CVS Flashcards
1
Q
What are some characteristics of coronary arteries?
A
They supply the myocardium with oxygenated blood.
They are functional end arteries.
They are prone to atheroma.
2
Q
What are the 3 types of arteries and what does the size of the artery depend on?
A
Large arteries are elastic arteries, such as the aorta.
Medium sized arteries are distributing arteries, such as the renal arteries.
Small arteries are resistance vessels, the arterioles - help control blood pressure.
The size of the arteries mainly depends on the thickness of the muscle.
3
Q
By what factor can the cardiac output increase by during exercise?
A
Between 4 and 7 times - the CO increases from 5L/min to 20-35L/min.
4
Q
What is serum?
A
It is plasma without the clotting factors.
5
Q
Why does turbulent flow occur, and where is it seen?
A
It occurs when the flow of blood is disorganised, when the pressure is greater than the flow can match.
It occurs when there is a change in direction of a vessel, and in stenoses.
6
Q
What is a stenosis?
A
An abnormal narrowing of an artery or a heart valve.
7
Q
Why is the velocity at the capillary level so slow?
A
Due to the large cross-sectional area, there is a much larger volume for the blood to fill.
8
Q
Below what pressure does organ perfusion become impaired?
A
70mmHg.
9
Q
What will the effect on pulse pressure be with exercise, and why?
A
Increase in pulse pressure because stroke volume increases, and vasodilation occurs, decreasing the afterload.
10
Q
What are the names referred to for blood flow that can be felt and heard?
A
Thrill can be felt.
Bruit can be heard.
11
Q
What are the two layers of the serous membrane around the heart adhered to?
A
The parietal layer is adhered to the fibrous pericardium.
The visceral layer is adhered to the epicardium.
12
Q
What is central venous pressure and arterial pressure?
A
CVP = the pressure in the large veins draining into the heart.
Arterial pressure = the pressure in the large arteries.
13
Q
How does smooth muscle work to meet the demands of tissues, close to their targets?
A
The arterioles and pre-capillary sphincters will dilate.
14
Q
What does the ventricular compliance curve state?
A
The higher the venous pressure, the more the ventricles fill.
The more the heart fills, the higher the left ventricular pressure.
15
Q
What does the ventricular filling depend on?
A
The greater the venous pressure, the greater the filling.
The greater the compliance of the ventricles, the greater the filling.
16
Q
What is calcium sensitivity of the heart influenced by?
A
The stretch of the muscle fibres - the greater the stretch of the muscle fibres, the greater the calcium sensitivity.
17
Q
What is contractility?
A
The force of contraction, for a given fibre length.
18
Q
What happens to the total peripheral resistance when metabolism increases, and what is the effect on arterial and venous pressure?
A
It decreases to supply more blood to meet the demand.
This means that arterial will decrease and venous pressure will increase.
19
Q
What is the response of the heart to a decrease in arterial blood pressure?
A
It will increase contractility and heart rate to increase cardiac output, and so the arterial blood pressure will also increase.
20
Q
What is jugular venous pressure measured in?
A
Cm of H2O.
21
Q
What is the length of a cardiac action potential?
A
Relatively long at 280ms.
22
Q
How long is the action potential held at the AV node for, and why does this occur?
A
120ms.
This is because the ventricles need time to fill before contracting.
23
Q
What percentage of ventricular filling is accounted by atrial contraction?
A
10%.
24
Q
What is the average EDV and ESV?
A
EDV = 120ml.
ESV = 50ml.
25
When is the S3 sound normal and abnormal?
It is normal in ventricular filling in children, but abnormal in adults.
26
What is heard in:
- Aortic valve stenosis.
- Aortic valve regurgitation.
- Mitral valve regurgitation.
- Mitral valve stenosis.
Aortic stenosis = systolic murmur: crescendo-decrescendo.
Aortic regurgitation = diastolic murmur: early decrescendo diastolic murmur.
Mitral regurgitation = systolic murmur: holosystolic.
Mitral valve stenosis = diastolic murmur: snap as the valve open - diastolic rumble.
