LSM3212

Cardiovascular physiology

A/Prof Lina Lim Dept of Physiology linalim@nus.edu.sg (x5515)

Overview and objectives (3 lectures)

1. 2. 3. 4. 5. 6. 7.

Cardiac electrical activity ECG Regulation of heart function Cardiac output Cardiac mechanics Circulatory system Blood pressure

Circulatory tree-different functions

Heart Pump Artery
Mass rapid transit vessels

Arteriole Capillary Venules Veins

Resistance vessels
Gaseous exchange

Leukocyte recruitment
Capacitance vessels

Battery: Nodes Conductor- conducting pathway Engine power- muscles

How it starts. Pacemaker cells (nodes)

Driven by Action potentials

brief, rapid, large changes in membrane potential where the inside of the cell membrane becomes more positive than the outside
Membrane potentials are formed by distribution of ions (cations and anions) inside and outside the plasma membrane

Anionic (-ve; intracellular large proteins), cationic (+ve; Na+, K+) High A- inside; High K+ inside (to counterbalance A-); High Na+ outside (maintained by Na+/K+ pump).

Concentration gradient Electrical gradient

Potassium is important in the generation of the membrane potential across the plasma membrane

+ Na

- Cl

-A
+K

80% of MP caused by passive diffusion of K and Na down their concentration gradients 20% of MP maintained by Na-K pump (active) 3 Na out :2 K in

Action potentials in the heart

Self-induced action potential

Threshold potential Slow depolarization (pacemaker potential)

The fastest player wins.

Action potential in a cardiac contractile (muscle) cell

Very different from the pacemaker cell
rapid repolarization prevented
Plateau phase of action potential

Threshold potential

ECG: Electro-cardiogram
The electrical currents generated by cardiac muscle during depol and

repol spread into the tissues surrounding the heart and are conducted through the body fluids. A certain portion of this electrical activity reaches the body surface. Records comparisons in voltage detected by electrodes at different points on body (leads) not a single cell recording, but a complex recording of overall spread of activity of the heart

Direction

The direction of the deflection on the electrocardiogram depends on direction of electrical impulse to a detecting electrode.

Meek, S. et al. BMJ 2002;324:415-418

The same 12 leads routinely used in all ECGs: 6 leads : different configurations from limbs and 6 chest leads at different locations around the heart. Can be used to diagnose abnormal heart rates, murmurs.

4 5

RIGHT ARM LEFT LEG

LEFT ARM

Limb leads

aVR: right arm

Lead I: Right arm to left arm

aVL: left arm

Lead II: Right arm to left leg

Lead III: Left arm to left leg

aVF: left leg

Vertical and horizontal perspective of the leads

The limb leads "view" the heart in the vertical plane & the chest leads in the horizontal plane
Meek, S. et al. BMJ 2002;324:415-418

ECG

ECG questions

Where is the SA node firing? Where is wave for atrial repoln? Why P wave smaller? What are the 3 occasions where there is no electrical activity?
AV node delay; PR
Vents completely depol, and cardiac cells undergoing plateau phase

(vents contracting) ST Heart muscle at rest, ventricles filling. TP

Why is T wave positive?

P: Atrial Depol; QRS: Vent Depol; T: Vent Repol;

Cardiac cycle

Figure 9.21 (1) Page 322

A: Passive filling B Atrial contraction C:Isovolumetri c contraction D: Ventricular ejection E: Isovolumetric ventricular relaxation

5L/ min (blood flow) needs to flow through circulatory tree

How is blood flow maintained?

Arteries Arterioles

To capillaries
From veins Heart contracting and emptying

Arteries Arterioles

From veins
Heart relaxing and filling

To capillaries

Pressure in arterial system increases as vessels inflate with blood As heart relaxes, elastic recoil of arteries forces blood into arterioles Elastic properties of arteries help convert pulsatile flow of blood from heart into more continuous flow.

