CVS Flashcards
(652 cards)
1
Q
Diffusion resistance is dependent on 3 things, what are they?
A
Nature of the molecule, nature of the barrier, path length
2
Q
What will the concentration gradient between a capillary and tissue be dependent on?
A
The rate of substance use by the tissue
The rate of blood flow to the tissue through the capillary bed
3
Q
Normal cardiac output for a 70kg man at rest is:
A
5l.min-1
4
Q
State 2 tissues that need a constant level of blood flow.
A
Brain and kidneys
5
Q
What 3 things influence the exchange of substances between the capillaries and surrounding tissues?
A
Surface area (capillary density), diffusion resistance & concentration gradient
6
Q
What blood flow does the brain receive at rest and during exercise?
A
750ml.min-1 (0.75L.min-1) at both rest and exercise
7
Q
What is the blood flow of the heart at rest and during exercise?
A
300ml.min-1 (0.3L.min-1) at rest.
Increases to 1200ml.min-1 (1.2L.min-1) during exercise.
8
Q
What is the normal blood flow to the gut? When does this increase, and by how much?
A
Normally, 1400ml.min-1 (1.4L.min-1).
This increases following a large meal for absorption of nutrients.
Increases up to 2400ml.in-1 (2.4L.min-1)
9
Q
Which tissue can increase its blood flow by the most?
Give values.
A
Skeletal muscle - by 16 times.
At rest only 1L.min-1. Increases up to 16L.min-1 during exercise.
10
Q
Define resistance in terms of blood vessels.
A
Reducing the ease with which some vessels are perfused in order to re-direct blood to areas that are more difficult to perfuse. (E.g. To the brain against gravity)
11
Q
Define capacitance in terms of vessels.
A
The ability of the veins to provide a temporary and variable store of blood so that the rate of blood return to the heart and total flow in the system can be varied.
12
Q
Describe the distribution of blood volume in the circulation at any point in time.
A
67% of blood is in the capacitance vessels (veins).
17% within the heart and lungs.
11% within the arteries and arterioles.
5% within the capillaries.
13
Q
In which area of the mediastinum is the heart situated?
A
Inferior, middle mediastinum
14
Q
What landmark separates the inferior mediastinum from the superior?
A
Sternal angle (angle of Louis / manibriosternal joint)
15
Q
As well as the heart, what else is found in the middle mediastinum?
A
Great vessels (aorta, pulmonary trunk, superior vena cava, pulmonary veins), nerve (e.g. Phrenic), trachea bifurcation and lymph nodes.
16
Q
What is found anterior (anterior mediastinum) and posterior (posterior mediastinum) to the heart?
A
Anterior - very little - some fatty tissue and thymus gland in children.
Posterior - oesophagus, aorta and thoracic duct
17
Q
Which ribs does the heart lie between?
A
Ribs 1 to 6
18
Q
What is found at the 4 borders of the heart?
A
Superior border = superior vena cava, aorta and pulmonary arteries.
Left border = mostly left ventricle. Some pulmonary artery and the auricle of the left atrium.
Inferior border = right ventricle.
Right border = right atrium
19
Q
What is the function of the pericardium?
A
Limits the hearts motion in the mediastinum, prevents excessive dilation on volume overload, lubricates to prevent friction during pumping & protects the heart from infections spreading from surrounding organs.
20
Q
What are the 4 layers of pericardium From superficial to deep?
A
- Fibrous Pericardium
- Parietal serous pericardium
- Pericardial cavity
- Visceral layer of serous pericardium
21
Q
Phrenic nerve is derived from spinal nerves…
A
C3, C4, C5
22
Q
Do the phrenic nerves pass anteriorly or posteriorly to the lungs?
What about the lung roots?
Which phrenic nerve passes more posteriorly than the other?
A
They both pass posteriorly to the lungs.
Both pass anteriorly to the roots of the lungs
Right phrenic nerve passes more posteriorly (across the right atrium) compared to the left (left ventricle).
23
Q
Within the heart and related structures, what does the phrenic nerve supply?
A
The fibrous pericardium and the parietal layer of the visceral pericardium.
24
Q
What is pericarditis?
A
inflammation of the pericardium
25
Give 3 causes of pericarditis.
Infection, inflammatory conditions (e.g. RA or SLE) or metabolic conditions (e.g. Renal failure, hypothyroidism)
26
What is the main problem associated with pericarditis?
Thickening of the fibrous pericardium can cause constriction of the heart and limit filling during diastole.
27
What is pericardial effusion?
An abnormal amount of fluid between the heart and pericardium (in the pericardial space).
28
Give 3 causes of pericardial effusion.
1. Pericarditis
2. Infection
3. Trauma (e.g. Stabbing) - post-operative
29
What is the main complication of pericardial effusion?
Cardiac tamponade - fluid constricts the heart leading to reduced ventricular filling during diastole and therefore haemodynamic compromise.
30
How many pulmonary arteries normally enter the heart?
4
31
Where is the transverse pericardial sinus found?
Behind the pulmonary trunk and ascending aorta when the heart is in situ
32
Where is the oblique pericardial sinus found?
On the posterior surface of the heart - primarily behind left atrium
33
Where do the 2 coronary arteries branch from the aorta?
At the left and right aortic sinuses - buldges just above the aortic valve at the origin of the ascending aorta
34
Name the 2 branches of the left coronary artery, and approximately where they are located.
1. Left circumflex artery - around the left superior heart to the posterior surface with the marginal branch branching off to supply the left border.
2. Left anterior descending artery - down the anterior surface of the heart (approximately between the two ventricles)
35
Name the 3 branches of the right coronary artery and where they are approximately located.
1. Posterior descending artery - down the posterior surface of the heart.
2. Right marginal artery - along the inferior border of the anterior heart.
3. Sinuatrial nodal branch - around the top of the heart to the posterior surface and to right atrium.
36
Name the 3 major branches of the cardiac veins.
| What do they drain into?
Small cardiac vein - inferior, anterior surface (RHS).
Middle cardiac vein - posterior surface (LHS).
Great cardiac vein - anterior surface and wrap around inferior surface (LHS).
Draining into the coronary sinus.
37
What are the 3 unpaired arteries branching off the abdominal aorta?
1. Celiac trunk
2. Superior mesenteric artery
3. Inferior mesenteric artery
38
Which arteries are major elastic arteries?
Large arteries - aorta, pulmonary arteries, brachiocephalic, left common carotid, left subclavian and common iliac arteries.
39
What is meant by elastic conducting arteries being 'pressure reservoirs' or 'auxiliary pumps'?
Walls of the arteries stretch during systole as left ventricle contracts.
Walls record during diastole to maintain blood pressure.
40
Under the microscope, how are muscular distributing arteries clearly defined?
Well developed internal elastic lamina.
41
What is an 'end artery'?
A terminal artery supplying all or most of the blood to a body part without collateral circulation.
42
Name 3 end arteries.
Coronary, splenic and renal arteries
43
Name 2 absolute end arteries.
Central artery to retina, labyrinthine artery to the internal ear.
44
What are meta-arterioles?
Those arterioles that supply blood to the capillaries.
45
What is the process of 'bridging' in reference to the coronary circulation?
Muscle grows around one of the larger coronary arteries. The artery becomes compressed during systole
46
How wide is a normal capillary?
7-10um in diameter.
47
What are the 3 types of capillary?
Continuous, fenestrated and discontinuous
48
Post-capillary venules are more permeable than capillaries, true or false?
True
49
What size are post-capillary venules?
10-30um
50
Where do leukocytes primarily migrate out of the blood from?
The post-capillary venules
51
What are venae comitantes?
| Give 2 examples.
Deep veins that in certain anatomical positions accompany one of the smaller arteries on either side.
The artery promotes venous return and also warms the venous blood returning to the heart.
Ulnar venae comitantes and tibial venae comitantes.
52
Which type of artery has a discontinuous internal elastic lamina?
Elastic arteries
53
What would you find in the tunica media of elastic arteries?
40 to 70 layers of fenestrated elastic membranes (stained black), smooth muscle cells (red), collagen (blue).
Thin external elastic lamina.
54
What are vasa vasorum? Where would you find these?
Vessels supplying vessels - in the tunica adventitia of large arteries.
55
What would you find in the tunica media of muscular arteries?
40 layers of circularly arranged smooth muscle cells. Connected by gap junctions.
Prominent external elastic laminar.
56
What is the diameter of arterioles?
57
How many layers of smooth muscle might you find in the tunica media of arterioles?
1 to 3 layers. Sometimes a single SM cell in small arterioles.
58
Which vessel type has no external elastic lamina and very little tunica adventitia?
Arterioles.
59
Which vessel type has pre-capillary sphincters?
Meta-arterioles
60
Describe the structure and function of pre-capillary sphincters.
A single smooth muscle cell encircling the endothelium or a capillary. Controls flow into the capillary bed.
61
What is the structure of continuous capillaries?
| Where are they found?
A continuous endothelial layer with cell joined by tight junctions.
Muscle, nervous and connective tissue.
62
Describe the structure of fenestrated capillaries.
| Where are they found?
Pored exit across the endothelium.
| Found in the gut, endocrine glands and renal glomerulus.
63
Describe the structure of discontinuous capillaries.
| Where are they found?
Large gaps exist in the walls with an incomplete basement membrane. Allowing the movement of whole cells between blood and tissue.
Found in the liver, spleen and bone marrow.
64
Describe the structure of a venous valve.
| When do they appear?
Extensions of the tunica intima into the lumen.
| Appear in larger venules (>1mm).
65
What is the diameter of large veins?
>1cm
66
Describe the structure of veins.
Thicker tunica intima which merges with tunica media.
Tunica media is thin with only a few layers of smooth muscle (except in superficial veins of the leg).
Well developed tunica adventitia with vasa vasorum.
67
What is the total cross section of the aorta?
2.5cm^2
68
What is the total cross sectional area of the capillaries?
4500cm^2
69
Which cells produce the elastin, collagen and ECM of the tunica media?
Smooth muscle cells
70
Describe aortic dissection.
Blood breaks through the tunica intima of the aorta. It enters the regions between the elastic Lamellae of the tunica media so that layers of the tunica media begin to separate and weaken the aortic wall.
71
The lymphatic vessels junction with the venous vessels where?
Internal jugular and subclavian veins
72
Name 3 tissues that are not supplied by blood vessels.
Cartilage, cornea and epithelium
73
Define 'stroke volume'
The volume of blood ejected from the heart with each cycle. Or EDV - ESV.
74
Stroke volume is usually about...
70ml
75
The equation for cardiac output is:
HR X SV (70 X 70) = 4.9L/min
76
What prevents inversion of atrioventricular valves?
They are attached to the papillary muscles of the ventricles via chordae tendinae. These muscles contract during systole pulled the chordae tendinae taught and preventing inversion of atrioventricular valves and back flow of blood.
77
How long is electrical activity delayed at the AV node approximately?
120ms
78
How many of the cardiac cycle steps are systole and how many are diastole?
3 systole, 4 diastole
79
What are the 7 stages of the cardiac cycle starting with atrial contraction?
1. Atrial contraction.
2. Isovolumetric contraction.
3. Rapid ejection.
4. Reduced ejection.
5. Isovolumetric relaxation.
6. Rapid filling.
7. Reduced filling.
80
How much of ventricular filling does atrial contraction account for?
10-20% only
81
At what stage in the cardiac cycle is EDV reached?
At the end of atrial contraction
82
What is a normal EDV value?
120ml
83
At what stage in the cardiac cycle does the mitral valve close?
