Cardiovascular Flashcards
1
Q
Electrocardiography is a representation of what?
A
The electrical events of the cardiac cycle.
2
Q
Name 6 conditions that electrocardiography can help identify.
A
Arrhythmias. Myocardial ischaemia and infarction. Pericarditis. Chamber hypertrophy. Electrolyte disturbances. Drug toxicity.
3
Q
Name a drug which may cause arrhythmia.
A
Digoxin.
4
Q
Name the dominant pacemaker of the heart.
A
The sinoatrial node.
5
Q
What is the intrinsic rate of the SAN?
A
60-100bpm.
6
Q
What is the name for a cardiac rhythm in which depolarisation of the cardiac muscle begins at the SAN?
A
Sinus rhythm.
7
Q
What is the function of the AVN.
A
To manage electrical activity from the atria to the ventricles and act as a back-up pacemaker.
8
Q
What is the intrinsic rate of the AVN?
A
40-60bpm.
9
Q
In addition to the AVN, what also functions as a back-up pacemaker?
A
Ventricular cells.
10
Q
What is the intrinsic rate of ventricular cells?
A
20-45bpm.
11
Q
Describe the conduction pathway of the heart.
A
SAN to AVN to Bundle of His to Bundle branches to Purkinje fibres.
12
Q
On an ECG trace, the P wave represents what?
A
Atrial depolarisation.
13
Q
On an ECG trace, the PR interval represents what?
A
The time between atrial depolarisation and electrical activation through the AVN.
14
Q
On an ECG trace, the QRS complex represents what?
A
Ventricular depolarisation.
15
Q
On an ECG trace, the ST segment represents what?
A
The period between depolarisation and repolarisation.
16
Q
On an ECG trace, the T wave represents what?
A
Ventricular repolarisation.
17
Q
Why doesn’t atrial repolarisation appear on the trace?
A
It is hidden by the QRS complex.
18
Q
Define tachycardia.
A
An elevated heart rate, >100 bpm.
19
Q
Define bradycardia.
A
A reduced heart rate, <60 bpm.
20
Q
Define dextrocardia.
A
The heart is on the right hand side of the chest instead of the left.
21
Q
Define acute anterolateral myocardial infarction.
A
Elevated ST segment in the anterior (V3 and V4) and lateral (V5 and V6) leads.
22
Q
Define acute inferior myocardial infarction.
A
Elevated ST segment in the inferior (I, III, aVF) leads.
23
Q
On ECG paper, what does one large box represent horizontally?
A
0.2 seconds.
24
Q
On ECG paper, what does one small box represent horizontally?
A
0.04 seconds, 40ms.
25
On ECG paper, what does one large box represent vertically?
0.5mV.
26
Describe the location where the left ventricle can be palpated.
The left, 5th intercostal space on the mid-clavicular line.
27
What is the left ventricle responsible for?
The apex beat.
28
Define stroke volume.
The volume of blood ejected from each ventricle during systole.
29
Define cardiac output.
The volume of blood ejected from each ventricle as a function of time.
30
Define total peripheral resistance.
The total resistance to blood flow in the systemic blood vessels (between the aorta and the vena cava).
31
Which blood vessels have the highest resistance to blood flow.
Arterioles.
32
Define preload.
The volume of blood in the left ventricle before left ventricular contraction (end-diastolic volume).
33
Define afterload.
The pressure the left ventricle must overcome to eject blood during contraction.
34
Define contractility.
The force of contraction and change in myocardial fibre length.
35
Define cardiac elasticity.
The ability of the muscle to recover to its normal shape after systole.
36
Define diastolic dispensability.
The pressure required to fill the ventricles to the same diastolic volume.
37
Define cardiac compliance.
How easily the heart chamber expands when filled with blood.
38
What is Starling's law?
The contractility of the heart is directly proportional to the end-diastolic volume.
39
Explain why stroke volume decreases as you stand up.
The effect of gravity reduces venous return, reducing end-diastolic volume
40
The first heart sound is produced from which event in the cardiac cycle?
The closure of the mitral and tricuspid valves.
41
The second heart sound is produced from which event in the cardiac cycle?
The closure of the aortic and pulmonary valves.
42
The third heart sound occurs when during the cardiac cycle?
In early diastole during rapid ventricular filling.
43
The third heart sound is normal in which patients?
Children and pregnant women.
44
What conditions is the third heart sound associated with?
Mitral regurgitation and heart failure.
45
The fourth heart sound occurs because of what?
Blood being forced into a stiff hypertrophic ventricle.
46
When does the fourth heart sound occur in the cardiac cycle?
Late diastole.
47
Name the condition associated with the fourth heart sound.
Left ventricular hypertrophy.
48
Give another name for ischaemic heart disease.
Coronary heart disease.
49
Give examples of ischaemic heart disease.
Stable angina. Unstable angina. Myocardial infarction. Cardiac arrest.
50
Describe the mechanism by which ischaemic heart disease develops.
Atherogenesis causes atherosclerosis.
51
Define atherogenesis.
The formation of fatty deposits in the arteries.
52
Define atherosclerosis.
The narrowing of an artery due to a build up of plaque.
53
Atherosclerosis commonly develops in which three arteries?
The circumflex, left anterior descending and right coronary artery.
54
Name seven risk factors for atherosclerosis.
```
Age.
Smoker.
High serum cholesterol.
Obesity.
Diabetes.
Hypertension.
Family history.
```
55
Why is diabetes a risk factor for atherosclerosis?
Hyperglycaemia damages endothelium.
56
Why is smoking a risk factor for atherosclerosis?
Smoking cause endothelial erosion.
57
What is the first step of the development of an atherosclerotic plaque?
Damage to endothelium.
58
How does damage to the endothelium contribute to atherosclerosis.
Damaged endothelium releases chemoattractants.
59
What is the function of chemoattractants?
To attract leukocytes.
60
Give examples of chemoattractants involved in atherosclerosis.
IL-1
IL-6
IFN gamma
61
How do leukocytes contribute to atherosclerosis?
They accumulate and migrate into the vessel wall.
62
Atherosclerosis begins as which type?
Fatty streak.
63
At what age can fatty streaks be found in the body?
Less than 10 years old.
64
What are fatty streaks composed of?
Lipid-laden macrophages and T-lymphocytes in the intimal layer of vessel wall.
65
Lipid-laden macrophages are called what?
Foam cells.
66
Fatty streaks develop into what?
Intermediate lesions.
67
What are intermediate lesions composed of?
Layers of foam cells, vascular smooth muscle cells and T-lymphocytes.
68
Other than cells, what also contributes to intermediate lesions?
Adhesion and accumulation of platelets to the vessel wall.
69
Intermediate lesions develop into what?
Fibrous plaques.
70
What are fibrous plaques composed of?
Smooth muscle cells.
Foam cells.
Red blood cells.
T-lymphocytes.
71
The components of a fibrous plaque are covered by what?
A dense fibrous cap made of extracellular matrix proteins.
72
Name two proteins that form the cap of a fibrous plaque.
Collagen.
| Elastin.
73
The cap of the fibrous plaque keeps what contained?
Lipid core and necrotic debris.
74
Describe the two possible outcomes of atherosclerotic development.
Plaque grows and occludes the vessel, restricting blood flow.
Plaque ruptures, forming thrombus and causing death.
75
What condition is caused when a plaque occludes a blood vessel and restricts blood flow?
Angina.
76
How does angina present?
Chest tightness/heaviness that radiates to the arms, neck, jaw and teeth. Precipitated by exertion. Relieved by rest / GTN spray.
77
Angina is a result of what?
Reversible myocardial ischaemia causing a mismatch of blood supply and metabolic demand.
78
What is myocardial ischaemia?
Inadequate blood supply (due to narrowing of the coronary arteries, reducing blood and therefore oxygen supply).
79
How is stable angina characterised?
Induced by effort/exertion and relieved by rest.
80
How is unstable angina characterised?
More sever and more frequent. Occurs at minimal exertion or even at rest.
81
Unstable angina is associated with an increased risk of what?
Myocardial infarction.
82
Other than stable and unstable, name another type of angina?
Prinzmetal's angina.
83
How is Prinzmetal's angina characterised?
Caused by coronary artery spasm.
84
Other than mismatch of supply and demand, what else is responsible for angina?
Ischaemic metabolites stimulate nerve endings and cause pain.
Gender.
85
Give nine risk factors for angina.
Smoking. Sedentary lifestyle. Obesity. Hypertension. Diabetes. Family history. Genetics. Age. Hypercholesterolaemia.
86
How do arteries accommodate the growth of plaques?
By arterial remodelling.
87
What is arterial remodelling?
Arterial vessel growth.
88
At what point is arterial remodelling unable to accommodate plaque growth?
When the plaque is greater than 50% of the lumen size.
89
Give examples of a differential diagnosis of angina.
```
Pericarditis.
Pulmonary embolism.
Chest infection.
Dissection of the aorta.
GORD.
```
90
How is angina diagnosed on an ECG?
ECG typically normal but may show ST segment depression, a flat/inverted T wave or signs of past MI.
91
Other than the use of an ECG, give four other methods for diagnosing angina.
Treadmill test.
CT scan calcium scoring.
SPECT.
Cardiac catheterisation.
92
How does a CT scan for calcium scoring help diagnose angina?
The CT scan identifies calcium - a marker for atherosclerosis (calcified plaque).
93
How does SPECT help diagnose angina?
A radio-labelled tracer is injected into the patient, which is taken up the coronary arteries to highlight areas of good blood supply (and inversely poor blood supply - as a result of atherosclerosis).
94
Angina treatment can be separated into which three categories?
Modify risk factors.
Pharmacological intervention.
Surgical intervention.
95
Give five pharmacological options for the treatment of angina.
```
Aspirin.
Statin.
Beta-blockers.
Glyceryl trinitrate spray.
Calcium channel antagonists.
```
96
Describe two ways by which aspirin helps treat angina.
Inhibits platelet aggregation - avoiding platelet thrombosis.
Inhibits COX.
97
How does COX inhibition help treat angina?
By reducing prostaglandin synthesis thereby reducing platelet aggregation.
98
Describe how statins help treat angina.
Reduce cholesterol production by the liver.
99
Describe how beta-blockers help treat angina.
By slowing the heart and reducing the force of contraction - lower oxygen demand.
100
Give five contra-indicators for treating angina with beta-blockers.
```
Asthma.
Hypotension.
COPD.
LVF.
Bradycardia.
```
101
Describe how glyceryl trinitrate spray helps to treat angina.
