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ESA 2 > CVS > Flashcards

CVS Flashcards

0
Q

Which 3 factors increase the rate of diffusion?

A

Large surface area available for exchange, low diffusion resistance and a high concentration gradient.

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1
Q

What does the CVS include?

A

A pump (heart), a distribution system (vessels and blood), an exchange mechanism (capillaries) and a way to control flow (arterioles and pre-capillary sphyncters)

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2
Q

What is the perfusion rate?

A

The rate of blood flow

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3
Q

Properties of Cardiac muscle?

A

Striated, 1/2 central nuclei, intercalated disks (for electrical & mechanical coupling with adjacent cells), branching, gap junction (for electrical coupling), T-tubules in line with the z-line, sarcoplasmic reticulum and t-tubules form diad.

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4
Q

What are the two main arteries?

A
  • Pulmonary trunk: from right ventricle splits into 2 pulmonary arteries to enter lungs.
  • Aorta: arises from left ventricle, goes up then descends. 3 branches off the aorta to supply head and upper limbs (brachiocephalic, common-carotid and left subclavian arteries).
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5
Q

What happens during systole?

A

Left ventricle contracts, increasing blood pressure in aorta. Walls of aorta stretch.

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6
Q

What happens during diastole?

A

Aortic semilunar valve closes, walls of aorta recoil, as well as sub-endothelial layer of connective tissue.

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7
Q

What are the three layers that make up an artery?

A
  • Tunica intima: endothelial cells parallel to axis of artery. Also sub-endothelial layer of connective tissue.
  • Tunica media: 40-70 elastic membranes. Smooth muscle cells & Collagen. Also thin external elastic lamina.
  • Tunica adventitia: thin layer of fibroelastic connective tissue with lymphatic and nerve vessels.
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8
Q

What are arterioles?

A

Arteries with a diameter of <0.1mm. They have only 1-3 layers of smooth muscle in their tunica media. With no external elastic lamina.

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9
Q

What are metarterioles?

A

They are arteries that supply blood to capillary beds. Their smooth muscle layer is not continuous. Individual muscle cells are spaced apart. Each muscle cell acts as a sphincter, controlling blood flow.

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10
Q

What is the role of lymphatic capillaries?

A

They drain away extracellular fluid, returning it to blood at junctions of the internal jugular and subclavian veins.

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11
Q

What are the 3 types of capillaries?

A
  1. Continuous: most common, cells joined by tight junctions e.g. in nervous tissue
  2. Fenestrated: There are windows in the thin parts of the endothelium that are covered by thin membrane e.g. in endocrine glands
  3. Sinusoidal: Slower blood flow, gaps in walls so whole cells can move between blood and tissue e.g. in the liver/spleen.
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12
Q

What are venules?

A

They have a diameter <1mm. Endothelium is associated with pericytes (on external surface to divide into muscle cells/fibroblasts). Valves prevent back-flow of blood.

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13
Q

What is the structure of a vein?

A

Larger diameter than accompanying artery & thinner wall. More connective tissue, fewer elastic and muscle fibres. Most do not have prominent tunica media.

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14
Q

What are Venae Comitantes?

A

Deep paired veins, accompanying one of the smaller arteries on each side of an artery. =3 vessels wrapped in one sheath.

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15
Q

What is the mediastinum?

A

The central compartment of the thoracic cavity. It contains all thoracic structures except the lungs. It is a highly mobile region. (bordered by thoracic spine, sternum, mediastinal pleura, thoracic inlet, diaphragm)

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16
Q

Where is the sternal angle of Louis?

A

It’s part of the sternum, inline with the 2nd ribs.

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17
Q

What is the structure of the Pericardium?

A

It is a closed sac with 2 layers. A tough, external fibrous layer and an inner serous membrane (which itself consists of 2 layers, the outer parietal layer and the inner visceral layer). Pericardial cavity is between the parietal and visceral layers.

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18
Q

What is cardiac tamponade?

A

When there is too much fluid in the pericardial cavity (pericardial effusion), which compresses the heart, not allowing it to expand fully. This is potentially lethal.

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19
Q

Where is the Oblique Sinus?

