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Y4 Cardiology > Physiology (ignore) > Flashcards

Physiology (ignore) Flashcards

1
Q

What is the heart ?

A

An ELECTRICALLY CONTROLLED muscular pump which sucks and pumps blood

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2
Q

Where are the electrical signals which control the heart generated?

A

WITHIN THE HEART itself

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3
Q

Where does excitation of the heart normally originate and what cells initate the heart beat ?

A
  1. Excitation of the heart normally originates in the sino-atrial node (SA) located in the upper RIGHT ATRIUM close to where the Superior Vena Cava enters the right atrium
  2. The pacemaker cells within the SA node initate the heart beat
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4
Q

The SA node normally sets the pace for the entire heart ==> a A heart controlled by the SA node is said to be in what?

A

Sinus rhythm

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5
Q

How does the initiation of cardiac excitation (heart beat) occur in the SA node within the pacemaker cells ?

A
  1. The pacemaker cells in the SA node generate regular spontaneous pacemaker potentials, each pacemaker potential takes the membrane potential to a threshold.
  2. Every time the threshold is reached an action potential (AP) is generated
  3. The result is regular spontaneous APs in the SA nodal cells
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6
Q

What is the pacemaker potential in SA node pacemaker cells (i.e. the slow depolarisation of membrane potential to a threshold) due to ?

A
  1. Decrease in K+ efflux
  2. Na+ and K+ influx (the funny current)
  3. Transient Ca++ influx
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7
Q

What is the rising phase (i.e. depolarisation) of action potential in SA node pacemaker cells due to ?

A

Ca++ influx

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8
Q

What is the falling phase (i.e. repolarisation) of the action potential in SA node pacemaker cells due to ?

A

K+ efflux

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9
Q

Describe how cardiac excitation normally spreads across the heart

A

From the SA node through both atria and from the SA node to the AV node (both these routes from the SA node are via cell-cell spread using gap junctions)

Then from AV node to the ventricles (travelling to the bundle of his, then left and right branches of the bundle of his and then the purkinjie fibres) within the ventricles gap junctions are used as well.

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10
Q

Where is the AV node located and what is special about it ?

A
  1. It is located at the base of the right atrium; just above the junction of atria and ventricles
  2. The AV node is the only point of electrical contact between atria and ventricles
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11
Q

What happens to the electrical conduction in the heart at the AV node and why? and then state what happens to the electrical conduction after the AV node

A
  1. Electrical conduction is delayed in the AV node. This allows atrial systole (contraction) to precede ventricular systole
  2. The Bundle of His and its branches and the network of Purkinje fibers allow rapid spread of action potential to the ventricles
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12
Q

The APs in contractile cardiac muscle cells differ considerably from the APs in pacemaker cells, describe the stages of AP generation in cardiac muscle cells

A
  1. Phase 2 (in pic) is called the plateau phase which is unique to cadiac muscle cells, it is where the membrane potential is maintained near the peak of action potential for few hundred milliseconds
  2. Phase 3 is referred to as the falling phase
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13
Q

What is heart rate (HR) mainly influenced by ?

A

The autonomic nervous system (ANS)

  • Sympathetic stimulation speeds up HR
  • Parasympathetic stimulation slows down HR
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14
Q

Describe the parasympathetic supply to the heart

A

The Vagus nerve is the parasympathetic supply to the heart and exerts a contiuous influence on the SA node under resting conditions known as vagal tone.

Vagal tone dominates under resting conditions to produce normal resting HR.

Vagus nerve supplies SA node and AV node

Vagal stimualtion slows HR andincreases AV nodal delay

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15
Q

Through what neurotransmitter does vagal stimulation of the heart act ?

A

Acetylcholine via M2 muscarinic receptors

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16
Q

What is the mechanism of action of Atropine and what is it used for ?

A

It is a competitive inhibitor of acetylcholine - used in extreme bradycardia to speed-up the heart

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17
Q

Describe the sympathetic supply to the heart

A
  • Cardiac sympathetic nerves supplies SA node and AV node and Myocardium
  • Sympathetic stimulation increases HR and decreases AV nodal delay and increases force of contraction
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18
Q

What neurotransmitter does sympathetic supply to the heart act via ?