GTN sprays are venodilators, meaning they dilate the systemic veins. Venodilation reduces the venous return and reduces preload, therefore the force of contraction decreases and the heart has a lower oxygen demand.
102
Describe how calcium channel antagonists help to treat angina.
Calcium channel antagonists are arteriodilators, meaning they dilate the systemic arteries. Arteriodilation reduces the blood pressure and reduces afterload, therefore the force of contraction decreases and the heart has a lower oxygen demand.
103
Give two surgical options for the treatment of angina.
Percutaneous transluminal coronary angioplasty (or percutaneous coronary intervention).
Coronary artery bypass graft.
104
Describe how percutaneous transluminal coronary angioplasty helps to treat angina?
Atheromas are dilated by inflating a balloon within a vessel, then removing the balloon to leave behind a stent.
105
Give risks and benefits of percutaneous transluminal coronary angioplasty.
Risk of stent thrombosis.
| PCTA is minimally invasive and has a short recovery time.
106
Describe how a coronary artery bypass graft can help treat angina.
The left internal mammary artery is used to bypass a proximal narrowing in the left anterior descending artery.
107
What are negatives of the use of coronary artery bypass grafts?
An invasive procedure with a long recovery time.
108
What is acute coronary syndrome?
A syndrome due to decreased blood flow in the coronary arteries, leading to improper functioning or death of the heart muscle.
109
How is acute coronary syndrome characterised?
With central chest pain lasting greater than 20 minutes.
110
ACS characteristic chest pain is associate with what other signs/symptoms?
Sweating, nausea, vomiting, dyspnoea and fatigue.
111
Chest pain may not present in which patients with ACS?
Diabetics and the elderly.
112
How may ACS present in diabetic and elderly patients?
Syncope, pulmonary oedema, epigastric pain and vomiting.
113
Give five examples of signs of ACS other than chest pain.
Distress and anxiety. Pallor. Increased pulse and reduced blood pressure. Reduced fourth heart sound. Tachy/bradycardia.
114
Give six risk factors for ACS.
Age. Male. Family history of IHD. Smoking. Hypertension, diabetes mellitus, hyperlipidaemia. Obesity.
115
Describe how ACS develops.
Rupture/erosion of fibrous cap of coronary artery plaque leads to platelet aggregation and adhesion. Platelets cause vasoconstriction and localised thrombosis which results in reduced blood flow and ischaemia.
116
The risk of rupture of a coronary artery plaque increases due to which factors?
Presence of rich lipid pool beneath the fibrous cap.
| The fibrous cap is thin.
117
What are the three types of ACS?
STEMI.
NSTEMI.
UA.
118
What is STEMI?
ST-elevation myocardial infarction is full thickness damage of heart muscle that occurs due to the complete occlusion of a major coronary artery.
119
How is STEMI diagnosed using ECG?
ST elevation. New left bundle branch block. Pathological Q wave will be present some time (days) after MI. Hyperacute T waves.
120
What is NSTEMI?
Non-ST-elevation myocardial infarction is partial thickness damage of heart muscle due to partial occlusion of a major coronary artery or complete occlusion of a minor coronary artery.
121
How is NSTEMI diagnosed?
Retrospectively after troponin results are available.
122
How may NSTEMI present on an ECG?
ST depression and/or T wave inversion. Hyperacute T waves.
123
What is UA?
Unstable angina of recent onset (less than 24 hours). A deterioration of previously stable angina.
124
What is the difference between NSTEMI and UA?
In NSTEMI an occluding thrombus causes myocardial necrosis and increased serum troponin or CK-MB.
125
What is myocardial infarction?
Myocyte death due to myocardial ischaemia.
126
What is Type 1 MI?
Spontaneous MI with ischaemia due to a primary coronary event.
127
Give three examples of a primary coronary event.
Plaque rupture. Fissuring. Dissection.
128
What is Type 2 MI?
MI secondary to ischaemia due to increased oxygen demand or decreased supply.
129
What conditions may lead to a decreased supply of oxygen to cause ischaemia?
Coronary spasm.
Coronary embolism.
Anaemia. Arrhythmia. Hyper/hypotension.
130
What is Type 3 MI?
MI due to sudden cardiac death.
131
What is Type 4 MI?
MI related to PCI (including stent thrombosis).
132
What is Type 5 MI?
MI related to CABG.
133
Give six possible differential diagnosis' of ACS.
```
Angina.
Pericarditis.
Myocarditis.
Aortic dissection.
Pulmonary embolism.
Oesophageal reflux.
```
134
Name three biochemical markers of ACS.
Troponin T & I.
CK-MB.
Myoglobin.
135
Which biochemical marker is the best for diagnosing ACS?
Troponin T & I.
| The most sensitive and specific markers of myocardial necrosis.
136
How are Troponin T & I used to diagnose ACS?
3 to 12 hours from the onset of chest pain, serum Troponin T & I levels will be increased.
137
When do Troponin T & I levels peak?
24 to 48 hours after the onset of chest pain.
138
When do Troponin T & I levels return to baseline?
Over a period of 5 to 14 days.
139
Give another use, other than identifying ACS, for measuring Troponin T & I levels.
Peak levels can be used as prognostic indicator for risk of mortality. As well as determining which patients would benefit the most from aggressive medical therapy and early coronary revascularisation.
140
What is CK-MB?
A creatine kinase isoenzyme mainly found in heart muscle.
141
How is CK-MB used to diagnose ACS?
3 to 12 hours from the onset of chest pain, serum CK-MB levels will increase.
142
When do CK-MB levels peak?
Within 24 hours from the onset of chest pain.
143
When do CK-MB levels fall to baseline?
After 48 to 72 hours.
144
How is myoglobin used to diagnose ACS?
1 to 4 hours from onset of chest pain, serum myoglobin levels will increase.
145
Why is myoglobin unreliable?
It isn't specific. Myoglobin is also found in skeletal muscle.
146
How can a chest x-ray be used to diagnose ACS?
Identification of pulmonary oedema, cardiomegaly and widened mediastinum.
147
Suggest nine groups of treatments that may be used to treat ACS?
```
Pain relief.
Antiemetic.
Oxygen.
Anti-platelet.
Beta-blockers.
Statins.
ACE inhibitors.
Coronary revascularisation.
Modifiable risk factors.
```
148
What options are available for pain relief treatment for ACS?
GTN spray.
| IV opioid.
149
What is the purpose of an antiemetic?
Effective against nausea and vomiting.
150
What is an ideal oxygen saturation?
94-98%
151
What is an ideal oxygen saturation for a patient with COPD?
88-92%
152
Give three examples of antiplatelet therapies.
Aspirin.
P2Y12 inhibitors.
Glycoprotein IIa/IIIb antagonists.
153
What is the route of administration of P2Y12 inhibitors?
Oral.
154
Name three drugs that are P2Y12 inhibitors and used in the treatment of ACS.
Clopidogrel.
Prasugrel.
Ticagrelor.
155
What is a side effect of using P2Y12 inhibitors?
Increased risk of bleeding.
156
What is a caution for using P2Y12 inhibitors?
Avoid if CABG planned.
157
When are glycoprotein IIa/IIIb inhibitors used?
In combination with aspirin and P2Y12 inhibitors in patients with ACS undergoing PCI.
158
Name three drugs that are glycoprotein IIa/IIIb inhibitors and used in the treatment of ACS.
Abciximab.
Tirofiban.
Eptifbatide.
159
What is a side effect of using glycoprotein IIa/IIIb inhibitors?
Increased risk of major bleed.
160
How are glycoprotein IIa/IIIb inhibitors administered?
By IV only.
161
Name two beta-blockers used in the treatment of ACS.
Atenolol.
| Metoprolol.
162
How are beta-blockers administered?
By IV then orally.
163
Explain the use of statins in the treatment of ACS.
HMG-CoA inhibitors inhibit cholesterol production.
164
Name three statins used in the treatment of ACS.
Simvastatin. Pravastatin. Atorvastatin.
165
Name two ACE inhibitors used in the treatment of ACS.
Ramipril. Lisonopril.
166
Ramipril and lisonopril are administered by which route?
Orally.
167
What is the incidence of ACS in the UK per year?
5/1000.
168
Define acute myocardial infarction.
Necrosis of cardiac tissue due to prolonged myocardial ischaemia due to complete occlusion of an artery by thrombus.
169
Of deaths, how many people die from STEMI per annum?
5/1000.
170
STEMI has a worse prognosis in which groups of patients?
The elderly.
| Those with left ventricular failure.
171
Give examples of risks for acute myocardial infarction.
```
Premature ménopause.
Those with CHD.
Age.
Male.
Hyperlipidaemia.
Hypertension.
Diabetes mellitus.
Family history of IHD.
Obesity.
Smoking.
```
172
Describe how acute myocardial infarction occurs.
Rupture/erosion of a vulnerable fibrous cap of coronary artery plaque. Platelet accumulation, adhesion, localised thrombosis, vasoconstriction result in distal thrombus embolisation - arterial occlusion.
173
Myocardial necrosis occurs how long after complete arterial occlusion?
15 to 30 minutes.
174
Infarction initially affects which area following complete coronary artery occlusion?
Sub-endocardial myocardium.
175
If ischaemia continues after initially affecting sub-endocardial myocardium, which area becomes affected?
Sub-epicardial myocardium.
176
What is the difference between the endocardium and the epicardium?
The endocardium is the inner layer of the heart wall.
| The epicardium is the outer layer of the heart wall.
177
What can the MI be called when infarct zone spreads to the epicardium?
Transmural Q wave MI.
178
Define transmural.
Occurs across the entire wall of the organ.
179
How may regions of the myocardium be salvaged after MI?
Early reperfusion.
180
How does MI present?
Severe central chest pain lasting greater than 20 minutes.
181
How is the pain of MI described?
```
Substernal pressure.
Sharp.
Squeezing.
Aching.
Burning.
```
182
How effective is GTN spray for treating MI pain?
Pain doesn't usually respond.
183
Other than chest pain, how else does MI present?
```
Breathlessness.
Distress and anxiety.
Significant hypotension.
Fatigue.
Tachy/bradycardia.
Pale, clammy and marked sweating.
```
184
How does STEMI present on an ECG?
ST elevation.
Hyperacute T waves.
LBBB.
T wave inversion and pathological Q wave follow.
185
An anterior infarct causes what changes on an ECG?
ST elevation in leads V1 to V3. ????????
186
An inferior infarct causes what changes on an ECG?
