Cardio Flashcards

(71 cards)

1
Q

Functions of CV system

A
  • Transports O2 and other nutrients to tissues
  • Removes waste products (CO2)
  • Spreads hormones
  • Helps to maintain body temp by shift heat around body. Exercise heats blood around muscle and cardio moves it to be cooled.
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2
Q

Effects of muscle thickness within the heart

A

Remember that each side of the heart pumps the same amount of blood.

Left sides has thicker muscles

Pressure in left during systole 120 and in right is 30

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3
Q

What determines blood flow

A

Blood flow is determined by cardiac output (stroke volume x HR) and vessel diameter

Velocity of blood flow is inversely related to total CSA. Increased CSA means decreased velocity

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4
Q

What is normal arteriolar tone

A

Normal arteriolar tone means that they are slightly contracted to hold shape, this is also why vasodilation can occur giving decreased resistance (increased flow).

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5
Q

Systemic blood vessels

A
  • Arteries
    • Thick highly elastic walls, large radius
    • low resistance, high pressure, low volume. ‘Pressure reservoir’
  • Arterioles
    • Highly muscular, well innervated (dilation/constriction)
    • Determine blood flow to tissues
  • Capillaries
    • Very thin walls for nutrients exchange (large CSA)
  • Veins
    • Thin walled, highly distensible meaning low resistance and low pressure with high volume
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6
Q

Pulse pressure

A

Blood pressure is highest and systole and lowest in diastole, the pulse pressure is the difference between these two values.

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7
Q

How do arteries maintain blood flow

A

Arteries are highly elastic which helps maintain blood flow. Elastic recoil maintains pressure and blood flow, this occurs constantly.

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8
Q

Measuring BP

A

Done with a sphygmomanometer

Sounds cannot be heard when no blood is flowing (occluded artery) or when it is flowing smoothly (laminar flow) only when blood is turbulent can heard pulses

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9
Q

Mean arterial pressure

A

Average blood pressure in the arteries, this is closer to diastolic pressure as the heart spend longer in diastole. The body uses this to regulate blood pressure as it is more constant. Dia and sys change with exercise but if dia decreases and sys increases then MAP will remain constant.

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10
Q

Layers of the heart

A

Endothelium - lines the inner

Myocardium - contractile layer, middle cardiac muscle

Epicardium - covers the heart

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11
Q

How is the pattern of blood flow maintain within the heart

A
  1. Inter connected muscle cells
  2. Self excitation (generates own heart beat)
  3. Conduction system
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12
Q

Similarities and differences between skeletal and cardiac muscle

A

Similarities - both have a striated appearance meaning they form cross bridges using actin myosin. Both have similar t-tubule system. Action potential do NOT summate

Differences - voluntary vs involuntary contraction

Cardiac cells are smaller and connected via intercalated disks to form functional syncytia allowing for coordinated contraction. Cardiac muscle AP lasts 10 times as long while also having a longer refractor period and slower AP propagation.

This means that cardiac muscle will never be able to reach tetanus (summation of contractions)

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13
Q

Cardiac muscle cell features

A

Desmosomes hold the cells together and gap junction allow the flow of ion to ensure the spread of the action potential can occur at a fast rate. This allows the cardiac muscle cells to act (contract) together

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14
Q

Auto Rhythmic cells of heart

A

These cells don’t stay at RMP, they continually slowly depolarise back to threshold.

The initial slow depolarisation is from Na moving into the cell (Na permeability increases while K permeability decreases)

Permeability for Ca+ increases with Na decreasing meaning Ca+ moves in

Once reaching threshold the transient Ca channels close and the long lasting Ca channels open causing a large amount of CA influx.

Depolarisation then occurs with K moving out of the cell (K permeability decreases and Ca decreases)

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15
Q

Action potentials in auto rhythmic cells

A

These cells don’t stay at RMP, they continually slowly depolarise back to threshold.

The initial slow depolarisation is from Na moving into the cell (Na permeability increases while K permeability decreases)

Permeability for Ca+ increases with Na decreasing meaning Ca+ moves in

Once reaching threshold the transient Ca channels close and the long lasting Ca channels open causing a large amount of CA influx.

Depolarisation then occurs with K moving out of the cell (K permeability decreases and Ca decreases)

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16
Q

Action potentials in contractile cells

A

There is a notable plateau phase in cardiac contractile cells. This is due to the activation of the slow L-type (long lasting) Ca channels.

