Cardiology Flashcards
1
Q
outline the RAAS system
A
- liver produces and secretes angiotensinogen
- kidney secretes renin (secretion is stimulated by low fluid volume moving through nephrons)
- renin converts angiontensinogen to angiotensin I
- angiotensin converting enzyme secreted by the lungs converts angiotensin I to angiotensin II
- ANG II causes ADH secretion, stimulates thirst and vasoconstriction and acts on the adrenal gland to produce aldosterone
- increase in blood pressure
2
Q
cardiac output equation
A
CO = HR x Stroke Volume
3
Q
Define angina.
A
Angina is a type of IHD. It is a symptom of O2 supply/demand mismatch to the heart experienced on exertion.
4
Q
What is the most common cause of angina?
A
Narrowing of the coronary arteries due to atherosclerosis.
5
Q
Give 5 possible causes of angina.
A
- Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
- Increased distal resistance = LV hypertrophy.
- Reduced O2 carrying capacity e.g. anaemia.
- Coronary artery spasm.
- Thrombosis.
6
Q
Give 5 modifiable risk factors for angina.
A
- Smoking.
- Diabetes.
- High cholesterol (LDL).
- Obesity/sedentary lifestyle.
- Hypertension.
7
Q
Give 3 non-modifiable risk factors for angina
A
- Increasing age.
- Gender, male bias.
- Family history/genetics
8
Q
What are the three main risk factors for IHD
A
Advancing age
Cigarette Smoking
Family history (first degree relatives who died of heart trouble under the age of 60)
9
Q
Briefly describe the pathophysiology of angina that results from atherosclerosis.
A
On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.
10
Q
Briefly describe the pathophysiology of angina that results from anaemia.
A
On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 carrying capacity-> myocardial ischaemia -> angina.
11
Q
How do blood vessels try and compensate for increased myocardial demand during exercise.
A
When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!
12
Q
Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?
A
In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!
13
Q
How can stable angina be reversed?
A
Resting - reducing myocardial demand.
14
Q
How would you describe the chest pain in angina?
A
Crushing central chest pain. Heavy weight on chest
15
Q
Give 5 symptoms of angina.
A
- Crushing central chest pain.
- The pain is relieved with rest or using a GTN spray.
- The pain is provoked by physical exertion.
- The pain might radiate to the arms, neck or jaw.
- Breathlessness.
16
Q
What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?
A
Pre-test probability of CAD. It takes into account gender, age and typicality of pain.
17
Q
What investigations might you do in someone you suspect to have angina?
A
- ECG - usually normal, there are no markers of angina.
- Echocardiography.
- CT angiography - has a high Negative Predictive Value (NPV) and is good at excluding the disease.
- Exercise stress test ECG - induces ischaemia.
- Invasive angiogram - tells you FFR (pressure gradient across stenosis).
- Blood tests (FBC, U&Es)
18
Q
Describe the primary prevention of angina.
A
- Risk factor modification.
2. Low dose aspirin.
19
Q
Describe the secondary prevention of angina.
A
- Risk factor modification (stop smoking, exercise, diet)
- Pharmacological therapies for symptom relief and to reduce the risk of CV events.
- Interventional therapies e.g. PCI.
20
Q
Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.
A
- Beta blockers.
- Nitrates e.g. GTN spray (symptom relief)
- Calcium channel blockers.
21
Q
Describe the action of beta blockers.
A
Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. This reduces cardiac output and so decreases oxygen demand
22
Q
Give 3 side effects of beta blockers.
A
- Bradycardia.
- Tiredness.
- Erectile dysfunction.
- Cold peripheries.
23
Q
When might beta blockers be contraindicated?
A
They might be contraindicated in someone with asthma or in someone who is bradycardic.
24
Q
Describe the action of nitrates.
A
Nitrates e.g. GTN spray are venodilators. Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
25
Describe the action of Ca2+ channel blockers.
Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.
26
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
1. Aspirin.
| 2. Statins.
27
How does aspirin work?
Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Caution: Gastric ulcers!
28
What are statins used for?
They reduce the amount of LDL in the blood.
29
What is revascularisation?
Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.
30
Name 2 types of revascularisation.
