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Cardiovascular > Basic Science > Flashcards

Basic Science Flashcards

1
Q

Where are the electrical signals that control the heart generated?

A

In the heart itself

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2
Q

What does autorhythmmicity mean?

A

The heart is capable of beating rhythmically in the absence of external stimuli e.g. nerve innervation

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3
Q

Sino-atrial node
Where is it located?
What does it consist of?
What is its function?

A

Upper RA, close to the entrance of the SVC
A cluster of specialized pacemaker cells
The SA normally drives (i.e. sets the pace for) the entire heart

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4
Q

How does the cardiac action potential originate?

A

The cells in the SA node do not have a stable resting membrane potential - they exhibit spontaneous pacemaker potential.
The spontaneous pacemaker potential takes the membrane potential to a threshold to generate an action potential in the SA nodal cells

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5
Q

What is the main factor which is responsible for the spontaneous depolarization of the SA node?
What are the two components of this?

A

The most significant is a small influx of Na ions into the cell.
Two components:
1. Background inward current (Ib)
2. ‘Funny’ current (If) i.e. the pacemaker current
NB The term ‘funny’ current denotes ionic flow through channels activated in hyperpolarized cells (-60 mV or greater), unlike other tie and voltage dependent channels activated by depolarization.

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6
Q

Which ion are the pacemaker cells most permeable to at rest?

A

K+

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7
Q

What causes the initial slow depolarization of membrane potential to a threshold in pacemaker cells?

A

Decrease in K+ efflux superimposed on an increase in Na+ influx (the funny current)

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8
Q

Once the threshold is reached, what is the rising phase of the AP (i.e. depolarization) caused by?

A

Activation of voltage - gated Ca2+ cells

—> resulting in Ca++ influx

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9
Q

What is the falling phase of the AP (i.e. repolarization) caused by?

A

Activation of K+ channels

–> resulting in K+ efflux

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10
Q

AV node
Where is it located?
Why is it important?
What it its function?

A

It is located at the base of the RA, just above the junction of atria and ventricle.
The AV node is the only point of electrical contact between the atria and ventricles.
–> The AV node delays the pulse of electricity giving time for the atria to contract before the ventricles contract.

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11
Q

What is the brief pathway that the electrical impulse takes through the heart?

A

SA node –> AV node –> Bundle of His –> Left & right bundle branches –> Purkinje fibres

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12
Q

Give two features of the AV node cells.

A
  1. Small in diameter

2. Slow conduction velocity

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13
Q

How are impulses from SA to AV node; SA node through both atria spread between cells?

A

Via gap junctions?

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14
Q

Ventricular Muscle Action Potential
What is the resting membrane potential?
How is the resting potential maintained?
What is the rising phase (i.e. depolarization) caused by?

A
  • 90 mV –> maintained by a small inflow of K+ ions; at this stage Na and Ca channels are closed.
    The arrival of adjacent APs triggers the opening of voltage gated Na channels, leading to the rising phase, where fast Na+ influx rapidly moves the membrane potential to +30 mV.
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15
Q

Describe the four phases of ventricular muscle AP?

A

Phase 0 - Fast Na+ influx
Phase 1 - Closure of Na+ channels and Transient K+ efflux
Phase 2 - Mainly Ca++ influx
Phase 3 - Closure of Ca++ channels and K+ efflux
Phase 4 - Resting membrane potential

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16
Q

What is a unique characteristic of cardiac muscle cells?

What ion causes this?

A

The plateau phase

Mainly due to influx of Ca2+ through voltage gated Ca2+ channels

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17
Q

What is the repolarization phase caused by?

A

K+ efflux

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18
Q

What nerve & nervous system typically controls HR under resting conditions?
What is the neurotransmitter and what receptor does it act through?
What drug can be used to reverse this?

A

Vagus nerve - parasympathetic supply to the heart exerts a continuous influence on the SA node
The neurotransmitter is acetyl choline acting through M2 Receptor
Atropine is a competitive inhibitor of acetylcholine - used in extreme bradycardia to speed-up the heart

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19
Q

What does vagal stimulation do to pacemaker potentials?