27
What are the cardiogenic fields derived from?
The mesoderm.
28
What do the 6 parts of the primitive heart tube go on to form?
Aortic roots - forms the arteries of the aortic arch.
Truncus arteroisus - forms the pulmonary trunk and aorta.
Bulbous cordis - forms the pulmonary trunk and aorta.
Primitive ventricle - forms the ventricles.
Primitive atrium - forms the atria.
Sinus venosus - forms part of the right atrium and vena cava.
29
What is the sinus venosus split into?
The left and right sinus horns.
30
What does the left sinus horn become?
The coronary sinus - drains blood from the coronary vessels into the right atrium.
31
Where does the trabeculated and smooth muscle of the heart come from?
Trabeculated is from the primitive atrium and ventricle.
Smooth is from the pulmonary veins.
32
What are the 5 different aortic arches?
I, II, III, IV, VI.
V does not form.
33
What do the left and right aortic arches of the 6th, 4th, and 3rd arches form?
The 6th left and right aortic arches form the pulmonary arteries.
The 4th left aortic arch form the arch of the aorta.
The 4th right aortic arch forms the right subclavian.
The 3rd left and right aortic arches form the common carotids and the first part of the internal carotids.
34
Why does the laryngeal nerve only loop behind the 4th aortic arch on the right and not left?
Because some of the 6th aortic arch on the right is remodelled.
35
What is central cyanosis?
Where the partial pressure of oxygen in the systemic tissues is low, leading to a blue discolouration of the face, mouth and tongue.
36
Why does patent ductus arteriosus result in right-sided heart failure?
Blood flows from the aorta to the pulmonary artery, increasing after load of the right side of the heart, which increases the workload and oxygen demand of the right side of the heart, leading to right-sided heart failure.
37
Why does pulmonary hypertension and oedema occur with atrial septal defects? What else can it lead to?
Blood flows from the left atrium into the right atrium, increasing the blood volume and pressure being pumped to the lungs. This increases the hydrostatic pressure in the lungs, which can cause a small amount of pulmonary oedema, but it can also cause fibrosis of the arteries of the lungs, increasing the hydrostatic pressure further.
Due to the increase in pulmonary pressure, there can be right-sided heart failure.
38
Eventually, what happens in an atrial septal defect, and what is it referred to as?
The increased after load increases the pressure in the right side of the heart sufficiently to lead to blood being pumped into the left side of the heart, referred to as Eisenmenger’s syndrome.
39
Why is patent foramen ovale not classed as an atrial septal defect?
It is a unidirectional shunt from the right to left atria (but the blood doesn’t actually tend to move in any direction due to the increased pressure in the left atrium). There is no defect in the septum of the atria.
40
What is the hole called that is formed during embryology and persists, most commonly, in a ventricular septal defect? If left untreated, what will form?
Primary interventricular foramen.
Pulmonary hypertension and right-sided heart failure.
41
What causes hypoplastic left heart?
Mitral or aortic valve stenosis, causing less blood to flow into the left ventricle, leading to its underdevelopment.
42
When do right to left shunts occur?
When there is a defect in the atrial or ventricular septa, with an obstruction, increasing the pressure in the right side of the heart.
43
What is Ek?
The equilibrium position at which the movement of potassium ions inside and outside the cell are equal, around -95mV.
44
What is the main factor that affects the resting membrane potential of ventricular myocytes?
The leaky potassium channels.
45
What type of channels are used in the funny current? What do they allow the movement of, and in what direction?
HCN channels - hyperpolarisation-activated cyclic nucleotide-gated channels.
They allow the influx of sodium ions.
46
What is the plasma potassium concentration range?
3.5 - 5.5mM.
47
Give some examples of where M2 and M3 receptors are found.
M2 are seen in the heart.
M3 are seen in the pupil of the eye, the airways of the lungs and sweat glands.
48
What nerve gives parasympathetic input to the heart, and what receptor is acted upon for what result?
The vagus nerve releases ACh onto M2 receptors.
These are located on the SA and AV nodes to decrease the rate of contraction.