A

Noradrenaline acting through b1 adrenoceptors

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19
Q

What are the main histological features of cardiac muscle ?

A
  1. It is striated
  2. Has no neuromuscular junctions
  3. Has gap junctions (intercalated discs)
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20
Q

What is the function of desmosomes found in the intercalated discs between cardiac muscle cells ?

A

They provide mechanical adhesion between adjacent cardiac cells and ensure that the tension developed by one cell is transmitted to the next

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21
Q

What is the contractile units of cardiac muscle and describe what they are comprised of ?

A

Myofibrils - comprised of actin and myocin filaments arranged into SARCOMERES

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22
Q

Describe the stages of cardiac muscle contraction

A
  1. Muscle fiber relaxed; no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin- tropomyosin complex
  2. Muscle fiber excited; Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs
  3. Binding of actin and myosin cross-bridge triggers power stroke that pulls thin filament inward during contraction
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23
Q

State what the refractory period is and what its purpose is in terms of cardiac excitation

A
  • It is a period following an AP in which it is not possible to produce another AP
  • The long refractory period is protective for the heart preventing generation of tetanic contractions in the cardiac muscle
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24
Q

State what happens to the ventricular muscle during diastole and systole

A
  • During diastole is relaxes
  • During systole is contracts
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25
Q

Define what stroke volume is and state what it is regulated by

A
  • The volume of blood ejected by each ventricle per heart beat
  • SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV
  • It is regulated by intrinsic (within the heart) and extrinsic (nervous and hormonal) controls
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26
Q

Considering the intrinsic control of stroke volume what are changes in stroke volume (SV) are brought about by?

A
  1. By changes in the diastolic length/ diastolic stretch of myocardial fibres (called cardiac preload)
  2. Which is in turn determined by the end diastolic volume (the volume of blood within each ventricle at the end of diastole) (EDV)
  3. Which inturn is determined by venous return
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27
Q

State starlings law of the heart (frank-starling mechanism)

A

The more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)

Note - optimal length in cardiac muscle is achieved by stretching the muscle

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28
Q

Describe what afterload is and what an increase in it can cause

A

Afterload = the resistance into which heart is pumping

  1. If afterload increases: at first, heart unable to eject full SV, so EDV increases
  2. Force of contraction rises by Frank-Starling mechanism
  3. If increased afterload continues to exist (e.g. untreated HTN), eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
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29
Q

What is meant when it is said sympathetic stimulation has a positive ionotropic effect on the heart ?

A

It increases force of contraction

Peak ventricular pressure rises, and duration of diastole and systole decrease

Remember Stimulation of sympathetic nerves to the heart also causes a positive chronotropic effect (i.e. increase the HR and decreases AV nodal delay)

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30
Q

What is the effect of sympathetic stimulation on the frank starling curve ?

A

The increased peak ventricular pressure due to sympathetic stimulation causes - contractility of heart at a given EDV to increase which causes a greater SV at a given EDV

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31
Q

What is the effect of heart failure on the frank-starling curve ?

A

Shifts it to the right - decreased SV at a given EDV due to decreased contractility of the heart

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32
Q

What is the effect of vagal (parasympathetic) stimulation of the ventricles

A
  • Very little innervation of ventricles by vagus ==> little, if any, direct effect on SV
  • Vagal stimulation has major influence on rate, not force, of contraction
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33
Q

What 2 hormones have a ionotropic and chronotropic effect on the heart?

A

Adrenaline and noradrenaline released from adrenal medulla

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34
Q

Define what cardiac output (CO) is and state how it is regulated

A
  • CO = the volume of blood pumped by each ventricle per minute
  • CO = SV x HR

If we regulate the SV and HR, we will regulate the CO

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35
Q

Normally when does a heart valve produce a sound ?

