Cardiovascular System Flashcards
1
Q
Define cardiovascular
A
organs and tissues involved in circulating blood and lymph through the body
2
Q
primary purposes of cardiovascular system
A
delivery of dissolved gasses (o2) and substrates for metabolism, growth and repair
removal of byproducts of cellular metabolism
3
Q
secondary purposes of cardiovascular system
A
- enable fast cell communication
- heat transfer (from internal organs)
- inflammatory and defence responses to foreign organisms
4
Q
3 essential parts to the CVS
A
- the heart (biological pump)
- blood and lymph (carrier)
- And vessels (transport paths)
5
Q
What are the two circuits in series for the CVS
A
– systemic and pulmonary
circuits, united by the heart.
6
Q
systemic circuit
A
- high pressure circuit
- perfuses most of the tissues and organs with blood
7
Q
pulmonary
circuit
A
- low pressure circuit.
- takes blood to and from the lungs
8
Q
three key things about circulation
A
- the blood flow in both systemic and pulmonary circuits over time should be matched, otherwise blood will likely pool in one of the circuits
- the cardiac output of the right side
of the heart is linked/matched with the cardiac output on the left side of the heart. - heart acts as a functional syncytium. both left and ride ventricles contract together to ensure coordinated blood flow in the circuit.
9
Q
Distribution of Blood
A
blood volume in circulation is unevenly distributed
- pulmonary 9%
- heart 7%
- systemic 84%
- most of blood is in systemic
- systemic veins are blood volume reservoirs and the reserve can be used whenever needed
10
Q
Blood Pressure & Flow - equations
A
Pressure = Force/Area
Flow = Pressure (1) – Pressure (2)/Resistance
OR
∆Pressure/resistance
11
Q
Resistance and viscous resistance
A
Resistance = a measure of the opposition to blood flow in a vessel
Viscous resistance = the friction between two layers of fluids next to each other flowing at different speeds (velocities)
(reflects the frictional interaction between adjacent layers of fluid, each of which moves at a different velocity.)
note: Think about the viscosity of blood as a measure of the internal ‘slipperiness’ between layers of fluid.
12
Q
Factors affecting resistance
A
- geometry of blood vessels and type of flow
- blood viscosity
- vessel length
- vessel width - radius
13
Q
Implications of Poiseuille’s law: (3)
A
- Flow is directly proportional to the axial pressure difference, Δ P.
- Flow is directly proportional to the fourth power of vessel radius.
- Flow is inversely proportional to both the length of the vessel and the viscosity of the fluid.
14
Q
Pressure requirements!
A
- A pump is required to create pressure
- Requirement = 5L per minute (400 million L in a lifetime) it needs a biological pump, with no room for error!
15
Q
How does the heart keep up with
flow requirements?
A
Cardiac Output: the amount of blood the heart pumps through the
circulatory system in a minute.
CO = SV x HR
SV: Volume of blood expelled from the left ventricle with each contraction
HR: Number of contractions per minute
16
Q
Haemodynamics
A
equations
CO = ΔP / TPR
CO = (MAP – CVP) / TPR
But CVP is close to zero (so disregard here)
CO = (MAP) / TPR
rearrange formula
MAP = CO x TPR
17
Q
Total Peripheral Resistance
A
TPR = R(arteries) + R(arterioles) + R(capillaries) + R(venules) + R(veins) in both circuits
= the overall resistance of the circulation reflects the contributions of the network of vessels in both the
systemic and pulmonary circuits.
18
Q
Mean Arterial Pressure
A
average pressure through one cardiac cycle
ie. the pressure that drives blood flow
don’t forget! blood pressure is not constant – it is pulsatile!
19
Q
What happens when: to the MAP equation
A
- increase MAP and SV
- increase TPR
- increase MAP and TPR
20
Q
Blood vessel general structure (excluding microcirculation)
A
- inner lumen: passageway for blood flow
- surrounded by an endothelium: tunica intima
- smooth muscular layer of varying thickness: tunica media
- an outer fibrous layer: tunica externa
with a variable amount of elastic connective tissue.