Cardiac output

= Stroke Volume x Heart Rate

Cardiac output = volume of blood pumped by each ventricle per min Heart rate =number of time the heart pumps per minute

Stroke volume = how much blood the heart can pump in one beat

Cardiac Output
Cardiac output: How much blood is pumped per min?
~70 beats per minute ~70ml /beat CO = beats x volume ~ 5 L /min Increases to 25 L/min during exercise

Regulation of cardiac output

Autonomic nervous system
Sympathetic Parasympathetic

Mediates rate and strength of contraction Resting conditions: S and PS cardiac fibres both active (P dominates) The ANS consists of motor neurons and is part of the nervous

system.
Efferent division of the peripheral nervous system makes adjustments to ensure optimal support for body activities. operates via subconscious control. Helps to regulate our internal environment

The Autonomic Nervous System (ANS) = independent

An autonomic nerve pathway has two

neurons: a preganglionic fiber and postganglionic fiber.

The ANS releases only two different

neurotransmitters on the structures it controls: acetylcholine (parasymp)and norepinephrine/noradrenaline (symp)

ANS effect on the target organ is

dependent upon the neurotransmitter released and the receptor type of the effector.

Divisions of the ANS

The two divisions of the ANS are the sympathetic and parasympathetic The sympathetic mobilizes the body during

extreme situations The parasympathetic performs maintenance activities and conserves body energy The two divisions counterbalance each others activity

Roles of the Parasympathetic Division

Roles of the Sympathetic Division

The sympathetic division is

the fight-or-flight system Involves E activities exercise, excitement, emergency, and embarrassment Activity is illustrated by a person who is threatened Heart rate increases, and breathing is rapid and deep The skin is cold and sweaty, and the pupils dilate

Concerned with keeping body energy use low Involves the D activities digestion, defecation, and diuresis (increased excretion of urine) Activity is illustrated in a person who relaxes after a meal Blood pressure, heart rate, and respiratory rates are low Gastrointestinal tract activity is high The skin is warm and the pupils are constricted
29

Heart rate and ANS

Resting conditions: S and PS cardiac fibres both active (P

dominates) Acetylcholine, vagus stimulation of M2 receptors increase K+ perm

Membrane potential (mV) Sympathetic stimulation Normal Parasympathetic stimulation

Threshold Seconds

Heart rate and ANS

SA node normally driven by PS, increasing time taken to reach threshold Noradrenaline (epinephrine, nor-) on b1 receptors in heart decrease K+ perm Symp NS stimulates SA node to increase rate of depolarization, reaching threshold faster, thus fire more rapidly, vice versa with parasymp
Membrane potential (mV)

Sympathetic stimulation

Normal

Parasympathetic stimulation

Threshold Seconds

Nor-adrenaline
Bind to a1 adrenoreceptors on vessel smooth muscle: Induces generalized vasoconstriction Brain only organ that does not have arteriolar vasoconstriction as brain blood flow must remain constant

Adrenaline
Sympathetic stimulation of adrenal gland:-secretion of

adrenaline
Binds to b2 adrenoceptors in the heart and skeletal muscle
Induces vasodilation

Not the gut, which has no b2 receptors

Shunting of blood to heart/muscle

Adrenaline- more affinity for b2 receptors = vasodilation in

arteriolar smooth muscle, especially in muscle and heart Nor-adrenaline affinity for a1 receptors = generalized vasoconstriction - a receptors (such as the skin, spleen, GIT)

EXERCISE

Ventricular fibrillation (VF).

chaotic quivering due to erratic electrical activity during pulselessness Deteriorates to total lack of activity

Defibrillator
Delivers electrical current through heart muscle, temporarily ceasing all electrical activity in the heart, In the hope that when that electrical impulse returns, it will return in an organized pumping action instead of VF.

What about Stroke volume?

Amount of blood pumped by heart each beat
Controlled Intrinsic and extrinsic factors Extrinsic: ANS Intrinsic: Adjust in response to venous return (FrankStarling Law of the Heart)

The heart pumps whatever it receives Increased stretch of cardiac muscle fibers.

increased cross-bridge formation increased calcium influx

both increases force of contraction

increased stretch on SA node

increases heart rate

Stroke volume regulation: extrinsic factors

Sympathetic influence (adrenaline) Sympathetic stimulation: heart pumps stronger Due to Ca influx (triggered by adrenaline and nor-adr) Leads to more forceful contractions through greater cross-bridge cycles Also inducing venous vasoconstriction to squeeze

veins, causing higher venous return

Stroke volume: intrinsic regulation Frank Starling Law of the heart SV = volume of blood ejected by left ventricle (ml / beat)
normal range for human: 60 - 130 ml 2 components: EDV = end diastolic volume (filling) ESV = end systolic volume (emptying)