1. PCI (percutaneous coronary intervention)
| 2. CABG (coronary artery bypass graft)
31
Give 2 advantages and 1 disadvantage of PCI.
1. Less invasive.
2. Convenient and acceptable.
3. High risk of restenosis.
32
Give 1 advantage and 2 disadvantages of CABG.
1. Good prognosis after surgery.
2. Very invasive.
3. Long recovery time.
33
Stable angina
Induced by exertion and relieved by rest
34
three environmental factors that can exacerbate angina
cold weather
heavy meals
emotional stress
35
how much stenosis does there have to be for angina to present
70% stenosis
| rapidly declines
36
what is unstable angina
critical ischaemia but not quite so bad that it has caused an infarct
will have pain on rest
37
what is the gold standard investigation for angina
perfusion MRI
38
side effects of calcium channel blockers
flushing
postural hypotension
swollen ankles
39
how do statins work
HMG CoA reductase inhibitors (the enzyme that produces cholesterol)
40
when would you use a PCI
STEMI
NSTEMI
Stable angina
41
When would you use CABG
NSTEMI
| Stable angina
42
Define atherosclerosis.
A hardened plaque in the intima of an artery. It is an inflammatory process.
43
What can an atherosclerotic plaque cause?
1. Heart attack.
2. Stroke.
3. Gangrene.
44
What are the constituents of an atheromatous plaque?
1. Lipid core.
2. Necrotic debris.
3. Connective tissue.
4. Fibrous cap.
5. Lymphocytes.
45
Give 5 risk factors for atherosclerosis.
1. Family history.
2. Increasing age.
3. Smoking.
4. High levels of LDL's.
5. Obesity.
6. Diabetes.
7. Hypertension.
46
In which arteries would you be most likely to find atheromatous plaques?
In the peripheral and coronary arteries.
47
Which histological layer of the artery may be thinned by an atheromatous plaque?
The media.
48
What is the precursor for atherosclerosis.
Fatty streaks.
49
What can cause chemoattractant release?
A stimulus such as endothelial cell injury.
50
What are the functions of chemoattractants?
Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!
51
Describe the process of leukocyte recruitment.
1. Capture.
2. Rolling.
3. Slow rolling.
4. Adhesion.
5. Trans-migration.
52
Describe in 5 steps the progression of atherosclerosis.
1. Fatty streaks.
2. Intermediate lesions.
3. Fibrous plaque.
4. Plaque rupture.
5. Plaque erosion.
53
Progression of atherosclerosis: what are the constituents of fatty streaks?
Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.
54
Progression of atherosclerosis: what are constituents of intermediate lesions?
- Foam cells.
- Smooth muscle cells.
- T lymphocytes.
- Platelet adhesion.
- Extracellular lipid pools.
55
Progression of atherosclerosis: what are the constituents of fibrous plaques?
- Fibrous cap overlies lipid core and necrotic debris.
- Smooth muscle cells.
- Macrophages.
- Foam cells.
- T lymphocytes.
Fibrous plaques can impede blood flow and are prone to rupture.
56
Progression of atherosclerosis: why might plaque rupture occur?
Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.
57
What is the treatment for atherosclerosis
Percutaneous coronary intervention (PCI).
58
Major limitation of PCI
restenosis
59
How can restenosis be avoided following PCI?
Drug eluting stents: anti-proliferative and drugs that inhibit healing.
60
What is the key principle behind the pathogenesis of atherosclerosis?
It is an inflammatory process!
61
Define atherogenesis.
The development of an atherosclerotic plaque.
62
What are acute coronary syndromes (ACS)?
ACS encompasses a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI.
63
What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.
64
What are uncommon causes of ACS?
1. Coronary vasospasm.
2. Drug abuse.
3. Coronary artery dissection.
65
Briefly describe the pathophysiology of ACS?
Atherosclerosis -> plaque rupture -> platelet aggregation -> thrombosis formation -> ischaemia and infarction -> necrosis of cells -> permanent heart muscle damage and ACS
66
what is the significance of troponin in ACS
when myocardial cells are damaged, troponins are released and enter the bloodstream
MIs have troponin rises, unstable angina does not
67
Describe type 1 MI.
