Capítulo 4 Fundamentos para proponer una Metodología Forense
4.6. Herramientas de Análisis Forense en Celulares
CHAPTER 6
Figure 6.1 Factors affecting the stroke volume of a heart. Total peripheral resistance, which is located mainly in the arterioles and terminal arteries, is represented by the narrow tube in series with the aorta.
Total peripheral resistence Stroke volume
Contractility:
– sympathetic nerves – circulating agents
Energy of contraction Filling pressure (preload):
Starling’s law of the heart
Arterial pressure opposing ejection (afterload)
LV RV
Isolated dog heart
Filling pressure (mmHg) (a)
0 20 40
12
6
Stroke volume (ml)
Human heart in situ
Left ventricle EDP (mmHg) (b)
0 5
60
40
Stroke volume/m2 (ml)
10 15 20 25
20
Control Pacing Phlebotomy Phlebotomy + pacing Reinfusion
Dextran 400 ml
U S
Figure 6.2 Ventricular function curves of dog (a) and human (b). (a) Effect of filling pressure (central venous pressure, dashed line; left atrial pressure, solid line) on stroke volume of isolated dog heart (Starling’s data). (b) Human ventricular function curve. LV end-diastolic pressure (LVEDP) was varied in vivo by phlebotomy (venous bleeding) and other manoeuvres. Stroke volume is expressed per unit body surface area (stroke index). Grey bands mark normal human LVEDP when supine (S) and upright (U).
Figures 161
Figur es - Chapter 6
Figure 6.3 Pump function curves for normal heart, failing heart and laboratory roller pump. W, normal work point. Increasing the peripheral resistance raises pressure but depresses stroke volume (point 1). Ventricular distension can restore the stroke volume by shifting the pump function curve to a higher energy level (point 2) – the Frank–Starling mechanism. Impaired contractility (heart failure) shifts the curve to a lower energy level (point 3). The stroke volume of a failing heart can be improved by pressure-reducing drugs (point 4).
0 100 200
Active tension (g) Velocity of shortening (mm/s)Shortening (mm)
(b)
Figure 6.4 Contractile behaviour of isolated cat papillary muscle. Preload weight sets resting length. If preload is clamped, shortening is prevented and the electrically stimulated contraction is isometric. Graph (a) shows effect of resting length on isometric contractile force. If the muscle is allowed to shorten, it lifts a constant weight, the afterload, and the contraction is isotonic (b, c). Isotonic contractions starting from 10 mm resting length (high preload) are stronger than from 8 mm resting length (low preload).
162 Figures
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100
50
0
Contractile force (tension) as %maximum
Skeletal muscle
Cardiac muscle
60 80 100
Resting length as % of optimum (%Lmax)
Figure 6.5 Length–tension relation of cardiac muscle compared with skeletal muscle. Cardiac muscle has a much steeper curve than skeletal muscle at physiological lengths (80–100% of Lmax), even though the filament overlap is the same. This is because stretch increases the Ca2⫹sensitivity of cardiac myocytes.
Figure 6.6 Effect of stretch (%Lmax) on isometric contractile force and Ca2⫹transients (light signal) in isolated papillary muscle. Note immediate, large increase in force at d without any increase in the Ca2⫹transient. This is followed by a smaller, slow force response and Ca2⫹ increase (the Anrep effect).
Figure 6.7 Effect of curvature of a hollow sphere on the conversion of wall stress S into internal pressure P (Laplace’s law). (a) Hollow sphere with an ‘exploded’ segment, showing the two circumferential wall stresses. Stress is force per unit cross-sectional area, of thickness w.
The wall stress in the ejecting heart is the afterload on the myocytes. (b) Cross section showing how the wall stresses (tangential arrows) give rise to an inwardly directed stress equal and opposite to the pressure. The thick red line represents a muscle segment exerting tension. Arrow length is proportional to stress magnitude. (c) Increasing the radius reduces the curvature, and therefore the inward com-ponent of the wall stress; so pressure falls (Laplace’s law).