49
Why does the parasympathetic nervous system not decrease the force of contraction of the heart?
There are no M2 receptors on the myocardium.
50
How does noradrenaline increase the force of contraction of the heart?
It activates the Gs GPCR which the alpha-s subunit dissociates to activate the adenylyl cyclase.
The adenylyl cyclase synthesises cAMP which activates PKA.
PKA phosphorylates the Ca2+ channels on the cell membrane and sarcoplasmic reticulum, increasing release of Ca2+.
The Ca2+ then binds to more troponin-C increasing the force of contraction.
More Ca2+ is also taken back into the SR.
51
Arteries supplying where also contain Beta-2 receptors?
The heart and skeletal muscle.
52
Explain how activation of beta-2 adrenoceptors promote vascular smooth muscle relaxation.
53
What nerves of the baroreceptor reflex are associated with the carotid sinus and aortic arch?
Carotid sinus = glossopharyngeal nerve.
Aortic arch = vagus nerve.
54
Why can the baroreceptor reflex not be used for long-term control of blood pressure?
The set point can increase.
55
How does the baroreceptor reflex work?
Stretch is sensed by the baroreceptor, due to an increase in blood pressure.
They then send signals to the medulla oblongata to decrease the sympathetic innervation and increase the parasympathetic innervation.
This causes a decrease in heart rate and force of contraction, and vasodilation of the vessels, decreasing blood pressure.
56
What is hypertension?
A sustained increase in blood pressure.
57
Where is renin released from, and what stimulates its release?
The granular cells of the juxtaglomerular apparatus:
- Reduced NaCl delivery to the distal tubule.
- Sympathetic stimulation of the JGA.
- Reduced renal perfusion.
58
What are the 2 types of angiotensin II receptors?
AT1 and AT2.
59
What do prostaglandins do to blood pressure?
Act as vasodilators.
Enhance glomerular filtration, reducing sodium and water reabsorption, decreasing blood volume and pressure.
60
What does dopamine do to blood pressure?
Causes vasodilation, increasing blood flow to the kidneys, increasing glomerular filtration rate.
Decreases reabsorption of sodium and water.
61
How do diuretics work?
Inhibit the reabsorption of sodium and water.
62
Name the following vessels:
63
What is superficial vein thrombophlebitis, and what are the complications?
It is inflammation of a superficial vein, appearing on the skin as streaks of erythema, that often follows on from varicose veins, due to a clot.
It increases the risk of DVT.
64
What is venous ulceration, its symptoms and cause?
Ulceration around hard nodular areas of skin, that are painful and red.
It is a result of venous hypertension, with poor perfusion of the skin.
65
What is venous eczema and what can it lead to?
It is a chronic, itchy, red and swollen skin condition, due to chronic venous insufficiency.
It can lead to lipodermatosclerosis.
66
What can revascularisation in acute limb ischaemia cause?
Compartment syndrome.
67
What is the management of chronic peripheral arterial disease?
Exercise, smoking cessation, antiplatelet drugs, angioplasty, bypass graft.
68
What value on an ankle-brachial pressure index suggests peripheral artery disease?
An ankle systolic divided by the brachial systolic being less than 0.8
69
What is critical limb ischaemia?
Where chronic peripheral vascular disease progresses to pain at rest, not just exercising.
It required strong pain relief.
70
What does untreated critical limb ischaemia lead to?
Ulceration and gangrene.
71
What is an example of a re-entry loop syndrome?
Wolff-Parkinson-White syndrome.
72
When is lidocaine usually given, and what is its mechanism of action?
In ventricular tachycardia to bind to the VGNC of the damaged tissues, preventing automatic firing of depolarised myocytes.
73
What do beta-blockers do to the action potential?
Decrease the slope of the pacemaker potential and upstroke, increasing the length of the action potential.
74
How do cardiac glycosides work?
Block the sodium/ potassium ATPase, causing the sodium/ calcium exchanger to reverse, so there is an influx of calcium into the cell, increasing the force of contraction.