Spontaneous MI with ischaemia due to plaque rupture.
68
Describe type 2 MI.
MI secondary to ischaemia due to increased O2 demand.
69
Why do you see increased serum troponin in NSTEMI and STEMI?
The occluding thrombus causes necrosis of cells and so myocardial damage. Troponin is a sensitive marker for cardiac muscle injury and so is significantly raised in reflection to this.
70
Give three signs of unstable angina
1. cardiac chest pain at rest
2. cardiac chest pain with cresecendo pattern as pain has an increased frequency and severity
3. new onset of angina occuring at rest
4. no significant rise in troponin
71
diagnosis of unstable angina
history
ECG shows no clear evidence of MI
Troponin has no significant rise
72
why is there no significant rise of troponin in unstable angina
because there is no damage (infarction) to the heart only ischaemia
73
Give 6 signs/symptoms that are typical of an MI.
1. Unremitting and usually severe central cardiac chest pain.
2. Pain occurs at rest.
3. Sweating
4. Breathlessness.
5. Nausea/vomiting.
6. 1/3 occur in bed at night.
74
Give 5 potential complications of MI.
1. Heart failure.
2. Rupture of infarcted ventricle.
3. Rupture of interventricular septum.
4. Mitral regurgitation.
5. Arrhythmias.
6. Heart block.
7. Pericarditis.
75
What investigations would you do on someone you suspect to have ACS?
1. ECG.
2. Blood tests; look at serum troponin.
3. Coronary angiography.
4. Cardiac monitoring for arrhythmias.
76
What might the ECG of someone with unstable angina show?
The ECG from someone with unstable angina may be normal or might show T wave inversion and ST depression.
77
What might the ECG of someone with NSTEMI show?
The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression. There also might be R wave regression, ST elevation and biphasic T wave in lead V3.
78
how do you diagnose a STEMI
ST-elevation can usually be diagnosed at the time of presentation on an ECG
79
What might the ECG of someone with STEMI show?
The ECG from someone with STEMI will show ST elevation in the anterolateral leads. After a few hours, T waves invert and deep, broad, pathological Q waves develop.
80
how do you diagnose an NSTEMI
retrospective diagnosis
| troponin levels
81
A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?
1. Gram negative sepsis.
2. Pulmonary embolism.
3. Myocarditis.
4. Heart failure.
5. Arrhythmias.
82
what test can you do that is an indicator for heart failure?
where is it produced?
Why does it indicate HF?
B-type natriuretic peptide is a hormone that helps to regulate blood volume. Produced by the left ventricle. Heart releases more of this hormone when the left ventricle is stretched from having to work harder
83
Management of someone having an ACS
```
Get to hospital ASAP!!! I STEMI call PCI centre for transfer
ROMANCE
Reassure
Oxygen (if hypoxic and below 94)
Morphine
Aspirin 300mg immediately
Nitrates
Clopidogrel (ST elevation)
Enoxaparin (heparin)
```
84
What is the treatment of choice for STEMI?
PCI.
85
how does aspirin work as an antiplatelet drug
irreversibly inhibits prostaglandin H synthase in platelets and megakaryocytes blocking the formation of thromboxane A2
86
what happens if you inhibit the P2Y12 receptor
decreased thromboxane production and decreased platelet aggregation
87
What is the function of P2Y12?
It amplifies platelet activation.
88
what is dual antiplatelet therapy
aspirin + P2Y12 inhibitor
89
when is dual antiplatelet therapy used
management of ACS
90
three oral options of P2Y12 inhibitors
clopidogrel
prasugrel
ticagrelor
91
action of clopidogrel
binds to the P2Y12 receptor
| to stop its effects have to wait until all the platelets have been replaced (10-12 days)
92
action of ticagrelor
binds reversibly to the P2Y12 receptor
| its effects relate to the presence of the drug in the plasma
93
3 side effects of P2Y12 inhibitors
increased bleeding
rash
GI disturbances
94
Describe the secondary prevention therapy for people after having a STEMI.
