SISTEMA CIRCULATORIO: FUNCIONES PRINCIPALES

SISTEMA CIRCULATORIO:

FUNCIONES PRINCIPALES

• Transporte y distribución de O2 y CO2,

sales, nutrientes, metabolitos, hormonas,

células inmunes y Acs.

• Producción de ultrafiltrado renal.

• Regulación de temperatura corporal.

• Comunicación humoral (hormonas, factores

inmunes).

Sistemas abiertos

- Corazón, arterias, válvulas

- Hemocele (30% vol. corporal)

- Baja presión (4-10 mmHg)

Sistemas cerrados

- Corazón, arterias, capilares, venas, válvulas

- Sangre (5-10% vol. corporal)

PUMP

DISTRIBUTING

TUBULES

THIN

VESSELS

COLLECTING

TUBULES

reservorio de PRESIÓN

reservorio de VOLUMEN

VEINS

CAPACITY

VESSELS

HEART

80 mmHg

120 mmHg

SYSTOLE

DIASTOLE

ARTERIES (LOW COMPLIANCE)

Que se puede simplificar

SERIES AND

PULMONARY

CIRCULATION

1. LOW RESISTANCE

2. LOW PRESSURE

(25/10 mmHg)

SYSTEMIC

CIRCULATION

1. HIGH RESISTANCE

2. HIGH PRESSURE

(120/80 mmHg)

PARALLEL

SUBCIRCUITS

UNIDIRECTIONAL

FLOW

Structure

of the

SINCITIO

conexión mecánica

y eléctrica

Cardiac muscle

SINCITIO

conexión mecánica

y eléctrica

Na

+

K

+

-70 mV

RESTING

THRESHOLD

-0

Gradually

increasing P

AUTOMATICITY

POTENCIAL MARCAPASOS

- Canales de fuga para Na+ (If) abiertos a Vm ~ -60 mV (PNa+ >> PK+)

- Vm ~ -40 mV, despolarización rápida por Ca+ (insensible a TTX)

- Canales de K+ retrasados open to start repolarization and close Ca2+ channels, then close themselves to allow next pacemaker potential to start.

2 _— PK and PCa

3a

3b

a slow K+ channels open b fast K+ channels reopen; Ca2+ channels close

P_K and P_Ca

— PK/PNa ≈ 100 (higher than in axon, so Vm)

"delayed rectifier" channels

Initial spike of P

involves

fast Na

channels (as in

axons). Late, low level of

P

is because slow Ca

channels have a small

permeability to Na

.

(Initial PNa spike is shown

as lasting far too long on this time scale; it should be only a few msec.)

Changes in P

result from

depolarization's effects on

at least two types of K

channels, one that closes

shortly after the P

spike

and one that opens much

later and very slowly.

Fast K closes Slow K opens

Fast K reopens ("Delayed rectifier")

In cardiac muscle, the action potential — and therefore

the refractory period — lasts almost as long as the

complete muscle contraction, so no tetanus, or even

summation, is possible. Sequential contractions are at

the same tension, though gradual increases and

PACEMAKERS (in order of

their inherent velocity)

• Sino-atrial (SA) node (0.8 m/s)

• Atrio-ventricular (AV) node (0.05 m/s)

• Bundle of His (5 m/s)

• Bundle branches (5 m/s)

• Purkinje fibers (5 m/s)

Conduction of pacemaker potential from nodal tissue to adjacent contractile cells and beyond, through gap junctions in intercalated disks.

Increased open probability

Acetylcholine (muscarinic)

Gi protein

Ca

signaling in cardiac muscle

Inhibited by digitalis & ouabain;

indirectly Na+_/Ca2+ exchange 

[Ca2+_] in

Electrocardiograma

Suma de la actividad eléctrica en el corazón

AV NODE AND AV BLOCKS

FOCUS ON N REGION

ECG

Systole — contraction of ventricles (systolic P = peak pressure per heartbeat in major systemic arteries)

Diastole — relaxed filling of ventricles (diastolic P = lowest pressure per heartbeat in major systemic arteries)

First heart sound (lub) — sound of atrioventricular valves closing as ventricles start contracting

Second heart sound (dup) — sound of semilunar valves closing as ventricles stop contracting and ventricular pressure drops below pressure in the major arteries

Pulse pressure (PP) — systolic P - diastolic P

Mean arterial pressure (MAP) — diastolic P + 1/3 PP

Stroke volume (SV) — vol. at end of diastole - vol. at end of systole; usually ~70 ml ( = ~130 ml - ~60 ml )

Cardiac output (CO) — heart rate (HR) x SV

CO can increase by a factor of 6 or more, initially due to HR & SV; at higher CO, increase is mostly due to HR.