A

It lies behind the left atrium, between the 2 pairs of pulmonary veins.

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20
Q

Where is the Transverse Pericardial Sinus?

A

It passes underneath the aorta and the pulmonary trunk, and above the superior vena cava. In front of the left atrium.

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21
Q

What is the role of the Phrenic nerve?

A

Supplies the diaphragm and the pericardium.

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22
Q

What is the Vagus Nerve?

A

Supplies parasympathetic fibres to all organs, except adrenal glands. It is responsible for heart rate, digestion, sweating etc.

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23
Q

What is the route of blood through the heart?

A

Enters heart via inferior and superior vena cava, into the right atrium (deoxygenated blood). Blood then enters the right ventricle via the tricuspid valve. Blood then forced out into the pulmonary artery and to the lungs to be oxygenated. Pulmonary veins then empties blood into the left atrium, which then contracts, forcing blood into left ventricle, through the mitral valve. Post contraction, this blood is forced out to the rest of the body via the aorta.

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24
Q

Which coronary artery supplies the left ventricle?

A

The left anterior descending artery.

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25
Q

Which coronary artery supplies the right atrium?

A

The right coronary artery.

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26
Q

What is the role of the pacemaker cells?

A

Fires action potential which spreads over whole heart and produces a coordinated contraction. Pacemakers generate action potentials at regular intervals.

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27
Q

Describe the cardiac cycle

A

Pacemaker in SAN spreads impulse over atria. This reaches the AVN. Excitation spreads down septum between ventricles, then through ventricular myocardium from inner to outer surface. Ventricle then contracts from apex up, forcing blood towards outflow valves.

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28
Q

How long does ventricular systole last?

A

280ms

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29
Q

How long between one ventricular systole and the next?

A

700ms

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30
Q

What causes the A/V valves to close?

A

A brief backflow of blood from ventricles to atria closes these valves. = Isovolumetric Contraction.

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31
Q

What causes the 1st heart sound?

A

A/V valve closure. The onset of ventricular systole.

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32
Q

What causes the 2nd heart sound?

A

Outflow valve closure. End of ventricular systole.

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33
Q

What causes heart murmurs?

A

Turbulent blood flow caused by narrowing of valves (stenosis) or valves not closing properly.

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34
Q

How do you calculate cardiac output?

A

Stroke volume x heart rate = cardiac output (total volume pumped per minute)

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35
Q

Give two roles of embryological looping

A

Causing convolution of the heart tube, ensuring:

  • primordium of right ventricle is near to outflow tract
  • primordium of left ventricle is near to inflow tract.
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36
Q

what are the five sections of the primitive heart tube?

A 
Aortic roots
Truncus arteriosus
Bulbus cordis
Atria
Sinus venosus
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37
Q

How does the oblique pericardial sinus form?

A

As LA expands, it absorbs the pulmonary veins and stretches out pericardial cavity.

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38
Q

What does RA develop from?

A

Most of the primitive atrium and sinus venosus.

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39
Q

What does the LA develop from

A

Small portion of primitive atrium and absorbs proximal parts of pulmonary veins.

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40
Q

Describe the route of blood through through fatal heart

A

Oxygenated blood from mother enters IVC via ductus venosus. This blood enters right atrium, and is then shunted to left atrium via the foramen ovale. This blood then goes via left ventricle to aorta to the fetal body. Deoxygenated blood then returns to placenta via the umbilical arteries.

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41
Q

What is the role of the ductus arteriosus?

A

Shunts blood that is used for muscle development from the pulmonary trunk to the aorta.

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42
Q

Which nerve is linked to the 6th arch of the aorta?

A

The recurrent laryngeal nerve that innervates intrinsic muscles of the larynx.

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43
Q

What happens after looping has taken place?

A

An atrioventricular canal links the atrium and ventricle.

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44
Q

What is the role of septation?

A

To create 4 chambers and to achieve selective outflow

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45
Q

Which three divisions of the heart must be formed?

A

An interatrial septum, an interventricular septum and septation of the ventricular outflow tract (to create pulmonary trunk and aorta).

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46
Q

Where do endocardial cushions develop during septation?