SV = EDV - ESV

The innermost region that lines the lumen (L) of the heart, the Endocardium (EN), consists of a thin layer of endothelial cells and some loose connective tissue. Most of the mass of the heart is contained within the muscular Myocardium (MYO). The outermost region of the wall of the heart is the Epicardium (EPI), an envelope of dense connective tissue containing both collagenous and elastic fibers.
Endocardium Myocardium Epicardium

Cardiac muscle structure

Skeletal muscles:- bundles of long cylindrical muscle cells

known as muscle fibres wrapped in connective tissue Cardiac muscle:- Also striated Each fibre is packed with myofibrils Each consisting of alternating, slightly overlapping thick and thin filmanents Thus, striated under microscope: dark A bands, light I bands At each junction (A and I), surface membrane dips into muscle fibre to form a transverse (T)-tubule

Cardiac muscle contraction

Stimulated by action potentials from auto-rhythmic

cells Not attached to bones! Factor: of diastolic filling

More you put in, bigger it becomes, the more it is

stretched Greater extent of diastolic filling, larger the end-diastolic volume, the more stretched is the heart

Structure and function

Thin filament: contains actin, troponin and tropomyosin

 Thick filament: contains myosin

Helical cross bridges made of myosin molecules

globular head projecting from each thick filament towards thin filament

Together
Forms a sarcomere Thin filaments extend into thick filaments so action of cross bridge draws them inward from both directions:- contraction
Portion of myofibril
Z line A band I band

M line

H zone

Sarcomere
Thick filament Thin filament A band I band

Cross bridges

M line

H zone

Z line

T-tubules

Action potential spreads down from membrane to T-tubule Rapid transmission of electrical activity Induction of permeability changes in a separate membranous

network within fibre: sarcoplasmic reticulum

Release of Ca2+ from SR

Actin Tropomyosin

Binding sites exposed

Ca2+ Ca2+

Covered

Troponin complex

Tropomyosin

In the muscle fiber the contraction begins with the release of Ca2+

Membrane depolarization by action potential causes release of Ca2+ ions from the sarcoplasmic reticulum

1 Ca2+ binds to the TnC subunit of the Troponin-Tropomyosin complex. This initiates a conformation change which ultimately shifts tropomyosins position and exposes the myosin binding site on actin. Pi is then released. If Ca2+ is present, crossbrdige cycles continue.

Inorganic P

If Ca2+ is taken away, the cycle stops here and the muscle relaxes. If ATP is taken away crossbridges remain attached and rigor mortis will occur. Cycle stops here. 4 ATP binds to the myosin head releasing the crossbridge. It remains bound as the hydrolyzed from of ADP and Pi. Membrane repolarization allows uptake of Ca2+ ions by the sarcoplasmic reticulum

The release of Pi triggers 2 the power stroke of contraction, the energy being supplied by the hydrolysis of ATPADP+Pi+E. During the power stroke the myosin head rotates 45 bringing the Z line closer to the thick filament. ADP is then released.

As long as Ca2+ and ATP are resent the cycle continues. The Z line is pulled closer and closer to the ends of the thick filaments.

3 Myosin remains in the bound position until ATP binds to the myosin head or Ca2+ is removed. fig 16-19, pg 501

Action potential in cardiac contractile cell

Travel down T-tubule

Entry of small amount of Ca2+ from ECF Release of large amount of Ca2+ from SR in cytosolic Ca2+

Troponin-myosin complex in thin filaments pulled aside X-bridge sliding Thin filaments slide inward between thick filaments

CONTRACTION

Cardiac muscle mechanics

Structural and functional characteristics

shared with skeletal and smooth muscle

Striated Clear length - tension relationship Have T-tubules and SR Ca enters the cytosol from both the ECF and SR during cardiac excitation Interconnected by gap junctions Innervated by ANS

Like skeletal muscle

Like smooth muscle

Difference in cardiac muscle vs skeletal muscle

Tetanic contractions are

additive activation of muscle to shorten to full extent Do not occur in cardiac muscle. Why? Ca2+ entry from ECF induces more Ca2+ release from SR Responsible for long period of cardiac contraction

Action potential

Contractile response

Refractory period

Optimal length

Stroke volume (SV) (ml) (related to muscle tension)

Increase in SV

B1 A1

(Cardiac muscle does not normally operate within the descending limb of the length tension curve.)

