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ESA 4 revision > CVS > Flashcards

CVS Flashcards

1
Q

Functions of CVS you always forget?

A

Infrastructure for immune system

Thermoregulation

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2
Q

Feature of metabolically active tissues that aid diffusion?

A

High capillary density leading to greater perfusion and SA

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3
Q

What molecules diffuse easiest?

A

Small, uncharged polar molecules

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4
Q

Nature of barrier?

A

Number of pores and size

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5
Q

Maintenance of conc gradient t?

A

constant high perfusion flow

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6
Q

What is in blood?

A

RBCs,
WBCs
Platelets

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7
Q

What is blood flow?

A

5L/min

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8
Q

Constant flow to which organs?

A

Brain & kidneys

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9
Q

What type of verses have faster flow?

A

Low cross-sectional area, like veins

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10
Q

Feature of capillaries affecting flow?

A

Many branches, increasing cross-sectional area of vascular bed > slows down flow for exchange

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11
Q

What are arteries?

A

resistance vessels regulating flow to direct perfusion

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12
Q

What are end arteries?

A

terminal arteries supplying blood to a body part without significant collateral circulation

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13
Q

Examples of end arteries?

A

Splenic, coronary and renal

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14
Q

What are elastic arteries?

A

large & conducting

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15
Q

What are the layers of arteries?

A

Tunica intima - endothelium
Tunica media - smooth muscle & collagen
Tunica adventitia - CT, vasa vasorum and nerves

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16
Q

Describe elastic arteries?

A

TI - elastic lamina
TM - fenestrated elastic membranes
TA - thin fibroelastic connective tissue with nerves & vast vasorum

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17
Q

What are muscular arteries?

A

Medium sized & distributing

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18
Q

Describe muscular arteries?

A

circularly arranged smooth muscle. Contain nerve endings for sympathetic stimulation of vasoconstriction

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19
Q

What are arterioles?

A

Narrowest arteries with thin CT, single smooth muscle layer and thin layer of fibroblasts

Able to constrict and dilate

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20
Q

What are Metarterioles?

A

Arteries supplying blood to a capillary bed with non-continuous regions of smooth muscles = pre-capillary sphincters

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21
Q

What do pre-capillary sphincters do?

A

regulate flow to capillary beds

CONTRACTED = REDUCED CAPILLARY FLOW

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22
Q

Features of capillaries?

A

Mono-layer of endothelium and basement membrane

RBC fills entire lumen

Low blood velocity

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23
Q

Types of capillaries?

A

Continuous - tight cell junctions (muscle, exocrine, lungs)

Fenestrated - interruptions of endothelium with thin diaphragms (endocrine, glomerulus and gut)

Sinusoidal/ discontinuous - gaps in wall for whole cells to more (liver, spleen and bone marrow)

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24
Q

Features of post-capillary venuoles?

A

More permeable than capillaries with lower pressure:

Tissue fluid drains back into vessels.

Site of emigration of leukocytes from blood

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25
Q

What are veins?

A

Capacitance vessels - distend to cope with changes to CO

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26
Q

Features of veins?

A

Thin and distend able walls = reservoir

Low pressure with thin smooth muscle

Valves to prevent retrograde flow. Work with muscles in legs to propel blood to heart

Large diameters

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27
Q

What are venue comitantes?

A

2 paired deep veins accompanying smaller arteries wrapped in a vascular sheath.

The pulsing artery helps venous return.

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28
Q

What is ventricular systole pressure?

A

120mmHg

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29
Q

What is ventricular diastole pressure?

A

80mmHg

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30
Q

What happens to BP as you go further from the heart?

A

Decreases with distance

Fluctuating in sync with ventricular systole & diastole > drops are capillaries > constant low at veins

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31
Q

Describe cardiac muscle?

A

Discrete cells connected electrically with intercalated discs.

Involuntary, striated and myogenic branching muscle

1/2 central nuclei per cell

Diad (t-tubules) occurs at Z-line

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32
Q

How long is systole?

A

280 ms

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33
Q

How long is diastole?

A

700ms

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34
Q

What is pulse pressure?

A

Systolic = Diastolic pressure = 40mmHg

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35
Q

What is Mean Arterial Blood Pressure?

A

Diastole + 1/3 systolic pressure

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36
Q

What are the names of heart valves?

A

Atrioventricular:
Tricuspid (RH)
Bicuspid (LH)

Outflow:
Pulmonary
Aortic

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37
Q

What is the SAN?

