BP = CO x TPR. (stroke volume x heart rate) BP = blood pressure CO = cardiac output TPR = Total peripheral resistance

BP = CO x TPR (stroke volume x heart rate)

BP = blood pressure

CO = cardiac output TPR = Total peripheral resistance

Stroke volume = End-diastolic volume (EDV) – End-systolic volume (ESV) EDV depends on:

ESV depends on:

1.

Filling pressure

1.

Prelod (i.e. EDV)

2.

Filling time

2.

Afterload

3.

Ventricular compliance

3.

Heart rate

4.

Contractility

5

Starling’s law of the heart (1914) ‘The energy of contraction - - - is proportional to the muscle fibre length at rest. Stroke volume (human)

(Arterial pressure held constant)

Plateau

ml 70 Normal, rest

5

10

15

Central venous pressure (mmHg) Filling pressure The ’ventricular function curve’ or ‘Starling curve’

How are RV and LV stroke volumes kept equal?

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 STARLING’S  LAW OF THE Right ventricle energy of contraction HEART  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 STARLING’S  LAW OF THE Left ventricle energy of contraction HEART  10 Left ventricle stroke volume

12

13

Laplace´s law states that, for a hollow sphere, the internal pressure (P) is proportional to the wall tension (T) and is inversely proportional to the internal radius (r):

2T P= r Tension is a force equal to wall stress (S) times Wall thickness (w):

2Sw P= r

Increasing the radius reduces the curvature, and therefore the inward component of the wall stress, so pressure falls. 16

The Laplace effect and the Frank-Starling mechanism clearly have opposite effects on ventricular performance:

Distension of the ventricle raises its force of contraction – due to Starling´s law X Distension also reduces the pressure generated by a given contractile force – due to Lapace´s law. Fortunately, under physiological conditions (i.e. in a healthy heart) the gain in contractile energy resulting from Moderated distension (Starling´s law) greatly outweighs the fall in pressure-generating efficiency (Laplace´s law)

In contrast, the failing heart is often grossly dilated, making the Laplace effect the dominant one. An increase in radius in an already swollen heart causes little to no increase in contractile force, because the ventricle is on the plateau of the Starling curve, but the increase in radius impairs the generation of systolic pressure and hence ejection (Laplace´s law).

Reduction of cardiac distension is an important therapeutic goal in heart failure

∆P = CVP - RAP CVP = central venous pressure RAP = right atrial pressure

∆P = pressure difference (i.e. driving force) for the return of blood from the periphery to the right atrium. Thus, the cardiac output steadily rises as RAP falls.

Independent variable

Dependent variable

Change in the venomotor tone, by constriction or dilatation of only veins, is equivalent to change in the blood volume. Because most of the blood volume is in the veins, a pure increase in venomotor tone would be equivalent to a blood transfusion.

Because arterioles contain only minor fraction of the blood volume, changes in the arteriolar tone have only little effect on MSFP and thus on the x-intercept. However, changes in the arteriolar tone can have a marked effect on the CVP

Normal situation ∆P = CVP – RAP = 6 mmHg – 2 mmHg = 4 mmHg Vasodilatation ∆P = CVP – RAP = 8 mmHg - 2 mmHg = 6 mmHg

venous return 5 L/min (1.25 L/1 mmHg) venous return 7.5 L/min (6 x 1.25)

There is no absolute dependent and independent variable in this closed circuit. (Imagine what would happen if RAP transiently increased from 2 to 4 mmHg)

∆P = CVP - RAP Cardiac output: • By sucking the right atrium dry, it will tend to lower RAP. • By pumping blood out of the heart towards the veins, it will increase CVP.

Thus, the only way to produce a permanent change in cardiac output, venous return and RAP is to change at least one of the two function curve

Akutní mechanizmy regulace krevního tlaku

1. Arteriální baroreflex 2. Arteriální chemoreceptory 3. Bainbridgeův reflex 4. Ischemické receptory CNS

Procenta výskytu

7,0 6,0 5,0 4,0 3,0 2,0 1,0 0,0

Normální

Denervovaný

1

50

2 100

3150

4 200

Střední arteriální tlak (mmHg)

5 250

Počet impulzů (impulz/sek)

„Normální“

I „Znovu nastavený“

P

100

Arteriální tlak (mmHg)