Normal resting length Increase in EDV End-diastolic volume (EDV) (ml) (related to cardiac-muscle fiber length)

Maximum contraction = optimal length before onset of

contraction= optimal overlap of thick filament cross-bridges and thin filament binding sites (most binding sites)

Cardiac muscle length vs tension

Within limits as cardiac fibers are stretched the force of contraction is increased
more cross bridge formation as actin overlap is removed more Ca++ influx into cell associated with the increased stretch

Frank-Starling Law of the Heart:

venous return ( EDV)

stretch of cardiac muscle fiber

force of contraction (ESV)

What governs EDV and ESV

Preload:- forced exerted by blood on ventricular

muscle at the end of diastole (also EDV) Afterload: force resisting pumping of blood out of the heart usually resistance (high aortic pressure)

Stroke volume is regulated by venous return

Return of blood to heart =venous return = EDV

Veins: Capacitance vessels Blood reservoir Muscle pump Valves

Venous return & capacity

Venous return (volume of blood returning to atria)
DP If atrial pressure high - blood accumulation in venous system

Venous capacity (amount of blood veins can hold) Inversely proportional to venous return
If high circulating volume Depends on distensibility of vessel walls and external pressure

Regulation of venous return

Sympathetic innervation
Skeletal muscle activity Cardiac pump/suction effect Respiratory pump

Negative effects of Gravity Planes, pregnancy, standing still

Effect of gravity
Scenario
Person stands still for long time, blood flow to brain reduced ( in

circulating volume), leads to fainting- horizontal positioning After sitting for a long time, better to get up and get blood moving Postural hypotension

Evidence of valves William Harvey 1628

Varicose veins
Venous valves are incompentent
Can no longer support the column

of blood above it, and collapse

Aggravated by frequent,

prolonged standing, very distended veins valves cannot form seal

Blood pools in them and edges of

Cardiac output

Stroke volume

End-diastolic volume Venous valves (mechanically prevent backflow of blood)

Passive bulk-flow shift Salt and water of fluid from interstitial fluid retention into plasma Blood volume ( venous pressure pressure gradient)

Venous return

Cardiac suction effect ( pressure in heart pressure gradient) Sympathetic vasoconstrictor activity ( venous pressure pressure gradient; venous capacity)

Respiratory pump ( pressure in chest veins pressure gradient)

Pressure imparted to blood by cardiac contraction ( venous pressure pressure gradient)

Skeletal muscle pump ( venous pressure pressure gradient)

= Short-term control measures

= Long-term control measures

In summary
Cardiac output = heart rate x stroke volume
Stroke volume regulated by frank starling law optimal muscle contraction ANS venous return, heart contractility Heart rate regulated by ANS directly on heart

receptors

Dr Lina Lim

Pressure vs flow
Blood pressure:
Force exerted by the blood against a vessel

Blood flow (Q):

Flow rate of blood is directly proportional to pressure gradient

and inversely proportional to resistance

Pressure gradient (DP)

Difference in pressure between the beginning and the end of a

vessel

Ohms law

Q= P/R

Where Q is blood flow, P is pressure gradient and R is resistance

0 mmHg 150 mmHg 150 mmHg

0 mmHg 150 mmHg

0 mmHg

Resistance is governed by 1. Viscosity 2. Vessel Radius (R = 1/r4) 3. Vessel length

Poiseuilles law
By integrating the velocities of all the concentric rings

of flowing blood and multiplying them by the areas of the rings, one can derive the following formula, known as Poiseuille's law: Q = ( Pr4)/8 l
where Q is the rate of blood flow, P is the pressure difference between the ends of the vessel, r is the radius of the vessel, l is length of the vessel, and is viscosity of the blood.

Like a dam

Modes of flow in vessles

Blood flow can either be laminar or turbulent

Laminar Flow
When blood flows through a long smooth vessel it flows in straight lines, with each layer of blood remaining the same distance from the walls of the vessel throughout its length When laminar flow occurs the different layers flow at different rates creating a parabolic profile, whre the centre of the vessel is fastest

Turbulent flow
Turbulent flow means that the blood flows crosswise in the

vessel as well as along the vessel, usually forming whorls in the blood called eddy currents. When whirlpool currents are present, the blood flows with much greater resistance than when the flow is streamline because eddies add tremendously to the overall friction of flow in the vessel. This happens when the rate of blood flow becomes too great; when it passes by an obstruction in a vessel; when it makes a sharp turn; or when it passes over a rough surface

Pressure-recording device

Figure 10.8 (1) Page 350

Inflatable cuff

Stethoscope

Cuff pressure Blood pressure

1,2
When cuff pressure is greater than 120 mm Hg: No blood through the vessel - laminar No sound is heard.