Figures 163
Figur es - Chapter 6
Figure 6.8 Equalization of right and left ventricular outputs by Starling’s law.
Central venous pressure (CVP)
Right atrial pressure (RAP)
Right ventricle end-diastolic pressure (RVEDP) Right ventricle end-diastolic volume (RVEDV) Right ventricle end-diastolic fibre length Right ventricle energy of contraction RV stroke volume
Pulmonary blood volume and pressure Pulmonary vein pressure, filling left atrium
Left atrial pressure (LAP)
Left ventricle end-diastolic pressure (LVEDP) Left ventricle end-diastolic volume (LVEDV) Left ventricle end-diastolic fibre length Left ventricle energy of contraction Left ventricle stroke volume
Figure 6.9 Venous blood redistribution by gravity on moving from supine (a) to standing (b). The thoracic compartment includes the central veins, heart and pulmonary blood. Numbers are cmH2O pressure above atmospheric. HIP, hydrostatic indifferent point. (c) Immersion raises pressure around the veins, displacing the ‘pooled’ blood centrally and raising CVP.
Foot Thorax Head
164 Figures
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Figure 6.10 Effect of exercise on ventricular dimensions and contraction, measured by M-modeechocardiography during rest (b) and upright exercise (c). The end-diastolic dimension (ED) increased and end-systole dimension (ES) fell. The ED–ES difference, an index of stroke volume, increased by 24%.
Transducer
(a)
LA
LV A
RV
Rest Exercise
ECG
Septum
Cavity
Posterior wall
ES ED
(b) (c) Time
Figure 6.11 Shift in ventricular function curves (Starling curves) brought about by sympathetic stimulation (dog heart). Sympathetic activity in range 0–4 s⫺1increased contractility. Arrows show how enhanced contractility reduces filling pressure, as well as raising stroke volume.
60
50
40
30
20
10
0 5
Sympathetic stimulation
Starling's law
10 15 20 25
Mean left atrial pressure (cmH2O)
Stroke work (g/m)
4.0 2.0
1.0 0.5
0.2 0
Figures 165
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Figure 6.12 Pressure–volume loops for human left ventricle. (a) Relation to aortic pressure wave. A, mitral valve opens; AB, filling phase; B, mitral valve closes at onset of systole; BC, isovolumetric contraction; C, aortic valve opens; CD, ejection phase; D, aortic valve closes; DA, isovolumetric relaxation.
Stroke work is sum of allΔP ⭈ dV strips inside the loop, i.e. total loop area. Sketches illustrate high energy expenditure and O2consumption by the myocardial manikin during isovolumetric contraction, achieving no external work, followed by lower energy cost of ejection. The subject is probably middle aged/elderly, since aortic pressure was 130/85 mmHg. (b) Set of pressure–volume loops for a constant contractility.
Lower boundary is passive pressure–volume curve of relaxed ventricle (compliance curve). Upper boundary is systolic pressure of a purely isovolumetric contraction at increasing end-diastolic volumes (Frank–Starling mechanism). Loop 1 is basal. Raising end-diastolic volume to B increases stroke volume (loop 2), due to Starling’s law. Note that end-systolic volume increases too. Raising peripheral resistance increases arterial pressure but reduces stroke volume (loop 3), due to the ‘pump function’ effect (Figure 6.3). A purely isovolumetric contraction (loop 4) reaches the upper boundary.
Pressure (mmHg)
(b) Volume of left ventricle (ml) Passive
166 Figures
Figur es - Chapter 6
200100
Volume of left ventricle (ml)
Pressure in the left ventricle (mmHg)
Exercise
Figure 6.13 Effect of increased left ventricular contractility on human pressure–volume loop. (a) Loop 1 is basal state. Loop 2 shows effect of increased sympathetic activity. Ejection fraction is increased, so end-diastolic volume falls. Loop area (stroke work) is increased. (b) During exercise (loop 3), contractility is raised by sympathetic activity but end-diastolic volume too is raised, by peripheral venoconstriction and the skeletal muscle pump.