21
Q
Arteries & Arterioles
A
Elastic Arteries
Muscular Arteries
Arterioles
Arteries convey blood from the heart to the capillaries.
- thicker walls than veins
- lot more connective tissue and more muscle than veins
- they’re rapid passageways
- don’t have much resistance to blood because of their large radii
- arterial pressure fluctuates in relation to systole and diastole
22
Q
Elastic Arteries
A
- Transport blood away
- Large lumen (1.5cm)
- More elastic (elastin in tunica intima)
23
Q
Muscular Arteries
A
- Smaller lumen (4mm)
- More smooth muscle than elastin
24
Q
Arterioles
A
- Very small lumen (30 µm)
- Smooth muscle
25
Blood Pressure in Systemic Circulation
BP is maintained in arteries
Arterioles are the main resistance vessels = loss of BP
(slide)
26
The Control of Vascular Tone
Vascular tone = partial constriction of arteriolar smooth muscle
radii of arterioles can be adjusted to variably distribute cardiac output among systemic organs and to help regulate MAP
27
Extrinsic vs Intrinsic control of Vascular tone
Extrinsic
control the arteriolar diameter
a) autonomic nervous system
- SNS releases NA (acts on a-1 adrenoreceptors to induce vasoconstriction)
- SNS also releases A (acts on ß-2 adrenoreceptors to indice vasodilation)
b) endocrine
- angiotension + vasopressin (vasoconstriction)
- atrial natriuretic peptide and bradykinin (vasodilation)
Intrinsic
- alters the radii of arterioles within a tissue through chemical and physical influences on the smooth muscle of the tissue's arterioles. These include:
- metabolic factors: blood gases
- local signals: NO (vasodilation), Endothelin (vasoconstriction), Histamine (vasodilation), Prostaglandins (both)
- local temperature (heat vs cold, dilation vs constriction)
- stretch: myogenic response
28
Capillaries
Capillaries
* Microscopic lumen (5 – 10 µm)
* Supply blood to tissues via perfusion
* Only a single endothelial cell thick
Interstitial fluid is between plasma & cells
Fluid movement (bulk flow) is driven by 2 opposing pressure gradients
* Hydrostatic Pressure
* Oncotic Pressure = Colloid Osmotic Pressure
Lymph vessels also important in fluid uptake
29
Lymphatics
Lymph: fluid flows through lymphatic system
part of the ECF- is similar in ionic composition to interstitial fluid
main difference is where its located
lymphatic system is a system of branched network of ducts which terminate in small, blind-ended capillaries
30
Functions of lymph
- Returning excess fluid back to circulation
- Immune defence
- Transport of lipids from the GIT
1. Interstitial fluid enters the lymphatic system via pores in the lymph capillaries that allow the entry of large molecules, like proteins and chylomicrons (fats).
2. Lymph is propelled along the lymphatic system by smooth muscle contraction, and external pressure from SkM contraction squeezing the
lymph vessels. Plus there are valves to prevent back-flow (like veins).
31
Oedema
Oedema is swelling in soft tissues as a result of fluid accumulation.
It occurs as a result of a shift in the balance in the capillaries.
Whilst there are many pathophysiological causes of oedema the main outcome is a build up or excess of interstitial fluid.
Functional consequences
- excess interstitial fluid -> increased distance between blood and cells -> decreased rate of diffusion -> inadequate nutrient supply
1. increased blood pressure
2. decrease oncotic pressure
3. increase permeability
4. blockade lymph
32
Venous System
Veins act as blood reservoirs
- approximately 64% of body’s blood
- convey blood back to heart (R atrium)
- large lumen, with thin walls
- have valves prevent backflow
- high volume (capacitance)
- low resistance, low pressure
33
Compliance
How readily a lumen of a blood vessel is able to expand
34
Arteries vs Veins
Arteries
- Thick layer of smooth muscle & elastin
- Capable of withstanding high pressure & recoils well.