A

Sino-atrial node in the RA

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38
Q

How long is the delay at the AVN?

A

120ms

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39
Q

What is the AVN?

A

Atrio-ventricular node

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40
Q

What direction do the ventricles contract?

A

Endocardium to epicardium, from the apex up

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41
Q

What is the tissue in the septum?

A

Bundle of His

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42
Q

How doe the ventricular muscles contract?

A

figure of 8 contraction movement for most effective ejection

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43
Q

What are the important stages of cardiac contraction?

A

Rapid filling phase
Isovolumetric contraction
Rapid ejection phase
Isovolumetric relaxation

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44
Q

What is the 1st heart sound - S1?

A

Atrioventricular valves closing (beginning of systole)

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45
Q

What is the 2nd heart sound - S2?

A

Outflow valves closing (end of systole)

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46
Q

What creates murmurs?

A

Turbulent flow through valves:

narrowed valve or back flow through incompetent valve

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47
Q

What is the most common congenital heart defect?

A

Ventricular septal defect

VSD

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48
Q

Which Congenital Heart defects are acyanotic?

A 
Atrial septal defect
Patent Foramen Ovale
Ventricular septal defect
Patent Ductus Arteriosus
Coarctation of Aorta
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49
Q

Which Congenital heart defects are cyanotic?

A

Tetralogy of Fallot
Tricuspid atresia
Transposition of the great arteries
Hypoplastic left heart

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50
Q

Why are Patent Foramen Ovale not a true ASD?

A

Clinically silent as high LA pressure functionally closes flap valve

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51
Q

What is dangerous about PFOs?

A

Route for venous embolism to reach systemic circ. if RA pressure transiently > LA pressure

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52
Q

Most common site for VSD?

A

membranous portion of septum

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53
Q

What is the ductus arteriosus?

A

In foetuses, shunt from pulmonary art. to aorta due to underdeveloped lungs. Shunt closes after birth.

Patent DA leads to blood flowing from aorta –> pulmonary artery creating a mechanical murmer

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54
Q

What is the consequence of PDA?

A

Increase volume cause vascular remodelling of pulm. circa > increase in resistance > increase pressure > revere direction from pulm. to aorta = Eisenmenger Syndrome

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55
Q

What is coarctaction of the aorta?

A

narrowing of the lumen at the ligament arteriosum (former DA) increasing resistance leading to Left Ventricular Hypertrophy.

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56
Q

In CoA, why are some body regions under-perfused?

A

Coarctation occurs after B,C,S arteries branching, hence not compromised. But the rest of the flow is compromised - weak and delayed femoral pulses, upper limb hypertension.

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57
Q

What are the 4 lesions in Tetralogy of Fallot?

A

VSD
Overriding Aorta
Pulmonary stenosis
Right ventricular hypertrophy

Pulmonary stenosis > RVH due to resistance > increased RV pressure > blood shunt R–>L due to VSD & Overriding Aorta > mixture of deoxy & oxy blood in systemic circ > cyanosis

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58
Q

What is tricuspid atresia?

A

Lack of development hence X inlet into RV.

Need to have an ASD or PFO (shunting RA –> LA) and VSD (shunting LV –> RV for oxygenation)

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59
Q

What is Transposition of the Great Arteries?

A

Incompatible with life, unless there is a shunt - Ductus Arteriosus or ASD

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60
Q

What is Hypoplastic Left Heart?

A

Underdeveloped LV and Ascending aorta

Requires a PFO or ASD, and a PDA

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61
Q

Where is the Sympathetic Nervous System outflow?

A

Thoraco-lumbar

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62
Q

Sympathetic pre & post-ganglionic lengths?

A

Short pre

Long post

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63
Q

What type of neurones are sympathetic pre-gang?

A

Cholinergic releasing nicotinic Ach

64
Q

What type of neurones are sympathetic post-gang?

A

Noradrenergic releasing NA to either Alpha 1/2 or Beta 1/3

65
Q

Where is the parasympathetic Nervous System outflow?

A

Cranio-sacral

66
Q

Parasympathetic pre & post-ganglionic lengths?

A

Long pre

Short post

67
Q

What type of neurones are parasympathetic pre-gang?

A

Nicotinic cholinergic

68
Q

What type of neurones are parasympathetic post-gang?

A

muscarinic cholinergic –> G-protein coupled receptors

69
Q

What are the receptors of the heart?