This amplifies the increase in stroke volume.
Figure 6.14 Effect of a pump on input and output pressure. At zero pumping rate, the central venous pressure (CVP) and arterial pressure equalize (mean circulatory pressure, MCP). When the pump starts, its removes fluid from the input line, so it reduces input pressure, CVP, as well as raising output pressure (arterial pressure). CVP changes less than arterial pressure, because venous compliance (volume accommodated per unit pressure change) is greater than arterial compliance.
Arterial pressure
Figures 167
Figur es - Chapter 6
Venous pressure 10–15 mmHg P = 250 mmHg
Total occlusion, flow = 0
VENOCONSTRICTION = VENOUS PRESSURE
Occlude Deep breath
Cold Startle Graded exercise Head-up
tilt
LBNP
Venous pressure (mmHg)
40
20
0
Figure 6.15 Sympathetic-mediated venoconstriction in human skin. During exercise, this helps shift blood into the thoracic veins to maintain/raise CVP
Figure 6.16 Normal chest X-ray (left) and dilated heart in patient with cardiac failure (right).
168 Figures
Figur es - Chapter 6
Figure 6.17 An acute rise in arterial pressure, resulting from a rise in total peripheral resistance (TPR), affects stroke volume through two negative and two positive mechanisms. TPR may be increased acutely by sympathetic vasomotor activity, or chronically by clinical hypertension.
Hypertrophy,
Figure 6.18 Multiple mechanisms by which acute ischaemia, due usually to coronary atheroma, impairs contractility and causes arrhythmia.
Coronary artery atheroma
ACUTE ISCHAEMIA (hypoxia, acidosis, cardiac pain)
ATP, ADP, PO4– intracellular H+
activation Impaired Ca2+– troponin C binding
Figures 169
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Figure 6.19 Effect of sympathetic stimulation (noradrenaline) on cardiac performance. (a) Left ventricular pressure climbs faster (dP/dtmax), systolic pressure increases, systole shortens, relaxation is quicker and end-diastolic pressure (EDP) falls. (b) Increased ejection fraction and stroke volume reduce filling pressure and ventricular volumes, which limits the increase in stroke volume (Starling’s law). Restoring the filling pressure (B) allows the effect of contractility on stroke volume to emerge fully. Vertical bar shows size of control stroke volume.
Right atrial pressure (cmH2O)
Stroke volume
Figure 6.20 Effect of catecholamine-driven increase in cardiac output and oxygen consumption on coronary blood flow. N, normal resting value (canine).
4 8 12 16
N
Oxygen consumption (ml/min per 100 g) 120
Coronary blood flow (ml/min per 100g)
Figure 6.21 Reflex effect of an imposed rise in arterial pressure upon autonomic fibre activity and heart rate. The reflex is mediated by the arterial baroreceptors.
170 Figures
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Figure 6.22 Human cardiovascular response to exercise. Stroke volume measured by pulsed Doppler method.
180
90
0
0.4 0.8 1.2 1.6 O2 consumption (l/min) 60
120 8 16
Stroke volume (ml)Heart rate (per min)Cardiac output (l/min)
200
100
0
0.4 0.8 1.2 1.6 BloodO2 content (ml/l)
O2 consumption (l/min) Mixed venous 20
10 200
100
Arterial TPR (mmHg per l/min)Blood pressure (mmHg)
Systolic Mean Diastolic
‘Sample volume’
Spectrum analyser
Doppler probe
Ergometer
VEVO2
Figures 171
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Figure 6.23 Effect of posture and exercise on pulmonary circulation.
Alveolar-arterial difference in PO2(mmHg) Supine Upright
5
Arterial PCO2 (mmHg) 30
40
Figure 6.24 Blood oxygen transport curves, showing very high oxygen extraction by myocardium.
200
Partial pressure of oxygen (mmHg) Coronary sinus blood