With K leaving the cell (hyperpolarising) the long lasting calcium channels allow some Ca to enter the cell and counter the K leaving.

This is important as it ensure adequate ejection time (time between contractions).

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17
Q

Why does summation of contraction not occur

A

The plateau phase (caused by long lasting calcium channels) as well as the long refractory period prevents the summation (tetanus) in cardiac muscle.

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18
Q

Conduction system of heart

A
  • Sinoatrial node (SA node) - right atria near opening of sup vena cava
  • Atrioventricular node (AV node) - located at base of right atrium
  • Bundle of His - originate at AV node and end at interventricular septum
  • Purkinje fibers - from bundle of His to ventricular myocardium
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19
Q

Movement of AP through the heart

A

Starts at the SA node, spread through right and left atria.

Goes through AV node to move into the ventricles, a brief delay occurs here to ensure the atria have finished contracting before the ventricles starts.

AP travels down interventricular septum via Bundle of His and then through Purkinje fibers, ventricles contract from the base contracting from the base upwards.

Remained of ventricular cells activated by AP moving through gap junctions

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20
Q

ECG key points

A

ECG is the sum of all the electrical activity in the heart:

  • P wave - atrial depolarisation (SA node fires)
  • QRS complex - ventricular depolarisation (atrial depolarisation occurs here but is masked)
  • T wave - ventricular depolarisation
  • PR segment - AV node delay
  • ST segment - ventricles are contracting
  • TP interval - ventricles are relaxing and filling
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21
Q

Blood flow through the heart

A

Blood flows through the heart in a defined pattern. This is ensured by both the valves present and the phases of both diastole and systoles that the chambers go through.

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22
Q

Valves of the heart

A

Prevent backflow and ensure forward flow occurs at the right time. A value will open if the pressure behind it is greater than the pressure in front of it and close if pressure behind is lower.

  • Atrioventricular - tricuspid (R) and bicuspid (L)
  • Semilunar valves - aortic (L) and pulmonary (R)
    Chordae tendineae and papillary muscles help to prevent backflow
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23
Q

Cardiac cycle

A
  1. Ventricular diastole (passive filling when atria relaxed but actively filling when atria contract) - ventricles fill with blood
  2. Isometric ventricular contraction - ventricles contract with valves closed meaning there is an increase in pressure (no volume change)
  3. Ventricular ejection
  4. Isovolumetric ventricular relaxation (all valves closed)
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24
Q

Left ventricle pressure loop

A

The result of above mention cardiac cycle is a pressure loop.

AV valves opens at one allowing for passive then active filling.

At 4 the AV valve closes and end diastolic volume is reached.

Isovolumetric ventricle contraction occurs, increasing pressure

Semilunar valve opens and stroke volume is ejected.

Note that there is always some blood in the ventricles (even after systole)