At the end of atrial contraction / beginning of isovolumetric contraction of the ventricles.
84
What is isovolumetric contraction?
Contraction of the ventricular walls but will all valves closed so there is no change in the volume of blood contained within them. Causes a huge increase in intraventricular pressure.
85
At what stage of the cardiac cycle does the aortic valve open?
Beginning of rapid ejection / end of isovolumetric contraction.
86
What is happening to the atria while there is reduced ejection from the ventricles?
They are increasing in pressure as blood flows passively into them.
87
What causes the aortic valve to close?
A very brief back flow of blood as the ventricle becomes lower in pressure than the aorta at the beginning on isovolumetric contraction (end of reduced ejection).
88
What is the dicrotic notch?
A very brief increase in aortic pressure as the aortic valve closes.
89
When is ESV reached?
At the end of reduced ejection / beginning of isovolumetric relaxation.
90
What is meant by isoelectric relaxation?
Relaxation of they ventricular walls but since all valves are closed, there is no change in blood volume inside the ventricles. This leads to a huge decline in ventricular pressure.
91
When does the mitral valve open?
When the pressure in the ventricles falls below that of the atria at the end of isovolumetric relaxation.
92
Is rapid filling a passive or active process?
Passive - no contraction involved.
93
What is another word for the cardiac cycle stage of reduced filling?
How full are the ventricles at the end of this stage?
Diastasis.
| Should be 80-90% full
94
Which stages of the cardiac cycle does systole comprise of?
Isovolumetric contraction.
Rapid ejection.
Reduced ejection.
95
How long is the entire cardiac cycle on average?
0.9s
96
How long does systole last?
| What proportion of the cardiac cycle is this?
0. 35s
| 0. 35 / 0.9 = 0.38 = about 1/3
97
How long does diastole averagely last?
| What proportion of the cardiac cycle is this?
0. 55s
| 0. 55 / 0.9 = 0.61 = 2/3
98
What are the changes in jugular venous pressure a reflection of?
The changes in atrial pressure during the cardiac cycle.
99
What do the following parts of the jugular venous pressure graph correspond to: A wave, C wave, X descent, V wave, Y descent.
```
A wave = atrial contraction
C wave = tricuspid valve closure.
X descent = pulling of atrial base downwards during ventricular contraction.
V wave = atrial filling
Y descent = rapid ventricular filling
```
100
Where do you listen for the aortic valve?
2nd intercostal space, right sternal border
101
Where do you listen for the pulmonary valve?
2nd intercostal space, left sternal border.
102
Where do you listen for the tricuspid valve?
4th intercostal space, left sternal border.
103
Where do you listen for the mitral valve?
5th intercostal space of the mid-clavicular line (at the apex).
104
What is Erb's point?
| Where is it?
The point where S2 is best auscultated.
| 3rd intercostal space on left sternal border.
105
What is the 'lub' heart sound?
S1 = atrioventricular valves closing
106
What is the 'Dub' heart sound?
S2 = semi-lunar valves closing
107
When might S3 heart sound be heard? Is this normal?
Early diastole due to deceleration of blood from left atrium to ventricle.
Normal in children, pathological in adults (congestive heart failure).
108
When might S4 be heard? What causes it?
Late diastole during atrial contraction.
| Associated with stiff, low compliant ventricles.
109
What are the 5 broad categories that murmurs can be divided into?
1. Ejection systolic.
2. Pan systolic.
3. Early diastolic.
4. Mid-diastolic.
5. Systolic & diastolic = continuous.
110
What type of murmur (when does it occur) would aortic valve stenosis cause?
Ejection systolic - occurring at the beginning of systole.
| Between S1 and S2.
111
When is an atrial septal defect murmur heard?
Ejection systolic - when atria are filling during early systole.
112
What 2 causes of murmur are pansystolic?
```
Mitral regurgitation (or tricuspid).
Ventricular septal defect.
```
113
What is the main cause of an early diastolic murmur?
Semi-lunar valve regurgitation (aortic or pulmonary valves).
114
When would atrioventricular valve (mitral and tricuspid) stenosis be heard?
Mid-diastolic - when atria contract
115
Give 2 causes of a murmur that is heard throughout both diastole and systole.
Pericarditis and patent ductus arteriosus
116
Why can S2 sometimes be heard physiologically as split?
During inspiration it can be split as the lower intrathoracic pressure aids venous return and results in pulmonary valve closing slightly after the aortic.
117
On a radiograph, when can cardiomegaly be diagnosed?
When the cardio thoracic ratio is >50%. (Heart takes up more than 50% of thorax).
118
Name 5 features of the right atrium.
```
Superior and inferior vena cava opening.
Fossa ovalis.
Atrioventricular orifice.
Sinus vanarum.
Orifice of the coronary sinus.
```
119
What is the name for the muscular ridges found in the ventricles?
Trabeculae carneae
120
What is the conus arteriosus / infundibulum?
The anterior superior part of the right ventricle that forms the entrance to the pulmonary trunk and is conical in shape.
121
Which cardiac veins drain directly into the right atrium, rather than the coronary sinus?
The anterior cardiac veins on the anterior, right heart
122
What is the crista terminalis?
The boundary between the rough and smoothed walled parts of the right atrium. Divides the 2 different embryological origins of the atrium (primitive atrium and sinus venosus).
123
Where are the pectinate muscles found?
On the surface of the rough walled part of the atrium.
124
How many papillary muscles are in the left and right ventricles?
3 in the right, 2 in the left
125
What is the moderator band?
A band of tissue in the right ventricle running from the inter ventricular septum to the papillary muscles. Carries part of the right bundle branch of the conduction system to allow co-ordinated contraction of papillary muscles.
126
What is the aortic vestibule?
Smooth walled, Outflow region of the left ventricle derived from the bulbus cordis.
127
Which heart valve is the odd one out? Why?
Mitral valve - only has 2 cusps rather than 3.
128
What embryological tissue does the cardiogenic field form from?
Splanchonopleuric mesoderm
129
What brings the two endocardial tubes of the cardiogenic region together at the midline?
Lateral folding of the embryo
130
What initially brings the fused endocardial tube into the thoracic region?
Cephalocaudal folding of the embryo
131
What are the 6 regions of the developing heart tube In order from top to bottom?
Aortic roots, truncus arteriosus, bulbus cordis, primitive ventricle, primitive atrium, sinus venosus.
132
What causes the heart tube to fold?
Growth into a fixed space - fixed by the pericardial sac. And differential growth of the different regions.
133
During looping of the heart tube, in what direction does the cephalic / cranial end fold?
Inferiorly / caudally, anteriorly / ventrally & to the right (VCR)
134
During looping of the heart tube, in what direction does the caudal end fold?
Superiorly, posteriorly / dorsally and to the left
135
What does the left sinus horn of the sinus venosus form?
The coronary sinus
136
Describe the formation of the vena cavae from the sinus venosus.
Sinus venosus divided into right and left sinus horns. Venous system remodels so that all systemic blood drains into right sinus horn via the superior and inferior vena cava. Left sinus horn ceases to grow. The right sinus horn is absorbed by the enlarged right atrium.
137
Describe the formation of the pulmonary veins and left atrium.
Primitive atrium sprouts a pulmonary vein which bifurcates and bifurcates again forming 4 branches. As the left atrium grows it absorbs the first 2 sets of branches into its posterior wall. Means that most of the LA wall comes from the pulmonary veins and only a small part from the primitive atrium which is displaced left.
138
The ductus venosus does what?
Shunts blood from the umbilical vein into the IVC past the liver.
139
What type of blood (oxygenated or deoxygenated) does the superior vena cava contain during embryology?
Deoxygenated.
140
What is the role of the ductus arteriosus?
Shunts deoxygenated blood from the pulmonary trunk to the aorta from high to low pressure in order to bypass the non-functioning lungs.
141
What causes closure of the ductus arteriosus at birth?
Increased oxygen saturation of blood causes muscular contraction in ductus arteriosus walls.
Later undergoes fibrosis to anatomically close.
142
Where is the ligamentum venosum found? What is it a remnant of?
On the posterior liver. A remnant of the ductus venosus.
143
What is the remnant of the umbilical vein?
Ligamentum teres
144
How many aortic arches are there?
5 - 1, 2, 3, 4 & 6
145
What do the two 4th aortic arches form on the left and right hand sides?
Right - proximal right subclavian artery.
| Left - arch of the aorta
146
What do the two 6th aortic arches form on the left and right hand sides?
Right - right pulmonary artery
| Left - left pulmonary artery and ductus arteriosus
147
Where is the recurrent laryngeal nerve found on the left and right hand sides?
Right - hooked around right subclavian artery level T1-T2.
| Left - hooked around ductus arteriosus level T4-T5.
148
Put the following into order: ostium secundum, foramen ovale, septum primum, ostium primum, septum secundum.
Septum primum, ostium primum, ostium secundum, septum secundum, foramen ovale.
149
What is the primary interventricular foramen?
The small gap left by the muscular portion of the interventricular septum between itself and the endocardial cushions. Will be filled in by the membraneous portion.
150
What is the conotruncal septum?
The septum that separates the outflow tract into aorta and pulmonary trunk.
151
Why are the aorta and pulmonary trunk twisted around one another?
The bulbar ridges that form on opposite wall in the inferior truncus arteriosus grow towards the midline separating the outflow tract into left and right sides. This septation proceeds superiorly and inferiorly and as it does so, it twists.
152
What 3 things does the bulbus cordis form?
```
Trabeculared RV (proximal 1/3).
Outflow tract (conus cordis portion).
Roots and proximal aorta & pulmonary trunk (truncus arteriosus portion).
```
153
What is the normal oxygen saturation of arteries?
Close to 100%
154
What is the normal oxygen saturation of the veins?
About 67%
155
What are the 3 main causes of congenital heart defects?
Genetic, environmental (e.g. Teratogenicity) or maternal infection
156
What is the main risk of a left to right shunt?
Increased pulmonary arterial and venous pressure
157
In what 4 places can a left to right shunt occur?
Atrial, ventricular, atrioventricular (abnormal formation of ECs) or aorto-pulmonary / ductal.
158
Why are left to right shunts acyanotic?
There is no deoxygenated blood entering the systemic circulation so that the oxygen saturation of the systemic circulation remains the same. Oxygenated blood entering the deoxygenated circulation.
159
Give 3 possible complications of an atrial septal defect (ASD).
Pulmonary hypertension, right heart failure and atrial arrhythmia.
160
Explain why pulmonary hypertension is rare in ASD.
The difference in pressures between the left and right atria is minimal so that not so much blood flows from left to right, and the effect on the pulmonary pressure will be low.
161
What percentage of the population has a patent foramen ovale (PFO)?
Why are most Asymptomatic?
20%.
| Because the higher pressure in the left atrium causes functional closure of the flap valve.
162
What is a paradoxical embolism?
A transient increase in pressure in the right side of the heart causes opening of a patent foramen ovale and a pulmonary embolism to pass through to the systemic circulation.
163
Why is a VSD more severe than an ASD?
The difference in pressure between the two ventricles is greater, meaning there is a greater flow from left to right through the defect in a VSD. Increases pulmonary venous congestion.
164
What do patients with a VSD commonly present with? Why, and at what age?
Left heart failure due to the left heart working harder to maintain cardiac output in the lower volumes.
Usually present in infancy.
165
What is Eisenmenger syndrome?
When a patient has a left-to-right shunt (congenital heart defect) causing the pulmonary resistance and pressure to increase beyond that of the systemic circulation (due to remodelling). Means the shunt reverses direction, becoming right-to-left as right heart pressures increase. Patient becomes cyanotic.