- Lower compliance
Veins
- Less smooth muscle, little elastin.
- Stretchy, but no recoil.
- Readily expand when filled with blood.
- Higher compliance
35
Venous Return
= The flow of blood back to heart via the veins
Directly affects
* End Diastolic Volume
= Vol. of blood in ventricles, before contraction
* Stroke Volume
= Vol. of blood pumped out of heart
* Cardiac Output
= Vol. of blood pumped out per minute
1) One-way valves prevent backflow
2) Compression of large veins is aided by skeletal muscle contractions
3) Respiration acts like a pump.
The pressure within the chest cavity is 5mmHg less than atmospheric pressure during inspiration.
4) Venoconstriction. Veins contain smooth muscle that is innervated by SNS
5) “Cardiac suction”. When atrial cavity enlarges during ventricular contraction (systole) atrial pressure < 0mmHg
36
ANS regulation of CO
Sympathetic activation
^ heart rate
^ force contraction
vessel constriction
adrenaline and noradrenaline released
Parasympathetic activation
> heart rate
> force contraction
dilation (penis and clitoris)
no hormones
37
What is Heart Rate, tachycardia, bradycardia
Heart rate is the number of heartbeats per minute, specifically
ventricular contraction. Usually measured as pulse rate eg. wrist.
Tachycardia is high resting heart rate. In adults > 100 bpm.
When heart rate so rapid, the efficiency of pumping is an issue and blood flow can be compromised. Blood flow to heart itself is a potential issue.
Bradycardia is when heart rate is too slow, defined in adults and
children < 60 bpm.
Athletes often have a lower than normal heart rate due to training.
Resting heart rate normally decreases with age.
38
ANS + sinus rhythm
ANS: balance of sympathetic to
parasympathetic tone.
At rest PSNS is dominant, as
spontaneous activity = 110 bpm
Recall sinus rhythm is set by SA node
39
Chronotropic Agents
‘chronotropic agents’ include drugs affect the heart rate.
Beta blockers eg. atenolol = slow heart rate
Ca channel blockers eg. verapamil
have direct negative chronotropic effect
40
Stroke volume
(SV) is the volume of blood ejected in each ventricular contraction.
SV = EDV - ESV
It is the difference between ventricular end diastolic volume
(EDV), the volume when relaxed and ventricular end systolic volume (ESV) the volume when fully contracted).
SV is typically around 70 ml/beat at rest.
41
Cardiac Length-Tension Relationship
The thick/thin filaments, mainly myosin and actin respectively, are similar in skeletal and cardiac muscle. For cardiac muscle contraction occurs by the sliding of the thick and thin filaments, like in skeletal muscle fibres
EXCEPT note there is no descending limb on the figure for cardiac muscle
42
3 main factors that affect stroke volume:
1. Pre-load
= defined as the myocardial sarcomere length, just prior to contraction. It is not measurable without removing the heart but is approximated by EDV
Pre-load is a function of:
* Ventricular filling
= intra-thoracic pressure, respiration, blood volume
* Ventricular and pericardial compliance
= reduced compliance decreases pre-load
* Ventricular wall thickness
= hypertrophy decreases pre-load
2. After-load
= the force against which the ventricles must act in order to eject blood. It is the sum of the elastic and kinetic forces.
For example, with increased arterial resistance (atherosclerosis) stroke volume will initially decrease, but over time will increase via compensatory mechanisms to maintain blood flow.
3. ‘Contractility’
= there are other factors, including pharmacological agents, that affect
stroke volume and therefore cardiac output.
Thes factors change the ventricular function curve.
Shift to right = negative inotropy
Shift to left = positive inotropy
43
The Frank-Starling Law of the heart
Law states that the strength of cardiac contraction is dependent on initial fibre length.
44
Inotropic Agents
An inotrope is an agent which increases or decreases the force of muscular contraction (nervous and
hormonal input, drugs).