A

when it shuts

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36
Q

Appreciate the normal blood flow through the heart

A

Appreicate

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37
Q

Define what the cardiac cycle is

A

It refers to all events that occur from the beginning of one heart beat to the beginning of the next (atrial and ventricular contractions and relaxations)

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38
Q

Define what diastole and systole is and state roughly the normal duration of each

A
  • Diastole = the heart ventricles are relaxed and fill with blood. Roughly 0.5s
  • Systole = the heart ventricles contract and pump blood into the: aorta (LV) and pulmonary artery (RV). Roughly 0.3s
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39
Q

List the 5 events which make up the cardiac cycle

A
  1. Passive Filling
  2. Atrial Contraction
  3. Isovolumetric ventricular Contraction
  4. Ventricular Ejection
  5. Isovolumetric ventricular Relaxation
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40
Q

Describe what happens during the passive filling phase of the cardiac cycle

A
  1. Pressure in atria and ventricles close to zero
  2. AV (tricuspid and mitral) valves open so venous return flows into the ventricles
  3. Pressure in the aorta is 80 mmHg > than in LV ==> aortic valve is closed
  4. Similar events happen in the right side of the heart, but the pressures (right ventricular and pulmonary artery) are much lower
  5. Ventricles become 80% full by passive filling
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41
Q

Describe what happens during the atrial contraction phase of the cardiac cycle

A
  1. The P-wave in the ECG signals atrial depolarisation
  2. The atria contracts between the P-wave and the QRS
  3. Atrial contraction complete the EDV (130 ml in resting normal adult)
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42
Q

Describe what happens during the isovolumetric ventricular contraction phase of the cardiac cycle

A
  1. Ventricular contraction starts after the QRS (signals ventricular depolarisation) in the ECG
  2. Ventricular pressure rises as contraction occurs
  3. When the ventricular pressure exceeds atrial pressure the AV (tricuspid and mitral) vlaves shit producing the 1st heart sound (LUB)
  4. The tension rises around a closed volume “Isovolumetric Contraction” as the aortic valve is still shut, so no blood can enter or leave the ventricle
  5. The ventricular pressure rises very steeply
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43
Q

Describe what happens during the ventricular ejection phase of the cardiac cycle

A
  1. When the ventricular pressure exceeds aorta/pulmonary artery pressure
  2. Aortic/pulmonary valve open - Remember this is a silent event
  3. Stroke Volume (SV) is ejected by each ventricle, leaving behind the End Systolic Volume (ESV)
  4. Aorta pressure ==> rises
  5. The T-wave in the ECG signals ventricular repolarisation
  6. The ventricles relax and the ventricular pressure start to fall. When the ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut. This produces the 2nd heart sound (DUB)
  7. The valve vibration produces the dicrotic notch in aortic pressure curve
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44
Q

Describe what happens during the isovolumetric ventricular relaxation phase of the cardiac cycle

A
  1. Closure of aortic/and pulmonary valves signals the start of the isovolumetric ventricular relaxation
  2. Ventricle is again a closed box, as the AV valve is shut
  3. The tension falls around a closed volume “Isovolumetric Relaxation”
  4. When the ventricular pressure falls below atrial pressure, AV valves open (Remember this is a silent event), and the heart starts a new cycle
45
Q

State what causes the 1st and 2nd heart sounds and what they indicate

A
  • The first heart sound (S1) is caused by closure of mitral and tricuspid valves. It sounds like a “lub”. S1 heralds the beginning of SYSTOLE
  • The second heart sound (S2) is caused by closure of aortic and pulmonary valves. It sounds like a “dub”. S2 heralds the end of systole and the beginning of DIASTOLE
  • Note additional heart sounds (S3 or S4) may be heard
46
Q

Go over the cardiac ascultation areas

A
47
Q

What do the different parts of the JVP pulse indicate

A
  • “a” is atrial contraction
  • “c” bulging of tricuspid valve into atrium during ventricular contraction
  • “v” is rise of atrial pressure during atrial filling: release as AV valves open
48
Q

Define what blood pressure is

A

It is the outwards (hydrostatic) pressure exerted by the blood on blood vessel walls

49
Q

In clinical practice what type of blood pressure is measured ?