166
What is coarctation of the aorta?
A narrowing of the aortic lumen in the region of the ligamentum arteriosus.
167
Give some complication of coarctation of the aorta.
Increased afterload leads to LV hypertrophy, weak femoral pulse, congestive heart failure, renal hypertension, volume overload, radial-radial delay.
168
What causes a congenital heart condition to be cyanotic?
When there is mixing of deoxygenated blood with the systemic, oxygenated, circulation so that this blood bypasses the lungs and lowers the oxygen saturation of the systemic circulation.
169
What is required for a cyanotic heart defect to occur?
A right to left shunt - requires a hole in the septum and distal obstruction to raise the pressure in the right side of the heart.
170
What causes tetralogy of fallot?
Abnormal development of the outflow portion of the inter-ventricular septum.
171
What are the 4 abnormalities in TOF?
1. VSD
2. Pulmonary stenosis
3. RV hypertrophy
4. Over-riding aorta
172
What is pulmonary atresia?
A lack of development of the tricuspid valve and right atrioventricular connection. Resulting in right to left shunt of entire venous return via an atrial septal defect.
173
Why do babies born with pulmonary atresia not die straight away?
Because the ductus arteriosus remains open for some time, allowing some flow to the lungs as the blood passes from the aorta to the pulmonary trunk.
May also have a ventricular septal defect which will also allow flow to the lungs.
174
Name 2 congenital heart defects that are neonatal emergencies.
Transposition of the great vessels.
| Hypo plastic left heart.
175
What is transposition of the great arteries?
The aorta is attached to the right ventricle while the pulmonary trunk is attached to the left ventricle giving 2 unconnected circuits (pulmonary and systemic).
176
How are patients with transposition of the great vessels kept alive prior to surgery?
By giving drugs to keep the ductus arteriosus open - so there is some connection between the two circuits.
Or by making or enlarging any existing septal defects to allow bloods to mix and some oxygenated blood to enter the systemic system.
177
What is hypoplastic left heart syndrome?
Hypoplasia (underdevelopment) of the left ventricle and ascending aorta
178
Explain how patients with a hypoplastic left heart survive.
They usually have an atrial septal defect (patent foramen ovale) through which all the blood flows from the left atrium to the right, and enters the pulmonary trunk. A patent ductus arteriosus allows blood to flow into the aorta and supplies the systemic circulation.
179
What happens to the blood in pulmonary atresia?
Same as tricuspid atresia. Right to left shunt (usually through PFO), blood enters aorta but can enter the pulmonary circulation through a PDA.
180
In 100,000 births, how common is ASD?
67 / 100,000
181
How common is a VSD in 100,000 births?
150-350 VSDs
182
How common is a PDA in 100,000 births?
20-40 PDAs
183
How common is TOF in 100,000 births?
50 / 100,000 births
184
How common is transposition of the great vessels in 100,000 births?
40 / 100,000 births
185
How common is hypoplastic left heart syndrome in 100,000 births?
16-36 in 100,000 births
186
Which of the following are cyanotic heart defects: ASD, VSD, PDA, transposition of the great vessels, Eisenmenger Syndrome, TOF, coarctation of the aorta, pulmonary stenosis, aortic stenosis, tricuspid atresia, hypoplastic left heart syndrome, pulmonary atresia.
```
Transposition of the great arteries.
Eisenmenger syndrome.
TOF
Tricuspid atresia
Hypoplastic left heart syndrome.
Pulmonary atresia.
```
187
How long is the average ventricular myocyte action potential?
300ms
188
What is the resting membrane potential of a ventricular myocyte?
-90mV
189
To what membrane potential does a ventricular myocyte depolarise during an action potential?
+30mV
190
What is the most negative membrane potential reached in a sino-atrial nodal cell?
-60mV
191
How long is a sino-atrial nodal action potential?
200ms
192
To what membrane potential does a sino-atrial nodal cell depolarise during an action potential?
+30mV
193
During stage 2 of a ventricular myocyte action potential, are potassium channels open or closed?
Open
194
Why is depolarisation by the funny current in sino-atrial nodal cells slow?
Because the funny channels are permeable to potassium as well as sodium
195
Why are sinoatrial-nodal action potentials known as slow response?
The upstroke of depolarisation is slightly less steep than a ventricular myocyte action potential
196
What is the main difference between cardiac and skeletal muscle in excitation-contraction coupling?
Cardiac muscle = calcium induced calcium release (L type calcium channels in membrane open due to membrane depolarisation, calcium binds calcium channels in SR and opens them).
Skeletal muscle = conformational change in SR calcium channels triggers their opening.
197
During cardiac muscle contraction, approximately what proportion of the calcium comes from the extracellular fluid and what proportion from the sarcoplasmic reticulum?
25% from ECF
| 75% from SR
198
What type of GPCR are alpha1 receptors alpha1 receptors on vascular smooth muscle?
Linked to Gq G-protein.
199
How many molecules of calcium bind calmodulin in smooth muscle contraction?
4
200
What is the action of activated calmodulin in smooth muscle contraction?
Binds to myosin-light-chain-kinase (MLCK) to activate it so that it can now use ATP hydrolysis to phosphorylate heads of myosin light chain to initiate cross bridge cycling.
201
What is the action of myosin light chain phosphatase (MLCP)?
| What inhibits it?
MLCP removes the phosphate group from myosin light chain to terminate cross-bridge cycling and contraction in smooth muscle cells.
Inhibited by phosphorylation by PKC (in turn activated by DAG).
202
What mechanism inhibits myosin light chain kinase?
Binding of adrenaline to beta adrenoceptors results in PKA activation which Phosphorylates MLCK and inhibits it. Leads to smooth muscle relaxation.
203
What 3 things within the CVS does the autonomic nervous system regulate?
Heart rate, force of contraction and peripheral resistance
204
Where are the parasympathetic ganglions in the heart?
On the epicardial surface or within the heart walls at the SA and AV nodes only.
205
How does the parasympathetic nervous system act to slow heart rate?
Via release of ACh onto M2 receptors - Gi G-proteins. Increase potassium conductance (hyperpolarisation) and decrease cAMP production (decreases slope of pacemaker potential).
Also slows AV conduction velocity.
206
What parts of the heart does the cardiac accelerator nerve innervate?
A sympathetic nerve = SA node, AV node and myocardium.
207
What type of sympathetic adrenoreceptor is mainly present in the heart?
Beta1
208
What type of GPCR are beta1 receptors?
Coupled to Gs G-protein
209
In what 3 ways does the sympathetic innervation of the heart increase inotropy?
1. Activation of PKA results in phosphorylation of calcium channels ( = increase calcium entry).
2. Increased calcium entry results in build up of calcium stores in the SR so that subsequent contractions are more forceful.
3. Increased sensitivity of contractile machinery to calcium
210
What is vasomotor tone?
The basal level of activity of the sympathetic nervous system at blood vessels - the basal level of vasoconstriction.
211
What is the most common adrenoceptors found at vessels?
Alpha1 adrenoceptors
212
In addition to alpha1 adrenoceptors in their vessels, which 3 tissue types also have beta2 adrenoceptors? And which single tissue has only beta2 adrenoceptors?
Liver, myocardium and skeletal muscle has both.
| Coronary vessels have beta2 only.
213
What is the advantage of some tissues having beta2 adrenoceptors present in their vessels as well as alpha1?
Increases their response to circulating adrenaline. Beta2 results in active vasodilation by activation of PKA to open potassium channels and inhibit MLCK.
214
What is the most important stimulus for vasodilation?
Local metabolites - adenosine, K+, H+ and CO2
215
How are changes to the state of the CVS communicated to the brain?
Via sensory neurones from baroreceptors (in glossopharyngeal and vagus nerves).
Afferent neurones from the atrial volume receptors.
216
Name 3 sympathomimetics (adrenoceptors agonists) and when they are used.
Adrenaline - in cardiac arrest and anaphylactic shock.
Dobutamine - in cardiogenic shock (beta1 agonist) = increased inotropy.
Salbutamol - in asthma (beta2 agonist) = relaxation of bronchial smooth muscle.
217
Name 3 adrenoceptors antagonists and their uses.
Prazosin- hypertension (alpha1 antagonist)
Propranolol - angina and hypertension (beta1 and beta2 antagonist) = slowed HR and reduced inotropy.
Atenolol - angina and hypertension (beta1 antagonist).
218
What receptor is pilocarpine an agonist for?
| What is used for?
M3 cholinergic receptor.
| Used for treatment of glaucoma - constricts pupil allowing aqueous humour to drain.
219
What type of drug is atropine?
| What is it used for?
A cholinergic receptor antagonist.
| Used to dilate pupils, increase HR and dilate bronchioles.
220
Which cranial nerves does the parasympathetic nervous system originate from?
CNIII, VII, XI and X
221
Which thoracolumbar spinal nerves does the sympathetic nervous system originate from?
T1 - L2
222
What are the 2 co-transmitters released with noradrenaline at post-ganglionic sympathetic neurones?
NPY and ATP
223
At what stage of the ventricular action potential are calcium channels inactivated?
Stage 4 - repolarisation after the plateau
224
What type of calcium channel is responsible for the plateau stage?
L-type calcium channel
225
Which potassium channel type is responsible for the initial repolarisation of the ventricular action potential?
Voltage gated Ito channel = transient outward
226
What potassium channel type is responsible for full repolarisation during the cardiac action potential?
Delayed rectifier channels (Ik)
227
Why is depolarisation of the pacemaker potential slow?
Because the If funny current channels are also permeable to potassium ions, as well as sodium.
228
At what membrane potential are the funny channels activated?
More negative than +50mV
229
What is the proper name for funny current channels? Therefore what activates them?
HCN - hyperpolarisation-activated, Cyclic Nucleotide-gated channels.
Activated by hyperpolarisation of the membrane and cAMP.
230
Why is the sink-atrial node usually responsible for setting the rhythm of the heart?
Because it has the fastest rhythm / steepest pacemaker potential.
231
If the SA node was removed, what would take over as the rhythm setter?
AV node
232
If both nodes were removed, what would take over as the rhythm setter?
The purkinje fibres
233
Cardiac myocytes are joined structurally by ..... And electrically by ..... These are both found at the .......
Structurally by desmosomes.
Electrically by connexins of gap junctions.
Both found at the intercalated disk.
234
The actin filaments of smooth muscle are cross linked at attached to.....
Attached to dense bodies
235
Define 'flow' in terms of vessels.
The volume of fluid passing a given point per unit time (ml/min)
236
An increased pressure gradient along a vessel will do what to flow?
Increase flow
237
If there is no change to the pressure gradient along a tube, an increase in resistance will do what to flow?
Decrease flow
238
Define 'velocity' in the CVS.
The rate of movement of fluid particles along a tube (cm/sec)
239
What 3 things is resistance of a vessel dependent on?
1. Viscosity of the blood
2. Shear forces of vessel walls
3. Vessel diameter
240
Give an equation link ing flow to pressure gradient and resistance.
Q = P / Res.
241
If flow remains the same along a vessel, but cross sectional area decreases, what will happen to velocity?
Velocity will increase
242
Give an equation linking flow to velocity and cross sectional area.
Q = Velocity X Cross Sectional Area (r^2)
243
Explain why the aorta has a very high velocity of blood compared with the capillaries despite the same flow.
Velocity is inversely proportional to the radius^2 of a vessel so that if radius doubles in size, the velocity decreases by 1/4. The aorta has a cross sectional area of about 2.5cm^2 whereas that of the capillaries is 4500cm^2. Therefore the overall cross sectional area of the capillaries is much larger and much slower than the aorta.