* Negative inotropic agents weaken the force of contraction.
* Positive inotropic agents increase the strength of contraction.
(both positive and negative inotropes are used in the management of various cardiovascular conditions)
Positive inotropic agents
* Cardiac Glycosides:
Digitalis (blocks Na-K ATPase)
* Catecholamines:
Epinephrine or Norepinephrine (activates beta Adrenergic Receptors)
Isoproterenol (also activates beta Adrenergic Receptors)
Negative inotropic agents
* Beta blockers (blocks beta Adrenergic Receptors)
* Diltiazem (blocks DHPR Ca channels)
* Verapamil (also blocks DHPR Ca channels)
45
Integrated Cardiovascular Control
Regulation of blood pressure occurs in cardiovascular control centres in the medulla oblongata in the brain
3 subdivisions (groups of neurons)
* Cardiostimulatory centres stimulate cardiac output via SNS activation
* Cardioinhibitory centres decrease cardiac output via PSNS activation
* Vasomotor centre that control vascular tone, mainly SNS activation
46
Inputs (afferent pathways)
Higher-order brain regions cerebral cortex, limbic system & hypothalamus
* Proprioceptors
detects changes in joint movements
* Baroreceptors
detects changes in blood pressure and stretch
* Chemoreceptors
detects changes in chemical substances in blood (O2, CO2, pH)
47
Outputs (efferent pathways)
- Blood vessels vasoconstriction arterioles and venoconstriction of veins
- Heart mainly decreased heart rate
- Heart increased rate and contractility
48
Baroreceptor Reflex
Arterial baroreceptors afferents innervate mainly the carotid sinus and aortic arch.
Impulses are relayed to the CVS centres in the medulla.
Baroreceptor reflex is a rapid negative feedback loop that controls mean arterial pressure it maintains BP within a narrow range
In experimental animals, denervation of the arterial baroreceptors results in increased blood pressure variability
49
Chemoreceptor Reflex
Central chemoreceptors
* Within medulla oblongata
* Detect changes in cerebral spinal fluid
* Respond to high PCO2 - low pH
Peripheral chemoreceptors
* Carotid and aortic bodies
* Respond to low PO2 in blood
CVS responses
- Hypocapnia/Hypoxia - increased CO and peripheral resistance
- Hypercapnia – bradycardia, decreased CO.
50
Integrated Cardiovascular Control (2)
Involves neural and endocrine control mechanisms
Sensors: baroreceptors, chemoreceptors, & proprioceptors
Integration: CVS control in medulla oblongata
Effectors: autonomic NS & hormones (adrenaline)
The baroreceptor reflex is the most important short-term regulator of MAP
Chemoreceptor input also important with changes in arterial PCO2 and PO2 but mainly about respiratory control
51
Regulation of Blood Pressure
Cardiopulmonary baroceptors are located within the atria, at the junctions of the large veins, and in the pulmonary artery
Impulses are sent via the vagus nerve to the CVS centres in medulla oblongata
52
Vasopressin (ADH)
Neurohormone, released from posterior pituitary aka ‘anti-diuretic hormone’
Actions
* Decrease water excretion kidneys “anti-diuretic”
* Vasoconstriction
Secretion is regulated by
* [solute] in ECF - osmoreceptors
* blood volume – cardiopulmonary baroreceptors
High solute concentration - osmoreceptors – increase ADH
High blood volume - baroreceptors – decrease ADH
53
Integrated Control of Blood Pressure system
1. increase sympathetic activity
(ß- ^ HR, ^ contractility = ^CO)
(a1- venocon, ^ venous return - ^CO)
(a1- arteriolar vasocon - ^TPR)
2. ^ Mean Arterial Pressure
(Angiotensin II, vasocon - ^TPR)
(Aldosterone, ^ Blood volume- ^CO)
3. ^ RAAS System
(JGA in kidney, decrease MAP)
4. decrease MAP
(medullary CVS centre senses decrease baroreceptor firing
1. back to = increases sympathetic
54
Regulation of Blood Pressure
Involves neural and endocrine control mechanisms
Sensors: baroreceptors, chemoreceptors, & proprioceptors
Integration: in medulla oblongata
Effectors: autonomic NS & hormones (adrenaline)
Baroreceptor reflex is most important short-term control.