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25
Ejection fraction
proportion of EDV pumped out with each heart beat (SV/EDV x 100)
26
Afterload
pressure against which the heart must work to eject blood during systole. This increases in hypertension.
27
When HR increases why does SV not decrease
Faster HR reduces filling time however, passive filling occurs quite fast at the start of diastole then slows before being increased by active filling. With increase HR the rapid filling still occurs and the time lost in diastole only effects the period in which filling is slower (right before active filling) meaning SV is not effected.
28
Normal heart sounds
Normal heart produces two sounds a lub (S1) and a dub (S2) S1 is caused by closing of AV (beginning of systole) and S2 is caused by closing of semilunar (right before diastole) However you dont actually hear the closing of the valves, you hear the turbulence of the remain blood bouncing against them.
29
Extra heart sounds
S3 is the end of the rapid filling phase in early diastole, it is from the recoil of blood from ventricular walls S4 is with atria contraction (indicates pathology of strong atrial contraction
30
Heart murmurs
These are always pathological and are caused from the failure of the valves to open or close properly resulting in abnormal turbulence Regurgitation - valves cant close tightly enough, blood can flow in wrong direction Stenosis - Passages contain valves decrease in size (cant open properly), blood flow in the right direction is effected.
31
Autonomic nervous system in relation to the heart
Contains parasympathetic (longer post ganglionic neuron) and sympathetic (longer pre ganglionic neuron). Both act on AcH with their pre ganglionic neurons. Sympathetic innervates SA node, AV node, myocardium and conduction system Parasympathetic: SA node, AV node and atrial muscle
32
Controlling heart rate
Both para and symp have chronotropic effects (change heart rate) and inotropic effect (activate or deactivate voltage gated ion channels). Heart rate is balance between the two inputs, if this did not occur then HR would be at extrmeities. It is under constant inhibitory (parasympathetic) control referred to as vagal tone.
33
Sympathetic and parasympathetic control on heart rate
Parasympathetic control: - Via AcH - Causes a slower depolarisation (decerases slow inward Na and Ca) as well as increased hyperpolarisation (more K out) meaning it takes longer time to reach threshold agian. Sympathetic control: - Via noradrenaline - Causes faster depolarisation (increases slow inward Na and Ca) as well as decreasing hyperpolarisation (less K out) meaning it takes lees time to reach threshold agian.
34
Controlling stroke volume
Altered by sympathetic nervous system Extrinsic control - direct increases in muscle contraction result in large SV Intrinsic control - adrenal (produced in adrenal medulla) increases venous return, increased EDV and therefore increased SV through frank starling la
35
Frank starling law
Heart will adjust its output (SV) to meet its input (EDV) Fibre length is below optimal length for cardiac muscle, increased in EDV will move fiber length closer to optimal length
36
How does systole effect coronary circulation
Difficult for this to occur in systole because: - Coronary arteries branch off the aorta close to semilunar valve. During contraction, when valve is open, it partially blocks the coronary arteries. - Contracting myocardium is compressed meaning major branches of coronary arteries are as well
37
Why does blood flow match cardiac needs
Heart is good at getting nutrients out of blood as it can remove 65% of O2 (skeletal does 25%). However, it has little capacity to increase this therefore blood flow must increase through vasodilation. This happens due to local release of adenosine) This can lead to complications when the coronary arteries have pathological changes that limit blood flow.
38
Features of different blood vessels
Arteries: Thick, highly elastic, muscular and large radius Pressure reservoir Arterioles: Highly muscular and well innervated Determine flow to tissues through resistance Capillaries: Very thin but large CSA Site of exchange Veins: High compliance and large radius Volume reservoir (largest volume)
39
Blood distribution around the body
There is a parallel arrangement of vessels, this ensure that adequate blood flow is able to reach all organs. More blood goes to organs responsible for reconditioning blood, meaning that they need blood not only for their own function but other bodily functions. Organs such as kidneys, skin, liver ect. This parallel arraignment also means that blood flow to each organ can change independently. With exercise the blood supply to the brain is constant at the expensive of the reconditioning organs.
40
Blood flow determinants
Flow rate is directly proportional to pressure gradient and inversely proportional to resistance. However, the radius is the only factor that can alter resistance so it can be said that blood flow is pressure gradient x radius of vessel (^4)
41
Pressure gradient in blood flow
- Difference between start and end of vessel. Blood flows down pressure gradient - Contraction of the heart establishes the pressure gradient, it then gets lower along the vessel due to frictional losses. - The larger the pressure gradient the greater the flow
42
Resistance in blood flow