244
Describe laminar flow.
A gradient of velocity of blood from the centre of the vessel, where velocity is highest, to the edge of the vessel, where fluid is stationary.
245
Describe turbulent flow.
The velocity gradient from the centre of periphery of a vessel breaks down and fluid tumbles over. Causes an increase in flow resistance.
246
Generally, what 3 things increase the chances of turbulence?
1. Irregular lumen
2. High velocity of blood
3. High viscosity of blood
247
How is turbulence detected?
By auscultation - heart as a Bruit
248
Define viscosity.
The extent to which fluid layers slide over one another.
249
If all else remains the same, what will happen to flow if viscosity is increased?
Flow will decrease
250
What 3 things is resistance to flow determined by?
| Give an equation linking these together.
1. Vessel diameter
2. Vessel length
3. Blood viscosity
Resistance = (length of vessel X viscosity of flood) / vessel diameter (r^4)
251
Is viscosity of blood higher in the capillaries or aorta?
Aorta - where sheer stresses are low
252
Give 3 scenarios where the viscosity of blood would be increased.
Hyper-proteinaemia.
Infection - increase white blood cells in the blood.
Fluid loss / dehydration.
253
What relationship does viscosity have with average velocity of laminar flow?
Increased viscosity slows the central layer of laminar flow and therefore the average velocity of flow decreases. (Inversely proportional)
254
If you have a 2 fold increase in the radius of a vessel lumen, but nothing else changes, what will happen to the resistance?
Decreases by 16 fold (2^4)
255
Define resistance.
What must be overcome to push blood through a vessel and create flow.
256
Give Poiseuille's law.
Q = (P X r^4) / viscosity X tube length
257
Explain why a very small decrease in radius dramatically decreases flow.
According to Poiseuille's law, flow is proportional to radius^4.
258
What factor has the dominant influence on resistance and flow?
Vessel radius
259
Give an equation linking pressure to resistance and flow.
Pressure = flow X resistance
260
If 2 tubes are connected in series, the resistance is...
The sum of the 2 resistances from each tube added together = massive increase.
261
If 2 tubes are connected together in parallel, the resistance...
Falls
262
Capillaries have a low or high: resistance, velocity and pressure gradient.
- Low resistance (parallel arrangement)
- Low velocity (large cross sectional area)
- Low pressure gradient (due to low resistance)
263
Arteries have high or low: resistance, pressure gradient, velocity, compliance, blood pressure
- Low resistance
- Low pressure gradient (due to low resistance)
- High velocity
- Low compliance
- High blood pressure
264
Arterioles have a high or low: resistance and pressure gradient
- High resistance
| - High pressure gradient (due to high resistance)
265
Venules & veins have a high or low: resistance, pressure gradient, compliance
- Low resistance
- Low pressure drop (due to low resistance)
- High compliance
266
Describe the graph of pressure against flow in a distensible tube.
Curved graph, as pressure increases, flow increases but effect greater at higher pressures (graph gets steeper at higher pressures)
267
Explain why the graph of pressure against flow for a distensible tube is not linear.
The increased pressure within a distensible vessel creates transmural pressure across the vessel wall and the walls distend / stretch. As the walls distend, resistance decreases and flow can occur more easily.
268
Define compliance in terms of blood vessels.
The ability of a vessel to distend and increase in volume due to a pressure increase.
269
Define capacitance in blood vessels.
A measure of relative volume increase per unit increase in pressure.
270
If the smooth muscle of a distensible vessel contracts, what happens to the curve of flow against driving pressure?
Shifted to the right so that there is less flow at any given driving now pressure (becomes more like rigid tube).
271
What is meant by the total peripheral resistance?
The sum of all arteriolar resistances
272
What is the Windkessel effect and why is it relevant to the CVS?
The recoil of elastic arteries during diastole smooths out flow through arteries during the cardiac cycle. Means that because arteries are elastic, they can store mechanical energy of pressure as it rises during systole and dissipate it during recoil in diastole so that flow never reaches 0.
273
Define systolic pressure.
The highest arterial blood pressure of a cardiac cycle occurring immediately after systole of the ventricles.
274
Define diastolic pressure.
The minimum arterial blood pressure of a cardiac cycle occurring during diastole of the ventricles.
275
What 3 things affect systolic and diastolic pressures?
| Give an equation for blood pressure.
CO, arterial compliance and TPR
BP = CO X TPR
276
How would you calculate pulse pressure?
Systolic pressure - diastolic pressure
277
How would you calculate average blood pressure?
Diastolic pressure + 1/3 pulse pressure
278
Why is the average blood pressure not just the average of diastolic and systolic blood pressures?
Because systole (0.3s) takes up a small portion of the cardiac cycle than diastole (0.55s)
279
Why does pulse pressure decrease down the arterial tree?
Because of reduced capacitance - less elastic in the walls of smaller arteries
280
What is vasomotor tone?
The amount of tension in the smooth muscle inside the walls of blood vessels.
281
How is ensured that blood supply matches metabolic demand?
Increased metabolism leads to build up of metabolites, some of which act as vasodilators to causes vasodilitation.
282
Name 5 metabolites that act as vasodilators.
H+, CO2, adenosine, K+, lactate
283
Why is vasodilitation usually only acute?
Because it is mostly controlled by build up of metabolites, which when flow is increased by vasodilitation are washed away - returns to resting vasomotor tone.
284
What is reactive hyperaemia?
When blood flow to a region is briefly lost, on return there is excess flow to remove build up metabolites.
285
Define vasoconstriction.
Narrowing of blood vessels due to contraction of smooth muscle in their wall.
286
Define vasodilitation.
Widening of blood vessels due to relaxation of smooth muscle in their walls.
287
As total body demands for blood increases, TRP will...
Decrease
288
What is the compliance percentage of veins?
10%
289
What is the pressure in the veins overall determined by?
The amount of blood contained within them
290
What 4 things will affect venous pressure?
1. Cardiac output
2. BMR
3. Gravity / muscle pumping
291
Why is central venous pressure important?
Reflects the amount of blood returning to the heart
292
What is the normal range of central venous pressure?
3-8mmHg
293
What does the systolic upstroke on the arterial pressure waveform account for?
Rapid ventricular ejection.
294
What does the dicrotic notch account for on the arterial pressure waveform?
Closing of the aortic valve - small decrease in pressure. Transition from systole to diastole.
295
Give 1 reason why pulse pressure might be wider than normal?
Aortic regurgitation
296
Give 1 reason why pulse pressure might be narrower than normal.
Low cardiac output - e.g. Cardiac tamponade
297
What is meant by autoregulation in terms of the CVS?
The intrinsic ability of an order to maintain constant blood flow despite changes in perfusion pressure.
298
How is autoregulation in the CVS carried out?
A decreased perfusion pressure will result in build up of metabolites and endothelial factors resulting in vasodilitation, decreased resistance and increased flow.
299
If cardiac output remains the same but total peripheral resistance increases, what will happen to arterial and venous pressure?
Arterial pressure will increase.
| Venous pressure will decrease.
300
If CO is not changed but TPR is decreased, what will happen to arterial and venous pressures?
Venous pressure will increase
| Arterial pressure will decrease
301
If CO is increased by TPR remains the same, what will happen to arterial and venous pressures?
Arterial pressure will increase.
| Venous pressure will decrease.
302
What is meant by demand-led pumping? Why is it essential?
When there is an increased demand for blood by the body, there will be vasodilation in the areas that require it. This will result in reduced TPR, which would lead to reduced arterial pressure and fainting if no change was made. In response, the heart increases CO which raises arterial pressure and maintains normal arterial and venous pressures.
303
Give an equation for calculation of cardiac output.
CO = HR X SV
304
Define the stroke volume.
The volume of blood ejected by the left ventricle in one cardiac cycle (EDV - ESV).
305
Define the EDV.
The volume of blood in one ventricle at the end of diastole.
306
Define end systolic volume.
The volume of blood in one ventricle at the end of systole.
307
What determines how much the ventricles fill during diastole?
The venous pressure. Since the ventricle is connected freely to the veins during diastole, the ventricle will fill until the walls stretch enough to produce an intra-ventricular pressure equal to that of the veins.
308
What is a ventricular compliance curve? Describe its shape.
Relates end diastolic volume (X axis) to venous pressure (Y axis). Gradually increases then peaks at the end (Suddenly increases).
309
Define the pre-load.
The volume of blood in the ventricles at the end of diastole that causes stretch of cardiac myocytes.
310
Define after-load.
The resistance that the left ventricle must overcome to eject blood.
311
What is the Frank-Starling mechanism?
The ability of the heart to change its force of contraction, and therefore stroke volume, in response to changes in venous return.
312
Why does the SV only increase up to a limit with increase venous pressure?
Because the fibrous pericardial sac limits the filling of the ventricle after a point.
313
Describe the Starling curve.
Plots LVEDP (mmHg) against SV (ml). A curved graph where SV increases with LVEDP before starting to level off at higher LVEDP values.
314
What can cause a shift of the Starling curve to the left? (I.e. The slope becomes steeper at line becomes straighter).
Increased inotropy or decreased afterload.
315
The slope of the Starling Curve represents what?
Contractility / inotropy
316
What 2 things cause a shift of the Starling curve to the right? (Downwards)
Decreased inotropy or increased afterload.
317
Define contractility / inotropy.
A change in the efficiency of contraction of cardiac myocytes by a length-of-fibre independent mechanism.
318
How is contractility increased?
Sympathetic activity or other chemicals - e.g. Adrenaline
319
What 2 factors determine the force of contraction of cardiac muscle?
Contractility & pre-load (muscle fibre length)
320
Why does an increase in afterload decrease stroke volume?
It increases the end systolic volume.
321
What will an increase in afterload do to the peak systolic pressure of the ventricle?
Will increase the peak systolic pressure of the ventricle, in order to overcome the afterload.
322
If arterial pressure increases, stroke volume will ....
| If venous pressure increases, stroke volume will.....
Increases in arterial pressure = decreased stroke volume (increased afterload)
Increases in venous pressure = increased stroke volume (increased preload)
323
Where is the carotid sinus baroreceptor located?
At the bifurcation of the common carotid artery
324
Out of the 2 baroreceptors, which detracted lower pressure changes?
The carotid sinus
325
How do the baroreceptors work?
They respond to stretch of the arterial wall. Increased stretch increase firing to the medulla which reflexes to the heart.
326
A fall in arterial pressure will do what to the heart rate and how?
Increase the heart rate by reduced parasympathetic activity to the SA node, and if HR needs to be increased past 100bpm, then increases sympathetic activity to the SA node also.
327
Why is increase the heart rate after a fall in arterial pressure only productive after a point?
Because you are decreasing the length of the cardiac cycle which decreases the duration of diastole = a reduced filling time. Eventually will lead to a reduced stroke volume.
328
A fall in arterial pressure will do what to the ventricular contractility And how?
Increase the contractility via increased medulla output to the myocardium via increased sympathetic activity
329
What is the Bainbridge reflex?
Detection of high venous pressure in the right atrium. Fed back to the medulla which results in reduced parasympathetic activity and increased heart rate to increase cardiac output (decrease venous pressure).
330
What is the name of the internodal tract of the conducing system that branches over to the left atrium?
Backman's bundle
331
Where does the bundle of his run from?
The AV node to the top of the septum.
332
The cardiomyocytes depolarise from ..... To ......
Endocardium to epicardium.
333
What is the role of the conducting system of the heart?