A

Between the primitive atria and primitive ventricle. Dividing the heart tube into left and right channels.

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47
Q

Describe the stages of atrial septation

A
  • septum primum grows down towards the fused endocardial cushions. The gap between the two prior to fusion is called the ostium primum.
  • before this fuses, a second hole, the ostium secundum appears due to apoptosis.
  • a second septum, the septum secundum forms. The gap in this is called the foramen ovale. Which provides a shunt from R to L atrium.
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48
Q

Describe ventricular septation

A

The large muscular component grows upwards towards the fused endocardial cushions, leaving a small gap, the primary interventricular foramen. This is closed by tissue derived from the endocardial cushions that grows downwards (membranous ventricular septum).

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49
Q

Describe outflow tract septation

A

Endocardial cushions appear on the truncus arteriosus. They grow towards each other, twist around each other, forming a spiral septum. Creating a pulmonary trunk (from right ventricle) and an aorta (from left ventricle).

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50
Q

Why does the foramen ovale close at birth?

A

LA pressure > RA pressure so the septum primum is pushed against the septum secundum.

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51
Q

Why does the ductus venosus close at birth?

A

As the placental support is removed

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52
Q

What are the derivatives of the following embryological structures?:

  • foramen ovale
  • ductus arteriosus
  • ductus venosus
  • umbilical vein
A
  • foramen ovale -> fossa ovalis
  • ductus arteriosus -> ligamentum arteriosum
  • ductus venosus -> ligamentum venosum
  • umbilical vein -> ligamentum teres
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53
Q

Give three causes of congenital heart disease

A
  • genetic e.g. Downs, turners, marfans.
  • environmental e.g. Due to drugs/alcohol etc.
  • maternal infections e.g. Rubella
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54
Q

Describe Acynotic CHD.

A

Shunting of blood from L to R side of heart. Remains normal levels of oxyhaemoglobin in systemic circulation. E.g. ASD, VSD or patent ductus arteriosus.

55
Q

Describe cyanotic CHD

A

Shunting from R to L side of heart. So deoxygenated blood in the systemic circulation. E.g. Tetralogy of fallot or transposition of great arteries.

56
Q

Which four abnormalities are present with tetralogy of fallot?

A
  • Pulmonary Stenosis – a narrowing at, under or above the valve between the right ventricle and the pulmonary artery.
  • Ventricular Septal Defect – a hole between the right and left ventricles.
  • Over-riding Aorta – the entrance to the aorta is next to the ventricular septal defect, allowing oxygen-poor blood to flow through it.
  • Thick Right Ventricle – the heart has to work harder to pump blood through the narrowed pulmonary artery, causing the muscle to thicken.
57
Q

Give four examples of Acynotic CHDs.

A

VSD
ASD
Patent Ductus Arteriosus
Coarction of the Aorta

58
Q

Give two examples of Cyanotic CHD

A
  • Transposition of great vessels

- Tricuspid atresia

59
Q

What is coat toon of the aorta?

A

Narrowing of the lumen in region of ligamentum arteriosum. Increasing overload on the left ventricle. Blood flow to lower body is compromised as vessels distal to coarction.

60
Q

What is the resting membrane potential of cardiac myocytes?

A

-90mV.

61
Q

Describe the stages of the ventricular cardiac action potential.

A

1) rapid upstroke due to opening of voltage-gated Na+ channels, which open on depolarisation. Influx of Na+.
2) drop due to inactivation of Na+ channels and opening of transient outward K+ channel.
3) voltage-gated Ca2+ channels open, Ca2+ enters giving plateau region. K+ channels also open.
4) over time, these L-type Ca2+ channels inactivate. More K+ channels open, bringing membrane potential down to rest. K+ leaves = repolarisation.

62
Q

Describe the stages of the SA Node action potential.

A

1) pacemaker potential caused by If (funny current). Na+ ion influx, depolarising the cells, to reach threshold.
2) upstroke caused by opening of L-type Ca2+ channels.
3) repolarisation by opening of K+ channels. Lowering membrane potential.

63
Q

What is the pacemaker potential?