A

The cell hyperpolarizes and is not longer able to reach threshold
–> slope of pacemaker potential decreases
–> frequency of AP decreases
This is a negative chronotropic effect - i.e. it decreases the HR

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20
Q

What is the neurotransmitter and receptor for sympathetic stimulation of the heart?

A

Noradrenaline acting through B1 adrenoceptors

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21
Q

Starlings Law of the Heart

Describe the physiology behind this

A

As with all other types of muscle, the velocity of contraction of myocardial tissue is reduced by increasing the load against which the tissue must contract.
However, in the non-failing heart, pre-stretching of cardiac muscle improves the relationship between the force and velocity of contraction.
This phenomenon was described in the intact heart as an increase of stroke volume (ventricular performance) with an enlargement of the diastolic volume (preload), and is known as Starling’s law of the heart.
Basically, stroke work is increased as ventricular end-diastolic volume is raised.

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22
Q

What is the nervous supply and receptor for the SA and AV nodes?

A

Cholinergic nerves from the vagus via M2 muscarinic receptors.

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23
Q

What external nerves supply the myocardium and what receptor is used?

A

Adrenergic nerves via B1 receptors

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24
Q

Briefly describe the events in the cardiac cycle.

A

The first event is atrial depolarization followed by right atrial and then left atrial contraction.
Ventricular activation follows after a short interval.
Left ventricular contraction starts and then right ventricular contraction.
The increased ventricular pressures exceed the atrial pressures, and close first the mitral and then the tricuspid valves.
The ventricular pressure then rises until it exceeds the aortic and pulmonary valve pressures, which then open and ejection occurs.
A ventricular pressure falls, the aortic and pulmonary valves close.
After the ventricular pressure falls below the atrial pressures, the mitral and tricuspid valves open.

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25
Q

What supplies the SA and AV nodes?

How is this important in disease?

A

Supplied by the right coronary artery in most, therefore disease in this artery may cause sinus bradycardia and AV nodal block

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26
Q

What are blood vessels mainly controlled by?

A

Endocrine system

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27
Q

What do sympathetic and parasympathetic nerves do to the vessels?

A 
Sympathetic = vasoconstrictor
Parasympathetic = vasodilator
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28
Q 
Nitric Oxide
What is it and where is it produced?
What triggers it?
What effect does this have?
What does this protect the cardiovascular system against?
A

NO is a diffusible gas with a very short half life produced in endothelial cells
It is produced in response to various stimuli such as sheer stress; agonists; inflammation
It causes SM relaxation (vasodilation); inhibits platelet aggregation; inhibits transcription of adhesion molecules.
This protects the CVS against atherosclerosis, hypertension, heart failure & thrombosis

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29
Q 
Prostacyclin (PGI2)
How does it relate to NO?
Stimulus?
Function?
What drug acts in a similar way?
A

It is synergistic to NO
Stimulated by agonists and thrombin inflammation
Function is to vasodilate and inhibit platelet aggregation
Drug = Fast acting heparin preparations

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30
Q 
Endothelin
What does it counteract?
Stimulus?
What is it's production inhibited by?
Effects?
A

Counteracts the effects of NO.
Stimulated by angiotensin II and thrombin
Inhibited by sheer stress
Effects - profound vasoconstriciton

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31
Q

von Willebrand factor
Stimulus
Effect

A

Promotes platelet aggregation & stabilizes factor 8

Stimulated by agonists - thrombin, epinephrine

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32
Q

Is cardiac muscle striated?
What causes this?
Are there any neuromuscular junctions between cardiac myocytes?
What are cardiac myocytes electrically coupled by?

A

Yes
Regular arrangement of contractile protein
No neuromuscular junctions
Electrically coupled by gap junctions

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33
Q

What are gap junctions?
What do they ensure re electrical excitation & cardiac myocytes?
What is the role of the desmosomes in the intercalated disks?
What do they ensure?

A

Protein channels which form low resistance electrical communication pathways between neighbouring myocytes.
They ensure that each electrical excitation reaches all the cardiac myocyctes (All-or-none Law of the heart).
The Desmosomes within the intercalated discs provide mechanical adhesion between adjacent cardiac cells.
They ensure that the tension developed by one cell is transmitted to the next.