A

The Systemic Arterial Blood Pressure and express it as “Systolic” and “Diastolic” blood pressures

50
Q

Define Hypertension

A
  • Clinic blood pressure of 140/90 mmHg or higher and day time average of 135/85 mmHg or higher
51
Q

What is pulse pressure and its normal range ?

A
  • It is the difference between systolic and diastolic blood pressures
  • It is normally 30-50
52
Q

What is the normal fashion for blood to flow through a normal patent artery and does it produce sound ?

A

In a laminar fashion - this produces no sound

53
Q

If external pressure (e.g. cuff pressure) exceeding the systolic blood pressure is applied to an artery will you hear anything on your stethoscope ?

A

No - because the flow in that artery would be blocked and no sound is heard through a stethoscope

54
Q

Describe the 5 korotkoff sounds and state when you record systolic and diastolic BP

A

Blood pressure cuff is pumped up higher than systolic BP (so that no sound is initially heard then slowly decrease pressure.

  1. 1st sound is heard at peak systolic pressure (record this as the systolic BP)
  2. Sounds 2-3 are heard as intermittent sounds due to turbulent spurts of blood flow exceeding the cuff pressure exerted
  3. The 4th sound is the last sound heard and it is muffled/muted and represents minimum diastolic BP
  4. The 5th sound is when no sound is aduible again and represents smooth laminar blood flow again (record diastolic BP here)
55
Q

What drives the blood around the systemic circulation ?

A
  • A Pressure Gradient between the Aorta (AO) and the Right Atrium (RA) drives the blood around the systemic circulation
  • Pressure gradient = Mean Arterial Pressure (MAP) – Central Venous (right atrial) Pressure (CVP)
  • The RA Pressure is close to zero so the main driving force for blood flow is the MAP
56
Q

Define what mean arterial blood pressure (MABP) is

A

It is the average arterial blood pressure during a single cardiac cycle

57
Q

State the equation used to calculate MABP and its normal range

A

Normal range = 70 - 105 mm Hg.

58
Q

A MABP of what is needed to perfuse the coronary arteries, brain, and kidneys?

A

60

59
Q

Why must MABP be regulated within a narrow range ?

A

To ensure Pressure is high enough to perfuse internal organs including the brain, heart, and kidneys but not too high to damage the blood vessels or place an extra strain on the heart

60
Q

Define what systemic vascular resistance (SVR) is

A
  • It is the sum of resistance of all vasculature in the systemic circulation

Note - (sometimes referred to as “Total Peripheral Resistance”)

61
Q

What are the major resistance vessels contributing to the systemic vascular resistance (SVR)?

A

Arterioles

62
Q

Using CO and Systemic vascular resistance (SVR) what is the equation used to calculate MABP?

A

MABP = CO x SVR

63
Q

Appreciate the summary of the effect of the ANS on MABP

A
64
Q

What controls the short-term regulation of MABP?

A

The baroreceptor reflex

65
Q

What are the main 3 components of the baroreceptor reflex and what type of feedback regulates this reponse ?

A

Negative feedback - The heart and blood vessels are the effectors which exert negative feedback on the baroreceptors

66
Q

What 2 locations are the baroreceptors mainly located ?

A

The carotids and aorta

67
Q

What is the baroreceptor reflex important for the regulation of BP ?

A

It is important in moment-to-moment regulation of arterial blood pressure including prevention of postural changes

68
Q

Describe the baroreceptor response to decreased BP

A
  1. Decreased BP causes decreased barorceptor firing
  2. Medulla then signals to decreased vagal activity and increase cardiac sympathetic activity and sympathetic constrictor tone
  3. Results in increased CO and SVR which increased the BP
69
Q

Describe the baroreceptor response to increased BP

A
  1. Increased BP causes increases barorceptor firing
  2. Medulla then signals to increase vagal activity and decrease cardiac sympathetic activity and sympathetic constrictor tone
  3. Results in decreased CO and SVR which decreases the BP
70
Q

Describe how the baroreceptor reflex helps prevent postural hypotension

A

When a normal person suddenly stand-up from lying position:

  1. The venous return to the heart decreases - effect of gravity ==> mean arterial pressure (MABP) very transiently decreases
  2. This reduces the rate of firing of baroreceptors
  3. The vagal tone to the heart decreases and the cardiac sympathetic tone to the heart increases. This increases the heart rate (HR) and stroke volume (SV)
  4. The sympathetic constrictor tone increases. This increases the systemic vascular resistance (SVR) - arterioles are the main site for SVR
  5. The sympathetic constrictor tone to the veins increases the venous return (VR) to the heart and stroke volume
  6. The result is: rapid correction of the transient fall in MAP: HR INCREASES; SV INCREASES; SVR INCREASES
71
Q

What causes postural hypotension

A

This results from failure of Baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

72
Q

Define how postural hypotension is confirmed

A

A positive result is indicated by a drop, within 3 minutes of standing from lying position:

  1. In systolic blood pressure of at least 20 mmHg (with or without symptoms) or
  2. A drop in diastolic blood pressure of at least 10 mm Hg (with symptoms)
73
Q

What are the symptoms of postural hypotension

A

lightheadedness, dizziness, blurred vision, faintness and falls

74
Q

Baroreceptors only respond to what type of changes in blood pressure ?

A

Acute changes

  • Baroreceptors firing decreases if high blood pressure is sustained
  • Baroreceptors “re-set” - they will fire again only if there is an acute change in MAP above the new higher steady state level
75
Q

Control of MABP in the longer-term is mainly by controlled by what?

A

Blood volume

76
Q

Blood volume and ==> MABP can be controlled by controlling what?

A

The extracellular fluid volume (ECFV)

77
Q

What is the total body fluid in someone comprised of ?

A

Total body fluid = Intracellular fluid (2/3rd) + Extracellular Fluid (ECF) - normally 1/3rd of the total

Note - 60% of body weight in a 70 kg young man is water (~ 42 L)

78
Q

What is the extracellular fluid volume comprised of ?

A

ECF Volume (ECFV) = Plasma Volume (PV) + Interstitial Fluid Volume (IFV) - this is the fluid which bathes the cells and acts as the go- between the blood and body cells

79
Q

If plasma volume falls what do compensatory mechanisms do?

A

They shift fluid from the interstitial compartment to the plasma compartment i.e. insterstital fluid is moved to replace the lost plasma fluid

80
Q

What are the 2 main factors which affect extracellular fluid volume ?

A
  1. Water - excess or deficit
  2. Na+ - excess or deficit

Healthy people stay in a stable water and salt balance, where water input = water output

81
Q

What role do hormones play in regulating the extracellular fluid volume and what 3 hormones can do this ?

A

​Hormones act as effectors to regulate the ECFV (including Plasma Volume) by regulating the Water and Salt Balance in our bodies.

  1. The Renin-Angiotensin- Aldosterone System - RAAS
  2. Natriuretic Peptides – NPs
  3. Antidiuretic Hormone (Arginine Vasopressin) - ADH
82
Q

Describe how the RAAS plays an important role in the regulation of plasma volume (==> ECFV) and SVR and hence the regulation of MAP

A

The RAAS has three important components (1) Renin (2) Angiotensin (3) Aldosterone

  1. Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)
  2. Angiotensin I is converted to angiotensin II by Angiotensin converting enzyme - ACE
  3. Angiotensin II (1) stimulates the release of Aldosterone from the adrenal cortex (2) Causes systemic vasoconstriction which increases SVR. (3) Also stimulates thirst and ADH release contributing to increasing the plasma volume which is mainly done by aldosterones action
  4. Aldosterone (a steroid hormone) acts on the kidneys to increase sodium and water retention – increases plasma volume
83
Q

What 3 things stimulate renin release from the juxtaglomerular apparatus in the kidney?

A
  1. Renal artery hypotension -caused by systemic hypotension (¯ blood pressure)
  2. Stimulation of renal sympathetic nerves
  3. Decreased [Na+] in renal tubular fluid
84
Q

What are the 2 types of Natriuretic Peptides (NPs)?

