocal of compliance is an important factor in damping pressure oscillation and that pulse pressure will increase when arteries stiffen for example, with aging.
Moreover it also makes clear that changes in arterial stiffness per se should affect pulse pressure and not mean pressure. More detailed examination of the arterial pressure waveform in different segments of the arterial tree shows that it undergoes complex changes in shape 5 that cannot be explained by the Windkessel model. Perhaps most surprising is that there is a consistent rise in systolic pressure but not mean pressure in a peripheral artery such as the tibial artery or the brachial artery compared with the aorta.
But during exercise or in some young individuals at rest the difference between brachial and aortic pressures can exceed 30 mm Hg. In the latter case this may give rise to spurious diagnoses of hypertension. Reflected pressure waves are clinically important since they may place an additional load on the heart and vasculature for example, in hypertension or heart failure.
Reflected pressure waves travel back towards the heart augmenting the forward pressure wave and reducing the forward flow of blood. In the aorta wave reflection is responsible for the late systolic augmentation of pressure that is often seen in elderly individuals and may impose an additional load on the heart and impair coronary blood flow. The contribution of reflected waves is often estimated non-invasively by measuring the augmentation index the proportional rise in late systolic pressure either from the pressure waveform measured in the carotid artery 7 w6 or after mathematical transformation of the radial artery waveform.
Differences in these account for the complex changes in the early systolic component of the pressure waveform at different sites. A different sort of pressure wave is evident at the end of systole—a forward travelling expansion wave. This is effectively a wave of suction generated by the left ventricle. This comes about when active myocardial shortening stops, but the aortic valve is still open.
For a short period aortic blood flow continues under its own momentum w8 and left ventricular pressure declines giving rise to the expansion wave. Patients with hypertension of several years standing but without target organ damage have increased PVR box 4.
Cardiac index and stroke volume are generally normal or reduced, although heart rate may be higher than in normals. Nevertheless, despite the normal cardiac index, modelling studies suggest that abnormal cardiac performance contributes significantly to elevated blood pressure in established hypertension, particularly in subjects with concentric hypertrophy of the heart. In established hypertension there is also a reduction in arterial compliance and a central shift in blood volume, which may be secondary to reduced venous compliance.
However, blood volume and extracellular fluid volume are generally found to be normal. While the basic haemodynamics of established hypertension are undisputed, there is less agreement about the haemodynamic pattern in young individuals with comparatively elevated blood pressures. In young individuals less than 19 years, most evidence suggests that subjects with the highest blood pressure have increased PVR, though small increases in cardiac index have been seen in some studies.
Interestingly, an increased left ventricular mass is a fairly consistent finding in young individuals with raised blood pressure 8 and is also seen in offspring of hypertensives, w14 although the functional determinants of this abnormality are not well understood.
In adults 18—40 years with raised blood pressure borderline or mild hypertension PVR is often in the normal range at rest, and the raised blood pressure is attributable to increased cardiac index and heart rate. Both heart and arteries adapt their structure in response to altered load.
This occurs physiologically for example, during somatic growth and pathologically in hypertension. More complex expressions for wall tension in the heart or blood vessels exist, but this is a reasonable approximation. A rise in tension results in increased wall tensile stress. Cardiac structure is influenced by pressure and volume loads. The increased pressure load in hypertension is primarily caused by the increased resistance, although reduced compliance and possibly altered magnitude and timing of reflected pressure waves make a contribution.
Hypertension is associated with a spectrum of structural change in the left ventricle. Major patterns of myocardial and vascular remodelling in hypertension.
Remodelling is seen in normal aging without hypertension w16 and is probably an adaptation to preserve ejection fraction despite reduced midwall fibre function. It has become apparent that myocardial fibre shortening is reduced in human hypertension. Early clinical investigations assessed cardiac function using endocardial measurements. Recently, it has been appreciated that there is a discrepancy between shortening measured at the endocardium and at the midwall.
Midwall shortening is commonly reduced in left ventricular hypertrophy and the process of wall hypertrophy allows total wall shortening to remain normal in spite of a depression in fibre shortening—that is, the change in left ventricular geometry allows the chamber function to remain normal. Normal myocardium contains an interstitial fibrous network upon which the myocytes are arranged. Although hypertrophy primarily involves myocytes, the interstitial network also changes.
This occurs initially in a perivascular distribution but progressively extends to cause a widespread interstitial fibrosis. In addition, replacement fibrosis may occur to replace necrotic or apoptotic myocytes.