EDV

Gasto cardíaco = volumen sistólico x frecuencia cardíaca

Volumen Sistólico

- presión venosa

- presión auricular

- distensión ventricular

- FC

Respuesta al ejercicio

- volumen sistólico constante

- estimulación simpática



FC, vel. llenado ventricular

Un poco de física

VELOCITY = DISTANCE / TIME

V = D / T

FLOW = VOLUME / TIME

Q = VL / T

VELOCITY -FLOW- AREA

V = Q / A

ÁREA SECCIONAL Y VELOCIDAD

Q=10ml/s

A= 2cm

10cm

1cm

V= 5cm/s 1cm/s 10cm/s

V = Q / A

a

b

c

TIPOS DE CAPILARES

músculo, tejido nervioso, pulmones

riñón, intestinos, glándulas endócrinas

CAPILLARIES

• Pressure inside is 35 to 15 mmHg

• 5% of the blood is in capillaries

• exchange of gases, nutrients, and wastes

• flow is slow and continuous

Distribution of Blood in the

Circulatory System

• 67% IN THE SYST. VEINS/VENULES

• 5% IN THE SYSTEMIC CAPILLARIES

• 11% IN THE SYSTEMIC ARTERIES

• 5% IN PULMONARY VEINS

• 3% IN PULMONARY ARTERIES

• 4% IN PULMONARY CAPILLARIES

• 5% IN HEART ATRIA/VENTRICLES

CARDIOVASCULAR

SYSTEM

HEART

(PUMP)

VESSELS

(DISTRIBUTION SYSTEM)

RE

GULA

TION

AUTOREGULATION

NEURAL

HORMONAL

RENAL-BODY FLUID

CONTROL SYSTEM

INCREASING HEART RATE

INCREASES CONTRACTILITY

Normal

Heart Rate

Ca

Ca

Fast

Heart Rate

Ca

Ca

Ca

Ca

Regulation of Cardiovascular System

Overview-

Regulation of Cardiovascular System

Overview-

HORMONAL REGULATION

• Epinephrine & Norepinephrine

– From the adrenal medulla

• Renin-angiotensin-aldosterone

– Renin from the kidney

– Angiotensin, a plasma protein

– Aldosterone from the adrenal cortex

• Vasopressin (Antidiuretic Hormone-ADH)

HYPERTENSION (140/90 mmHg)

Secondary Hypertension (10%) [e.g., Pheochromocytoma]

Essential Hypertension (90%)

- Normal cardiac output

- Cardiac hypertrophy [left ventricle]

- “Resetting” of the baroreceptors

- Thickening of vascular walls

ARTERIAL PRESSURE-URINARY OUTPUT THEORY

Hypertension causes thickening of vascular walls

NEUROGENIC THEORY

Thickening of vascular walls causes hypertension

TREATMENT:

Reduce stress

Sympathetic blockers

Low sodium diet

RESPONSE TO HEMORRHAGE

•



Sympathetic tone via baroreceptor reflex

–



Heart rate and contractility

– Venoconstriction (



MCP)

– Vasoconstriction (



arterial BP & direct blood to

vital organs)

• Restore Blood Volume

– Capillary fluid shift (



BP favors reabsorption)

–



Urinary output (



Arterial BP, ADH,

Renin-Angiotensin-Aldosterone)

CARDIAC FAILURE

CAUSES:

Impairment of electrical activity

Muscle damage

Valvular defects

Cardiomyopathies

Result of drugs or toxins

PROBLEM: Maintaining circulation with a weak pump

(



Cardiac output & cardiac reserve;



RAP)

SOLUTIONS:



Sympathetic tone via baroreceptor reflex

-



Heart rate and contractility

-Venoconstriction (



MCP)

-Vasoconstriction (



Arterial BP)

Fluid retention (



MCP)

-Capillary fluid shift

-ADH

MEASURING BLOOD PRESSURE

TURBULENT FLOW

1. Cuff pressure > systolic blood pressure--No sound.

2. The first sound is heard at peak systolic pressure.

3. Sounds are heard while cuff pressure < blood pressure.

4. Sound disappears when cuff pressure < diastolic pressure.

Blood pressures

and the vascular

system

Arterial

Pressure-

MEASUREMENT OF CARDIAC OUTPUT

THE FICK METHOD:

VO

= ([O

]

- [O

]

) x Flow

Flow =

VO

[O

]

- [O

]

Spirometry (250 ml/min)

Arterial Blood (20 ml%)

Pulmonary Artery Blood (15 ml%)

CARDIAC OUTPUT

PERIPHERAL

BLOOD FLOW

VENOUS RETURN

CARDIAC OUTPUT (Q) =

[O

VO

]

- [O

]

250 ml/min

20 ml% - 15 ml%

=

= 5 L/min

.

Q = HR x SV

.

SV =

Q

HR

.

=

5 L/min

70 beats/min

= 0.0714 L or 71.4 ml

CARDIAC INDEX =

Q

m

body surface

area

.

5 L/min

1.6 m

=

= 3.1 L/min/m