A

Initial slope to threshold, caused by the funny current. It is activated by hyperpolarisation. (More -ve than -50mv)
HCN channels are responsible for this current.

64
Q

Which are of the heart is the fastest to depolarise?

A

The SA Node so this sets the heart rhythm. Depolarisation spreads to AV node, down bundle of HIS, purkinjee fibres then out through ventricular myocytes.

65
Q

Explain excitation-contraction coupling

A

Intracellular calcium increase through activation of GPCRs.
Which in turn activate IP3, which acts on SR to release Ca2+ from stores.
In smooth muscles cells, this Ca2+ binds to calmodulin, which activates MLCK, which phosphorylates a regulatory light chain on myosin to allow it to bind to actin.

66
Q

Describe the sympathetic nervous system.

A

Thoracolumbar origin (T1-L2)
Most synapse with postganglionic neurones in the paravertebral chain of ganglia.
Short preganglionic axon.

67
Q

Describe the parasympathetic nervous system.

A

Craniosacral origin.
Synapse with neurones in ganglia close to target tissue.
Short postganglionic neurones.

68
Q

Which neurotransmitters and receptors are involved with pre-ganglionic neurones?

A

Always ACETYLCHOLINE which activates NICOTINIC ACh receptors on the postganglionic cell.

69
Q

Which neurotransmitters and receptors are involved with post-ganglionic neurones?

A
  • sympathetic: usually NORADRENERGIC (using noradrenaline). (Except sweat glands which release ACh for muscarinic ACh receptors)
  • parasympathetic: usually CHOLINERGIC (using ACh) for MUSCARINIC receptors. (Using GPCRs).
70
Q

What does Noradrenaline and adrenaline act upon?

A

Adrenoceptors (GPCRs).

Different tissues have different subtypes of receptors, allowing selectivity of drug action.

71
Q

What effects does the ANS have on the heart?

A

Controls heart rate, force of contraction and peripheral resistance.

72
Q

How is HR decreased by parasympathetic input?

A

Via vagus nerve. Synapses with postganglionic cells on epicardial surface, as well as at SA and AV nodes.
Releases ACh which acts on M2 receptors to decrease HR and rate of AVN conduction velocity.

73
Q

Now is heart rate increased by Sympathetic nervous system?

A

Via sympathetic trunk, to innervated SAN, AVN and myocardium. Done by releasing noradrenaline which acts on beta-1-adrenoceptors to increase HR and force of contraction.

74
Q

Sympathetic/parasympathetic effects on pacemaker potentials.

A

Symp: beta1 receptors (GPCRs) stimulate enzyme that produces cAMP, which speeds up pacemaker potential (slope becomes steeper)

Parasympathetic: m2 receptors cause inhibition of enzyme that produces cAMP. Also increases K+ conductance. Decreases slope.

75
Q

How do active tissues instigate vasodilation?

A

They produce more metabolites e.g adenosine, K+, H+. Local metabolites are strong vasodilators.

76
Q

Which receptors detect changes in blood pressure and where are they found?

A

Baroreceptors in the aorta and carotid sinus. They are sensitive to stretch, caused by increased arterial pressure. They send messages to medulla of the brain via afferent pathways, which then coordinates a response via efferent pathways.

77
Q

Describe ‘Flow’

A

The volume of fluid passing a given point per unit time. It is proportional to the pressure difference between the ends of a vessel. The higher the pressure difference, the greater the flow.

Flow = volume / time

78
Q

Describe velocity

A

The rate of movement of fluid particles along the tube. It can vary along the length of the vessel if the tube radius changes.
At a given flow, it is inversely proportional to cross sectional area. The bigger the area, the lower the velocity.

79
Q

Describe lamina flow

A

There’s a gradient of velocity from the middle to the edge of the vessel. Velocity is highest at the centre and stationary at the edge.

80
Q

What is turbulent flow?

A

As the mean velocity increases, the velocity gradient eventually breaks down and fluid rumbles over itself. Flow resistance is greatly increased.

81
Q

What is viscosity?

A

In lamina flow, the fluid layers move over each other. The extent to which the layers resist sliding over each other is the viscosity.
The higher the viscosity, the slower the central layers flow, and the lower the average velocity.