Increase the vagus activity of the heart to slow conduction of the AV node and heart rate.
75
How do nitric oxides cause vendoilation?
Activate guanylate cyclase, increasing cGMP synthesis.
cGMP activates PKG which phosphorylase’s the VGCCs.
This acts to lower intracellular calcium, causing relaxation of vascular smooth muscle.
76
Why is the depolarisation delayed in the AV node for 120-200ms?
To allow for blood to drain into the ventricles through atrial contraction before ventricular contraction.
77
What is the first 2 things that should be checked when analysing an ECG, after checking that it is the correct patient and the machine is programmed correctly?
1) Check for sinus rhythm - each QRS is preceded by a P wave.
2) Check the regularity of the rhythm and rate - whether it is regular/ irregular and bradycardia or tachycardia.
78
What is sinus tachycardia and sinus bradycardia?
ST = rate of depolarisation from the SA node greater than 100 per minute.
SB = rate of depolarisation from the SA node less than 60 per minute.
79
What is the difference in depolarisations in atrial fibrillation and atrial flutter?
In atrial fibrillation, the depolarisations are coming from ectopic sites, whereas in atrial flutter, they are coming from the SA node, just incredibly quickly.
80
What are the most common causes of first degree heart block?
Vagal activation.
Electrolyte disturbances.
Medication - calcium channel blockers or beta blockers.
81
What are the 2 types of second degree heart block?
Mobitz type I - the PR intervals continue to lengthen until there is a failure of conduction and no QRS complex occur, and the cycle starts again.
Mobitz type II - there is a ratio between the atrial depolarisations and ventricular depolarisations, most commonly 2:1 but can be greater. This is because not all the P waves are conducted to the ventricles.
82
What is seen on an ECG with a bundle branch block?
A wide QRS complex as the normal conduction pathway is not being followed, but still sinus rhythm.
83
What can be done to image the posterior aspect of the heart on an ECG?
Add leads 7 and 8.
84
What is sinus arrhythmia?
Where there is always a P-wave followed by a QRS complex but the there is irregular spacing between the QRS complexes.
85
What leads should be looked at with left and right axis deviation?
The limb leads, only:
- I, II, III.
- aVL, aVR, aVF.
86
What is left axis deviation and what can be the cause?
It is where the depolarisation follows a route that centres more to the left, making aVL more positive. It can be caused by:
- Left ventricular hypertrophy.
- Complete inferior MI.
- Wolf-Parkinson-White syndrome.
It can also be a normal variant.
87
What is right axis deviation and what can be the cause?
It is where the route of depolarisation follows a route more to the right, making lead III more positive. It can be caused by:
- Right ventricular hypertrophy.
- Wolf-Parkinson-White syndrome.
- Complete lateral myocardial infarction.
It can be normal in children.
88
What can be the cause of a short PR interval and a long PR interval?
Short PR interval = accessory pathway.
Long PR interval = first degree heart block.
89
What can a large R wave suggest?
Ventricular hypertrophy.
90
What are the mean arterial, capillary and venous pressures of the pulmonary circulation?
MAP = 12-15mmHg.
MCP = 9-12mmHg.
MVP = 5mmHg.
91
What gives the pulmonary circulation a low resistance?
It contains short, wide vessels.
It has a high capillary density.
It has arterioles with little smooth muscle.
92
Why does the systemic circulation need a greater lymphatic drainage than the lungs?
The oncotic pressure in the systemic circulation is lower than the pulmonary.
The capillary hydrostatic pressure is greater in the systemic than in the lungs.
93
At what pressure does the myogenic autoregulation response fail at?
Below 50mmHg.
94
Where do the right and left coronary arteries arise from?
The right and left aortic sinuses.
95
What does the coronary endothelium continuously produce to maintain high basal flow?
NO for vasodilation.
96
What are the functions of the skeletal muscle circulation?
To maintain oxygen and nutrient delivery, and removal of metabolites during exercise, to allow the skeletal muscle to continue to work.
Regulation of of arterial blood pressure to allow for perfusion of other organs.