A
  • Atrial Natriuretic Peptide (ANP) and Brian-type Natriuretic Peptide (BNP)
85
Q

Describe the action of natriuretic peptide hormones and how they regulate ECFV and ==> blood pressure

A
  1. Released in response to cardiac distension or neurohormonal stimuli
  2. They cause excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure
  3. Decrease renin release ==> decrease blood pressure
  4. Act as a vasodilators ==> decrease SVR and blood pressure

NPs act as a counter-regulatory system for the Renin-Angiotensin-Aldosterone System (RAAS)

86
Q

Where is Antidiuretic Hormone (ADH) also called “Vasopressin” produced and stored

A

synthesised by the hypothalamus and stored in the posterior pituitary

87
Q

What is ADH secretion stimulated by and describe its effect on ECFV and MABP

A

Secretion stimulated by (1) reduced extracellular fluid volume or (2) increased extracellular fluid(plasma) osmolality (main stimulus)

Plasma osmolality indicates relative solute-water balance - Plasma osmolality is monitored by osmoreceptors mainly in the brain in close proximity to hypothalamus

  1. ADH acts in the kidney tubules to increase the reabsorption of water (conserve water) - i.e. concentrate urine (antidiuresis) ==> increase extracellular and plasma volume and hence cardiac output and blood pressure
  2. ADH (vasopressin) also acts on blood vessels to cause vasoconstriction - increase SVR and blood pressure: the effect is small in normal people but becomes important in hypovolaemic shock (e.g. haemorrhage)
88
Q

State the 5 main components of the cardiovascular system and their function

A
  1. HEART: the Pump.
  2. ARTERIES: Passageways of blood from heart to tissues.
  3. ARTERIOLES: major Resistance vessels
  4. CAPILLARIES: site of Exchange of gas, nutrients and water between blood and tissues
  5. VEINS: Capacitance vessels (contain most of blood volume during rest); Passageways of blood from tissues to heart. Venous Return must provide heart with sufficient blood to pump
89
Q

What is SVR regulated by and state the major site of SVR

A

SVR is regulated by vascular smooth muscles (so all those in the pic regulate it) the main site of SVR is in the arterioles

90
Q

What effect does contraction and relaxation of vascular smooth muscles have on SVR and in turn MABP

A
  • Contraction of vascular smooth muscles causes vasoconstriction and increases SVR and MAP (i.e. pressure upstream)
  • Relaxation of vascular smooth muscles causes vasodilatation and decreases SVR and MAP
91
Q

What are vascular smooth muscles controlled by ?

A

Extrinsic and Intrinsic mechanisms

92
Q

What 3 things is SVR dependent on (referring to the equation here)

A

Resistance to blood flow is: directly proportional to blood viscosity and length of blood vessel; and inversely proportional to the radius of blood vessel to the power 4

93
Q

What are the 2 extrinsic controls of vascular smooth muscles ?

A

Nerves and hormones

94
Q

Describe how nerves control vascular smooth muscle

A

Vascular smooth muscles are supplied by SYMPATHETIC nerve fibers via the neurotransmitter NORADRENALINE acting on a receptors

At rest vascular smooth muscle is partially constricted (vasomotor tone) due to tonic discharge of sympathetic nerves resulting in continuous release of noradernaline

  • Increased sympathetic discharge will increase the vasomotor tone resulting in vasoconstriction
  • Decreased sympathetic discharge will decrease the vasomotor tone resulting in vasodilatation

Note - There is no significant parasympathetic innervation of arterial smooth muscle except in the penis and clitoris

95
Q

List 3 hormones which exert extrinsic control over the vascular smooth muscle

A
  1. Adrenaline
  2. Angiotensin II - causes vasoconstriction
  3. ADH - causes vasoconstriction
96
Q

Describe the selective effect of adrenaline on vascular smooth muscle and state why this is important

A

The effect of adrenaline is largely organ specific. It depends on the predominant type of receptor. This helps with strategic redistribution of blood e.g. during exercise

  • Adrenaline acting on alpha receptors causes vasoconstriction - alpha receptors are predominant in skin, gut, kidney arterioles
  • Adrenaline acting on beta2 receptors causes vasodilation - beta2 receptors are predominant in cardiac and skeletal muscle arterioles
97
Q

What are the main intrinsic control mechanisms of vascular smooth muscle how do they work and do these or extrinsic control mechanisms have overriding control ?