82
Q

Mean velocity is…

A
  • inversely proportional to viscosity

- directly proportional to cross sectional area

83
Q

Resistance…

A
  • increases as viscosity increases

- decreases with the 4th power of the radius (harder to push blood through smaller vessels)

84
Q

Explain resistance in terms of blood vessels in series/parallel

A

Series: Add resistances together. Re=R1+R2

Parallel: the resistance is lower. Re= (R1 x R2) / (R1 + R2)

85
Q

Which blood vessels have a high resistance and which have a low resistance?

A 
Arteries = low 
Arterioles = high 
Individual capillaries = high 
Venules = low
Veins = low
86
Q

What are distensible walls and why are they important?

A

The pressure within a vessel creates a transmural pressure between inside and out. This stretches the tube. As the vessel stretches, the resistance falls.
As the pressure in a distensible vessel falls, the walls eventually collapse, and blood flow ceases.
As vessels widen wirh increasing pressure, more blood flows in than out.
Distensible vessels store blood, they have capacitance (veins).

87
Q

What is total peripheral resistance?

A

The sum of resistance of all peripheral vasculature in the systemic circulation.

88
Q

What Is the role of resistance vessels?

A

Ensures each body part receives the correct amount of blood.

E.g. Arterioles and pre-capillary sphincters.

89
Q

What is the significance of vasodilator metabolites?

A

Metabolically active tissues produce these e.g. H+, K+, adenosine.
They cause the relaxation of local smooth muscle, lowering resistance, increasing blood flow.

90
Q

Explain reactive hyperaemia

A

If circulation to an organ is cut off then restored, a large amount of blood enters after a period of no flow.
As the organ continued to produce vasodilators, with no blood flow to remove them, when circulation is restored, the local arterioles dilate maximally (as vascular smooth muscle relaxes) and blood flow is very high.

91
Q

What is central venous pressure?

A

The pressure in the great veins supplying the heart. This depends on blood return from the body, pumping of the heart, gravity and muscle pumping.

92
Q

What is venous return?

A

The rate of flow of blood back to the heart. Limits cardiac output.

93
Q

Describe the arterial pulse waveform

A
  • dicrotic notch: due to pressure in left ventricle falling below aortic pressure and the subsequent backflow of blood.
  • dicrotic wave: the slight increase in pressure due to the recoil of blood off the closed aortic valve.
94
Q

What is end diastolic pressure & end systolic pressure?

A

End diastolic= the volume of blood in the ventricle at the end of diastole.

End systolic= the volume of blood in the ventricle at the end of systole.

95
Q

What effect does venous pressure have on ventricular filling?

A

The ventricles fill until the walls stretch, until it has filled with enough blood to equal the venous pressure.
Hence the higher the venous pressure, the more the heart fills in diastole.

96
Q

What is pre-load/after-load?

A

Preload: the end diastolic stretch of the myocardium, determined by venous pressure.
After load: the force necessary to expel blood into the arteries.

97
Q

What is contractility?

A

The stroke volume that you get for a given venous pressure. It is increased by increasing sympathetic activity.

98
Q

If venous pressure rises/falls, what happens to cardiac output?

A

If it falls: cardiac output decreases as decreased pre-load.
If it increases: cardiac output increases as increased pre-load.

99
Q

What is the CVS response to eating a meal?

A

Increased gut activity leads to increased metabolites and vasodilation. TPR falls, reducing arterial pressure and increasing venous pressure. This gives a rise in cardiac output.
Extra heart pumping reduces venous pressure and raises arterial. Demand is met.

100
Q

What is the CVS response to exercise?

A

Muscle pumping forces extra blood back to the heart.
Overfilling of ventricles prevented by rise in HR, driven by the brain.
When venous pressure starts to rise, heart rate is already high, keeping stroke volume down.

101
Q

CVS response to standing up.

A

Blood pools in superficial veins of legs, so central venous pressure falls. Hence cardiac output falls aswell as arterial pressure.
Baroreceptors detect fall in arterial pressure, and they raise the HR.
TPR increased to defend arterial pressure.
If the baroreceptors don’t work, leads to postural hypotension.