ST elevation in leads I, III and aVF.
187
A lateral infarct causes what changes on an ECG?
Leads I, AVL and V5 to V6 show change.
188
A posterior infarct causes what changes on an ECG?
ST depression V1 to V3.
ST elevation V5 to V6.
Dominant R wave.
189
A subendocardial infarct causes what changes on an ECG?
Any change.
190
Why is continuous ECG monitoring required after MI.
Likelihood of significant cardiac arrhythmia.
191
Minutes after STEMI: what does the ECG show?
T waves tall, pointed and upright.
| ST elevation.
192
Hours after STEMI: what does the ECG show?
T waves invert.
| Q waves develop as the R wave voltage increases.
193
Days after STEMI: what does the ECG show?
ST segment returns to normal.
194
Weeks/months after STEMI: what does the ECG show?
T waves may return upright.
| Q waves remain.
195
Other than ECG, what investigation could be performed to confirm MI?
Transthoracic echocardiography.
196
What can transthoracic echocardiography show?
Wall motion abnormalities.
197
How is prehospital MI treated?
Aspirin 300mg chewable.
GTN.
Morphine.
198
How is hospital MI treated?
IV morphine.
Oxygen.
Betablockers - atenolol.
P2Y12 inhibitor - clopidogrel.
199
Give two other options, other than pharmacological intervention, for the treatment of MI?
Coronary revascularisation (including percutaneous transluminal coronary angioplasty and coronary artery bypass graft) or fibrinolysis.
200
Describe how fibrinolysis is used as a treatment of MI?
To enhance the breakdown of occlusive thromboses by activation of plasminogen to form plasmin.
201
What are modifiable risk factors of MI?
```
Stop smoking.
Increase exercise.
Lose weight.
Eat a healthier diet.
Alcohol intake within recommended limits.
```
202
What drugs are used for secondary prevention post MI?
```
Statins.
Aspirin.
Beta-blockers.
ACE inhibitors.
Warfarin (if large MI).
```
203
Give a possible complication within hours of MI.
Sudden death.
204
Sudden death post MI is due to what?
Ventricular fibrillation.
205
Why may persistent pain occur post MI?
Due to progressive myocardial necrosis.
206
How soon may persistent pain occur following MI?
12 hours to days after.
207
Why may arrhythmias occur post MI?
Due to electrical instability following infarction, pump failure and excessive sympathetic stimulation.
208
Explain why heart failure may occur following MI.
Muscle necrosis causes ventricular dysfunction, reducing cardiac output to a level that is insufficient to meet metabolic demands.
209
What is mitral incompetence?
Failure of the mitral valve to close properly allowing the regurgitation of blood back from the left ventricle into the left atrium. (Mitral regurgitation).
210
Why does mitral incompetence occur following MI?
Myocardial scarring prevents valve closure.
211
Why may pericarditis occur following MI?
A transmural infarct would cause inflammation of the pericardium.
212
Early cardiac rupture is a result of what?
Shearing between mobile and immobile myocardium.
213
Late cardiac rupture is a result of what?
Weakening of the wall following muscle necrosis and acute inflammation.
214
What is a ventricular aneurysm?
Inward bulging of the ventricular wall. Begin from a weakened area of the ventricular wall - filled with blood.
215
Why are ventricular aneurysms concerning?
Although they won't usually rupture they can block passageways out of the heart and reduce blood flow.
216
Why may ventricular aneurysms occur post MI?
Due to stretching of newly formed collagenous scar tissue.
217
What is cardiac failure?
The inability of the heart to deliver blood (and therefore oxygen) at a rate that is commensurate with the requirements of the body's metabolising tissues.
218
What is the mortality rate of cardiac failure following diagnosis?
25% to 50% mortality within the five years following diagnosis.
219
What is the prevalence of cardiac failure among the population?
1% to 3%.
220
What is the prevalence of cardiac failure among elderly patients?
10%.
221
Give six causes of cardiac failure.
```
Ischaemic heart disease.
Cardiomyopathy.
Valvular heart disease.
Cor pulmonale.
Hypertension.
Alcohol excess.
```
222
What is cardiomyopathy?
Disease of the heart muscle, which becomes enlarged, thick and stiff.
223
What is cor pulmonale?
Pulmonary heart disease. Enlargement and failure of the right ventricle.
224
What causes cor pulmonale?
Increased pulmonary resistance (due to pulmonary stenosis or pulmonary hypertension) puts the right ventricle under greater stress - eventually it fails.
225
Give five risk factors for cardiac failure.
```
Aged over 65.
Of African descent.
Obesity.
Male.
People with a history of MI.
```
226
Heart failure brings about what kind of physiological changes?
Compensatory changes.
227
Why does heart failure cause compensatory changes?
Compensatory changes try to negate the effect of heart failure.
228
Compensatory changes for heart failure aim to maintain what?
Cardiac output.
| Peripheral perfusion.
229
How does the progression of heart failure effect the compensatory changes?
Further progression overwhelms the compensatory changes.
230
What term describes the state when the compensatory changes are overwhelmed?
Decompensation.
231
What are the four compensatory mechanisms?
Venous return (preload).
Outflow resistance (afterload).
Renin-angiotensin system.
Sympathetic stimulation.
232
Describe how preload is a compensatory mechanism for heart failure.
During heart failure the volume of blood ejected from the heart decreases (more blood remains) so preload increases. According to Starling's law, greater preload increases the force of contraction of the heart.
233
Why may the preload compensatory mechanism for heart failure be ineffective?
In patients with heart failure the failing myocardium isn't able to contract that much more in response to increased preload - cardiac output cannot be maintained and may decrease.
234
Outflow resistance is made up of which three things?
Pulmonary and systemic resistance.
Physical characteristics of the vessel walls.
The volume of blood that is ejected.
235
Why may the outflow resistance compensatory mechanism for heart failure be ineffective?
Increase in afterload increases end-diastolic volume (cardiac output decreases). Increase in end-diastolic volume means ventricle must work harder - exacerbating the problem.
236
Outflow resistance is made up of which three things?
Pulmonary and systemic resistance.
Physical characteristics of the vessel walls.
The volume of blood that is ejected.
237
Why may the renin-angiotensin compensatory mechanism for heart failure be ineffective?
RAA system asks the heart to beat more forcefully to increase cardiac output. This causes a mismatch between supply (inadequate oxygen due to IHD) and demand (increased respiration for contraction). Ultimately the cardiac myocytes die and cardiac output decreases.
238
Describe how activation of the sympathetic system is a compensatory mechanism for heart failure.
During heart failure, arterial pressure decreases and venous pressure increases. These changes are detected by baroreceptors, which send out sympathetic stimulation to beta-1-adrenoceptors to increase the force of contraction and the heart rate with the aim of increasing cardiac output.
239
Why may the renin-angiotensin compensatory mechanism for heart failure be ineffective?
RAA system asks the heart to beat more forcefully to increase cardiac output. This causes a mismatch between supply (inadequate oxygen due to IHD) and demand (increased respiration for contraction). Ultimately the cardiac myocytes die and cardiac output decreases.
240
Describe how activation of the sympathetic system is a compensatory mechanism for heart failure.
During heart failure, arterial pressure decreases and venous pressure increases. These changes are detected by baroreceptors, which send out sympathetic stimulation to beta-1-adrenoceptors to increase the force of contraction and the heart rate with the aim of increasing cardiac output.
241
Where are baroreceptors located?
In the arterial wall of the aorta and carotid. In the walls of the heart and in the major veins.
242
Why may activation of the sympathetic system as compensatory mechanism for heart failure be ineffective?
Chronic sympathetic stimulation causes down regulation of the beta-1-adrenoceptors (fewer receptors), reducing the sympathetic activation of the heart and reducing cardiac output.
243
Name the four main types of heart failure.
Systolic.
Diastolic.
Acute.
Chronic.
244
Name four other types of heart failure.
Left-sided.
Right-sided.
Low-output.
High-output.
245
Describe systolic heart failure.
The inability of the ventricles to contract normally.
246
Give two characteristics of systolic heart failure.
Cardiac output decreases.
| Ejection fraction < 40%.
247
Give three causes of systolic heart failure.
IHD, MI, cardiomyopathy.
248
Describe diastolic heart failure.
The inability of the ventricles to relax and fill fully.
249
Give two characteristics of diastolic heart failure.
Cardiac output decreases.
| Ejection fraction > 50%.
250
What is tamponade?
When the pericardial fluid builds up and constricts the heart.
251
Other than hypertrophy, name three other causes of diastolic heart failure.
Aortic stenosis.
Constrictive pericarditis.
Tamponade.
252
What is tamponade?
When the pericardial fluid builds up and constricts the heart.
253
Describe acute heart failure.
Almost exclusively new onset or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension.
254
Describe chronic heart failure.
Develops slowly. Venous congestion is common but arterial pressure is well maintained until very late.
255
What is venous congestion?
When arterial flow is greater than venous flow.
256
A diagnosis of heart failure is made using which criteria?
Framingham criteria.
257
Name nine major criteria for heart failure.
```
Paroxysmal nocturnal dyspnoea.
Crepitations.
S3 gallop.
Cardiomegaly.
Increased central venous pressure.
Weight loss.
Neck vein distension.
Acute pulmonary oedema.
Hepatojugular reflux.
```
258
What is paroxysmal nocturnal dyspnoea?
Attacks of severe shortness of breath or coughing, typically at night.
259
What are crepitations?
Crackles of the lung.
260
What is S3 gallop caused by?
Rapid ventricular filling. Occurs in early diastole.
261
Describe the hepatojugular reflux.
Distension of the neck veins occur when pressure is applied to the liver.
262
Name seven minor criteria for heart failure.
```
Bilateral ankle oedema.
Dyspnoea on ordinary exertion.
Tachycardia.
Decrease in vital capacity.
Nocturnal cough.
Hepatomegaly.
Pleural effusion.
```
263
How is a diagnosis of heart failure made using the Framingham criteria?
Diagnosis of heart failure can be made if (two major criteria) or (one major and two minor) criteria are met.
264
Give seven other signs of heart failure.
```
Cyanosis.
Cold peripheries.
Hypotension.
Narrow pulse pressure.
Ascites.
Murmurs.
Displaced apex beat.
```
265
Give four examples examples of tests which may be performed to diagnose heart failure.
Blood tests.
Chest X-ray.
ECG.
Echocardiography.
266
Which blood tests may be performed to diagnose heart failure?
BNP.
FBC.
U&E.
Liver biochem.