- Larger the R the lower the flow - Three factors in resistance - Directly proportional to viscosity of blood (doesn't change) and the length of vessel (doesn't change) - Inversely proportional to the radius of the vessel
43
Upon arterial stenosis (thus increased resistance), | how does ΔP increase to maintain adequate flow?
CO will increase, causing an increases in pressure therefore larger pressure gradient.
44
What is blood pressure
Blood pressure is the force exerted by blood against a vessel wall. It depends on volume of blood and compliance of vessel.
45
Mean arterial pressure
Mean arterial pressure - average pressure during each cardiac cycle diastolic + 1/3 (systolic-diastolic) This is because we spend more time in diastole (2/3)
46
Arterioles function
Branches of an artery within an organ that controls the flow of blood to tissues. They are very high resistance vessels meaning there is a large drop in pressure, this pressure difference helps to maintain blood flow (pressure gradient) resistance in arterioles alters to: - Distribute blood depending on activity - Regulate MAP
47
What causes vasocon/dilation in arterioles
Vascular tone is present in arterioles, this is baseline resistance due to myogenic activity and continuous sympathetic innervation, meaning there is some level of contraction (allows for dilation) **Vasocontraction/dilation** within arterioles is sensitive to various intrinsic and extrinsic factors and innervated by sympathetic nerves. It is also important to remember that vascular smooth muscle can undergo changes in force without APs meaning there is not an all or nothing response.
48
Intrinsic/local factors for vasocontraction in arterioles
Regulate blood distribution These factors will override the extrinsic factors - Chemical - Metabolic changes - Oc, CO2, lactic acid → vasoactive paracrines from the endothelia cells act on smooth muscle - Histamine release - not from local changes, important in pathology (swelling from injury) - Physical - Vessel/stretch → opening of mechanically gated cation channels cause Ca influx and increased flow - Shear stress - friction of blood on inner surface of vessels creates shear forces, releasing nitric oxide - Hot/cold - heat causes localised vasodilation and cold dose constriction
49
Extrinsic factors for vasocontraction in arterioles
Regulate blood pressure - Sympathetic nervous system - Innervates smooth muscle for vasoconstriction except the brain. Noradrenalin binds to receptors on smooth muscle - Contributes to ongoing vascular tone and generalised vasoconstriction increases TPR and therefore MAP (increased MAP will increase flow to the brain) - Hormonal - Noradrenalin and adrenalin normally reinforce the sympathetic nervous system (constrict), expect in skeletal and cardiac muscle where the beta receptors cause dilation - Anti diretic hormone and angiotensin 2 also important for blood volume and fluid balance
50
How is diffusion maximised in the capillaries
- Minimal distance - Single layer of endothelial cells - Small diameter meaning the RBCs have to flow single file and slightly deform, this pushes the plasma to the wall which is what carriers the nutrients. - Maximal surface area (large number of capillaires) - Maximal time - Velocity of blood is slow to due extensive branching (flow rate remains the same as CVS is closed loop), velocity is inversely proportional to total CSA
51
Capillary permeability
Capillaries have tightly joint endothelial cells with narrow water filled spaced between them meaning that small water soluble substance can pass through (varies in tissues). These are referred to as water pores/clefts. Lipid soluble substances pass through endothelia cell wall Substances such as proteins normally (hormones) still need to be exchanged via vesicle through the wall due to their large size.
52
How does permeability change in the capillaries
This permeability (tightness of endothelial cells) varies between organs. - Cerebra has tight junctions so no clefts are present (blood brain barrier, more selective) - Skeletal muscle and lungs with 4nm water filled clefts, small water soluble substance can pass (ions, glucose, amino acids) but proteins cannot and need to be transported via vesicles - Kidneys and intestines have large clefts meaning the capillaries are leaky for rapid movement - The liver has clefts that very large meaning proteins can pass Histamine can increases this leakiness
53
Control of blood flow through capillaries
- No smooth muscle present - Pre capillary sphincters are not innervated and sensitive to local factors - metabolic activity increase →sphincters relax increasing flow - If metabolic activity decreases → sphincters contract meaning flow is bypassed
54
Difference between diffusion and bulk flow
Exchange between blood and organs through the interstitial fluid occurs in two ways: - Diffusion (passive) - Down a concentration gradient - Specific to ion or molecule - Bulk flow (only occurs in capillaries as they have pores) - Regulates the distribution of ECF between plasma and interstitial fluid, maintains plasma volume - Hydrostatic (fluid pressure) and oncotic pressure (protein pressure) influce bulk flow. Increased blood pressure in vessel = hydrostatic pressure out of the vessels, movement into ECF
55
Lymphatic system functions