A

Symp = B1

Parasym = M2

70
Q

What are the receptors of the airways?

A

Symp = B2

Parasym = M3

71
Q

What are the receptors of the pupils?

A

Symp = A1 –> dilation

Parasym = M3 –> constriction

72
Q

What are the receptors of the sweat glands?

A

Symp:
Localised secretion = A1
General secretion = M3

No parasymp.

73
Q

What signals go to beta-adrenoreceptors?

A

Adrenaline or Noradrenaline

74
Q

What protein and effector occurs at Beta-adrenoceptors?

A

Gs –> stim. adenylyl cyclase

75
Q

What signals go to Muscarinic receptors?

A

muscarinic Acetylecholine

76
Q

What protein and effector occurs at M3 receptors?

A

Gq –> stim. phospolipase C > smooth muscle contraction

77
Q

What protein and effector occurs at M2 receptors?

A

Gi –> inhibits adenylyl cyclase

78
Q

Describe the relationship between sympathetic NS and blood vessels?

A

Innervates smooth muscle in the wall of vessels and cause vasoconstriction via A1 receptors.

Constant sympathetic stimulation = vasomotor tone. Less symp. stim = vasodilatation,
More symp. stim = vasoconstriction

79
Q

What is the vasomotor tone of skin?

A

High

arterioles, pre-capillary sphincters and artery-venous anastomoses are shut

80
Q

What is the vasomotor tone of skeletal muscle?

A

High at rest

Antagonised by vasodilator metabolites in exercise

81
Q

How is distribution of blood in the CVS controlled?

A

Balance between sympathetic vasoconstriction tone and vasodilator metabolites

82
Q

Where do the symp & parasymp. fibres innervate in the heart?

A

Both to SA and AV nodes

Symp also to ventricular myocytes to increase FoC –> increase CO

83
Q

What controls the symp/parasym stimulation?

A

Baroreceptors in the arch of the aorta & carotid sinuses –> sending signals via hypoglossal nerve

84
Q

What is HR without parasymp?

A

100BPM

85
Q

How does the heart increase in rate?

A

1) reduce parasymp stim

2) increase symp. swim

86
Q

What are all the signals that act of the heart?

A

Increase rate & FoC = Noradrenaline from post-gang sympathetic fibres & Adrenaline from Adrenal Glands acting on B1 receptors

Decrease HR & FoC = mAch from parasym. fibres acting on M2 receptors

87
Q

Define FLOW

A

volume of fluid passing a given point per unit of time

Flow = Volume/Time

88
Q

Define VELOCITY

A

rate of movement of fluid particles along a tube

Velocity = Distance/Time

89
Q

What is LAMINAR FLOW?

A

Gradient of velocity, highest in the centre and stationary at the edge.
Most blood vessels have laminar flow

90
Q

What is TURBULENT FLOW?

A

Increased mean velocity > gradient breaks down ? layers of fluid move over each other > tumble over each other > increased flow resistance

91
Q

What is VISCOSITY?

A

The extent that fluid layers slide over each other.

High viscosity = more overlap and slow central layer flow

Low viscosity = less overlap, fast central layer flow

92
Q

Relationship between diameter and flow?

A

The wider the tube, the faster the central layers flow. Mean velocity = proportional to cross sectional area of tube

93
Q

What is resistance and it’s relationship to flow?

A

Pressure = Flow X Resistance

R increases with viscosity (thicker blood)

R decreases with greater diameter - harder to flow in small vessels

94
Q

Vessels in series affect on resistance?

A

Add together

95
Q

Vessels in parallel affect on resistance?

A

Decreased, as more that 1 path for flow

96
Q

If the heart pumps more blood, but resistance is the same, what happens to pressure?

A

PRESSURE RISES

97
Q

Describe how the distensibility of blood vessels affect flow and pressure?

A

vessel pressure exerts a transmural pressure causing the vessel to stretch.

Stretch > increased diameter > reduced resistance > increases flow.

Hence with increased pressure > stretch > increased flow

Low pressure > walls collapse > no flow

98
Q

What affects systolic pressure?

A

FoC
TPR
Compliance of arteries

99
Q

What affects diastolic pressure?

A

Systolic pressure

TPR

100
Q

What is TPR?

A

Total Peripheral Resistance is the sum of the resistance of all the peripheral vasculature in the systemic circ.

101
Q

What is the pulse wave?