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34
Q

Structure of Striated Muscle Fibre
What does each muscle fibre contain lots of?
What are these?
What causes their striped appearance?

A

Myofibrils - contractile units of muscle
They have alternating segments of thick and thin protein filaments.
The actin (thin filaments) causes the lighter appearance in myofibrils and fibers.
The myocin (thick filaments) causes the darker appearance.

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35
Q

What does force generation depend on at a cellular level?

A

ATP-dependent interaction between thick (myosin) and thin (actin) filaments.

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36
Q

What molecule and ion are required for both contraction and relaxation?

A

ATP & Ca2+

37
Q

What is Ca2+ required to do re force generation in cardiac myocytes?
What does this process cause?

A

Required to switch on cross bridge formation - causes muscle contraction in the heart

38
Q

Is a raise in extra cellular or intra cellular Ca2+ required for SM contraction?
What does this cause inside the cell?

A

Extracellular calcium - important for the function of the heart
Causes release of Ca2+ from SR (sacroplasmic reticulum)

39
Q

Define stroke volume.

How does it relate to end systolic volume and end diastolic volume?

A

Defined as “ the volume of blood ejected by each ventricle per heart beat”
SV = EDV - ESV

40
Q

Intrinsic control of SV

What brings about changes in stroke volume?

A

Changes in the diastolic length of myocardial fibres

41
Q

What is the end diastolic volume determined by?

A

Venous return to the heart

42
Q

Define Starling’s law of the heart.

Clue - think EDV and SV

A

The more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be during the resulting systolic contraction (SV).

43
Q

How does starlings law match the SV of the RV & LV?

A

If venous return to right atrium increases, EDV of right ventricle increases.
Starling’s Law leads to increased SV into pulmonary artery.
Venous return to left atrium from pulmonary vein increases, EDV of left ventricle increases.
Starling’s Law leads to increased SV into aorta.

44
Q

The ventricular muscle is supplied by what kind of nerve fibre, using which neurotransmitter?
What does stimulation of these nerves cause?

A

Sympathetic through noradrenaline.
Stimulation causes an increase in the force of contraction (positive inotropic effect)
NB the EDV stays the same

45
Q

Define inotropic and chronotropic.

A 
Inotropic = change in force of contraction
Chronotropic = change in HR
46
Q

What does vagal stimulation of the heart influence?

A

Influence on rate, NOT FORCE of contraction

47
Q

A pressure gradient between what two things drive the blood around th body?

A

Aorta and RA

48
Q

What is the normal range for MAP?

What MAP is required to perfuse the coronary arteries, brain etc

A

70-105 mmHg

60 mmHg

49
Q

What is the relationship between MAP, CO and TPR?

A

MAP = CO x TPR

50
Q

Define CO

A

The volume of blood pumped by each ventricle of the heart per minute

51
Q

What is the relationship between CO, HR and SV?

A

CO = HR x SV

52
Q

What are the major resistance vessels in the body?

A

Arterioles

53
Q

What do baroreceptors detect?
Where are they located?
What are they important in?

A

Pressure
Aortic arch & carotid sinus
Moment to moment regulation of arterial blood pressure including prevention of postural changes

54
Q

Describe the steps in control of postural changes in blood pressure.

A
  1. Venous return to the heart decreases bc of gravity
  2. MAP transiently decreases, reducing the firing of baroreceptors
  3. The vagal tone th the heart decreases and the sympathetic tone increases - this increases the HR and SV
  4. Sympathetic constrictor tone increases, increasing the TPR
  5. The sympathetic constrictor tone to the veins increases the venous return to the heart and stroke volume
    The result is rapid cirrection of the transient fall in MAP - HR INCREASES, SV INCREASES, TPR INCREASES
55
Q

What does the baroreceptor reflex do when there is increased BP?

A
  1. Increased baroreceptor discharge
  2. Increased vagal activity; decreased cardiac sympathetic activity; decreased sympathetic constrictor tone, causing:
  3. Decreased HR & decreased SV (leading to decreased cardiac output); vasodilation (causes decreased TPT
  4. Fall in BP
56
Q

What is the extracellular fluid volume made up of?

What % of the total body fluid does this make up?

