4. Additional differences between Arteries & Veins
• Arteries and veins run side-by-side
• Arteries have thicker walls and higher blood
pressure
• Collapsed artery has small, round lumen
• Vein has a large, flat lumen
• Vein lining contracts, artery lining does not
• Artery lining folds
• Arteries more elastic
• Veins have valves
5. Arteries and Pressure
– Elasticity allows arteries to absorb pressure waves that come with
each heartbeat
– Contractility -Arteries change diameter
– Controlled by sympathetic division of ANS
______________________
Arteries & their diameter:
• Vasoconstriction -The contraction of arterial smooth
muscle by the ANS
• Vasodilatation- The relaxation of arterial smooth muscle
enlarging the lumen
• Both of them Affect:
– afterload on heart
– peripheral blood pressure
– capillary blood flow
8. Valves in the Venous System
Figure 21-6
Vein Valves
Folds of tunica
intima
Prevent blood
from flowing
backward
Compression
pushes blood
toward heart
9. Figure 21-7
Blood Distribution
•Heart, arteries, and
capillaries:
30–35% of blood
volume
•Venous system:
60–65%
•1/3 of venous blood is
located in the large
venous networks of the
liver, bone marrow, and
skin
11. Viscosity (R)
• R caused by molecules and suspended materials in
a liquid
• Whole blood viscosity is about 4 times that of water
Turbulence
• Swirling action that disturbs smooth flow of liquid
• Occurs in heart chambers and great vessels
• Atherosclerotic plaques & Abnormal Valves cause
abnormal turbulence
12. Pressures in the Systemic Circuit
• Systolic pressure: peak arterial pressure during ventricular systole
• Diastolic pressure: minimum arterial pressure during diastole
• Ideal BP: 120/80
Abnormal Blood Pressure:
• Hypertension: abnormally high blood pressure: greater than 140/90
• Hypotension: abnormally low blood pressure
• Pulse pressure:
– difference between systolic pressure and diastolic pressure
• Mean arterial pressure (MAP):
MAP = diastolic pressure + 1/3 pulse pressure
13. Venous Return
• Amount of blood arriving at right atrium each minute
• Determined by venous pressure
• Low effective pressure in venous system
• Low venous resistance Is assisted by:
– muscular compression of peripheral veins
– the respiratory pump
– Muscle contraction pushes blood toward heart (one-way valves).
• Capillary Exchange
• Vital to homeostasis
• Moves materials across capillary walls by diffusion, filtration, and
reabsorption
14. 4 Functions of
Blood and Lymph Cycle
1. Ensures constant plasma and interstitial fluid
communication
2. Accelerates distribution of nutrients, hormones,
and dissolves gases through tissues
3. Transports insoluble lipids and tissue proteins that
can’t cross capillary walls
4. Flushes bacterial toxins and chemicals to immune
system tissues
15. Blood flow & Tissue Perfusion
• Blood flow is the goal
• Total peripheral blood flow equals cardiac output
• BP overcomes friction and elastic forces to sustain blood flow
• If BP is too low: vessels collapse, blood stops & tissues die
• If BP is too high: vessel walls stiffen, capillary beds may rupture.
• Blood flow through the tissues
• Carries O2 and nutrients to tissues and organs
• Carries CO2 and wastes away
• Tissue perfusion Is affected by:
– cardiac output
– peripheral resistance
– blood pressure
16. 3 Regulatory Mechanisms
• Control cardiac output and blood pressure:
1. Autoregulation: causes immediate, localized
homeostatic adjustments
2. Neural mechanisms: respond quickly to
changes at specific sites
3. Endocrine mechanisms: direct long-term
changes
17. The elements of circulation
An effective
pump
(The heart)
(Normal vessels)
A clear channel
An effective return
(No peripheral
pooling)
19. shock
• A state of generalised hypoperfusion of all cells and
tissues due to reduction in blood volume or cardiac
output or redistribution of blood resulting in an
inadequate effective circulating volume.
• A systemic (whole body) event resulting from failure of
the circulatory system.
• It is at first reversible, but if protracted leads to
irreversible injury and death.
23. Stages of hypovoleamic shock
• Asymptomatic (< 10% loss)
• Early stage (15-25% loss)
– Compensated hypotension
• Progressive/Advance Stage
– Results when no therapeutic intervention is given for the early
stage, compensatory mechanisms become harmful. Auto-
regulation mechanisms breakdown.
• Irreversible shock
– Irreversible hypoxic injury to vital organs
24. Compensated hypotension
• Hypotension (low volume or low cardiac output)
• Sympathetico-adrenal stimulation (fight or fright)
• Release of catecholamines – resulting in peripheral
vasoconstriction – maintain BP
• Activation of renin-angiotensin-aldosterone system and
increased anti-diuretic hormone release
• Fluid retention by kidneys, further vasoconstriction
• Impaired renal perfusion and perfusion to other organs
with every effort made to maintain perfusion to brain
and heart (auto-regulation)
27. 3 Short-Term Responses to Hemorrhage
To prevent drop in blood pressure:
1. carotid and aortic reflexes:
• increase cardiac output (increasing heart rate)
• cause peripheral vasoconstriction
2. Sympathetic nervous system:
• triggers hypothalamus
• further constricts arterioles
• venoconstriction improves venous return
3. Hormonal effects:
• increase cardiac output
• increase vasoconstriction (E, NE, ADH, angiotensin II)
28. 4 Long-Term Responses to Hemorrhage
Restoration of blood volume take several days:
1. Recall of fluids from interstitial spaces
2. Aldosterone and ADH promote fluid retention
and reabsorption
3. Thirst increases
4. Erythropoietin stimulates red blood cell
production
29. Blood Flow to the Brain
• Is top priority
• Brain has high oxygen demand
• When peripheral vessel constrict, cerebral
vessels dilate, normalizing blood flow.