97
What two things is the increased blood flow to the skeletal muscle due to during exercise?
98
What are artereovenous anastomoses controlled by?
Sympathetic vasoconstrictor fibres - increase in innervation will decrease heat loss.
99
Why do patients with myocardial infarctions experience sympathetic nervous system symptoms?
Visceral afferents from the heart run with sympathetic nerve fibres and are stimulated when the visceral afferents are.
The sympathetic nervous system is also upregulated due to the falling cardiac output.
100
What are the different nerve fibres that are used for cardiac and pleuritic chest pain?
Cardiac uses visceral afferent nerves.
Pleuritic uses somatic afferent nerves.
101
What term is used to describe pain that moves from one place to another?
Referred pain.
102
Why is cardiac pain referred?
The visceral afferents of the heart are sent to the spinal cord at the level of T1-T4/5.
This is perceived by the brain as innervation from the somatic afferents.
The dermatomes of T1-4/5 are then perceived as the ones giving off the pain signals.
103
What are type I and type II MIs?
Type I = rupture of an atherosclerotic plaque, thrombus formation and occlusion of a coronary artery, leading to myocardial necrosis.
Type II = a condition other than coronary plaque instability, leading to an imbalance between myocardial oxygen supply and demand.
104
What can exacerbate pain during angina?
Exercise.
Stress, emotion and cold weather.
Eating.
105
How does the GTN spray work?
Predominantly by causing venodilation to increase the blood flow through the coronary arteries, decrease the venous return and decrease pre-load, decreasing the demand on the heart.
106
What is the management for a patient after a myocardial infarction?
Lifestyle changes - low fat diet, regular exercise, low salt.
Aspirin for life.
Statins to reduce the cholesterol.
Beta blockers.
ACE inhibitors.
107
What is the equation for ejection fraction?
(Stroke volume/ end diastolic volume) x 100.
108
What conditions can increase the demand on the heart sufficiently to cause heart failure?
Sepsis.
Thyrotoxicosis.
109
What does measuring ejection fraction allow a clinician to do for a patient in heart failure, and how is this done?
Determine whether the heart failure is due to an ejection or filling problem, determining the course of treatment.
It is measured using an echocardiogram.
110
What percentages determine whether the heart failure is HFrEF or HFpEF?
HFrEF = less than 40%.
HFpEF = 50% or above.
111
Why do people experience dyspnoea and fatigue with heart failure?
Due to tissue hypoperfusion.
112
What causes the activation of the RAAS system?
The decrease in renal perfusion.
Stimulation through the sympathetic nervous system (renin release).
113
What is the direct affect that long-term activation of the sympathetic nervous system and RAAS has on the heart?
Sympathetic nervous system, and the angiotensin II released, both have a direct cardiotoxic effect on the heart, which stimulates apoptosis of cardiac myocytes.
114
Explain why pulmonary and peripheral oedema may be present with left ventricular heart failure.
115
What is paroxysmal nocturnal dyspnoea?
Waking at night, suddenly gasping for breath. It is relieved by sitting up.
116
What is orthopnoea?
Shortness of breath that worsens when lying down.
117
Explain why peripheral oedema occurs with right ventricular heart failure.
118
What are the long-term deleterious effects of up-regulation of the SNS?
Down-regulation of beta-adrenergic receptors.
Induction of cardiac myocyte apoptosis/ hypertrophy.
Up-regulation of the RAAS.
119
State the abnormal calculation of measuring mean arterial blood pressure, and why this can be done.
1/3 systolic pressure + 2/3 diastolic pressure.
This is because in the cardiac cycle, 1/3rd of the time is spent in systole and 2/3rds of the time is spent in diastole.
120
What is oliguria?
Decrease in urine output.
121
What is pulseless electrical activity?
Where the cardiac myocytes do not respond to electrical activity.
122
What percentage of blood is required to be lost to cause hypovolaemic shock?
30-40% for it to be serious.
20-30% will cause a few signs.
123
What is the definition of septic shock?
Persisting hypotension requiring treatment to maintain blood pressure, despite fluid resuscitation.