267
Describe how BNP may be a marker for heart failure.
Brain natriuretic peptide is secreted from the ventricles in response to myocardial wall stress. Therefore BNP levels will be increased in patients with heart failure.
268
What may a chest X-ray of a person with heart failure show?
Alveolar oedema.
Cardiomegaly.
Dilated upper lobe vessels of lung.
Effusion (pleural).
269
What may an ECG show for a person with heart failure?
The underlying causes of the heart failure, including ischameia and left ventricular hypertrophy.
270
When is an echocardiogram performed on a patient with suspected heart failure?
If BNP and ECG are abnormal.
271
How is an echocardiogram used to diagnose a patient with heart failure?
Measure cardiac chamber dimensions.
Regional wall motion abnormalities, valvular disease and cardiomyopathies.
Signs of MI.
272
Give examples of treatment options for patients with heart failure.
```
Lifestyle changes.
Diuretics.
ACE inhibitors.
Beta blockers.
Spironolactone.
```
273
Give possible lifestyle advice to patient with heart failure.
Avoid large meals, lose weight, stop smoking, exercise and take vaccinations.
274
Why are diuretics used to treat patients with heart failure?
They reduce blood pressure by promoting water loss. Reducing preload and pulmonary/systemic congestion.
275
Give three examples of diuretics used in the treatment of patients with heart failure.
Loop diuretics.
Thiazide diuretics.
Aldosterone antagonist.
276
Give an example of a loop diuretic used in the treatment of heart failure.
Furosemide.
277
Give an example of a thiazide diuretic used in the treatment of heart failure.
Bendroflumethiazide.
278
Give an example of an aldosterone antagonist used in the treatment of heart failure.
Spirolactone, epelerone.
279
Why are ACE inhibitors used to treat patients with heart failure?
To reduce hypertension.
280
Give examples of ACE inhibitors used in the treatment of heart failure.
Ramipril.
Enalipril.
Captiopril.
281
Give side effects of ACE inhibitors used in the treatment of heart failure.
Cough. Hypotension. Hyperkalaemia. Renal dysfunction.
282
Give an alternative if cough is a problem when treating heart failure with ACE inhibitors.
Angiotensin receptor blockers, such as canderstan.
283
What are surgical options for patients with heart failure?
Mitral valve repair/replacement.
Aortic valve replacement.
Heart transplant.
284
Inotropes can also be prescribe to patients with heart failure. What are they?
Positive inotropes are drugs that increase the force of contraction of the heart.
285
What are surgical options for patients with heart failure?
Mitral valve repair/replacement.
Aortic valve replacement.
Heart transplant.
286
Describe acute heart failure.
Almost exclusively new onset or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension.
287
Describe chronic heart failure.
Develops slowly. Venous congestion is common but arterial pressure is well maintained until very late.
288
What is venous congestion?
When arterial flow is greater than venous flow.
289
A diagnosis of heart failure is made using which criteria?
Framingham criteria.
290
Name nine major criteria for heart failure.
```
Paroxysmal nocturnal dyspnoea.
Crepitations.
S3 gallop.
Cardiomegaly.
Increased central venous pressure.
Weight loss.
Neck vein distension.
Acute pulmonary oedema.
Hepatojugular reflux.
```
291
What is paroxysmal nocturnal dyspnoea?
Attacks of severe shortness of breath or coughing, typically at night.
292
What are crepitations?
Crackles of the lung.
293
What is S3 gallop caused by?
Rapid ventricular filling. Occurs in early diastole.
294
Describe the hepatojugular reflux.
Distension of the neck veins occur when pressure is applied to the liver.
295
Name seven minor criteria for heart failure.
```
Bilateral ankle oedema.
Dyspnoea on ordinary exertion.
Tachycardia.
Decrease in vital capacity.
Nocturnal cough.
Hepatomegaly.
Pleural effusion.
```
296
How is a diagnosis of heart failure made using the Framingham criteria?
Diagnosis of heart failure can be made if (two major criteria) or (one major and two minor) criteria are met.
297
Give seven other signs of heart failure.
```
Cyanosis.
Cold peripheries.
Hypotension.
Narrow pulse pressure.
Ascites.
Murmurs.
Displaced apex beat.
```
298
Give four examples examples of tests which may be performed to diagnose heart failure.
Blood tests.
Chest X-ray.
ECG.
Echocardiography.
299
Which blood tests may be performed to diagnose heart failure?
BNP.
FBC.
U&E.
Liver biochem.
300
Describe how BNP may be a marker for heart failure.
Brain natriuretic peptide is secreted from the ventricles in response to myocardial wall stress. Therefore BNP levels will be increased in patients with heart failure.
301
What condition is caused by an increase in pulmonary capillary pressure?
The increase in pressure will result in pulmonary oedema.
302
What may an ECG show for a person with heart failure?
The underlying causes of the heart failure, including ischameia and left ventricular hypertrophy.
303
When is an echocardiogram performed on a patient with suspected heart failure?
If BNP and ECG are abnormal.
304
How is an echocardiogram used to diagnose a patient with heart failure?
Measure cardiac chamber dimensions.
Regional wall motion abnormalities, valvular disease and cardiomyopathies.
Signs of MI.
305
Give three signs of mitral stenosis that are easily identified.
Progressive dyspnoea.
Haemoptysis.
Malar flush.
306
Give possible lifestyle advice to patient with heart failure.
Avoid large meals, lose weight, stop smoking, exercise and take vaccinations.
307
Why are diuretics used to treat patients with heart failure?
They reduce blood pressure by promoting water loss. Reducing preload and pulmonary/systemic congestion.
308
Give three examples of diuretics used in the treatment of patients with heart failure.
Loop diuretics.
Thiazide diuretics.
Aldosterone antagonist.
309
Give an example of a loop diuretic used in the treatment of heart failure.
Furosemide.
310
Give an example of a thiazide diuretic used in the treatment of heart failure.
Bendroflumethiazide.
311
Give an example of an aldosterone antagonist used in the treatment of heart failure.
Spirolactone, epelerone.
312
Why are ACE inhibitors used to treat patients with heart failure?
To reduce hypertension.
313
Give examples of ACE inhibitors used in the treatment of heart failure.
Ramipril.
Enalipril.
Captiopril.
314
Give side effects of ACE inhibitors used in the treatment of heart failure.
Cough. Hypotension. Hyperkalaemia. Renal dysfunction.
315
Give an alternative if cough is a problem when treating heart failure with ACE inhibitors.
Angiotensin receptor blockers, such as canderstan.
316
What is the use of spironolactone used in the treatment of heart failure?
Reduces fluid retention.
| Reduces mortality by 30%.
317
Inotropes can also be prescribe to patients with heart failure. What are they?
Positive inotropes are drugs that increase the force of contraction of the heart.
318
Give three markers from a chest x-ray that are used to diagnose mitral stenosis.
Left atrial enlargement.
Pulmonary oedema.
Calcified mitral valve.
319
Give four examples of valvular heart disease.
Mitral stenosis.
Mitral regurgitation.
Aortic stenosis.
Aortic regurgitation.
320
How is echocardiography used to diagnose mitral stenosis?
By assessing mitral valve mobility, gradient and area.
321
What is mitral stenosis?
A narrowing of the mitral valve that causes obstruction to blood flow into the left ventricle.
322
Mitral stenosis prevents what from happening?
The proper filling of the left ventricle during diastole.
323
What is the normal area of the mitral valve opening?
4 to 6cm^2.
324
At what point does mitral stenosis become symptomatic?
When the area of the mitral valve opening is less than 2cm^2.
325
What is the main cause of mitral stenosis?
Rheumatic heart disease secondary to rheumatic fever.
326
What causes rheumatic fever?
An infection of a group A beta-haemolytic streptococcus bacteria.
327
Name a bacteria that causes rheumatic fever.
Streptococcus pyogenes.
328
In percutaneous mitral balloon valvotomy, what step comes after the catheter is advanced across the mitral valve?
The balloon is inflated, separating the leaflets and increasing the size of the mitral valve opening.
329
What is commissural fusion?
The commissures define an area where the valve leaflets are inserted into the annulus. Fusion reduces mobility of the leaflets.
330
Describe the effect of rheumatic heart disease on mitral stenosis over many years.
Progression to valve thickening, cusp fusion, calcium deposition, severely narrowed orifice and greater immobility of the valve cusps.
331
How is the prevalence and incidence of mitral stenosis changing?
Both decreasing due to a reduction in rheumatoid heart disease.
332
Give two other causes of mitral stenosis, other than rheumatic heart disease.
Infective endocarditis.
| Mitral annular calcification.
333
What are two risk factors for mitral stenosis?
History of rheumatic fever.
| Untreated streptococcus infection.
334
Explain how and why mitral valve thickening leads to an increase in left atrial pressure.
Left atrial pressure increases due to left atrial hypertrophy and dilation. The increase in pressure works to maintain cardiac output.
335
Describe the effect of an increase in left atrial pressure on the pulmonary system.
Pulmonary venous pressure and pulmonary arterial pressure increase.
336
How does an increase in pulmonary capillary pressure effect the pulmonary system?
The increase in pressure will result in pulmonary oedema.
337
By what mechanisms does the body try to counter pulmonary oedema as a result of stenosis?
Alveolar and capillary thickening. Pulmonary arterial vasoconstriction.
338
Describe why do the body's efforts in countering pulmonary oedema fail.
Pulmonary hypertension causes right ventricular hypertrophy, dilation and ultimately right heart failure.
339
How quickly does an attack of rheumatic fever lead to mitral stenosis?
Not until several decades later.
340
Why is progressive dyspnoea caused by mitral stenosis?
Due to pulmonary congestion as a result of left atrial dilation.
341
What four heart sounds are heard from a patient with mitral regurgitation?
Soft S1.
Pan systolic murmur at the apex, radiating to the axilla.
Split S2.
Loud P2.
342
Why does haemoptysis occur in mitral stenosis?
Elevated pulmonary pressure ruptures bronchial vessels.
343
What is malar flush?
Bilateral, cyanotic or dusky pink discolouration over upper cheeks.
344
Why does malar flush occur in mitral stenosis?
Due to vasoconstriction as a result of reduced cardiac output.
345
What heart sounds are heard from a patient with mitral stenosis?
Low-pitched diastolic rumble.
| Loud opening S1 snap.
346
How is the low-pitched diastolic rumble best heard on a patient with mitral stenosis?
In expiration with the patient lying on their left side.
347
What causes the loud opening S1 snap in patients with mitral stenosis?