Increased interstitial fibrous tissue is probably important in cardiac dysfunction in hypertension, but the amount of fibrosis is not easy to measure clinically and so differential changes in myocyte hypertrophy and fibrosis cannot easily be assessed in patients.
Most hypertensives have normal left ventricular structure, but left ventricular hypertrophy predicts a poor prognosis, the almost threefold increased risk being independent of the blood pressure level. The increase in ventricular arrhythmias 13 and increased QT duration and QT dispersion seen in left ventricular hypertrophy 14 may account for the increased risk of sudden death, but other mechanisms such as impaired coronary perfusion could also be important. The electrical abnormalities are likely to be caused by heterogeneous conduction in the ventricle due to increased interstitial fibrosis.
There is now increasing evidence that regression of left ventricular hypertrophy with antihypertensive treatment provides cardiovascular protection over and above the reduction in blood pressure levels, 15 w17 but again the mechanism of the risk reduction is uncertain. Active relaxation is impaired in hypertrophy and remodelling. This may be caused by a number of mechanisms, including endothelial dysfunction, narrowing of small arteries, microvascular rarefaction, perivascular fibrosis, altered wall mechanics, and relative myocyte hypertrophy.
Impaired relaxation results in prolongation of isovolumic relaxation time from aortic valve closure to mitral valve opening because it takes longer for left ventricular pressure to decrease below atrial pressure.
Once the mitral valve is open the slowed relaxation means that left ventricular filling takes longer and there is more blood in the left atrium by the end of the early filling period. This leads to an increased force of atrial contraction. As diastolic dysfunction progresses there is a decrease in left ventricular compliance caused mainly by the increased interstitial fibrosis.
This impairs filling notably. As the heart becomes stiffer, pressure in all the chambers increases. The increased left atrial pressure results in a large pressure gradient in early diastole when the mitral valve first opens, so the peak velocity of the early filling wave is very high. Doppler echocardiographic records showing A normal diastolic function, B impaired relaxation, and C restrictive pattern that is, severe diastolic function with an increase in left atrial pressure.
Mild diastolic dysfunction is often clinically silent; however, if the deterioration of diastolic function is sufficient to significantly reduce ventricular filling and left ventricular end diastolic volume, a reduction in stroke volume will occur and patients may develop low output symptoms such as fatigue. As diastolic dysfunction progresses, left ventricular filling pressures become abnormally high and pulmonary congestion may occur.
Early studies have suggested that over a third of patients with a clinical diagnosis of heart failure have normal left ventricular systolic function w22 ; however, it is now becoming apparent that there is considerable overlap between diastolic and systolic dysfunction. Structural changes in hypertensive vasculature show similarities to those in the heart. In both cases the primary goal appears to be the normalisation of wall stress.
The elevated pressure causes an increase in wall tension that is largely experienced by vascular myocytes and the extracellular matrix of the blood vessel. The pattern of remodelling of the vasculature seems highly dependent on the size and function of the artery examined.
In part this may reflect the major influence of flow on arterial structure. The wall shear stress is sensed by the endothelial cells. In response to shear stress the endothelium releases a number of vasoactive factors that affect arterial tone and growth. Increased peripheral vascular resistance PVR is the hallmark of established hypertension, but altered cardiac function also probably contributes to the raised blood pressure.
Large elastic arteries are important in damping the pulsatile flow created by the heart. Pressure wave reflection from downstream affects the pressure waveform in arteries and this is responsible for raised brachial systolic blood pressure compared with central aortic systolic pressure.
Deceleration of left ventricular contraction causes an expansion suction wave, which is responsible for aortic valve closure. Hypertension causes cardiac and vascular remodelling and hypertrophy.
This helps to normalise left ventricular and arterial wall stress and may compensate for a reduction in myocardial fibre function to preserve cardiac output. Hypertensive vessels are not inherently stiffer than normal blood vessels. All vessels become stiffer as they are distended and the increased stiffness in hypertension is a reflection of this. Hypertension is associated with reduced vasodilator reserve and a reduction in microvascular density.
These arteries do not contribute to peripheral vascular resistance, but influence total arterial compliance and wave reflection. The diameter of large elastic arteries such as the aorta or carotid is increased in hypertension. There is also an increase in wall thickness or at least intima—media thickness IMT as measured by ultrasound.