A
  • They include local CHEMICAL and PHYSICAL factors - they match the blood flow of different tissues to their metabolic needs
  • They can OVER-RIDE the extrinsic control mechanisms
98
Q

Local metabolic changes (CHEMICAL) within an organ influences the contraction of arteriolar smooth muscles, what factors cause relaxation of arteriolar smooth muscles resulting in VASODILATATION and METABOLIC HYPERAEMIA?

A
  • Decreased local PO2
  • Increased local PCO2
  • Increased local [H+] (decreased pH)
  • Increased extra-cellular [K+]
  • Increased osmolality of ECF
  • Adenosine release (from ATP)
99
Q

In addition to metabolites, other local chemicals released within an organ (local humoral agents) influence the contraction of arterial and arteriolar smooth muscles, when are they released?

Note again this is CHEMICAL intrinsic control

A

They can be released in response to tissue injury or inflammation

100
Q

List examples of local humoral agents (CHEMICAL) which cause relaxation of arteriolar smooth muscles resulting in VASODILATATION

A
  • Histamine
  • Bradykinin
  • Nitric Oxide (NO) - most potent one
101
Q

List of examples of local humoral agents which cause contraction of arteriolar smooth muscles resulting in VASOCONSTRICTION

A
  • Serotonin
  • Thromboxane A2
  • Leukotrienes
  • Endothelin - most potent one
102
Q

List the physical intrinsic factors influencing control of vascular smooth muscles and their effect

A

TEMPRATURE:

  • Cold - causes vasoconstriction
  • Warmth - causes vasodilatation

MYOGENIC RESPONSE to Stretch:

  • If MAP rises resistance vessels automatically constrict to limit flow
  • If MAP falls resistance vessels automatically dilate to increase flow. Important in tissues like brain and kidneys

SHEER STRESS:

  • Dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate. This increases blood flow to metabolically active tissues
103
Q

State the different factors influencing venous return

A
104
Q

How does venomotor tone influence venous return

A

The veins are capacitance vessels that contain most of the blood volume under resting conditions.

  • Venous smooth muscles are supplied with sympathetic nerve fibres and stimulation gives venous constriction
  • Increased venomotor tone increases venous return, SV & MAP

Remember: INCREASED VASOMOTOR TONE INCREASES SVR & MAP

105
Q

How does the respiratory pump affect venous return

A
  • During inspiration, intrathoracic pressure decreases and intraabdominal pressure increases
  • This increases pressure gradient for VENOUS RETURN and creates a suction effects that moves blood from veins towards the heart
  • Increasing rate and depth of breathing increases VENOUS RETURN to the heart
106
Q

How does the skeletal muscle pump affect venous return

A
  • Large veins in limbs lie between skeletal muscles. Contraction of muscles aids venous return
  • One-way venous valves allow blood to move forward towards the heart
  • Muscle Activity ==> increases VENOUS RETURN to heart
107
Q

Describe the acute CVS response to exercise

A
  1. Sympathetic nerve activity increases ==> HR & SV increase ==> CO increases
  2. Sympathetic vasomotor nerves reduce flow to kidneys & gut - due to vasoconstriction
  3. In skeletal and cardiac muscle, metabolic hyperaemia overcomes vasomotor drive - causing vasodilatation
  4. Blood flow to skeletal and cardiac muscles increase in proportion to metabolic activity
  5. The increases in CO increases systolic BP. The metabolic hyperaemia decreases SVR and decreases DBP (i.e. the pulse pressure increases)
  6. Post exercise hypotensive response
108
Q

Describe the chronic CVS response to exercise

A

Regular aerobic exercise helps reduce blood pressure

Y4 Cardiology (27 decks)

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