The increased atrial pressure force the mobile valve leaflets far apart - further to snap.
348
Describe the signs of mitral regurgitation that can be identified using a chest x-ray.
Left atrial enlargement.
| Central pulmonary artery enlargement.
349
How do the heart sounds of a patient with mitral stenosis change as the condition progresses?
The diastolic rumble is longer and the opening S1 snap is closer to S2.
350
Give four signs of mitral stenosis that are harder to identify.
Right heart failure.
Atrial fibrillation.
Systemic emboli.
Prominent a wave in jugular venous pulsations.
351
Which three tools are used in the diagnosis of mitral stenosis?
Chest x-ray.
Electrocardiogram.
Echocardiogram.
352
Give three markers from a chest x-ray that are used to diagnose mitral stenosis.
Left atrial enlargement.
Pulmonary oedema.
Calcified mitral valve.
353
Give two markers from an ECG that are used to diagnose mitral stenosis.
Atrial fibrillation.
| Left atrial enlargement.
354
How is echocardiography used to diagnose mitral stenosis?
By assessing mitral valve mobility, gradient and area.
355
Describe the aortic valve of the heart.
The aortic valve separates the left ventricle from the aorta. It has three cusps. It is one of two semi-lunar valves, the other being the pulmonary valve.
356
Name a beta-blocker used in the treatment of mitral stenosis.
Atenolol.
357
What is the purpose of treating mitral stenosis with beta-blockers?
Slows the heart to prolong diastole and improve diastolic filling.
358
Name a diuretic used in the treatment of mitral stenosis.
Furosemide.
359
What is the purpose of treating mitral stenosis with diuretics?
To reduce fluid overload.
360
Give three causes of aortic stenosis.
Calcific aortic valvular disease.
Calcification of congenital bicuspid aortic valve.
Rheumatic heart disease.
361
In percutaneous mitral balloon valvotomy, where is the catheter directed?
The catheter is inserted into the right atrium via the femoral artery (under local anaesthesia). The intertribal septum is punctured and the catheter is advanced into the left atrium and across the mitral valve.
362
In percutaneous mitral balloon valvotomy, what step comes after the catheter is advanced across the mitral valve?
The balloon is inflated, separating the leaflets and increasing the size of the mitral valve opening.
363
What is mitral regurgitation?
The backflow of blood from the left ventricle to the left atrium during systole.
364
How common is mitral regurgitation in normal individuals?
Mild physiological mitral regurgitation is found in 80% of normal people.
365
Mitral regurgitation is commonly caused by abnormalities of what four structures?
Valve leaflets.
Chordae tendinae.
Papillary muscles.
Left ventricles.
366
Give an example of a structural problem of the chordae tendinae.
Myxomatous degeneration.
367
What is myxomatous degeneration?
Weakening of the chordae tendinae.
368
How does myxomatous degeneration cause mitral regurgitation?
Weakening of the chordae tendinae results in a floppy mitral valve and mitral valve prolapse.
369
Other than myxomatous degeneration, name four conditions that can cause mitral regurgitation.
```
Ischaemic mitral valve.
Rheumatic heart disease.
Infective endocarditis.
Papillary muscle dysfunction.
Dilated cardiomyopathy.
```
370
Give five risk factors for mitral regurgitation.
```
Lower BMI.
Female.
Ageing.
Renal dysfunction.
Prior MI.
```
371
Other than the classic triad, how else might aortic stenosis present?
Slow rising carotid pulse with narrow pulse pressure.
Soft/absent S2.
Prominent S4.
Ejection systolic murmur-crescendo-decrescendo character.
372
Volume overload in mitral regurgitation causes what?
Left ventricular hypertrophy.
| Left atrial enlargement.
373
Progressive left atrial dilation has what knock on effect?
Pulmonary hypertension which itself causes right ventricle dysfunction.
374
Progressive left ventricular volume overload has what eventual effect?
Progressive heart failure (due to dilation).
375
Describe the signs of aortic stenosis that can be identified using a chest x-ray.
Left ventricular hypertrophy.
| Calcified aortic valve.
376
Excluding heart sounds, how does mitral regurgitation present?
Exertion dyspnoea.
Fatigue and lethargy.
Increased stroke volume felt as palpitation.
Symptoms of LHF.
377
How long is the compensatory phase of mitral regurgitation?
10 to 15 years.
378
What two factors suggests an increase in risk of mortality?
Ejection fraction less than 60% and/or symptomatic.
379
What is the mortality rate for those with severe mitral regurgitation?
5%.
380
Describe the signs of mitral regurgitation that can be identified using an ECG.
Left atrial enlargement.
Atrial fibrillation.
Left ventricular hypertrophy.
381
Describe the signs of mitral regurgitation that can be identified using a chest x-ray.
Left atrial enlargement.
| Central pulmonary artery enlargement.
382
How is an echocardiogram used in the diagnosis of mitral regurgitation?
Left atrial and left ventricular size and function.
| Valve structure assessment.
383
Suggest a method of echocardiogram that can be undertaken to produce clearer images.
Transoesophageal echo.
384
Give four types of drug for treating mitral regurgitation.
Vasodilators.
Heart rate control.
Anticoagulants.
Diuretics.
385
Give four risk factors of aortic regurgitation.
SLE.
Marfan's and Ehlers-Danlos syndrome.
Aortic dilation.
Infective endocarditis / aortic dissection.
386
Give two examples of heart rate controllers used in the treatment of mitral regurgitation.
Beta-blockers - atenolol.
| Calcium channel blockers - amlodipine.
387
At what point is surgical intervention for treatment of mitral regurgitation considered?
Symptoms at rest / exercise.
| Ejection fraction < 60% or new onset atrial fibrillation.
388
What is aortic stenosis?
Narrowing of the aortic valve resulting in obstruction to blood flow from the left ventricle.
389
What is the normal area of the aortic valve opening?
3 to 4cm^2.
390
At what point does aortic stenosis become symptomatic?
When the area of the aortic valve opening is less than 25% of the normal area.
391
Name the three types of aortic stenosis.
Supravalvular aortic stenosis.
Valvular aortic stenosis.
Subvalvular aortic stenosis.
392
What is congenital aortic bicuspid valve?
Inherited heart disease where two of the aortic valve leaflets are fused - aortic valve has two cusps.
393
In aortic stenosis, the two causes: calcific aortic valvular disease and calcification of congenital bicuspid aortic valve are both examples of what?
Diseases of ageing.
394
Give two risk factors for aortic stenosis.
Congenital BAV predisposes to stenosis and regurgitation.
| Congenital BAV is predominant in males.
395
Describe how aortic stenosis results in left ventricular hypertrophy.
Obstructed left ventricular emptying produces a pressure gradient between the left ventricle and aorta (increasing afterload). Left ventricular pressure increases and the ventricle hypertrophies to compensate.
396
Give a consequence of LV hypertrophy as a result of aortic stenosis.
Myocardial ischaemia, which is characterised by angina, arrhythmia and heart failure.
397
Under what conditions are the problems of aortic stenosis exaggerated?
During exercise (when demand for blood is greater).
398
Describe the effects of exercise on a patient with aortic stenosis.
Cardiac output cannot increase to meet increased oxygen demands.
Blood pressure falls and myocardial ischaemia worsens, myocardium fails and arrhthymias develop.
399
For patients with aortic stenosis, at what point does LV function decline rapidly?
When compensatory hypertrophy has been exhausted.
400
Think aortic stenosis in any elderly patient with... (3).
Chest pain.
Exertional dyspnoea.
Syncope.
401
What is the classic triad for clinical presentation of patients with aortic stenosis?
Syncope.
Angina.
Heart failure.
402
Give two possible differential diagnosis for aortic stenosis?
Aortic regurgitation.
| Subactute bacterial endocarditis.
403
How is echocardiogram used to identify aortic stenosis in patients?
By measuring left ventricular size and function to identify possible hypertrophy, dilation and ejection fraction.
404
Describe how an ECG may show signs of left ventricular strain in patients with aortic stenosis.
Depressed ST segments and T wave inversion in leads orientated to the left ventricle.
405
Describe the signs of aortic stenosis that can be identified using a chest x-ray.
Left ventricular hypertrophy.
| Calcified aortic valve.
406
What precaution should those with aortic stenosis take?
Rigorous dental hygiene as they are at increased risk of infective endocarditis.
407
What pharmacological intervention is contraindicated for those with sever aortic stenosis.
Vasodilators.
408
Why are vasodilators contraindicated in the treatment of severe aortic stenosis?
May cause hypotension and syncope.
409
Aortic valve replacement is recommended in patients that meet which criteria?
Symptomatic patients with aortic stenosis.
Patients with decreasing ejection fraction.
Patient undergoing CABG with moderate/severe aortic stenosis.
410
Other than aortic valve replacement, name a procedure that may be used in the treatment of aortic stenosis.
Transcutaneous aortic valve implantation.
411
Describe how transcutaneous aortic valve implantation is performed (first step).
The catheter is passed up the aorta and balloon is inflated across the narrow valve to crack the calcification.
412
Describe how transcutaneous aortic valve implantation is performed (second step).
Another catheter is passed up which leaves a stent with a valve.
413
What is aortic regurgitation?
Leakage of blood into the left ventricle from the aorta during diastole due to ineffective coaptation of aortic cusps.
414
Give three examples of causes of aortic regurgitation.
Congenital bicuspid aortic valve.
Rheumatic fever.
Infective endocarditis.
415
Give four risk factors of aortic regurgitation.
SLE.
Marfan's and Ehlers-Danlos syndrome.
Aortic dilation.
Infective endocarditis / aortic dissection.
416
What is the immediate effect on the heart of aortic regurgitation?
Left ventricular dilation and hypertrophy to maintain cardiac output.
417
How does left ventricular dilation progress for those with aortic regurgitation?
Progressive dilation results in heart failure.
418
Other than structural changes, how else does aortic regurgitation effect the heart?
Regurgitation leads to a reduction in diastolic pressure and thus a reduction in coronary perfusion. Coronary arteries receive blood from the root of the aorta.
419
How does aortic regurgitation result in myocardial ischaemia?
Regurgitation stimulates hypertrophy which demands more oxygen. Demands can't be met.
420
How quickly do patients present with aortic regurgitation?
In chronic aortic regurgitation patients remain asymptomatic for years, until the 4th/5th decade.
421
Give seven signs of aortic regurgitation.
```
Exertional dyspnoea.
Palpitations.
Syncope.
Angina.