A

ECFV = plasma volume (PV) + interstitial fluid volume (IFV)

1/3 of total

57
Q

If plasma volume falls, where is extra fluid taken from?

A

Intertitium

58
Q

What two main factors affect extracellular fluid volume?
Is this the long or short term control of blood volume?
How are these factors regulated?
Name three of these

A
  1. Water excess or deficit
  2. Na+ excess of deficit
    Long term
    Regulated by hormones:
  3. RAAS
  4. Atrial Natriuretic Peptide (ANP)
  5. Antidiuretic hormone (arginine vasopressin)
59
Q

What is the rate limiting step in RAAS?

What three things control this?

A

Renin secretion

  1. Renal artery hypotension - caused by systemic hypotension
  2. Stimulation of renal sympathetic nerves
  3. Decreased [Na+] in renal tubular fluid
60
Q 
Atrial Natriuretic Peptide
What is it?
What is it released in response to?
What does it cause in the kidneys?
What does this cause?
What system does it counter regulate?
A

28 AA peptide synthesized by atrial muscle cells
Released in response to atrial distention (hypervolaemia)
Causes excretion of Na and water
Causes reduced blood volume –> reduced BP
(vasodilator)
It counter acts RAAS by decreasing renin release

61
Q 
ADH (Vasopressin)
What is it stimulated by?
How does it detect this?
What does it do to the kidneys?
What does this do to the cardiac output?
Where does it also act in hypovolaemic shock?
A

Reduced or increased extracellular fluid volume
Osmoreceptors close to the hypothalamus
Acts in the kidney tubules to increase the reabsorption of water
This increases extracelluar and plasma volume and hence cardiac output & BP
Acts as a vasoconstrictor in blood vessels - increases TPR and BP in hypovolaemic shock

62
Q

What is the pulse pressure?

A

The difference between systolic & diastolic blood pressure

63
Q

What is TPR controlled by?

A

Vascular SM

64
Q

Vascular SM is supplied through why type of nerve, using which neurotransmitter and which receptor?

A

Sympathetic
Noradrenaline
Alpha receptors

65
Q

What is vasomotor tone and what is it maintained by?
How does vasoconstriction/dilatation occur?
Is there parasympathetic innervation of vascular SM?

A

Vascular SM is partially contricted at rest - maintained by tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline
Increased sympathetic discharge will increase the vasomotor tone resulting in vasoconstriction.
Decreased sympathetic discharge will decrease the vasomotor tone resulting in vasodilatation.
There is no significant parasympathetic innervation of arterial smooth muscles - exceptions are penis and clitoris.

66
Q

Hormonal control of vascular SM
What is the hormone?
What receptors does it act on and what does this cause?

A

Adrenaline
Acting on alpha receptors (in skin, gut, kidney arterioles) causes vasoconstriction
Acting on beta receptors (in cardiac and skeletal muscle arterioles) causes vasodilation

67
Q 
Vagal manouvres
What is this?
What does it stimulate?
What does it do to the NS? 
When is it used?
A

Massage of the bifurcation of the carotid artery or valsalve maneuver - activates baroreceptors
This increases parasympathetic output and may be employed in atrial tachycardia (flutter or fibrillation) to suppress impulses through the AV node

68
Q

Phrenic and vagal nerves - which is medial and which is lateral?

A

Vagal is medial

Phrenic is lateral

69
Q

Which derm layer does the heat arise from?

A

Visceral mesoderm

70
Q

What are the three basic layers to every blood vessel?

Breifly describe each

A
  1. Inner layer - tunica intima made up of a single layer of squamous epithelial cells supported by a basal lamina and a thin layer of connective tissue
  2. Middle layer - tunica media, made up predominantly of SM (sometimes elastic tissue
  3. Outer layer - tunica adventitia made up of supporting connective tissue
71
Q

What are the three types of capillary?

Briefly describe each.

A
  1. Continuous - most common, found in muscle, connective tissue, lung, skin, nerve
  2. Fenestrated - have ~50nm pores in wall; found in mucosa of the gut, endocrine glands, glomeruli of kidney
  3. Sinusoidal - lack a basal lamina and have large gaps through which macromolecules can pass; found in liver, spleen & bone marrow
72
Q

What are valves inward extensions of?