Return excess fluid and protein that leaked out of capillaries (from bulk flow) back into the venous system, normally more proteins and fluid is filtrated than what is resorbed. Lymphatics vessels have overlapping endothelial cells, when there is increased pressure outside the vessel this pushes inwards creating an opening. Lymph is picked up around capillaries an deposited right before right atrium.
56
Odema
Accumulation of interstitial fluid = increased space therefore decreased efficiency for diffusion between blood and cells.
57
How can veins act as storage
They have a large diameter, low resistance, low elastic and little smooth muscles Making them highly compliant and large storage capacity. The blood is not stagnate, still flowing. When required vein capacity can decrease which will increase venous return to the heart
58
Why does blood still flow in the veins if they have such low pressure
Veins have really low pressure (lost has been lost) but atrial pressure is near zero so there is still a gradient to induce flow
59
What is MAP
MAP = diastolic + 1/3 (sytolic-diastolic) Main purpose of MAP is to drive blood into the tissues (pressure gradient for flow)
60
Three factors for determining blood flow to tissues
Blood flow to tissues depends on: - MAP - Resistance of arterioles (opening arterioles decreases pressure in arteries, therefore less MAP as TPR has decreases) - Vascularisation/open capillaries
61
Why is MAP regulation important
MAP must be closely monitored to ensure sufficient drive (despite local adjustments) and low enough to avoid damage to heart and vessels. MAP = COxTPR
62
Processes for detecting changes in MAP
Many mechanics can detect changes in MAP: - Baroreceptors in aortic arch and carotid sinus (short term) - Left atrial volume receptors and hypothalamic osmoreceptors (long term) - Chemoreceptors in carotid and aortic arteries sensitive to low O2 and high H (short term) - Cerebral cortex hypothalamic pathway sensitive to behaviour and emotion which influence MAP (fight/flight) - Hypothalamus sensitive to body temp, which affects cutaneous arterioles and overrides regulation of MAP
63
Baroreceptor reflex
Baroreceptors are mechanoreceptors that constantly monitor MAP, regulate short term response to MAP. - Baroreceptors fire APs in response to pressure in these arteries (increased Bp then increases firing rate, decreased…) - Afferent neurons to CV control center in medulla of brain stem for integration. Correct output is decided here (symp/para) - Sympathetic and parasympathetic outflow via efferent nervous - Para - decrease HR → decrease CO → BP - Sympathetic → HR and Contractile strength (therefore SV) → CO → BP - Sympathetic → Vasoconstriction of arterioles → TPR increase → BP - Sympathetic → Vasoconstriction → venous return → SV → CO → BP - Heart and blood vessel change status to restore MAP
64
Long term response to MAP changes
Left atrial volume receptors and hypothalamic osmoreceptors regulate long term responses. Related to regulating blood volume. Hypothalamic osmoreceptors: - Dominant factor (controls thirst and vasopressin secretion) - Both of these will increases ECF volume therefore decreasing ECF osmolarity Left atrial volume receptors: - Only important in large changes in ECF volume - ADH from vasopressin causes vasoconstriction therefore decreasing arterial BP
65
ECG interval
PR segment - AV node delay TP interval - ventricles are relaxed and filling ST interval - ventricles are contracting
66
What would happen to HR if vargus nerve was cut
HR would increase as constant inhibitory input (vagal tone) would be removed.
67
Why does sympathetic induced vasoconstriction causes decreased flow in arterioles and increased flow in veins
In the veins it increases the pressure gradient while also not really effecting the resistance as the radius is very large (r^4, so exponential effect)
68
Factors that increase venous return
- Sympathetic induced vasoconstriction - Increases venous pressure (therefore larger gradient) - This doesn't effect resistance due to large radius - Skeletal muscle pump - Large veins sit between muscles, contraction compresses veins → increasing venous pressure → venous return - Counter effects of gravity, blood pools in legs → increases hydrostatic pressure → decreases gradient - Venous valves - Help skeletal muscles pump, gravity and constriction by preventing backflow - Respiratory pump - Resp action creates external pressure gradient as pressure in chest veins decreases (sub atmopheric) causes blood in lower limbs to flow up to chest. This further increases with exercise - Cardiac suction - AV valves drawn down which increases volume in atria therefore decreasing pressure. Further increasing gradient → venous return - Increased blood volume - Short term = bulk flow → increased plasma volume - Long term = salt and water retention → increased plasma volume
69
Short and long term responses to MAP changes
Short - autonomic nervous system to heart, veins and arterioles → CO+TPR Long - kidney and thirst responses to regulate total blood volume → CO
70
Steps in blood presssure reading
Cuff inflated to pressure greater than systolic Slowly deflated until a sound is heard. This is systolic and is flowing turbulently Last sound heard is diastolic and flow becomes lamina
71
What would cause decreased respiratory volume
Pulmonary surfactant deficiency - seen in premature babies and is Infant Respiratory Distress Syndrome. Increases alveolar surface tension leading to increases in pressure gradient. Pneumothorax