Longer-term control mainly blood volume regulation.
More integrated control (hormones - Vasopressin & RAAS) is critical in
longer-term blood pressure regulation
55
The Central Ischaemic Response
activated when blood flow to brain is compromised
fall i blood pressure, stimulates vasomotor centres in medulla oblongata. Results in massive stimulation of SNS to increase heart rate, cardiac output and blood pressure.
A fall in blood pressure can directly stimulate the vasomotor
centres in the medulla oblongata. As a result, massive stimulation
of the SNS occurs to increase heart rate, cardiac output, and
blood pressure.
This reflex can effectively raise MAP > 200 mmHg for 10 minutes.
It does not become active until systolic blood pressure < 60 mmHg and is most effective around a systolic pressure of 15 to 20 mmHg.
initial baroreceptor
* then chemoreceptor
* then local (brain)
* lastly central reflex
56
Pulmonary Circulation
The pulmonary circulation system is the only system through which the entire cardiac output passes. The major role of pulmonary circulation is respiratory gas exchange.
Mean pulmonary arterial pressure = 15 mmHg = a low-pressure circuit.
57
Characteristics of pulmonary circuit
* Relatively short circuit.
* Branches immediately, increases exchange area, and lowers resistance.
* Arteries (less muscle) and therefore higher compliance vessels cf systemic.
* Minimal resting smooth muscle tone – normally near fully dilated.
* 'Passive factors' play an important role in determining flow eg. gravity
* Remember receives all cardiac output (from right ventricle).
An important difference is intrinsic response to hypoxia is vasoconstriction as opposed to vasodilation in other vascular beds.
There is diversion of blood to regions of better ventilation and is related to
minimising ventilation – perfusion (VQ) differences. Supplying blood to regions of the lungs that will most efficiently oxygenate it.
58
Pathophysiology - Hypertension
Hypertension - ”high blood pressure” is a major risk factor for chronic
diseases including stroke, coronary heart disease, heart failure and chronic kidney disease.
However, hypertension is classed itself as a cardiovascular disease.
Primary Hypertension
- high blood pressure that has a multi-factorial pathogenesis ie. not one distinct cause. It's also known as
essential hypertension or ‘idiopathic’.
High prevalance.
Secondary Hypertension -
is defined as elevated blood pressure
secondary to an identifiable cause. eg. end organ damage (kidneys).
Low prevalence.
59
Primary Hypertension
Various risk factors including:
* poor diet (particularly a high salt intake)
* obesity
* excessive alcohol consumption
* insufficient physical activity
Uncontrolled high blood pressure
Systolic BP > 140 mmHg,
or Diastolic BP > 90 mmHg
60
Why don’t baroreceptors respond
to bring blood pressure back to
normal in hypertensive patients?
Arterial baroreceptors have an
optimal response range around
normal MAP.
In hypertension, the baroreceptors
adapt or “reset” to operate at a
higher level i.e. they maintain a
higher MAP.
61
Hypertension effects on blood vessels
Blood flow shapes vasculature architecture
increased blood pressure
increased sheer stress
endothelial cell damage
fibrotic scar tissue
atherosclerotic plaque develops
narrows vessels and stiffer
Atherosclerosis consequences:
* stenosis – narrowing
* thrombosis or clot
* aneurysm - rupture wall
62
Hypertension effects on the heart
increased after load, decreases SV initial, then compensatory effects increase SV etc
muscle hypertrophy - change in shape – less efficient (thicker heart walls = less blood)
less compliant
less pre-load
lower EDV
lower SV
= potential heart failure
63