A

Tunica intima

73
Q

What are the three layers of the heart?

A

Endocardium - inner layer
Myocardium - middle layer
Epicardium - outer layer

74
Q

What lines the valves of the heart?

A

Endocardium

75
Q

What apoproteins make up HDL and LDL?

A

HDL - apoA1 and apoA2

LDL - apoB-100

76
Q

What are the key events in primary haemostasis?

A
  1. A local event occur, damaging the vessel wall and exposing the sub-endothelial matrix
  2. In response, circulating protein von Willebrand factor binds to the exposed collagen, to which platelets bind
  3. Platelets bind to collagen and platelet activation is initiated - they grow finger like projections and synthesize thromboxane A2
  4. TXA2 binds to platelet receptors, causing mediator release and vasoconstriction
  5. These mediators bind to platelet receptors, causing further platelet aggregation
  6. This exposes the platelet surface and facilitates clot formation
77
Q

What are they key events in coagulation? - INITIAL PHASE

A
  1. Tissue injury causes cells in the matrix of the vessel to reveal TF
    Cells bearing TF are exposed to factor 7A from the plasma forming a complex (TF:VIIa)
    The scene is now set for amplification which takes place on platelets
78
Q

What are they key events in coagulation? - AMPLIFICATION

A

Thrombin factor 11a activates further platelets and causes the release of factor 5 from the platelets
Thrombin also liberates factor 8 from vWf and acts it at the platelet membrane
The scene is now set for propagation

79
Q

What are the key events in coagulation?- PROPAGATION

A
  1. Factor 11a or TF:VIIIa activate factor IX, which forms a complex that powerfully activates factor 10
  2. Thrombin cleaves fibrinogen, forming fragments that join to form fibrin
  3. Factor VIIIa forms a fibrin fibre network and a solid clot
80
Q

What is Virchow’s triad?

A
  1. Injury to vessel wall
  2. Abnormal blood flow
  3. Increased coagulability of the blood
81
Q 
What type of thrombus forms in the arteries?
What is it made of?
Where is its site of origin?
Where does it often lodge?
What is it primarily treated with?
A

White thrombus
Made of mainly platelets in a fibrin mesh
Site of origin e.g. left heart, carotid artery
Often lodges in an artery in the brain or another organ
Treated with ANTIPLATELET drugs

82
Q

What type of thrombus forms in the veins?
What is it made of?
Where does it usually lodge?
What is it primarily treated with?

A

Red thrombus
White head, jelly-like red tail, fibrin rich
Lodges in the lung
Primarily treated with anticoagulants

83
Q

What is the significance of vitamin K and warfarin?

A

The liver uses vitamin K to produce blood clotting proteins, so plays a role in the body’s natural clotting process.
Warfarin reduces the liver’s ability to use vitamin K.
A significant change to intake of vitK can result in a dangerous change in INR.
If you reduce the amount of vitK, INR will increase (high INR = blood is too thin)

84
Q

What is the main summary of coagulation?

A

They key end point is the production of the protease thrombin – factor 2A. Thrombin cleaves the fibrinogen to fibrin which aggregates and then solidifies the plot.

85
Q

What role do smooth muscle cells play in ischaemic heart disease?

A

They migrate from the tunica media into the intima forming a fibrous capsule over the plaque

86
Q

What role do macrophages play in ischaemic heart disease?

A

They phagocytose LDL forming foam cells

87
Q

How does the brain ensure an optimum blood supply?

What range of blood pressure is cerebral blood flow maintained over?

A

The major cerebral arteries (internal carotids and vertebral) anastomose at the Circle of Willis - so cerebral perfusion should be maintained even in one carotid artery gets obstructed
60-160 mmHg

88
Q

What is the blood brain barrier (BBB) and what does it do?

A

Cerebral capillaries have very tight intercellular junctions.
These are highly permeable to O2, CO2 and glucose.
The capillaries are exceptionally impermeable to hyrophilic substances such as ions, catecholamines and proteins.
This helps to protect brain neurones from fluctuating levels of ions etc in the blood.

Cardiovascular (14 decks)

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