Quincke's sign.
de Musset's sign.
Pistol shot femoral.
```
422
How is pulse pressure affected by aortic regurgitation?
Pulse pressure is wide in patients with aortic regurgitation
423
Describe the heart sounds of a patient with aortic regurgitation.
Diastolic blowing murmur at the sternal border.
| Systolic ejection murmur due to increased blood flow across the valve.
424
Describe the pulse of a patient with aortic regurgitation.
Collapsing water hammer pulse.
425
What is Quincke's sign?
Capillary pulsation in the nail beds.
426
What is de Musset's sign?
Head nodding with each heart beat.
427
What is a pistol shot femoral sign?
A sharp bang is heard on auscultation.
428
What possible differential diagnosis may be made for aortic regurgitation?
Heart failure.
Infective endocarditis.
Mitral regurgitation.
429
How is echocardiogram used in the diagnosis of aortic regurgitation?
Evaluation of aortic valve and aortic root.
| Measurement of left ventricle dimensions and function.
430
Give two markers from a chest x-ray that are used to diagnose aortic regurgitation.
Enlarged cardiac silhouette and aortic root enlargement.
| Left ventricular enlargement.
431
Give two markers from an ECG that are used to diagnose mitral stenosis.
Tall R waves, deeply inverted T waves in the left side chest leads.
Deep S waves in the right sided leads.
432
What precaution should be taken in patients with aortic regurgitation?
Infective endocarditis prophylaxis.
433
What treatments are available for patients with aortic regurgitation?
ACE inhibitors, ramipril, for vasodilation to improve stroke volume and reduce regurgitation.
Valve replacement surgery.
434
What is infective endocarditis?
An infection of the endocardium or vascular endothelium.
435
What is a characteristic lesion of infective endocarditis?
Vegetation.
436
Describe what a vegetation is.
When valve leaflets develop infective or thrombotic nodules that impair normal valve motility.
437
Other than impairing valve motility, why are vegetations harmful?
They can fragment and embolise.
438
How does the prevalence of infective endocarditis differ between men and women?
Infective endocarditis is twice as common in men as in women.
439
Give examples of four groups of people who are especially at risk of endocarditis?
Patients with prosthetic heart valves.
The elderly.
IV drug abusers.
Congenital heart disease sufferers.
440
What is the most frequent pathology for elderly patients with infective endocarditis?
Calcific valve disease.
441
Give examples of predisposing factors for elderly patients with infective endocarditis.
GU infection. Diabetes. Tooth extractions. Pressure sores. Surgical procedures.
442
Describe two ways in which IV drug use puts people at risk of infective endocarditis.
Drug prep. done with water that contains virulent microorganisms that enter the circulation directly.
Bacterial cellulitis at the injection site. Injection through the inflamed skin results in bacteraemia.
443
In patients with infective endocarditis due to IV drug abuse, which side of the heart is more commonly affected?
The right side of the heart (injection into venous system).
444
How is infective endocarditis different in IV drug abusers compared to other patients?
Infection affects the right side of the heart, meaning tricuspid valve involvement. Vegetations can embolise to the lungs.
445
Name the bacteria responsible for most cases of infective endocarditis.
Staphylococcus aureus.
446
Other than staphylococcus aureus, which other two bacteria are common causes of infective endocarditis?
Streptococcus viridans.
| Pseudomonas aeruginosa.
447
In infective endocarditis, how does infection by streptococcus viridans often occur?
Dental problems/procedures.
448
What makes staphylococcus aureus and streptococcus viridans suitable candidates for causing infective endocarditis?
They are both gram positive bacteria with a thick protective mucopeptide layer.
449
Give six examples of risk factors for infective endocarditis.
```
Prosthetic heart valves.
Immunosuppression and haemodialysis.
Intravenous drug use.
Invasive procedures.
Poor dental hygiene and dental treatment.
Diabetes mellitus.
```
450
Which two factors lead to the development of infective endocarditis?
Bacteraemia and abnormal cardiac endothelium.
451
What is bacteraemia?
The presence of bacteria in the blood.
452
Explain how poor dental hygiene can cause infective endocarditis.
Bacteria in tooth plaque causes gum disease which leads to bleeding and inflammation of the gums. Bacteria can enter the blood and reach the heart.
453
Explain how damaged endocardium can cause infective endocarditis?
Damaged endocardium promotes platelet and fibrin deposition which allows organisms to adhere and grow, leading to infected vegetation.
454
Which valves are most commonly involved in infective endocarditis?
The aortic and mitral valves.
455
How does infected vegetation develop and cause further damage?
Virulent organisms destroy the valve they are on, causing regurgitation and resulting in worsening heart failure.
456
What happens when vegetations break away from their heart valves?
Embolise in the spleen, kidney and brain (common). As well as tiny haemorrhage lesions in the skin, mucous membranes and retina.
457
Give an example of a tiny haemorrhage lesion that occurs in infective endocarditis.
Splinter haemorrhage.
458
What is a splinter haemorrhage?
Linear haemorrhage beneath the tips of the nails.
459
Infective endocarditis should be assumed until proven otherwise in what circumstance?
When the patient presents with a fever and new murmur.
460
Give five examples of when a patient should be treat with high clinical suspicion for infective endocarditis.
New valve lesion / regurgitant murmur.
Embolic events of unknown origin.
Sepsis of unknown origin.
Haematuria, glomerulonephritis and suspected renal infarction.
Fever and prosthetic valve in the heart or fever and risk factor for IE.
461
What is haematuria?
The presence of red blood cells in the urine.
462
Give seven examples of visible presentation of infective endocaridits.
```
Finger clubbing.
Splinter haemorrhage.
Embolic skin lesions.
Osler nodes.
Janeway lesions.
Roth spot.
Petechiae.
```
463
What are Osler nodes?
Tender nodules in the digits.
464
What are Janeway lesions?
Haemorrhage and nodules on the palms.
465
What are Roth spots?
Retinal haemorrhage with white/clear centres on fundoscopy.
466
What is Petechiae?
Small red/purple spots caused by bleeds in the skin.
467
What criteria is used in the diagnosis of infective endocarditis?
Duke criteria.
468
Give the major criteria of Duke criteria.
Positive blood culture.
| Endocardium involved.
469
Duke criteria: define positive blood culture.
Typical organism in two separate cultures.
| Persistently positive blood cultures.
470
Duke criteria: define endocardium involvement.
Positive echocardiogram.
| New valvular regurgitation.
471
Give the minor criteria of Duke criteria.
Predisposition.
Fever > 38
Vascular / immunological signs.
Positive blood culture that doesn't meet major criteria.
Positive echocardiogram that doesn't meet major criteria.
472
When investigating infective endocarditis, how should blood cultures be taken?
Three sets taken at different sites over 24 hours.
473
In patients with infective endocarditis, suggest four things that blood tests would show.
Normochromic anemia.
Normocytic anaemia.
Neutrophilia.
Raised ESR and CRP.
474
What is normochromic anaemia?
Normal concentration of haemoglobin, reduced numbers of red blood cells.
475
What is normocytic anaemia?
Normal sized red blood cells, reduced haematocrit and haemoglobin.
476
What is the haematocrit?
Ratio of the volume of red blood cells to the total volume of blood.
477
Other than blood tests and blood cultures, what other analysis is done in the investigation of infective endocarditis?
Urinalysis.
CXR.
ECG.
Echocardiogram.
478
What may urinalysis show in a patient with infective endocarditis?
Microscopic haematuria.
479
What may CXR show in a patient with infective endocarditis?
Cardiomegaly.
480
What may ECG show in a patient with infective endocarditis?
Long PR interval at regular intervals.
481
What two options of echocardiogram may be used in the investigation of infective endocarditis?
Transthoracic echo.
| Transoesophageal echo.
482
State the positives and negatives of using transthoracic echo for diagnosing infective endocarditis.
Safe, non-invasive and no discomfort. Poor images (low sensitivity). Can identify vegetations but cannot be a negative test cannot be used to exclude IE.
483
Transthoracic echo can identify vegetations of what size?
Vegetations bigger than 2mm.
484
State the positives and negatives of using transoesophageal echo for diagnosing infective endocarditis.
Very uncomfortable. Good images (greater sensitivity).
| Useful for visualising mitral lesions and the development of aortic root abscess.
485
Which type of echocardiography is preferred for diagnosing infective endocarditis.
Transoesophageal echo is better for diagnosis.
486
How is infective endocarditis treated?
With antibiotics for 4 to 6 weeks.
487
How is infective endocarditis caused by staphylococcus treated?
Vancomycin and rifampicin (if MRSA).
488
How is infective endocarditis caused by non-staphylococcus treated?
Benzylpenicillin and gentamycin.
489
In what circumstances is surgery used to treat infective endocarditis?
If the infection can't be cured with antibiotics.
To remove infective devices.
To remove large vegetations before they embolise.
490
What recommendations should be given for the prevention of infective endocarditis?
Good oral health.
491
What is cardiomyopathy?
A group of disease of the myocardium that effect mechanical or electrical function of the heart.
492
What are the four types of cardiomyopathy?
Hypertrophic cardiomyopathy.
Dilated cardiomyopathy.
Restrictive cardiomyopathy.
Arrhythmogenic right ventricular cardiomyopathy.
493
Cardiomyopathies are generally...
inherited genetic conditions (although some are acquired).
494
All cardiomyopathies carry what risk?
Risk of arrhythmia.
495
Give five risk factors for cardiomyopathy.
```
Family history of cardiomyopathy.
Hypertension.
Obesity.
Diabetes.
Previous myocardial infarction.
```
496
What is hypertrophic cardiomyopathy?
Ventricular hypertrophy or thickening of the heart muscle without an obvious cause.
497
What is the prevalence of hypertrophic cardiomyopathy?
0.2%
498
Hypertrophic cardiomyopathy is passed on by what type of inheritance?
Autosomal dominant inheritance.
499
70% of patients with hypertrophic cardiomyopathy have mutations in genes encoding which proteins?
Beta-myosin.
Alpha-tropomyosin.
Troponin.
500
At what age does hypertrophic cardiomyopathy usually present?
HCM can present at any age.
501
Describe the pathology that arises from the associated mutations in patients with hypertrophic cardiomyopathy.
Hypertrophic and non-compliant ventricles:
- impairs diastolic filling, reducing stroke volume
- disarray of cardiac myocytes affects electrical conduction
502
In hypertrophic cardiomyopathy, which part of the myocardium is particularly affected?
Intraventricular septum.