In smaller more muscular large arteries, such as the femoral, brachial, and radial, arterial diameter is not increased, although IMT is increased and wall:lumen ratio is therefore increased.
Numerous studies have reported that arterial stiffness is increased in hypertension. With the possible exception of the carotid artery of young hypertensives, w23 this increase in stiffness is not caused by a change in the inherent wall properties of arteries despite the increase in wall thickness but is a result of the increased distending pressure.
When this is taken into account, the intrinsic elasticity of hypertensive arteries does not usually differ from normotensive arteries. Aging results in increased arterial stiffness probably through degenerative changes in elastin in the arterial wall. In contrast hypertension does not affect the elastic nature of the arterial wall, although the pressure induced increase in stiffness will worsen age related decreases in arterial compliance.
Deciphering the neural signature of human cardiovascular regulation
Correctly identify valve closings and openings, chamber pressures, and volume lines, and the ECG and heart sound scan lines on the diagram below by matching the diagram labels with the terms to the right of the diagram. Diastole Systole 1 2 b 3 4 f 1. AV valve closes g 7. AV valve opens o 8. ECG m Define the following terms: systole: Contraction of the ventricles general usage diastole: Ventricular relaxation general usage cardiac cycle: One complete heartbeat including atrial and ventricular contraction 3.
Tae-Heon Yang, Jaeuk U. Simulating physiologies of blood pressure, the compliance chamber in the simulator can control arterial stiffness to produce age-dependent pressure waveforms. The augmentation index was used to assess the pressure waveforms generated by the simulator. The test results show that the simulator can generate and control radial pressure waveforms similar to human pulse signals consisting of early systolic pressure, late systolic pressure, and dicrotic notch. The simulator is intended to serve as a platform for the development, performance verification, and calibration of wearable blood pressure sensors. The importance of real-time monitoring a radial artery pressure and its waveform is steadily increased in the medical science and healthcare field. This is because the radial pulsation is a surrogate maker to estimate a central aortic pressure and its waveform which is clinically imperative for predicting cardiovascular diseases [ 1 — 4 ].
SS. Sawo MDA WOMAN. MOON. QINDA cons. BMW. Sous. ASANA. S www. Box. Human Cardiovascular. Physiology-Blood Pressure and Pulse Determinations.
Arterial waveform analysis to determine cardiovascular parameters
Hypertension is one the earliest recorded medical conditions Nei Jin by Huang Ti around BC ; it has shaped the course of modern history 1 and the consequences of hypertension myocardial infarction, strokes, and heart failure will soon be the leading global cause of death. The role of the circulation is to deliver blood to the tissues and flow occurs because of the pressure difference established by the pumping action of the heart. This relation can be restated for the whole circulation in terms of mean arterial pressure, cardiac output, and peripheral resistance box 2. Although a simplification, this emphasises that an elevation of mean blood pressure can only come about as a result of an increase in cardiac output CO , an increase in total peripheral vascular resistance PVR , or a combination of both.
NORMAL CARDIAC AND VASCULAR PHYSIOLOGY
List the elements of the intrinsic conduction system in order, starting from the SA node. At what structure in the transmission sequence is the impulse temporarily delayed? AV node. Allows completion of atrial contraction before initiation of ventricular systole. Even though cardiac muscle has an inherent ability to beat, the nodal system plays a critical role in heart physiology. What is that role? Ensures that depolarization proceeds in an orderly manner from atria to ventricles; accelerates and coordinates heart activity to effectively pump blood Electrocardiography.
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Двигатели снизили обороты, и самолет с залитого солнцем летного поля въехал в пустой ангар напротив главного терминала. Вскоре появился пилот и открыл люк.
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Повсюду разбросаны грязные бумажные полотенца, лужи воды на полу. Старая электрическая сушилка для рук захватана грязными пальцами. Беккер остановился перед зеркалом и тяжело вздохнул. Обычно лучистые и ясные, сейчас его глаза казались усталыми, тусклыми. Сколько я уже тут кручусь.
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Попытка переделать Цифровую крепость - дело серьезное и хлопотное. Я не хотел тебя впутывать. - Я… понимаю, - тихо сказала она, все еще находясь под впечатлением его блистательного замысла.
Ну видите, все не так страшно, правда? - Она села в кресло и скрестила ноги. - И сколько вы заплатите. Вздох облегчения вырвался из груди Беккера.
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Сьюзан отчаянно пыталась встретиться взглядом со Стратмором. Коммандер. Северная Дакота - это Хейл.