To co-ordinate direction of depolarisation and contraction.
| To allow atria to contract before the ventricles at the AV node.
334
What do extracellular electrodes record?
Changes in membrane potential
335
What is the amplitude of a deflection on an ECG dependent on?
1. The amount of tissue being depolarised
| 2. How directly the signal is coming towards the electrode
336
Depolarisation towards an electrode causes a ..... Deflection.
Upwards
337
Depolarisation away from an electrode causes a ..... Deflection.
Negative
338
Repolarisation towards an electrode causes a ..... Deflection.
Negative
339
Repolarisation away from an electrode causes a ..... Deflection.
Positive
340
Why is the P wave small?
Atria only a small muscle mass
341
Why is the Q wave negative in lead II?
Because it corresponds to septal depolarisation which occurs from left to right - I.e. Away from the recording electrode.
342
Why is the R wave so large?
The depolarisation is spreading directly towards the recording electrode and corresponds to a large mass (the ventricles).
343
What does the S wave correspond to?
Depolarisation of the last parts of the ventricles via the purkinje fibres.
344
Why is the T wave a positive deflection?
Repolarisation moving away from the electrode
345
In what direction do the ventricles repolarise?
From epicardial to endocardial wall
346
If depolarisation is at a right angle to the electrode, what will be seen as the deflection?
No deflection - a flat line
347
Which electrode is the upside version of lead II?
AvR
348
What colour electrode does the right upper limb correspond to?
Red
349
What colour does the left upper limb electrode correspond to?
Yellow
350
What colour does the right lower limb electrode correspond to?
Green
351
What colour does the left lower limb electrode correspond to?
Black
352
Where would the following leads be placed: V1, V2, V3, V4, V5 V5
```
V1 = 4th intercostal space, right of sternum
V2 = 4th intercostal space, left of sternum
V3 = between V2 and V4
V4 = 5th intercostal space, mid-clavicular line
V5 = between V4 and V6
V6 = 5th intercostal space, mid-axillary line
```
353
How is an ECG recorded from 2 electrodes in bipolar leads?
Negative electrode signal is inverted and added to that of the positive electrode.
354
Give 4 confounders of ECG recording.
Mis-placement of electrodes.
Muscle contraction (movement).
inference (other electrical equipment),
Poor electrode contact - sweat, hair, cable pull
355
How do you determine whether an ECG trace is a sinus rhythm?
If every QRS complex is preceded by a P wave then it is sinus rhythm
356
Name a drug that can induce heart block (prolonged P-R interval).
Beta blockers
357
What on the ECG is indicative of left ventricular hypertrophy?
Very large amplitude R waves in V5 and V6
358
What is it called when there are long pauses between QRS complexes?
Sinus arrest
359
Which leads view the heart in the coronal plane?
Leads I, II, III, aVL, aVR and aVF.
360
What view of the heart do the chest leads have?
Horizontal plane on the anterior surface
361
What is meant by a 'bipolar lead'? Which leads are bipolar?
Uses one positive and one negative electrode from the standard limb leads.
Leads I, II and III are bipolar
362
What is meant by a 'unipolar lead'?
Read from the labelled positive electrode and use several other electrodes as negative.
363
Which lead usually has the most positive R deflection?
Lead II
364
Which lead has the opposite deflection pattern to lead II?
aVR
365
What is the first thing you do when assessing an ECG?
Assess the rhythm
366
How would you calculate heart rate from a rhythm strip of a regular rhythm ECG?
300 / (number of large squares between R waves)
367
When might an irregular rhythm be normal in physiology?
As the heart speeds up during inspiration but slows during expiration.
368
How would you calculate the heart rate from an ECG with irregular rhythm?
Number of R waves in 30 large squares X 10
369
Define sinus tachycardia.
>100 bpm originating at the sinoatrial node.
370
Define sinus bradycardia.
Heart rate of less than 60bpm originating in the sino atrial node
371
What is the difference between a irregularly irregular and regularly irregular heart rhythm?
Regularly irregular = R waves different distanced apart but reoccur in a pattern.
Irregularly irregular = no pattern at all to R waves
372
How might you determine whether a heart rate is regular, irregular or irregularly irregular?
Use a piece of paper, mark the distance between R waves on the edge and move it along the rhythm strip.
373
What are the 3 characteristics of an atrial fibrillation ECG?
Irregularly irregular rhythm, absent P wave, uneven/fluctuating baseline
374
Explain the atrial fibrillation ECG.
Atria have ectopic pacemakers that are randomly conducting causing the uneven baseline. Only a few of these depolarisations will be conducted through the conduction system to the ventricles - which ones is random.
375
How long does each large square of the ECG correspond to?
0.2s
376
How long does each small square of the ECG correspond to?
0.04s
377
How long is the normal P-R interval?
0.12 - 0.2s (3-5 small squares)
378
Where is the P to R interval measured from / to?
Start of P wave to start of QRS complex
379
How is first degree heart block defined on an ECG?
PR interval >0.2s (more than 5 small squares)
380
What would you see on the ECG in second degree heart block mobitz I?
Progressive lengthening of PR interval until one atrial depolarisation (P wave) is not conducted (QRS dropped)
381
What would you see in second degree heart block, Mobitz II?
A normal PR interval with no progressive lengthening but not all P waves are conducted.
382
What would you see on an ECG in third degree heart block?
Normal rate and rhythm of P waves.
QRS complex completely disconnected from P waves.
Slow ventricular rhythm (30-40bpm).
Wide QRS.
383
Why is the QRS complex wide in third degree heart block?
Ventricular depolarisations are not originating in the atria, but from the ventricles. Therefore they do not travel through the conducting system, but through the myocardial tissue itself - this is not as rapid.
384
What is the treatment for 3rd degree heart block and why?
Pacemaker. Slow heart rate means blood pressure will be too low to maintain perfusion.
385
If you see a single, abnormal QRS complex on a rhythm strip, what is the diagnosis?
Ventricular ectopic beat
386
How is ventricular tachycardia defined?
More than 3 consecutive ventricular ectopic beats
387
What does ventricular fibrillation look like on an ECG?
Abnormal, chaotic, fast ventricular depolarisation
388
What is happening in ventricular fibrillation of the heart?
Numerous ectopic sites present in the ventricles so that there is no co-ordinated contraction and very little to no cardiac output.
389
How is ventricular fibrillation treated?
Defibrillation - electric shock to put all myocardial cells into refactory period in order to re-coordinate electrical activity.
390
What is meant by the ECG 'axis'?
The average direction of spread of ventricular depolarisation.
391
What axis are the following leads placed at: aVR, aVF, aVL, I, II, III.
```
aVR = -150
aVF = +90
aVL = -30
I = 0
II = +60
III = +120
```
392
What is the normal axis of the heart?
Between -30 and +90 degrees
393
What axis occurs in left axis deviation?
-30 to -90
394
What axis occurs in right axis deviation?
+90 to 180
395
What is the most common cause of left axis deviation?
Left, anterior conduction block (sometimes left ventricular hypertrophy)
396
What is the most common cause of right axis deviation?
RV hypertrophy
397
What do you see on the ECG in left axis deviation?
Positive lead I but negative lead III when both should normally be positive
398
What do you see on the ECG in right axis deviation?
Lead I is negative but lead III is positive
399
What is the QT segment measured from?
From start of Q to end of T
400
How is long QT syndrome defined in males and females?
>0.45s in males or >0.47s in females
401
What causes long QT syndrome?
Prolonged depolarisation / delayed repolarisation
402
Why can you not defibrillate sinus arrest?
There is no electrical activity in the heart to be re-coordinated.
403
In normal axis, which of leads I, II and III should be positive?
All 3
404
What are wide Q waves on an ECG indicative of?
A previous myocardial infarction
405
What is the normal width of a Q wave?
0.04s (1 small square)
406
What is wide QRS complexes indicative of?
Bundle branch block
407
How might you differentiate between myocardial ischaemia, pericarditis and aortic dissection whilst taking a history in a patient presenting with chest pain?
```
Ischaemia = a tightening pain
Pericarditis = a sharp pain
Dissection = tearing pain
```
408
When might you suspect pneumonia as a cause of chest pain?
Lateral chest pain, fever and progressive
409
What is meant by 'tender'? What might you think if somebody presented with tender chest pain?
Tender = more painful when you press on the area
| Probably a musculoskeletal problem
410
Myocardial ischaemia is primary caused by...
An imbalance between myocardial oxygen supply and demand
411
Why is sub endocardial muscle of the heart most vulnerable to ischaemia?
Receives coronary blood flow last. Blood flows from epicardium to endocardium as vessels penetrate from the epicardial surface at right angles.
412
Explain why tachycardia worsens ischaemia.
Coronary arteries are compressed during systole and so coronary blood flow occurs during diastole. During tachycardia, diastole shortens and reduces the time available for coronary blood flow.
413
What is the commonest cause of ischaemic heart disease (IHD)?
Fixed narrowing of the coronary artery due to atherosclerosis
414
Explain why the myocardium is particularly prone to ischaemia.
There are no collateral arteries between the main coronary arteries.
415
What 2 things is oxygen supply of the myocardium dependent on?
Coronary blood flow and oxygen carrying capacity of the blood
416
What 2 things is the coronary blood flow dependent on?
Perfusion / diastolic pressure and coronary artery resistance
417
What 3 things is the myocardial oxygen demand dependent on?
Heart rate, contractility and wall tension
418
Myocardial wall tension is dependent on ...
Afterload and preload
419
How does anaemia affect the balance between myocardial oxygen supply and demand?
Decreases the supply by reduced oxygen carrying capacity of the blood.
Also increases the demand by increasing heart rate.
420
Give 3 non-modifiable risk factors of coronary arterial disease.
Family history, age (increasing) and gender (male)
421
Name 5 modifiable risk factors of coronary arterial disease.
Obesity, hyperlipidaemia, hypertension, diabetes, smoking
422
Describe the structure of a stable plaque in atherosclerosis.
Thick fibrous cap and small necrotic core.
423
Describe the structure of a vulnerable fibrous cap in atherosclerosis.
Large necrotic core with thin fibrous cap.
424
What happens on plaque rupture of atherosclerosis?
Blood is exposed to thrombogenic material causing generation of a platelet clot followed by a fibrin thrombus. This can completely block the lumen of the artery.
425
The clinical condition 'stable angina' corresponds to which type of atherosclerotic plaque?
Stable, fixed atherosclerotic plaque with a large fibrous cap and small necrotic core.
426
Name the 3 types of acute coronary syndrome.
1. Unstable angina
2. Non-ST-segment elevation myocardial infarction (NSTEMI)
3. ST-segment elevation myocardial infarction (STEMI)
427
Unstable angina corresponds to what stage of atherosclerosis?
Unstable plaque disruption causes platelet aggregation reducing blood flow.
428
NSTEMI correspond to what stage of atherosclerosis?
Unstable plaque rupture and thrombus formation significantly, but not fully, occludes the vessel.
429
STEMI corresponds to what stage of atherosclerosis?
Unstable plaque rupture followed by thrombus formation and complete occulsion of the vessel lumen.
430
What actually causes the pain during ischaemic chest pain?
The accumulation of metabolites stimulating pain fibres
431
What are the 3 characteristic features of ischaemic chest pain?
Central
Tightening / constricting / crushing
Radiates down arms, to jaw and shoulders
432
Stable angina patient presents with:
No pain at rest, but pain precipitated by stress or exertion.
Relieved by rest or nitrates within 5 minutes.
Typical risk factors of coronary arterial disease.
Normal ECG at rest.