A

The contraction of the ventricles propagated along the arteries

102
Q

List vasodilator metabolites:

A

H+, adenosine and K+

103
Q

What doe vasodilator metabolites do?

A

Relax the local smooth muscle > decrease resistance > increase flow

104
Q

Whats reactive hyperaemia?

A

Cut off circ. to limb > cells continue metabolising > produce vasodilators which are not removed > circulation restored > dilated arterioles > max. blood flow

105
Q

What s auto-regulation?

A

Organs automatically take the blood flow supply they require matching their demand, as long as arterial pressure is within a certain range

106
Q

What is venous return?

A

Venous return = rate of flow back to the heart - determines CO

107
Q

What is Central Venous Pressure?

A

Central Venous Pressure = pressure of the great veins supplying heart

108
Q

what is stroke volume?

A

The differences between end diastolic & end systolic volume

109
Q

Describe the relationship between venous pressure and ventricle filling?

A

The amount ventricles fill is determined by the venous pressure. Ventricle walls stretch to equal the venous pressure.

Higher VP = more heart filling in diastole = increased end diastolic volume.

End diastolic stretch of myocardium = Pre-load - determined by venous pressure

110
Q

What is after load?

A

the pressure needed to expel blood through arteries

111
Q

What is the Starling’s curve?

A

The more the heart stretched, the harder it contracts giving a bigger stroke volume - shown by starling’s curve.

If the heart is over-filled, the myocardium is overstretched.

Gradient = contractility of the heart, not FoC.

112
Q

What is postural hypotension?

A

Failure of baroreceptor reflex.

Standing - blood pools in legs > reduced VP > reduced CO > reduced AP = both low VP & AP –> solved by increased HR (detected by baroreceptors) and increased TPR

113
Q

When do coronary arteries fill with blood?

A

During diastole, via the left & right coronary sinuses.

Cardiac muscle = high capillary density for O2 delivery & constant NO production for keep basal flow high

114
Q

What is angina?

A

Narrowest coronary artery.
Stress & cold causes sympathetic coronary vasocontriction, as well as extra O2 demand, as well as shorter diastole so reduced blood delivery

115
Q

What is syncope?

A

Loss of consciousness

116
Q

what is the cushion’s reflex?

A

impaired blood flow to vasomotor control regions of brainstem (due to haemorrhage or tumour) leads to increased peripheral vasomotor activity increased art. BP > maintaining cerebral blood flow

117
Q

How is blood supply to brain controlled/maintained?

A

Many anastomoses, myogenic auto-regulation (vasoconstriction with increased BP, vice versa), metabolic regulation - panic hyper vent > hypercapnia > cerebral vasoconstriction > dizziness & fainting
Areas with increased neural activity have increased blood flow as adenosine is a powerful vasodilator

118
Q

Temperature regulation in skin?

A

Blood flows via atria-venous anastomoses to remove heat

119
Q

What are non-modifiable risk factors for coronary atheroma?

A

Age, male and family history

120
Q

Modifiable risk factors for coronary atheroma?

A

Hyperlipideamia, smoking, hypertension and diabetes

121
Q

What is Ischeamic Chest Pain?

A

central, retrosternal/left-sided pain, radiating down left shoulder, arm, neck or jaw

122
Q

What is ischeamic chest pain described as?

A

heavy, crushing, tightening pain

123
Q

Describe stable angina?

A

Atheromatous plaques with thin necrotic centre & thick fibrous cap that occlude coronary lumen

Isheamic chest pain on exertion - physically / emotionally

124
Q

At what level of occlusion does angina occur?

A

> 70%

125
Q

Stable angina Tx?

A

Acute: Sub-lingual nitrate spray
Preventative: B-blockers, Ca channel blockers, oral nitrates, aspirin, statins, ACE inhibitors

126
Q

What is unstable angina?

A

Progression of the formation of atheromatous plaque with increase occlusion. Thin fibrotic cap and thick necrotic centre.

127
Q

Main characteristic of unstable angina?

A

ICP at rest - severe pain

128
Q

What is a MI?

A

Myocardial Infarction - complete occlusion of coronary artery > ischeamic death of myocardium.

129
Q

Cause of MI?

A
  • The thin fibrous cap has ruptured leading exposure of blood to thombogenic necrotic core causing a platelets blot that has occluded the vessel.
  • embolism broken off
130
Q

Presentation of MI?