Stroke
• Also called cerebrovascular accident (CVA)
• Blockage or rupture in a cerebral artery
• Stops blood flow
30. Blood Flow to the Heart
• Through coronary arteries
• Oxygen demand increases with activity
• Increase Lactic acid and low O2 levels:
– dilate coronary vessels / increase coronary blood flow
• Epinephrine:
– dilates coronary vessels
– increases heart rate & strengthens contractions.
• A blockage of coronary blood flow Can cause:
–angina
–tissue damage (MI)
–heart failure / death
31. Blood Flow to the Lungs
• Regulated by O2 levels in alveoli
• High O2 content: --- vessels dilate
• Low O2 content:----- vessels constrict
Pulmonary Blood Pressure :
• In pulmonary capillaries: --- is low to
encourage reabsorption
• If capillary pressure rises: --- pulmonary edema
occurs
35. Cardiogenic shock
• Failure of myocardial pump.
– Intrinsic – due to myocardial damage
– Extrinsic
• Due to external pressure –e.g. cardiac tamponade
• Due to obstructed flow – e.g. thrombosis
36. Heart Pump Failure
Cardiogenic Shock
Vessel injury
Physical injuries such as wounds, ruptures of
aneurysms, etc (Hypovoleamic)
Toxins , infection and immune-complexes
(DIC, Anaphylaxis, Septiceamic)
Peripheral Pooling
Hypoalbumineamia, Ascites,
Renal failure,
(Hypovoleamic)
Septiceamic, Anaphylaxis
(Capillary pooling)
37. Compensated heart failure
• Here the situation is one of a compromised cardiac
pump which has been “compensated” by an increase
in right atrial pressure ( increased blood volume
caused by retention of fluid ). Thus cardiac output is
maintained.
• It may not be noticed as it would have developed
gradually over time. However any strain on the heart,
eg sudden increase in exercise would tip the balance
and lead to a “decompensated heart failure”.
38. Decompensated heart failure
• The pump is so damaged that no amount of fluid
retention can maintain the cardiac output.
• This failure also means that the renal function
cannot return to normal, thus fluid continues to
be retained and the person gets more and more
edematous with eventual death.
• In short, failure of the pump to pump enough
blood to the kidneys.
39. Anaphylactic shock
• Usually due to prior sensitisation
• Exposure to specific antigens
• Mediated by histamines, complements and
prostaglandins
• Vasodilatation of micro-circulation associated
with pooling and fluid extravasation
40. Septic shock
• Commonly due to gram-negative endotoxin
producing bacteria. May also accompany
gram-ve bacteria.
• Predisposing factors include:-
– Debilitating diseases
– Complications of instrumentation and treatment
– Burns
41. Septic shock
• Pathogenesis include:-
– Inflammatory reaction – vasodilatation mediated by
histamines and complements
– Disseminated intravascular coagulopathy – activation
of clotting factors and platelets together with
consumption of clotting factors
– Endothelial damage – extensive due to endotoxins
– Release of interleukin-1 and TNF-alpha (Tumor
necrosis factor alpha) from macrophages
42. Pathological changes after shock
• Hypoxic injury to vital organs – infarction
• Necrosis of tissues
• Lysis of cells
• The extent of pathological changes is dependent on
the duration of decompensation before death.
• In acute deaths, often no significant findings are
found.
43. Pathological changes after shock
• Brain
– Hypoxic and ischaemic damage
– Initially found at “boundary” zones
– May also be associated with marked cerebral
oedema.
44. Pathological changes after shock
• Heart
– Focal myocardial necrosis
– Subendocardial infarction (vulnerable region of
blood supply)
– If there is pre-existing coronary artery diseases,
may also lead to acute transmural myocardial
infarction
45. Pathological changes after shock
• In cardiogenic shock
– Due to previous ischaemic heart diseases – the
ventricular chambers may well be dilated and
distended. The walls are often thin and may be
replaced by non-elastic fibrous scars
– In intrinsic myocardial diseases leading to pump
failure, the myocardium may be unusually
thickened and rigid.
46. Pathological changes after shock
• Lungs
– Diffuse alveolar damage (adult respiratory distress
syndrome)
– Damage to Type 1 pneumocytes and to
endothelial cells – oedema as well as hyaline
membrane due to decreased surfactant
production
– Haemorrhages, fibrosis, atelectasis and infection
47. Pathological changes after shock
• Kidneys
– Acute tubular necrosis – often associated with
remarkably well preserved glomeruli