3,4,
When cuff pressure is between than 120 and 80 mm Hg: Blood flow through the vessel is turbulent whenever blood pressure exceeds cuff pressure. Intermittent sounds are heard as blood pressure fluctuates throughout the cardiac cycle.

5
When cuff pressure is less than 80 mm Hg: Blood flows through the vessel in smooth, laminar fashion. No sound is heard.

Clinical blood pressure

Pressure
Systolic pressure

drops from arteries to veins increasingly nonpulsatile (high resistance in arterioles)

Mean pressure

Diastolic pressure

Left ventricle

Large arteries

Arterioles Capillaries Venules and veins

Systolic pressure: peak arterial pressure which occurs during

contraction of the ventricle Diastolic pressure: minimum pressure after relaxation Systolic /diastolic = 120/80

Why is blood pressure up and down?

Arteries are Pulsatile Lowest pressure at ventricular diastole Highest during systole Aorta and artery walls stretch and increase in diameter in response to blood PULSE PRESSURE = difference between systolic and diastolic pressure (if 120/80 then pp= 40 mmHg) pulse

Pulsatile pressure
Systolic pressure

Mean pressure

Diastolic pressure

Mean arterial pressure

Main driving force for blood flow: average pressure
MAP =2/3 diastolic + 1/3 systolic
At resting HR, 2/3 of cardiac cycle is spent in diastole and 1/3 in systole Eg., race car 80 mph for 40 min and 120 mph for 20 min:average speed is 93mph

What regulates blood pressure?

Mean arterial pressure = cardiac output x total peripheral resistance = (Heart rate x Stroke volume) x total peripheral resistance =Q x TPR

Total peripheral resistance

reflects the status of the resistance arterioles.

The higher the resistance, the lower the flow, the higher the pressure in the artery upstream, and thus higher the mean arterial pressure.

Total peripheral resistance

Arterioles: thick layer of smooth muscle innervated by sympathetic nerve fibres

Resistance 1/r4 while Flow r4

A small reduction in radius leads to a large

increase in resistance and a large reduction in flow

What regulates TPR?

Local vasoregulation of arterioles
Vasoconstriction Vasodilatation

Local changes within a tissue: intrinsic factors affecting tone

SM sensitive to local chemical changes and hormonal signals
resistance, flow resistance, flow

Arteriole Smooth muscle cells

Caused by SM relaxation Vasodilatation O2, CO2 and metabolites, sympathetic stimulation, Heat NO

Normal tone

Caused by SM contraction Vasoconstriction O2, CO2 and metabolites, sympathetic stimulation, Cold Endothelin

 E.g., skeletal muscle contracting

Local O2 levels CO2 levels
Trigger local arteriolar vasodilatation blood flow

Vasoactive substances
NO causes vasodilatation Endothelin

made in endothelium, causes vasoconstriction very potent R antagonists in clinical trials for hypertension

Suggested reading:- Galie N, Manes A, Branzi A. The endothelin system in pulmonary arterial hypertension. Cardiovasc Res. 2004 Feb 1;61(2):22737. Review.

Figure 10.35 Page 376

Short term control of BP: Baroreceptor reflex

Carotid sinus baroreceptor

Figure 10.36 Page 377

Common carotid arteries (Blood to the brain)

Neural signals to cardiovascular control center in medulla

Aortic arch baroreceptor

Aorta (Blood to rest of body)

Long term control of BP : blood volume

blood volume results in arterial BP Control of blood pressure :- alteration in normal salt and water balance (takes days) Regulation of urine output, thirst Eat more/less salt?