433
If you are unable to diagnose angina by history alone, what might you do?
Exercise stress ECG test.
434
When would you terminate an exercise stress test?
1. When target heart rate reached if no symptoms (and increased gradient and speed).
2. If ECG changes are seen
3. If chest pain occurs
435
What ECG changes do you see in stable angina stress test?
ST segment depression of more than 1mm (more than 1 small square).
436
The anatomical / physiological cause of stable angina is...
Sub-endocardial ischaemia on exercise
437
The ST segment is measured from.... And to....
The end of the S wave to the start of the T wave
438
What is the most common treatment for stable angina? How do they work?
Sublinguinal nitrates. Cause venodilation to decrease the preload of the heart.
439
Other than nitrates, give 5 other ways you might treat a patient with stable angina.
Modification of lifestyle, beta blockers, calcium channel blockers, statins and aspirin.
440
How are calcium channel blockers useful in stable angina?
Reduce afterload by causing peripheral vasodilatation.
441
Name the 2 methods of revascularisation for treatment of coronary arterial disease.
1. Percutaneous coronary intervention (PCI)
| 2. Coronary artery bypass grafting
442
Before performing a revascularisation technique, what must first happen?
Coronary angiography - injection of dye to identify site of occlusion and study coronary anatomy
443
What is Percutaneous coronary intervention (PCI)?
Insertion of a catheter through the arterial system into the affected coronary artery to the region of the plaque, expansion of stent in this region to compress plaque and widen artery.
444
Coronary bypass grafts are grafted onto which arteries?
From the left subclavian artery or ascending aorta to the affected coronary artery beyond the blockage.
445
Name the 3 vessels commonly used for coronary bypass grafts.
Internal thoracic artery, radial artery or great saphenous vein.
446
What must you do when using the great saphenous vein as a coronary bypass graft?
Must reverse the vein segment so that valves face downwards so that blood flow along the vessel is not prevented.
447
Which two types of acute coronary syndrome cause incomplete obstruction to flow?
Unstable angina and NSTEMI
448
Why does the ST segment become elevated in a STEMI?
The total occlusion of the artery lumen causes transmural (full-thickness) injury - including sub-epicardium.
449
Define unstable angina.
An unprovoked or prolonged episode of chest pain raising suspicion of acute myocardial infarction.
450
What ECG characteristics might you see during unstable angina?
ST depression, T wave inversion, no change/normal.
451
What ECG changes might you see during NSTEMI?
ST depression, T wave inversion or no changes/normal
452
How is unstable angina differentiated from NSTEMIs?
Through lab tests - NSTEMI will show release of troponins whereas unstable angina will not
453
Which area of the myocardium becomes ischaemic in unstable angina or NSTEMI?
Subendocardial areas only
454
Which 2 troponins are released on myocyte death?
Troponin I and Troponin T
455
How might a patient with unstable angina present?
Worsening of stable angina.
Central, compression pain at rest.
Recent onset new, effort-limiting angina.
456
How will a patient with a myocardial infarction typically present?
```
Pain at rest
Severe, persistent, crushing chest pain with radiation.
Pain not relieved by nitrates.
Sweating
Pallor
Nausea
Vomiting
Breathlessness
Faint
Typical risk factors of coronary arterial disease
Tachycardia
Low blood pressure
```
457
Sweating and pallor in myocardial infarction is the result of what?
Increased sympathetic output due to decreased blood pressure
458
What are the 3 ECG features of a fully evolved STEMI?
1. ST elevation
2. T wave inversion
3. Pathological Q waves
459
What do the pathological Q waves seen in STEMI indicate? What does this mean for the fate of the Q wave?
Areas of necrosis - hence only develop over time and won't occur if myocardium if reperfused quickly enough. Also remain forever after the MI has been treated (good way of identifying previous MI).
460
Describe a pathological Q wave.
Greater than 1 small square wide.
| Deeper than 25% of QRS complex.
461
If an infarction occurred in the inferior heart, which leads would you see it in? Which vessel is this most likely to correspond to?
Leads II, III and aVF.
| Right coronary artery.
462
If an infarction occurred in the antero-septal heart, which leads would you see it in? Which vessel is this most likely to correspond to?
Leads V1 and V2.
| Left anterior descending artery.
463
If an infarction occurred in the anterior apical heart, which leads would you see it in? Which vessel is this most likely to correspond to?
Leads V3 and V4.
| Distal left anterior descending artery.
464
If an infarction occurred in the anterior lateral heart, which leads would you see it in? Which vessel is this most likely to correspond to?
Leads I, aVL, V5 and V6.
| Circumflex artery.
465
If an infarction occurred in the entire anterior heart, which leads would you see it in? Which vessel is this most likely to correspond to?
Leads I, aVL, V2, V3, V4, V5 and V6.
| Proximal left coronary artery.
466
What ECG changes are seen in a posterior myocardial infarction?
Which vessel causes this?
Tall R wave in V1.
| Caused by right coronary artery.
467
Describe the life cycle of cardiac troponins following MI.
Rise about 4 hours after MI.
Peak at 18-36 hours.
Decline slowly and can take up to 14 days to reach basal levels.
468
Explain why creatine kinase is more useful in a new episode of chest pain within 10 days of an MI than troponins.
Creatine kinase levels also rise after MI but go back to normal levels within 72 hours. Troponins can take up to 14days. In a second episode of chest pain, troponins would still be raised from the first MI so raised levels would not necessarily be indicative of a second MI but raised CK levels would be.
469
How else might a STEMI be diagnosed other than ST elevation?
ECG showing left bundle branch block.
470
What is classed as 'ST elevation'?
More than 1mm in limb leads or 2mm in chest leads.
471
What is everybody who presents with acute coronary syndrome treated with despite diagnosis (STEMI, NSTEMI or unstable angina)?
Aspirin (anti-platelet), oxygen and pain relief (opioids)
472
What is the primary / first treatment for STEMI?
Emergency Percutaneous coronary intervention
473
If emergency PCI is unavailable, how might you treat STEMI?
Fibrinolytic therapy
474
What is the primary / first treatment for NSTEMI and stable angina?
Anti thrombotic therapy
475
How is it assessed whether a patient with NSTEMI or unstable angina requires revascularisation treatment?
They undergo a risk assessment using a GRACE score.
476
What are the 5 drug types used for long term management following an MI?
Aspirin, beta blockers, ace inhibitors, statins, life style modification.
477
Give 7 complications of myocardial infarction.
```
Sudden cardiac death = ventricular fibrillation or asystole.
Sinus tachycardia.
Sinus bradycardia.
Heart block.
Ventricular tachycardia or fibrillation.
Heart failure
Cardiogenic shock.
```
478
Why might you get sinus tachycardia following an MI?
Pain, anxiety or heart failure
479
Why might you get sinus bradycardia following an Mi?
If there was ischaemia of the SA node
480
Why might you get heart block following an Mi?
If there was ischaemia of the AV node.
481
When do you get cardiogenic shock following an MI?
If more than 40% of the myocardium was infarcted so that cardiac output severely decreased, resulting in decreased blood pressure and inadequate perfusion.
482
How many bundle branches does the right bundle branch have?
One
483
How many bundle branches does the left tract have and what are they called?
Two - anterior and posterior bundle branches
484
What is the pneumonic used for identifying bundle branch blocks on the ECG?
WiLLiaM MaRRoW
485
What do you see on the ECG in left bundle branch block?
Wide W shaped peak in V1
| Wide M shaped peak in V6
486
What do you see on the ECG in right bundle branch block?
Wide M shaped peak in V1
| Wide W shaped peak in V6
487
Describe and explain the V1 normal wave.
Small positive Q as septum has a small volume. V1 is on the right and septal depolarisation occurs left to right.
Large negative R as this occurs right to left and is a larger mass.
488
Describe and explain the V6 normal ECG wave.
Very small negative Q wave due to small volume of muscle depolarising from left to right (away from V6).
Large positive R wave as a large muscle mass moving from right to left.
489
What are the 2 blood supplies to the lungs and what is the difference?
Bronchial and pulmonary circulations.
Bronchial for metabolic requirements of the lungs.
Pulmonary for gas exchange.
490
How much blood per minute does the pulmonary circulation receive?
Entire cardiac output = 5L/min
491
What is the pressure in the right atrium of the heart?
0-8mmHg
492
What is the pressure in the left atrium of the heart?
1-10mmHg
493
What is the pressure in the left ventricle of the heart?
100-140 / 1-10mmHg
494
What is the pressure in the right venticule of the heart?
15-30 / 0-8 mmHg
495
What is the pressure in the pulmonary artery?
15-30 / 4-12 mmHg
496
What is the pressure in the aorta?
100-140 / 60-90 mmHg
497
The pulmonary circulation is at ****** pressure and ****** resistance.
Low pressure and low resistance
498
What is the mean capillary pressure of the pulmonary circulation?
9-12 mmHg
499
Why is the pulmonary circulation low resistance?
Has a lot of branching in parallel arrangement
| Arterioles contain relatively little smooth muscle
500
What 2 factors in the lungs allow efficient gas exchange?
Large surface area (lots of capillaries) and short diffusion distance (single cell of endothelium and epithelium only 0.3um)
501
The combined diffusion distance for gas exchange in the lungs is...
0.3um
502
Why is the pressure in the left atrium higher than the right?
Because pulmonary circulation is low resistance so there is not the same drop in pressure around the circulation
503
Give 2 differences between the pulmonary and systemic circulations.
Pulmonary is low resistance and low pressure.
| Pulmonary circulation is supply driven whereas systemic circulation is demand led.
504
Why does left atrial pressure increase on inspiration?
Pulmonary vessels hold more blood during inspiration
505
What is the normal pressure in the pulmonary veins?
5mmHg
506
What is the optimal ventilation : perfusion ratio value?
5 / 4 = 0.8 (close to 1)
507
How is the V/Q maintained?
Diversion of blood away from poorly ventilated alveoli
508
How is blood diverted away from poorly ventilated alveoli?
Hypoxic pulmonary vasoconstriction - alveolar hypoxia results in vasoconstriction of local pulmonary vessels.
509
What is the main determinant of pulmonary vascular tone?
Hypoxic pulmonary constriction
510
Explain how altitude and lung disease can lead to right ventricular heart failure.
Altitude and lung disease can lead to chronic hypoxia of the alveoli. This results in hypoxic pulmonary vasoconstriction which increases vascular resistance. This results in a high afterload on the right ventricle and right ventricular hypertrophy and heart failure.
511
Why do normal lungs have some ventilation-perfusion mismatch?
There is high blood flow to the base of the lungs but air is delivered primarily to the apex.
512
What is the physiological shunt in the pulmonary circulation?
Blood passes through the pulmonary arteries without being oxygenated due to the ventilation perfusion mismatch
513
What is the difference in diameter of vessels in the superior and inferior lungs? Why?
Greater hydrostatic pressure in vessels below the heart level - hence they tend to be distended. Vessels above the heart tend to collapse during diastole. All due to gravity.
514
What happens in the lungs during exercise?
Small increase in pulmonary arterial pressure.
Capillaries open at lung apex.
Increased ventilation.
Increased capillary transit time from 1s to 0.3s.
515
What is the major cause of pulmonary oedema?
Rise in left atrial pressure
516
Give 2 reasons why left atrial pressure might rise leading to pulmonary oedema.
LV failure or mitral valve stenosis
517
How does a rise in left atrial pressure cause pulmonary oedema?
Increased LV pressure raises pulmonary venous pressure which leads to increased hydrostatic pressure in the pulmonary capillaries. More fluid is pushed out of the fluid at the arterial end of the capillary so that filtration becomes greater than reabsorption.