503
Give six ways in which hypertrophic cardiomyopathy may present.
```
Sudden death.
Chest pain, angina, dyspnoea, palpitation, syncope.
Left ventricular outflow obstruction.
Cardiac arrhythmia.
Ejection systolic murmur.
Jerky carotid pulse.
```
504
Give three methods of diagnosing hypertrophic cardiomyopathy.
ECG.
Echocardiogram.
Genetic analysis.
505
How may an ECG show signs of hypertrophic cardiomyopathy?
Signs of LVH.
Progressive T wave inversion.
Deep Q waves.
506
How may an echocardiogram show signs of hypertrophic cardiomyopathy?
Ventricular hypertrophy.
| Small left ventricle cavity.
507
Give examples of drugs used to treat hypertrophic cardiomyopathy.
Anti-arrhythmic drugs.
Beta-blockers.
Calcium channel blockers.
508
Name an anti-arrhythmic drug used in the treatment of hypertrophic cardiomyopathy.
Amiodarone.
509
If the risk of arrhythmia is high in patients with hypertrophic cardiomyopathy, what treatment may be used?
Implantable cardiac defibrillator.
510
Name a calcium channel blocker used in the treatment of hypertrophic cardiomyopathy.
Verampril.
511
Name a beta-blocker used in the treatment of hypertrophic cardiomyopathy.
Atenolol.
512
What is dilated cardiomyopathy?
Dilated left ventricle with thin muscle, therefore poor contraction.
513
What is the prevalence of dilated cardiomyopathy?
0.2%
514
Dilated cardiomyopathy is passed on by what type of inheritance?
Autosomal dominant inheritance.
515
Dilated cardiomyopathy is associated with what?
Alcohol.
High blood pressure.
Haemochromatosis.
Peri-/postpartum hyperthyroidism.
516
What is haemochromatosis?
Iron overload.
517
Give eight ways that dilated cardiopathy may present.
```
Fatigue, dyspnoea.
Heart failure and pulmonary oedema.
RVF.
Arrhythmia.
Thromboembolism.
Increased jugular venous pressure.
S3 gallop.
MR or TR.
```
518
Give three methods of diagnosing dilated cardiomyopathy.
CXR.
ECG.
Echocardiogram.
519
How may a CXR show signs of dilated cardiomyopathy?
Cardiac enlargement.
520
How may an ECG show signs of dilated cardiomyopathy?
Tachycardia.
Arrhythmia.
Non-specific T wave changes.
521
How may an echocardiogram show signs of dilated cardiomyopathy?
Dilated ventricles.
522
How is dilated cardiomyopathy treated?
Treat heart failure and atrial fibrillation.
523
What is the mortality of cardiomyopathy?
40% in two years.
524
What is restrictive cardiomyopathy?
Disease in which the walls of the heart are rigid but not thickened.
525
Give four examples of causes of restrictive cardiomyopathy.
Idiopathic.
Amyloidosis.
Sarcoidosis.
Endomyocardial fibrosis.
526
Explain the pathology behind restrictive cardiomyopathy.
Rigid myocardium means poor dilation and thus low compliance. Results in reduced diastolic ventricular filling and reduced cardiac output.
527
Restrictive cardiomyopathy presents similarly to which condition?
Constrictive pericarditis.
528
Give two ways in which restrictive cardiomyopathy presents.
With features of right ventricular failure.
| S3 and S4 heart sounds.
529
Give features of right ventricular failure that present in patients with restrictive cardiomyopathy.
Increased jugular venous pressure.
Hepatomegaly.
Oedema.
Ascites.
530
What is hepatomegaly?
Enlarged liver.
531
Describe the characteristic jugular venous pressure in patients with restrictive cardiomyopathy.
Increased JVP with prominent X and Y descents.
532
How is restrictive cardiomyopathy diagnosed?
CXR, ECG and Echo are abnormal but non-specific.
| Cardiac catheterisation.
533
How is restrictive cardiomyopathy treated?
The causes are treated and cardiac transplant is considered.
534
What is the prognosis for patients with restrictive cardiomyopathy?
Death with one year.
535
What is arrhythmogenic right ventricular cardiomyopathy?
Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium.
536
Describe how arrhythmogenic right ventricular cardiomyopathy is inherited.
Autosomal dominant inheritance with incomplete penetrance.
537
What mutation is observed in patients with arrhythmogenic right ventricular cardiomyopathy.
Desmosome gene mutation.
538
Describe how a desmosome gene mutation causes pathology in patients with arrhythmogenic right ventricular cardiomyopathy.
The RV is replaced by fat and fibrous tissue.
| Poor adhesion between cardiac myocytes leads to conduction issues.
539
How do patients with arrhythmogenic right ventricular cardiomyopathy present?
With arrhythmias and right heart failure.
540
How may an ECG show signs of arrhythmogenic right ventricular cardiomyopathy?
Normal but may show T wave inversion.
541
How may an echo show signs of arrhythmogenic right ventricular cardiomyopathy?
Normal or shows RV dilation.
542
What is used in the treatment of arrhythmogenic right ventricular cardiomyopathy?
Anti-arrhythmic drugs.
Beta-blockers.
Cardiac transplant.
543
Hypertension is a major risk factor for what?
Atherosclerosis and cerebral haemorrhage.
544
How does blood pressure affect mortality?
Mortality rises with increasing blood pressure.
545
Hypertension is responsible for what % of vascular deaths?
Around 50%.
546
Describe the prevalence of hypertension.
Hypertension is prevalent in those over 35 and is more common in men than women.
547
How does hypertension usually present?
Hypertension is usually asymptomatic.
548
Give that hypertension is usually asymptomatic, what is required?
Regular screening.
549
Define normotensive.
A blood pressure of less than 140/90mmHg.
550
Define stage 1 hypertension.
A clinic blood pressure of ≥ 140/90mmHg. An ABPM or HBPM of ≥ 135/85mmHg.
551
What is ABPM?
Ambulatory blood pressure monitoring.
552
What is HBPM?
Home blood pressure monitoring.
553
Under what conditions should stage 1 hypertension be treated?
If 10 year cardiovascular risk is greater than 20% or if there is end organ damage.
554
Define stage 2 hypertension.
A clinic blood pressure of ≥ 160/100mmHg. An ABPM or HBPM of ≥ 150/95mmHg.
555
Define severe hypertension.
A clinic systolic blood pressure of ≥ 180mmHg. A clinic diastolic blood pressure of ≥ 110mmHg.
556
What is essential hypertension.
Hypertension in which the cause is unknown.
557
Essential hypertension makes up what % of hypertension cases?
Around 95%.
558
What is a key feature of essential hypertension?
An increase in total peripheral vascular resistance.
559
Give five mechanisms responsible for essential hypertension.
Genetic susceptibility.
Excessive sympathetic nervous system activity.
Abnormalities in Na+/K+ membrane transport.
High salt intake.
Abnormalities in RAAS.
560
Name four things that may be responsible for secondary hypertension.
Renal disease.
Endocrine disease.
Coarctation of the aorta.
Drug therapy.
561
What is the most common cause of secondary hypertension?
Renal disease.
562
Give three examples why renal disease might develop as a cause of secondary hypertension.
Diabetes.
Glomerulonephritis.
Atheroma.
563
Give five examples why endocrine disease might develop as a cause of secondary hypertension.
```
Cushing's disease.
Conn's syndrome.
Phaemochromocytoma.
Acromegaly.
Hyperparathyroidism.
```
564
Explain how Cushing's disease can cause hypertension.
In Cushing's disease, the hypersecretion of corticosteroids enhance adrenalines to cause vasoconstriction.
565
Explain how Conn's syndrome can cause hypertension.
In Conn's syndrome, an adrenal tumours cause excessive aldosterone production leading to Na+ retention and thus water retention.
566
Explain how phaemochromocytoma can cause hypertension.
In phaemochromocytoma, adrenal tumours secrete catecholamines which stimulate alpha-adrenergic receptors (causing vasoconstriction and increased contractility) and beta-adrenergic receptors (causing increased heart rate and contractility).
567
What is coarctation of the aorta?
Congenital narrowing of the descending aorta.
568
What are signs of coarctation of the aorta?
Radiofemoral delay.
Weak femoral pulse.
Increased blood pressure.
569
What is radiofemoral delay?
The femoral pulse is delayed relative to the radial artery.
570
Give examples of drugs that can cause hypertension.
Corticosteroids.
Some contraceptive pills.
Some NSAIDs.
Alcohol, amphetamines and cocaine.
571
Give ten examples of risk factors for hypertension.
```
Age.
Race (black people have greater risk).
Family history.
Overweight.
Little exercise.
Smoking.
High salt intake.
Alcohol.
Diabetes.
Stress.
```
572
What is isolated systolic hypertension?
Hypertension as a result of atheroscelrosis. The most common form of hypertension.
573
How does isolated systolic hypertension affect a patient's risk for cardiovascular problems?
Doubles risk of MI.
| Triples risk of cerebrovascular accident.
574
Give three vascular effects of hypertension.
Accelerate atherosclerosis.
Thickening of media of muscular arteries.
Endothelial cell dysfunction.
575
What is the effect of endothelial cell dysfunction as a result of hypertension?
Impaired nitric oxide mediated vasodilation.
| Enhanced secretion of vasoconstrictors.
576
Other than vascular effects, give three effects of hypertension.
Ischaemic heart disease risk.
Intracerebral haemorrhage risk.
Renal disease.
577
What is malignant hypertension?
A rapid rise in blood pressure that causes vascular damage. Severe hypertension and retinal haemorrhage with or without papilloedema.
578
How does malignant hypertension present?
Headache with or without visual disturbance.
579
Malignant hypertension is most prevalent in which group of people?
Black males in their 30s - 40s.
580
Give six possible tests used to diagnose hypertension?
```
ECG.
Urine analysis.
Blood tests.
Fundoscopy.
Echocardiogram.
24 hour ABPM.
```
581
In patients with hypertension, what may an ECG show?
Left ventricular hypertrophy.
| Signs of past MI.
582
In patients with hypertension, what may urine analysis show?
Protein or blood.
583
In patients with hypertension, what is analysed in a blood test?
Serum creatinine.
eGFR.
Glucose.
U&E.
584
In patients with hypertension, what may fundoscopy show?
Retinal haemorrhage.
| Papilloedema.
585
In patients with hypertension, what may an echocardiogram show?
Left ventricular hypertension.
586
What is the goal of hypertension treatment?
To reduce blood pressure to < 140/90mmHg.