A

very severe pain, not relived by rest or nitrate spray, breathless, fainting (loss of LV function), feeling of impending doom, sweating, pallor, N/V

131
Q

What is a NSTEMI?

A

Non-ST elevating MI, infarct not full thickness of myocardium

132
Q

What is a STEMI?

A

ST elevated MI, infarct = full thickness of myocardium

133
Q

What are the investigations for angina?

A

Risk factors - corneal Arcus, elevated BP
LV dystfunction
Normal resting ECG (pathological Q wave)
Exercise stress test

134
Q

What is a pathological Q wave indicative of?

A

Previous MI

135
Q

What is the exercise stress test?

A

Graded exercise connected to ECG. Increase speed until target HR reached/ chest pain / ECG changes

+ve test = ST depression greater than 1mm

136
Q

What is Acute Coronary Syndrome?

A

Group of symptoms connected to obstruction of coronary arteries - caused by unstable angina, NSTEMI & STEMI

137
Q

What are the biomarkers in MIs?

A

Troponin I & T,

Creatine kinase can also be used after 24hours

138
Q

Do you know which ECG lead corresponds to an MI in which coronary artery?

A

Yes - great!

No - better go learn it!

139
Q

MI Tx?

A

Anti-thrombotics: aspirin, heparin
Surgery:
Percutaneous Coronary Intervention PCI = angioplasty & stunting

Coronary Artery Bypass Graft (CABG) from radial art or saphenous vein

140
Q

What are causes of acute pericarditis?

A

Infection - viral, TB
Post-MI
Autoimmune
Ureamia

141
Q

Symptoms of acute pericarditis?

A

Central/left-sided chest pain
Sharp pain,
worse with inspiration

142
Q

What is Heart Failure?

A

Heart fails to maintain adequate circulation needed for the body, despite adequate filling pressure

143
Q

Cause of HF?

A

Hypertension
Dilated cardiomyopathy - alcohol, pre, drugs
Congenital heart defect
Arrhythmia

144
Q

Describe the classes of HF?

A

1 - asymptomatic

2 - slight limitations in activity, asymptomatic at rest

3 - marked limitations, asymptomatic at rest

4 - inability to do physical activity and symptoms at rest

145
Q

What is congestive heart failure?

A

Heart failure of both ventricles

Left heart failure > increased pulmonary pressure > right heart failure

146
Q

Signs of Left HF?

A

Fatigue, SOB, pulmonary oedema

147
Q

Sign of Right HF?

A 
Raised JVP
Peripheral oedema
Ascites
pitting oedema
Fatigue, SOB
Hepatospenomegaly
148
Q

Causes of RHF?

A

Often 2ndary to LHF
Pulmonary embolism
Pulmonary hypertension
Left–> right shunt

149
Q

HF Tx?

A

B-blockers,
ACE inhibitors
Nitrates > veno-dilators > reduced BP
Cardiac Glycosides > increase CO & FoC

150
Q

What is shock?

A

Inadequate distribution of blood to tissues resulting in generalised lack of oxygen to cells.

Either affecting CO or TPR

151
Q

What is cardiogenic shock?

A

Inability of heart to eject enough blood.

Caused by arrhythmias or ischeamic cardiac damage

152
Q

What is mechanical shock?

A

Restriction on filling of heart due to cardiac tamponade - pressure on outside of heart, or obstructed blood through lungs - PE

153
Q

What is hypovolameic shock?

A

Loss of circulating blood volume due to burns / haemorrhage - falling venous pressure = falling CO = falling AP

Tx = IV fluids

154
Q

What is distributive shock?

A

Uncontrolled fall in TPR due to dramatic fall in AP, Sepsis (circulating bacteria > endotoxin triggering vasodilation) - tachy, red and warm skin- or anaphylaxis (mast cells release histamine causing vasodilation. Tx = adrenaline to trigger A1 receptors –> vasoconstriction) which is associated with bronchoconstriction

155
Q

What types of shock reduce CO?

A

Hypovoleamic, mechanical or cardiogenic shock

156
Q

What type of shock leads to reduced TPR?

A

Septic or anaphylactic shock

157
Q

What are the effects of HF in the body?

A
  • Activation of RAAS due to underperfusion of kidneys > reduced GFR> activates cells to release renin > Angiotensin 2 > vasoconstriction & Aldosterone > Na & Water retention > increased blood volume
  • ADH release > increased water uptake

ESA 4 revision (4 decks)

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