518
Where does pulmonary oedema mainly formed when standing and why? What effect will lying down have?
At the base of the lungs as this is where hydrostatic pressure is greatest.
Lying down reduces the effects of gravity so that oedema forms throughout the lung.
519
How is pulmonary oedema treated?
With diuretics
520
Describe the graph of coronary blood flow against myocardial oxygen demand.
As myocardial demand increases, coronary blood flow increases proportionately until a high oxygen demand is reached when it begins to level off.
521
How is an increased oxygen demand met by coronary supply?
Increased blood flow and a small increase in the amount of oxygen extracted.
522
How do coronary vessels increase their blood flow to the myocardium during exercise or increased demand?
Due to metabolic hyperaemia - build up of metabolites causes vasodilation.
523
What is the capillary density of cardiac muscle?
3000 / mm^2
524
How many cardiac fibres does one coronary capillary supply?
1 capillary to each fibre
525
How is the high basal flow in the coronary arteries maintain?
Continuous production of NO by the coronary endothelium.
526
How do stress and cold aggregate angina?
Through activation of the sympathetic nervous system resulting in coronary vasoconstriction and reduced blood supply to the myocardium.
527
At rest, how much of the total body consumption of oxygen does the grey matter of the brain account for?
20%
528
In what 4 ways is the high demand for oxygen by the brain met?
1. High capillary density
2. Small diffusion distance
3. High basal flow rate
4. High oxygen extraction.
529
Structurally, how is the blood supply to the brain secured?
Lots of anastomoses present - e.g. Between basilar and internal carotid arteries at the circle of Willis.
530
Functionally, in what 3 ways is the blood supply to the brain secured?
1. Myogenic auto regulation
2. Reactive hyperaemia (metabolite build up)
3. Cushing's reflex
531
What is meant by myogenic autoregulation in the brain?
A mechanism of keeping blood flow to the brain constant.
| Changes in blood pressure in cerebral resistance vessels results in a response to alter vasomotor tone.
532
An increase in systemic blood pressure will result in the cerebral vessels doing what?
Vasoconstriction
533
Decreased systemic blood pressure will result in the cerebral blood vessels doing what?
Vasodilation
534
Myogenic autoregulation keeps cerebral blood flow roughly the same between what blood pressures?
60 and 180mmHg
535
What does reactive hyperaemia in the brain ensure?
Ensures that the areas of the brain with the highest neuronal activity will have the greatest blood flow.
536
How can panic hyperventilation cause fainting?
Results in hypocapnia within the brain leading vasoconstriction = decreased cerebral blood flow
537
Name 3 metabolites important for regulating blood flow in cardiac and cerebral tissues.
Adenosine, H+ and CO2.
538
What is the Cushing's reflex in control of cerebral blood flow?
Impaired blood flow to vasomotor control centres of the brainstem results in increased sympathetic vasomotor activity to systemic arterioles. This raises arterial blood pressure and increases perfusion pressure / flow to the cerebrum.
539
Why is the cerebrum prone to ischaemia?
The rigid cranium does not allow for volume expansion so anything that causes an increase in intracranial pressure (e.g. Tumour or haemorrhage) will impair cerebral blood flow.
540
Why does the skeletal muscle have such a large impact on arterial blood pressure?
Accounts for 40% of total adult body mass. Changes in resistance will have massive impact on total peripheral resistance.
541
What type of skeletal muscle has a high capillary density?
Those with few glycolytic muscle fibres - e.g. Postural muscles
542
What percentage of skeletal muscle capillaries are perfused at rest? How does this compare with cardiac muscle capillaries?
Only 50% in skeletal muscle but 100% in cardiac
543
How does vasodilation occur in the skeletal muscle during exercise?
```
Metabolic hyperaemia (metabolite build up)
Adrenaline beta2 adrenoceptors
```
544
What are arteriovenous anastomoses (AVAs) and where are they found?
Vessels connecting arterioles directly to superficial venules in the skin that allow blood to bypass the capillary bed.
545
Describe the role of arteriovenous anastomoses (AVAs) in temperature regulation by the skin.
A rise in body temperature causes sympathetic outflow to the cutaneous vessels to reduce. Vasodilation occurs and AVAs open. This allows a low resistance shunt of blood to the venous plexus lying just beneath the apical skin. Skin temperature rises to dissipate heat.
546
A decrease in core body temperature will cause what in relation to arteriovenous anastomoses?
Increased sympathetic tone will increase tone in AVAs so that blood flow through them is reduced.
547
What type of skin are arteriovenous anastomoses present in?
Apical skin
548
Other than the skin, name 2 other mechanisms by which heat loss occurs.
Sympathetic innervation of sweat glands causes sweat release.
Bradykinin release from sweat glands causes local vasodilation.
549
More metabolic activity results in what in terms of TPR?
Lower TPR
550
What response does the CVS have to an increase heart rate?
Cardiac output rises. Venous pressure falls. Diastolic filling reduced. Reduces stroke volume. Cardiac output returned to normal.
551
Which of the baroreceptors is more sensitive to small changes in blood pressure?
Carotid sinus
552
Why does vasodilatation occur following digestion of a meal?
Because of production of vasodilator metabolites by the gut
553
Describe the changes in the cardiovascular system following eating a large meal.
Vasodilatation in the gut lowers TPR. Arterial pressure falls and venous pressure rises. Rises in venous pressure lead to increased stroke volume. Decreased arterial pressure activates baroreceptors resulting in increased contractility (stroke volume) and heart rate. Cardiac output rises so that arterial and venous pressures normalise.
554
Describe the changes in the CVS when a person stands from a lying position.
Blood pools in the legs. Central venous pressure decreases. Cardiac output falls (due to decreased stroke volume). Arterial pressure falls. Baroreceptors increase heart rate, contractility, venoconstriction and cause vasoconstriction in the skin and gut. TPR increases and cardiac output increases. Arterial blood pressure stabilised.
555
Why is someone who has recently eaten or is in a hot environment more likely to faint on standing up from a lying position?
Normally the CVS would cause vasoconstriction in the gut and skin vessels in order to increase TPR and maintain arterial blood pressure. In these individuals the blood flow to the gut and skin cannot be reduced as much (need to maintain digestion and temperature regulation) so TPR cannot be raised so significantly. More chance of blood pressure being too low to maintain perfusion pressure to the brain.
556
Explain why exercise should not be performed after eating a large meal.
Normally after eating a large meal the blood flow to the gut is hugely increased but perfusion pressure of other organs is maintained at rest. During exercise, perfusion of skeletal muscle takes priority over perfusion of the digestive system so that digestion becomes unpleasant as the increased perfusion cannot be maintain. Can lead to vomiting.
557
Why can the increase in venous pressure during exercise (fall in TPR and increased muscle pumping) not account entirely for the increased cardiac output?
Because the changes in venous pressures are so great that the heart is driven to the top of th starling curve - limiting its capacity to control cardiac output.
558
In addition to increased venous return, what other mechanisms account for the increase cardiac output during exercise?
Increased sympathetic activity = increased heart rate.
559
Why is there not a sudden increase in venous pressure during exercise / how is central venous pressure overfilling avoided?
Heart rate increases before a large change in arterial and venous pressure occurs. So extra venous blood is pumped immediately into the arteries.
560
Describe the initial CVS changes following haemorrhage.
Venous pressure falls. Results diastolic filling. Cardiac output falls. Arterial pressure falls. Baroreceptors raise heart rate and cause peripheral vasoconstriction.
561
What is the problem with the CVS causing an increased heart rate and vasoconstriction following haemorrhage?
Further decreases central venous pressure
562
How is venous pressure risen following haemorrhage?
Venoconstriction and auto-transfusion (fluid moving in from extracellular space to blood)
563
What is autotransfusion and what pathological process is this involved in?
Fluid moves into the circulation from the extracellular space. Occurs following haemorrhage.
564
What blood level is reached to cause hypovolaemic shock?
3.5 to 4 litres
565
What is a long term consequence of hypovolaemic shock? Why?
Kidney failure. Because perfusion to the heart and brain is maintained at the expense of other tissues which remain highly vasoconstricted to maintain mean arterial blood pressure.
566
What effect will a long term elevation in blood volume have on the CVs? How does it lead to hypertension?
Raised venous pressure. Increased diastolic pressure. Increased cardiac output. Increased arterial pressure. More blood perfusion in tissues. Vasoconstriction (increased vascular tone to limit perfusion). Increased total peripheral resistance. Further increase in blood pressure. = hypertension
567
How does initial hypertension due to raised blood volume become permanent?
The longterm vasoconstriction/increased vascular tone of vessels that occurs in fluid volume increases leads to remodelling of resistance vessel walls so that the TPR rise becomes permanent.
568
Define heart failure.
A state where the heart is unable to pump sufficient blood to meet the demands of the body despite an adequate filling pressure.
569
In what 2 ways is heart failure divided into subtypes?
Systolic versus diastolic.
| Left sided versus right sided (or congestive).
570
What is the 'problem' in diastolic heart failure?
The heart muscle is unable to pump with enough force during systole so that there is a reduced stroke volume. Usually caused by thin, fibrous walls of the ventricles increasing LV capacity.
571
What is the 'problem' in diastolic heart failure?
The heart is unable to fill with enough blood during diastole, leading to a reduced stroke volume. Usually caused by ventricular hypertrophy resulting in a smaller lumen size and decreased left ventricular compliance.
572
In which Type of heart failure is there always a change in ejection fraction? Explain.
Systolic heart failure as the stroke volume is reduced despite end diastolic volume remaining the same = a smaller ejection fraction.
573
What is the equation for ejection fraction?
SV / EDV. = (EDV-ESV) / EDV
574
At what ejection fraction is systolic heart failure diagnosed?
575
Explain how left sided heart failure results in pulmonary oedema.
As only a small amount of the LVEDV is being ejection, a large amount of blood remains in the LV and raises. This causes a backlog of blood and pressure, so that left atrial pressure also rises since it cannot empty into the LV so easily. This will then back up into the pulmonary veins and arteries, raising the hydrostatic pressure of pulmonary capillaries causing more fluid to be pushed out into the lungs.
576
What is the major cause of right sided heart failure?
Left sided heart failure - backlog of pressure
577
What is meant by congestive heart failure?
Both sides of the heart are affected, hence pulmonary and systemic systems are both affected. The result of congestion of blood from the left ventricle, through the pulmonary circulation and to the right ventricle.
578
Give 2 symptoms of the backward failure that occurs in left sided heart failure.
```
Pulmonary oedema (breathlessness and coughing).
Weight gain (fluid retention to increased preload).
```
579
Give 4 symptoms of the forward failure that occurs in left sided heart failure.
Tachycardia
Tiredness and fatigue (loss of skeletal muscle mass)
Decreased urine production (fluid retention)
Anaemia
580
Why do patients with left sided heart failure get anaemia?
Reduced perfusion of the kidneys results in loss of kidney mass and reduced production of erythropoietin.
581
Give 3 symptoms of backward failure of right-sided heart failure.
Peripheral oedema / ascites / pleural effusion.
Raised jugular venous pressure.
Increased urination at night.
582
Why would someone with right-sided heart failure need to urinate more frequently in the night?
Fluid built up in peripheral tissues will pass to the kidneys when lying down
583
Give 2 symptoms of the forward failure of right sided heart failure.
Weakness and fatigue (decreased oxygen exchange)
| Tachycardia
584
Give 4 causes of systolic heart failure.
Ischaemic heart disease.