587
What is the goal of hypertension treatment in diabetics / patients > 80 year?
In diabetics < 130/80mmHg.
| In 80+ < 150/90mmHg.
588
When should treatment for hypertension be taken?
When blood pressure is persistently greater than 160/100mmHg. Or if 10 year cardiovascular risk is greater than 20% or if there is end organ damage.
589
How should hypertension be treated?
Lifestyle changes.
| ACD pathway.
590
What lifestyle changes should be made to treat hypertension?
```
Stop smoking.
Low fat diet.
Reduce alcohol and salt intake.
Increase exercise.
Lose weight if obese.
```
591
What is the ACD pathway used in the treatment of hypertension?
ACE inhibitor.
Calcium channel blocker.
Diuretics.
592
Give two examples of ACE inhibitors used in the treatment of hypertension.
Ramipril.
| Enalapril.
593
What should be prescribed if ACE inhibitors are contraindicated in the treatment of hypertension?
Angiotensin receptor blocker.
594
Give an example of an angiotensin receptor blocker used in the treatment of hypertension.
Candesartan.
595
Give an example of a calcium channel blocker used in the treatment of hypertension.
Amlodipine.
| Nifedipine.
596
Give an example of a diuretic used in the treatment of hypertension.
Bendroflumethiazide.
| Furosemide.
597
Should beta-blockers be considered as treatment for those with hypertension?
In the young, yes.
598
What is a cardiac arrhythmia?
An abnormality of the cardiac rhythm.
599
Patients with bradycardia will usually show what symptoms?
Patients are usually asymptomatic unless the heart rate is very slow.
600
Bradycardia is normal in what group of people?
Athletes.
601
Why is bradycardia normal in athletes?
Due to increased vagal tone and thus increased parasympathetic activity.
602
What are the two subdivisions of tachycardia?
Supraventricular tachycardia.
| Ventricular tachycardia.
603
Give the sinus rhythm conduction pathway.
SAN > action potential > muscle cells of atria > depolarisation of AVN > delay > interventricular septum > bundle of His > R&L bundle branches > Purkinje cells > ventricular myocardial cells.
604
Where is the SAN located?
The SAN is found at the junction between the superior vena cava and the right atrium.
605
Where is the AVN located?
The AVN is found in the lower intertribal septum.
606
Why is the AVN delay important?
Allows complete contraction (and emptying of blood) of the atria before ventricles are excited.
607
Describe the function of the SAN.
The normal cardiac pacemaker. The SAN depolarises spontaneously.
608
What modulates the rate of SAN discharge?
The autonomic nervous system.
609
Of the sympathetic and parasympathetic nervous system, which predominates in modulation of SAN discharge?
The parasympathetic nervous system.
610
Describe the state of the autonomic nervous system that leads to tachycardia.
A reduction of parasympathetic tone or and increase in sympathetic stimulation.
611
Describe the state of the autonomic nervous system that leads to bradycardia.
An increased parasympathetic tone or a decrease in sympathetic stimulation.
612
Compare the difference in sinus rate between men and women.
The sinus rate is slightly faster in women than men.
613
Describe how inspiration affects heart rate.
Parasympathetic tone falls and heart rate increases.
614
Describe how expiration affects heart rate.
Parasympathetic tone increases and heart rate falls.
615
What is atrial fibrillation?
A chaotic irregular rhythm of the atria at 300 to 600bpm.
616
Describe the prevalence of atrial fibrillation between men and women.
Atrial fibrillation is more common in men than women.
617
Give the five classifications of atrial fibrillation.
```
Acute.
Paroxysmal.
Recurrent.
Persistent.
Permanent.
```
618
Define acute atrial fibrillation.
Onset within the previous 48 hours.
619
Define paroxysmal atrial fibrillation.
Stops spontaneously within 7 days. Self terminating.
620
Define recurrent atrial fibrillation.
More than 2 episodes.
621
Define persistent atrial fibrillation.
Continuous for more than 7 days and not self terminating.
622
Define permanent atrial fibrillation.
Cannot be corrected by treatment.
623
Give seven causes of atrial fibrillation.
```
Heart failure/ischaemia.
Hypertension.
Myocardial infarction.
Pulmonary embolism.
Mitral valve disease.
Cardiac surgery.
Alcohol.
```
624
Give six risk factors for atrial fibrillation.
```
Older than 60.
Diabetes.
High blood pressure.
Coronary artery disease.
Prior MI.
Structural heart disease.
```
625
What is structural heart disease?
Valve problems or congenital heart defects.
626
Describe the pathophysiology behind the development of atrial fibrillation.
The causes listed, such as hypertension, stress the cells in the atria leading to tissue heterogeneity. After which conduction becomes unpredictable.
627
What is tissue heterogeneity?
When cells develop different properties.
628
Give examples of tissue heterogeneity in atrial fibrillation.
Some cells conduct faster while others have a shorter refractory period.
629
Why does tissue heterogeneity lead to unpredictable conduction in atrial fibrillation?
Multiple meandering wavelets are produced by the SAN as well by rapidly depolarising ectopic foci.
630
What are ectopic foci?
An excitable group of cells that causes a heart beat outside the normal functioning of the SAN. An ectopic pacemaker.
631
Where ectopic foci located?
Predominantly located in the cardiac muscle around the pulmonary veins.
632
What is the response to the meandering wavelets in atrial fibrillation?
The atria respond electrically but without coordinated mechanical action.
633
What is the name for the lack of coordinated mechanical action in atrial fibrillation.
Atrial spasm.
634
What is the effect of the meandering wavelets (in Afib) on the ventricles?
Only a proportion of impulses are conducted to the ventricles resulting in irregular ventricular contraction.
635
Atrial spasm results in what missing feature from the cardiac cycle?
Atrial kick.
636
What is the atrial kick?
Atrial contraction which forces more blood into the ventricles.
637
What is the consequence of an absent atrial kick?
Cardiac output falls by around 20%
638
Why is atrial spasm problematic? Other than the loss of the atrial kick.
Can lead to thromboembolic events.
639
Describe how atrial spasm can lead to thromboembolic events.
Blood in the atria stagnates/pools and clots forming thrombi which may become emboli.
640
Give an example of a thromboembolic event as a result of atrial spasm.
Stroke.
641
How does atrial fibrillation present?
Symptoms are highly variable and patient may be asymptomatic.
Palpitations.
Dyspnoea and/or chest pain.
Fatigue.
Apical pulse rate > radial rate. S1 of varying intensity.
642
Give two differential diagnoses of Afib.
Atrial flutter.
| Supraventricular tachycardia.
643
How is Afib diagnosed?
On ECG:
No P waves.
Rapid and irregular QRS rhythm.
644
Give four focuses in the treatment of acute atrial fibrillation.
Treatment of precipitating event.
Control of ventricular rate.
Anticoagulation treatment.
Cardioversion.
645
How is ventricular rate controlled in patients with acute atrial fibrillation?
1st line: calcium channel blocker or beta-blocker.
| 2nd line: dioxin or anti-arrhythmic.
646
Name a calcium channel blocker used in the treatment of acute atrial fibrillation.
Verapamil.
647
Name a beta-blocker used in the treatment of acute atrial fibrillation.
Bisoprolol.
648
Name an anti-arrhythmic used in the treatment of acute atrial fibrillation.
Amiodarone.
649
What treatment is used for anticoagulation in patients with acute atrial fibrillation?
Low molecular weight heparin.
650
Name two anticoagulant medications in the class of low molecular weight heparin (used in treatment of Afib).
Enoxaparin.
| Dalteparin.
651
Why are anticoagulant medications prescribed for patients with acute Afib?
To minimise the thromboembolism risk associated with cardioversion.
652
Give the electrical cardioversion regime for treatment of patients with acute Afib.
Oxygen.
ITU/CCU.
GA or IV sedation.
Monophasic 200J, 360J, 360J (biphasic 200J).
653
Give the drug cardioversion regime for treatment of patients with acute Afib.
Amiodarone IV infusion or flecainide (anti-arrhythmic).
654
What are the main goals for treatment of chronic atrial fibrillation?
Rate control and anticoagulation.
655
When is rhythm control appropriate in the treatment of chronic atrial fibrillation?
When the patient is young, symptomatic, presenting for the 1st time or has AF from a corrected precipitant.
656
What treatment is used for anticoagulation in patients with chronic atrial fibrillation?
Warfarin.
657
What is the aim of anticoagulation in patients with chronic atrial fibrillation?
Achieve an INR of 2 to 3.
658
What are alternatives for warfarin in patients with chronic atrial fibrillation?
Aspirin.
| Dabigatran.
659
When should aspirin be used as an alternative for warfarin in the treatment of chronic Afib?
If warfarin is contraindicated or if there is a very low risk of emboli.
660
What treatment should be used for rate control in patients with chronic atrial fibrillation?
Beta-blocker or calcium channel blocker. If that fails add digoxin, then amiodarone.
661
What treatment is used for rhythm control in patients with chronic atrial fibrillation?
Cardioversion.
662
In patients with chronic Afib, what should be done before cardioversion if there is an increased risk of cardioversion failure?
Pretreat with amiodarone for ≥ 4 weeks.
663
What drug should be given for pharmacological cardioversion in the treatment of Afib if the patient has no structural heart defects?
Flecainide.
664
What drug should be given for pharmacological cardioversion in the treatment of Afib if the patient has structural heart defects?
IV amiodarone.
665
What is the function of the CHA2DS2-VASc score?
To estimate risk of stroke in patients with atrial fibrillation.
666
What does C represent in the CHA2DS2-VASc formula?
Congestive heart failure.
667
What does H represent in the CHA2DS2-VASc formula?
Hypertension.
668
What does A2 represent in the CHA2DS2-VASc formula?
Age ≥ 75 years.
669
What does D represent in the CHA2DS2-VASc formula?
Diabetes mellitus.
670
What does S2 represent in the CHA2DS2-VASc formula?
Prior Stroke / TIA / Thromboembolism.
671
What does V represent in the CHA2DS2-VASc formula?
Vascular disease, involving the aortic, coronary or peripheral arteries.
672
What does A represent in the CHA2DS2-VASc formula?
Age 65 - 74
673
What does Sc represent in the CHA2DS2-VASc formula?
Sex category: female.
674
How does a CHA2DS2-VASc score of 1 influence treatment?
Oral anticoagulants and/or aspirin should be considered.
675
How does a CHA2DS2-VASc score of 2+ influence treatment?
Oral anticoagulants are required.