102
Q

CVS response to haemorrhage

A

Reduced blood volume lowers venous pressure, so cardiac output falls.
Arterial pressure falls, detected by baroreceptors. HR and TPR rise.
Rise in HR lowers venous pressure even more.
Veno-constriction and blood transfusion to replace blood volume lost.

103
Q

CVS response to long term increase in blood volume?

A

If blood volume increases for days, the venous pressure increases.
So cardiac output and arterial pressure rise.
Forcing more blood through tissues, Auto regulating and increasing TPR.
So arterial pressure rises further and stays up.

104
Q

Explain the four possible electrode views

A

-repolarisation towards an electrode gives downwards signal.
-repolarisation away from an electrode gives upwards signal.
-depolarisation towards an electrode gives upwards signal.
-depolarisation away from an electrode gives downwards signal.
The more muscle depolarising and the more direct towards the electrode, the bigger the amplitude of the signal.

105
Q

Explain the PQRST waveform

A 
P= Atrial depolarisation
Q= Septal depolarisation spreading to ventricle
R= Main ventricular depolarisation 
S= End ventricular depolarisation 
T= Ventricular repolarisation
106
Q

How do you get just one view from multiple electrodes?

A

Use an amplifier. This takes the negative input signal, inverts it, and adds it to the signal from the positive input. Then amplifies the total.

107
Q

What view of the heart do the limb and chest leads give from an ECG?

A

Limb leads give a vertical view of the heart.

Chest leads give a horizontal view of the heart.

108
Q

Where are the 6 chest leads placed?

A

V1: 4th right intercostal space at sternal border
V2: 4th left intercostal space at sternal border
V3: between V2 and V4
V4: 5th intercostal space at midclavicular line
V5: level with V4 at left anterior Axillary line
V6: level with V5 at left mid-Axillary line

109
Q

How do you calculate heart rate using an ECG?

A

300/number of squares in the R-R interval.

110
Q

What is a ventricular ectopic beat?

A

When ventricular cells gain pacemaker activity, causing ventricular contraction before the underlying rhythm would normally depolarise the ventricles.
ECG often appears wider and taller.
May occur ever other beat/every third beat etc.

111
Q

How does atrial fibrillation present on an ECG?

A

P-wave will be absent, with irregular fibrillation in its place.

112
Q

What is ventricular fibrillation?

A

Uncoordinated contraction of ventricular myocardium causing it to quiver rather than contract properly.

113
Q

What is heart block?

A

Communication problem between the atria and the ventricles.

  • 1st degree: P-R wave elongated. Conduction delay through AV node. But all electrical signals reach ventricles.
  • T1 2nd degree: P-R wave erratic. Only some atrial beats reach ventricles.
  • T2 2nd degree: electrical excitation sometimes fails to pass through AV node/bundle of HIS. So not all atrial contraction are followed by ventricular contraction.
  • 3rd degree: no electrical conduction conveyed to ventricles. The ventricles generate their own signal, through an ectopic pacemaker.
114
Q

Three signs of MI on an ECG?

A
  • S-T elevation
  • pathological Q waves
  • inverted T-waves
115
Q

Explain the 2 circulations of the lungs

A
  • Bronchial is part of systemic circulation and meets metabolic demands of the lungs
  • Pulmonary circulation is the blood supply to the alveoli required for gas exchange. Must accept entire cardiac output.
116
Q

Explain ventilation-perfusion

A
  • optimal ventilation-perfusion ratio is 0.8.
  • to maintain this, blood must be diverted from alveoli that aren’t well ventilated.
  • this is done via hypoxic pulmonary vasoconstriction. This ensures greater flow to well ventilated areas, optimising gas exchange.
117
Q

How is tissue fluid formed?

A
  • hydrostatic pressure of blood within the capillary pushes fluid out.
  • oncotic pressure exerted by large molecules such as plasma proteins, draws fluid into the capillaries.
  • in low pressure pulmonary system, only a small amount of fluid leaves the capillaries.
  • if capillary pressure increase, pulmonary oedema can occur.
118
Q

What do the right and left coronary arteries Arise from?

A

Aortic sinuses.

They fill during diastole.