Renin-angiotensin system
blood volume and arterial BP = release of renin from kidneys Liver releases angiotensinogen Lungs secrete angiotensin-converting enzyme Angiotensin II strong vascoconstrictor

Angiotensinogen
Adrenal cortex Renin Aldosterone

Angiotensin I
ACE

Renal proximal tubule

sodium excretion

Blood volume arterial BP

Angiotensin II
Vasoconstriction

Peripheral arterioles

TPR

Vasopressin or anti-diuretic hormone (ADH)

ADH secreted from pituitary gland in hypothalamus

Plasma osmolality

Blood vessel

Vasoconstriction

plasma volume

ADH

Blood volume arterial BP

Increased reabsorption of water

Atrial natriuretic hormone

ANH secreted from specialized cells of right atrium
Blood volume arterial BP
Promote loss of Na+ in urine and increase urine volume

Blood pressure

ANH

Clinical hypertension
Defined as chronically increased systemic arterial

pressure (~140/90) Well established hyper T = due to increased TPR caused by abnormally reduced arteriolar radius

Hypertension
5% of cases of hypertension = the cause is known
Renal hypertension kidneys increased release of

renin and potent angiotensin II causes vasoconstriction 95% - primary or essential hypertension = cause unknown

Hypertension
High blood pressure
High afterload

http://video.healthhaven.com/High_Blood_Pressure.htm#item0

Micro-Control of blood volume swelling or edema

Normally retained plasma proteins

leak out and cause osmotic effect (water leaks out to balance osmotic equilibrium)

Bulk flow
Capillary hydrostatic pressure PC Plasma oncotic pressure

Interstitial fluid oncotic pressure IF

Interstitial fluid hydrostatic pressure, PIF

Filtration forces Net Filtration Pressure =

Absorption forces

Hydrostatic pressure (fluid pressure) P Colloid osmotic pressure (or oncotic pressure)

Net exchange of fluids in capillary

Oncotic pressure gradient Hydrostatic pressure gradient

Net filtration

Net absorption

At arterial end, HP > OP so fluid flows out- filtration At venous end, HP< OP so fluid flows in-absorption

fig. 19-19b; pg. 604

Arteriole

Capillary
VASODILATION

Venule

Effects of vasomodulation or sphincter opening

Vasodilation
Capillary hydrostatic pressure
Net filtration Net filtration

Filtration all through

VASOCONSTRICTION

Vasoconstriction
Capillary hydrostatic pressure Absorption all through
fig. 19-20; pg. 605

Net absorption

Net absorption

Overlapping endothelium one way

Edema formation
Edema formation too much interstitial fluid accumulation from:
in plasma protein concentration capillary

permeability venous pressure will also capillary pressure, Blockage of lymphatics

e.g filariasis mosquito parasite worms infect lymphatics and prevent lymph drainage elephantitis. removal of lymph nodes from breast cancer patients, damage of lymphatics swelling in arms

Symptoms of congestive heart failure

Swollen feet and water in lungs

During heart failure, heart works extra hard to

pump blood out of the heart High afterload (high aortic pressure) less blood pumped out Drop in pressure gradient, leading to higher pressure in ventricles Back log of pressure = back log of volume High venous pressure = high capillary pressure High hydrostatic pressure = more filtration Swollen feet and water in lungs

Importance of bulk flow

Regulating distribution of fluid between blood and tissue

Maintaining blood volume regulates blood pressure

If plasma volume (e.g blood loss), blood pressure too This extra fluid provides extra fluid for plasma, temporarily

compensating for plasma volume loss

If plasma volume , more plasma leaves blood

temporarily relieving expanded plasma volume

Long term compensatory reactions to drop in blood volume

After a moderate hemorrhage, circulating plasma volume restored in 12-72 hours (through urine output)
Fluid enters the circulation from intravascular stores (bulk flow), mostly protein free Preformed albumin also enters initially, but plasma protein loss replaced by hepatic synthesis Erythropoeitin appears in circulation and reticulocyte count increases (peak at day 10)

Figure 10.41 Page 384

Effects of Hemorrhage

Consequences

Compensations

Circulatory shock ( mean arterial pressure)

Cardiac output

Cardiac output

Total peripheral resistance

Loss of blood volume

Widespread vasodilation

Loss of fluids derived from plasma

Vasodilator substances released from bacteria

Histamine released in severe allergic reaction

Loss of vascular tone

Severe hemorrhage

Excessive vomiting, diarrhea, urinary losses, etc.

Weakened heart

Septic shock

Anaphylactic shock

Sympathetic nerve activity

Hypovolemic shock

Cardiogenic shock

Vasogenic shock

Neurogenic shock

When blood pressure falls so low that adequate blood flow to tissues can no longer be maintained, circulatory shock occurs

Conclusions