Dilated cardiomyopathy - infection, drugs, pregnancy
Valve disease - mitral regurgitation or aortic stenosis
Arrythmias
585
Give 4 causes of diastolic heart failure.
```
Pericardial disease = reduced compliance
Hypertension = hypertrophy
Valve disease - stenosis (hypertrophy)
Restrictive cardiomyopathy (e.g. Ameloidoses) = reduced compliance
```
586
What is high output heart failure? Give one cause.
The heart is ejecting a normal stroke volume, but the oxygen demand is increased. Can be caused by anaemia.
587
Why does remodelling of the heart occur in heart failure?
Reduced pumping ability will increase the workload of the heart to try and meet the oxygen demands of the body. This will increase the oxygen demand of the myocardium itself and since this cannot be met, will result in muscle cell death.
588
What are the main neurohormonal responses to heart failure?
```
Increased sympathetic output.
Increased stimulation of the renin-angiotensin-aldosterone system.
Decrease nitric oxide production.
Increased endothelial production.
Vasoconstriction.
```
589
In the short term, what effect will increasing sympathetic output have in heart failure?
Increases the inotropy and chronotropy of the heart, increasing stroke volume. Also cause vasoconstriction to maintain the perfusion pressure of organs.
590
In the short term, what effect will activation of the RAA system have in heart failure?
Increases sodium and fluid retention and causes vasoconstriction. This increases the preload of the heart and maintains the perfusion pressure of organs.
591
What structural chance might the heart make in order to compensate for heart failure?
Hypertrophy
592
Why does increased sympathetic output in heart failure become pathological and worsen symptoms?
The increased heart rate increases the oxygen demand of the heart, which cannot be met leading to cell death.
Also down regulation of beta receptors occurs in Longterm SNS stimulation so the high levels of noradrenaline cannot have the same beneficial effects.
Increases vasoconstriction which increases wall stress of myocardium.
Up regulates RAA system.
593
How does the activation of the RAA system in heart failure become pathological and worsen the condition?
The increased preload increases the oxygen demand of the heart which cannot be met leading to cell death.
Increases collagen synthesis leading to cardiac remodelling and reduced compliance.
Vasoconstriction increases the resistance the heart must overcome to perfuse tissues / increases wall stress and oxygen demand.
Causes endothelial dysfunction in the vasculature.
594
How does the Frank-Starling curve change in mild and severe heart failure?
In mild - the gradient of the line decreases so that an increase in filling pressure no longer has the same increase in stroke volume.
In severe - the gradient decreases further and drops off at the end so that at high filing pressures, the stroke volume actually decreases.
595
What is meant by decompensation?
When compensation by the heart for heart failure actually ends up worsening the condition.
596
In what 3 ways would you treat heart failure in the early stages.
Modify risk factors.
Decrease blood pressure.
Decrease sympathetic stimulation.
597
In what 2 ways is blood pressure reduced in heart failure?
Using ACE inhibitors to reduced fluid retention and cause vasodilation.
Using nitrates to cause venodilitation.
598
How is preload directly reduced pharmaceutically in heart failure?
Using nitrates and venodilators
599
What 2 additional treatments might you use in the late stages of heart failure?
Target congestion - with diuretics
| Calcium channel blockers to cause vasodilitation and decrease heart rate (maximise diastole)
600
When are calcium channels especially used for treatment of heart failure? Why?
In diastolic heart failure. Causes a reduction in heart rate to maximise diastole time.
601
Give 2 other treatments of end stage heart failure other than risk factor modification and drugs.
Medical devices - pacemakers, ventricular assist devices and defibrillators.
Transplant.
602
How is heart failure functionally classified?
Using the New York heart association classification. Based on how well the individual responses to physical exertion. Classes I to IV.
603
What is the role of natriuretic peptides in heart failure?
Released by the atria and ventricles response to excessive stretching. They decrease sodium and water retention, decrease renin and aldosterone production and cause vasodilation.
604
What causes the activation of the RAA system in heart failure?
Reduced renal blood flow and SNS induction.
605
Why does hypo-naturaemia occur in heart failure?
Water retention in excess of sodium retention due to thirst and actions of vasopressin.
606
How do ACE inhibitors cause vasodilation?
They inhibit the conversion of bradykinin to its inactive form. This means bradykinin can bind to its receptors to stimulate NO production - an active vasodilator.
607
Why is tiredness and weakness a common symptom in left sided heart failure? What does this result from?
Reduced skeletal muscle mass due to reduced blood flow to the skeletal muscle.
608
What percentage of heart failure patients have diastolic heart failure?
20-50%
609
Give the 3 main causes of arrhythmias.
1. Ectopic pacemaker activity
2. After depolarisations
3. Re-entry loops
610
How does ectopic pacemaker activity usually arise?
A damaged area of myocardium becomes depolarised and spontaneously active. This depolarisation spreads to neighbouring cells. Or damage to the SA node causes it to stop being the dominant pacemaker.
611
What is a common predisposing factor to early and delayed after depolarisations?
An abnormally long action potential duration - e.g. In long QT syndrome
612
What happens in early and after depolarisations?
Abnormal action potentials are triggered by a preceding action potential.
613
During which part of the action potential do early after depolarisations occur?
Phase 2 or 3 (whilst cell is already depolarised)
614
What stage of the action potenital do delayed after depolarisations occurs?
During stage 4 - when the cell has just depolarised
615
What are delayed after depolarisations associated with?
High intracellular calcium concentrations.
616
What are early are depolarisations generally associated with?
Prolonged action potential.
617
What is the underlying cause of a re-entrant arrhythmia?
Incomplete conduction damage - unidirectional block.
618
Explain how incomplete conduction damage leads to re-entrant arrhythmia.
Depolarisation spread cannot get through the region of damaged myocardium. Excitation therefore takes a long route to spread the wrong way through the damaged area. This spread can now reactivate previously activated tissue setting up a circuit of excitation.
619
Explain how re-entry arrhythmias can lead to atrial fibrillation.
Multiple small re-entry loops form in the atria leading to atrial fibrillation.
620
How does mitral stenosis predispose to atrial fibrillation?
Mitral stenosis causes stretching and hypertrophy of atrial walls. This damages the myocardium and increases the likelihood of forming incomplete conduction block and re-entrant loops.
621
Name the four classes of anti-arrhythmic drugs.
Class 1 = voltage gated sodium channel blockers
Class 2 = beta blockers
Class 3 = potassium channel blockers
Class 4 = calcium channel blockers
622
Name an anti-arrhythmic voltage gated sodium channel blocker drug.
Lidocaine
623
What is meant by lidocaine being a 'use-dependent block'b
Only binds to sodium channels that are in their open or inactivated state - I.e. Those that have been stimulated
624
When might lidocaine be used Clinically?
Following MI when the patient has ventricular tachycardia.
625
Explain how voltage gated sodium channel blockers work as anti-arrhythmics.
Damaged areas of myocardium, e.g. After MI, tend to be depolarised and fire automatically. This means more sodium channels are in their open or inactivated state in these regions, so lidocaine binds to these channels and prevents automatic firing of depolarised venticule tissue whilst leaving the normal, non-dopolarised tissue unaffected.
626
How do beta blockers affect the heart?
Decrease the slope of the pacemaker potential.
| Decrease conduction through the AV node.
627
Give 2 reasons why it is beneficial to give beta blockers after MI.
1. Reduces the oxygen demand of the heart
| 2. Prevention of ventricular arrhythmias due to increased sympathetic activity post-Mi.
628
How are beta blockers beneficial in prevention of supraventricular tachycardias?
They slow conduction through the AV node so that the ventricular rate slows despite atrial fibrillation - maintains cardiac output.
629
Theoretically, how are potassium channel blockers anti-arrhythmic?
They pro-long the action potential to lengthen the absolute refactory period - decreasing the change of a delayed after depolarisation occurring.
630
Realistically, why are potassium channel blockers not used as anti-arrhythmic drugs?
They increase the likelihood of early after depolarisations occurring
631
What is the one potassium channel blocker that is used clinically? What is it used for?
Amiodarone. Used to treat tachycardia associated with Wolff-Parkinson-White syndrome.
632
Name an L-type calcium channel blocker.
Verapamil
633
What effect do L type calcium channel blockers have on the heart?
Decrease the slope of the action potential at the SA node. = negative chronotropy.
Decrease AV node conduction.
Decrease the force of contraction. = negative inotropy.
Coronary and peripheral vasodilation.
634
Why are dihydropyridinesp calcium channel blockers not used as anti-arrhthmics? Name one.
They are no effective in the heart, but are at vascular smooth muscle. E.g. Nicardipine.
635
Name 1 other drug that is used as an antiarrhytmic that does not fit any of the classic classes. How does it work?
Adenosine. Binds A1 receptors at AV node to enhance potassium conductance and hyperpolarise the cells. Stops AV conduction briefly, allowing it to start again at a normal rhythm.
636
Name 2 classes of drugs that might be used INITIALLY in heart failure to relieve symptoms.
Cardiac glycosides.
| Beta-adrenergic agonists.
637
Name a cardiac glycoside drug. What is its mechanism of action?
Digoxin. Blocks the sodium pump to increase intracellular sodium concentration / reduce sodium gradient. This reduces the gradient for the sodium-calcium exchanger to work. Intracellular calcium rises and force of contraction is increased.
638
Why might cardiac glycosides be used in the context of heart failure with arrhythmia?
Because as well as increasing force of contraction, they increase vagal activity via the CNS. This slows AV conduction and the heart rate which will reduce the symptoms of atrial fibrillation.
639
Name a beta1 adrenoceptor agonist.
Dobutamine
640
When are beta1 adrenoceptor agonists used?
Acute Reversible heart failure.
| Cardiogenic shock.
641
Do ACE inhibitors affect the afterload of preload of the heart?
Both - vasodilation and decreased fluid retention.
642
Name 3 classes of drug you would use to treat angina.
Beta blockers.
Calcium channel antagonists.
Organic nitrates.
643
How are calcium channel antagonists useful in angina?
Reduce the workload of the heart - less calcium induced calcium release.
Reduce smooth muscle contraction.p = vasodilation.
644
How do organic nitrates work in angina treatment?
React with SH groups in vascular smooth muscle to cause NO2 release. This is reduced to NO - a vasodilator.
645
Name an organic nitrates used in angina treatment.
Glyceryl trinitrate.
646
Give the mechanism of action of nitric oxide.
Activate guanylate cyclase. Increases cGMP levels. Activates PKG which Phosphorylates calcium channels to decrease their activity. This lowers intracellular calcium levels and causes relaxation of vascular smooth muscle.
647
What is the primary action of organic nitrates in angina treatment?
Venodilation to reduce preload. Reduces workload of the heart - as force of contraction is reduced. Lowers the oxygen demand of the heart.
648
What is a secondary action of organic nitrates in angina?
Vasodilation of collateral coronary arteries improving oxygen supply to the myocardium.
649
Give 3 heart conditions that have an increased risk of thrombus formation.
Atrial fibrillation.
Acute myocardial infarction.
Mechanical prosthetic heart valves.
650
Give the 2 types of antithrombotic drugs and examples of each.
1. Anticoagulants = heparin and warfarin
| 2. Anti platelets = aspirin
651
What are the 3 possible targets in hypertension treatment?
Lower blood volume
Lower cardiac output by reducing contractility
Lower peripheral resistance
652
Name the 5 classes of drugs used in treatment of hypertension.
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Diruretics
ACE inhibitors.
Beta blockers.
Dihydropyridine calcium channel blockers.
Alpha1 adrenoceptor antagonists.
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