“The first slide of the lecturer, who was an intrepid young cardiovascular physiologist, was Figure 1 from Guyton and Coleman´s epic paper. It was clear that the audience was already becoming nervous. There was some whispering, shuffling, and a sense of unease. The lecturer´s second slide was met with a more definite response. There was derision, laughter, and spontaneous comments from the audience….. I witnessed, for the only time in my academic life, a lecturer being chased from the podium by the audience”

Christopher S. Wilcox

Vazodilatace

Vazokonstrikce

Filtration, Reabsorption and Excretion Rates of Different Substances by the Kidneys

Amount Filtered

Amount Reabsorbed

Amount Excreted

% of Filtered Load Reabsorbed

Glucose (g/day)

180

180

0

100

Bicarbonate (mmol/day)

4 320

4 318

2

99.9

Sodium (mmol/day)

25 560

25 410

150

99.4

Chloride (mmol/day)

19 440

19 260

180

99.1

Potassium (mmol/day)

756

664

92

87.8

Creatinine (g/day)

1.8

0

1.8

0

Autoregulation of Glomerular Filtration Rate and Renal Blood Flow

1. Myogenic Mechanism 2. Tubuloglomerular Feedback

Příjem nebo vylučování sodíku (x normálu)

8 6 4 Equilibrium

2 0 0

50

100

150

Renálně perfuzní tlak (mmHg)

200


8

Equilibrium B

6

4

Equilibrium A 2

0 0

50

100

150

200


250


8

A

B

6 4 Equilibrium

2 0 0

50

100

150


200


8 6

4

Equilibrium A

Equilibrium B

2 0 0

50

100

150

200


250


8 6

4

C 2

A

B

0 0

50

100

150

200


250

Formy Hypertenze A. Esentiální (Primární) Hypertenze B. Sekundární Hypertenze 1. Renovaskulární Hypertenze 2. Renální (parenchymatózní) Hypertenze 3. Endokrinně Podmíněné Formy Hypertenze a/ Primární hyperaldosteronismus b/ Pseudohyperaldosterinismus - Liddleuv syndrom c/ Pseudohyperaldosterinismus - způsobený defektem 11-ßHSD d/ Hyperaldosterinismus ovlivnitelný glukokortikoidy e/ Cushingův sysndrom f/ Feochromocytom

Primární hyperaldosteronismus Nadbytek mineralokortikoidů produkovaných adenomem (tzv. Connův syndrom) způsobí: 1. Zvýšenou aktivitu Na+-K+ pumpy v bazolaterální membráně.

2. Zvýšenou aktivitu epiteliálních kanálů pro Na+ (ENaC) v luminální membráně.

Primární hyperaldosteronismus intersticium

lumen

Na+ Cl-

3Na+

2K+

Na+

K+

Liddleuv syndrom - pseudohyperaldosteronismus

Tento syndrom je způsoben mutací jedné ze tří podjednotek ENaC kanálu, což způsobuje, že tento kanál zůstává konstitutivně aktivní

Liddleúv syndrom - pseudohyperaldosterinismus lumen

Na+

intersticium

Pseudohyperaldosteronismus způsobený defektem 11-beta-hydroxysteroiddehydrogenázy

Mineralokortikoidní receptor je nitrobuněčný cytoplazmatický

protein, který může vázat jak aldosteron, tak i glukokortikoidní hormon kortizol. Buňky (distálního tubulu) mají na svém povrchu enzym 11-ß-HSD, která mění kortizol na kortizon, což sekundárně

způsobí, že v okolí těchto buněk je lokálně dostupný pouze aldostern

intersticium

lumen

Na+ Cl-

3Na+

2K+

Na+

K+

Pseudohyperaldosteronismus příznivě ovlivnitelný glukokortikoidy

Dochází k nadprodukci aldosteronu a gen aldosteronsyntáza je napojen na regulační gen 11-betahydroxylázy, což dostává syntézu pod kontrolu ACTH.

Hyperaldosterinismus – ovlivněný glukokortikoidy intersticium

lumen

Na+ Cl-

3Na+

2K+

Na+

K+

Cushingův syndrom V případě nadměrného (farmakologického) podávání glukokortikodiů, tak i funkční 11-ß-HSD není schopna „odbourat“ všechen kortizol a dochází k aktivaci mineralokortikoidních receptorů

Cushingův syndrom intersticium

lumen

ALDO

N GR

Na+

Feochromocytom Nádor dřeně nadledvin produkuje enormní množství katecholaminů

Děkuji za pozornost

BP = CO x TPR. (stroke volume x heart rate) BP = blood pressure CO = cardiac output TPR = Total peripheral resistance

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