119
Q

How is the O2 demand of the brain met?

A

By having a large capillary density, with large SA for gas exchange, and reduced diffusion distance. It has a high basal flow rate and also high O2 extraction.

120
Q

How is a secure blood supply to the brain ensured?

A
  • anastamoses between basilar and internal carotid arteries.

- myogenic auto-regulation to maintain cerebral blood flow when BP changes.

121
Q

What are some consequences of panic hyperventilation?

A

Hypocapnia (low co2), cerebral vasoconstriction. Leading to dizziness and fainting.

122
Q

What is cushing’s reflex,

A

Increases in intracranial pressure impairs cerebral blood flow as rigid cranium doesn’t allow for volume expansion.
Impaired blood flow to vasomotor control regions of the brainstem increase sympathetic vasomotor activity, increasing arterial BP and maintaining flow.
Increasing arterial BP restores blood flow to the brain.

123
Q

What must change to blood flow to skeletal muscle during exercise?

A

Must increase O2 and nutrient delivery, aswel as removing metabolites.

124
Q

Describe the cutaneous circulation.

A

Most blood to the skin flows through arterio-venous anastamoses.
This circulation has a role in temperature control, influenced by sympathetic nervous system.
Increased core temperature, reduced vasomotor drive to AVAs, allowing them to dilate. Also a low resistance shunt of blood vessels to Venus plexus, close to surface, allowing dissipation of heat.

125
Q

What effects can drugs have on the CVS?

A

They can alter the rate and rhythm of the heart, the force of myocardial contraction and peripheral resistance.

126
Q

Give Three causes of arrhythmias.

A
  • ectopic pacemaker activity, either arising from damaged area of myocardium that becomes depolarised, or an area activated due to ischaemia. This may dominate over SA node.
  • after-depolarisation which are depolarisations following the normal action potential.
  • re-entry loop where there is an additional pathway from atria to ventricles, or there’s a conduction delay involved.
127
Q

4 types of anti-arrhythmic drugs

A

1) drugs that block voltage-sensitive Na+ channels. Only blocks open/inactive ones. Dissociates quickly for next AP.
2) beta-adrenoceptor antagonists that slow down slope of pacemaker potential of the SA node.
3) K+ channel blockers that prolong the AP, lengthening the absolute refractory period, preventing another AP too soon.
4) Ca2+ channel blockers that decrease slope of pacemaker AP at SA node, decrease AV node conduction and decreases force of contraction.

128
Q

What is the role of the drug adenosine?

A

It’s an anti-arrhythmic drug, that stops the heart to allow it to get back into rhythm. Acts on A1-receptors at AV node.

129
Q

Give two options for treatment of heart failure.

A

1) increase cardiac output via cardiac glycosides that block Na+ K+ ATPase. This increases Intracellular [Na+] so less Na+ taken in via Na+Ca2+exchanger, so less calcium extruded. So increased force of contraction.
2) reduce the workload of the heart via drugs that inhibit angiotensin converting enzyme. Preventing production of angiotensin 2 that acts on kidney to increase Na+ and water reabsorption aswell as being a vasoconstrictor making heart work harder.
- ACE inhibitors and beta-blockers also reduce workload of the heart.

130
Q

What is angina?

A

When O2 supply to the heart doesn’t meet its demand. Therefore causes ischaemia of heart tissue, causing chest pain on exertion. Due to narrowing of coronary vessels.

131
Q

What is the treatment for angina?

A

Reduce workload of the heart via beta-adrenoreceptor blockers, Ca2+ channel antagonists or organic nitrates.
Also improve blood supply to heart via organic nitrates.

132
Q

How do organic nitrates work?

A

React in vascular smooth muscle to produce Nitric oxide, which is a vasodilator. This reduces venous pressure and return of blood to heart, reducing workload of the heart.

133
Q

Which two types of drugs are antithrombic?

A

Anticoagulants and anti platelet drugs,

134
Q

Which drug types help with hypertension?

A 
Diuretics
ACE inhibitors
Beta-blockers
Ca2+ channel blockers 
Alpha1-adrenoceptor antagonists

ESA 2 (7 decks)

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