1. Aspirin.
2. Clopidogrel (P2Y12 inhibitor).
3. Statins.
4. Metoprolol (beta blocker).
5. ACE inhibitor.
6. Modification of risk factors.
95
what other drug category can you use as well as antiplatelet drugs
anti-coagulants
used during PCI
enoxaparin (low molecular weight heparin)
96
what is the pathway of electrical activity in the heart
SA node --> R+L atrium --> AV node --> bundle of His --> R+L bundle branches --> Purkinje fibres (left bundle splits into post and anterior fascicle)
97
the chest leads look at the heart in what plane?
horizontal
98
the limb leads look at the heart in what plane?
vertical
99
what does V1 look at
septal aspect of the heart
100
what does V2, V3, V4 look at
anterior aspect of the heart
101
what does V5 and V6 look at
lateral aspect of the left ventricle
102
which lead has the best view of the heart
lead II
103
ECG: what is the normal axis of the QRS complex?
-30° -> +90°
104
what is left axis deviation
past -30°
105
ECG: what does the P wave represent?
Atrial depolarisation.
106
ECG: how long should the PR interval be?
120 - 200ms.
107
ECG: what might a long PR interval indicate?
Heart block.
108
what is right axis deviation
past +90°
109
how to decide if someone has left axis deviation or right axis deviation
The Axis was Left Two the Right One
Lead II = negative = LAD
Lead I = negative = RAD
110
3 causes of left axis deviation
Left anterior fascicular block
Left BBB
LVH
111
2 causes of right axis deviation
Left posterior fascicular block
| right heart hypertrophy
112
equation to determine heart rate of a regular rhythm
rate = 300 / (number of large squares between R waves)
113
equation to determine rate of an irregular rhythm
rate = (QRS complexes in 10s) x 6
114
how many big squares on an ECG reading = 1 second
5
115
how many big squares on an ECG reading = 1 mV
2
116
what might M shaped P waves on an ECG suggest (p mitrale)
Left atrial hypertrophy
117
what might tall pointed p waves (p pulmonale) on an ECG suggest
right atrial hypertrophy
118
What is the dominant pacemaker of the heart?
The SA node. 60-100 beats/min.
119
How long should the QRS complex be?
Less than 110 ms.
120
In which leads would you expect the QRS complex to be upright in?
Leads 1 and 2.
121
In which lead are all waves negative?
aVR.
122
Give 3 signs of abnormal T waves
1. Symmetrical.
2. Tall and peaked.
3. Biphasic or inverted.
123
What happens to the QT interval when HR increases?
The QT interval decreases.
124
define heart failure
an inability of the heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
125
why are males more at risk of developing heart disease
do not have the protection that oestrogen provides
126
what is the most common cause of heart failure
ischaemic heart disease
127
name three causes of heart failure
hypertension
alcohol excess
cardiomyopathy
128
risk factors for developing heart failure?
Including ethnicity
```
Over 65
Male
Of african descent
obesity
history of MI
```
129
pathophysiology of heart failure
DIAGRAM IN NOTES
130
Three symptoms of heart failure
```
shortness of breath
fatigue
ankle swelling
cold peripheries
increased weight
```
131
Name three signs of heart failure
1. peripheral oedema
2. raised jugular venous pressure
3. S3 and S4 heart sounds
4. Crackles and tachycardia
5. Murmurs and displaced apex beat
132
Investigations for heart failure
Chest X-ray
Blood test : B-type natriuretic peptide
Echocardiography
133
What is the value of B-type natriuretic peptide that diagnoses heart failure
BNP > 400ng/L
134
Outline the New York Heart Association Classification
Class I : no limitation
Class II : slight limitation (milf HF), patient is comfortable at rest
Class III : marked limitation, less than ordinary activities causes dyspnoea which is limiting
Class IV: inability to carry out any physical activity without discomfort
135
Three examples of acute decompensation of chronic heart failure
acute MI
uncorrected increased BP
Obesity
136
Three complications of heart failure
Renal dysfunction
Arrhythmias
Systemic thromboembolism
137
Management of acute heart failure
Medical emergency
| ROMANCE
138
Lifestyle management of chronic heart failure
Stop smoking
Stop drinking alcohol
Eat less salt
Optimize weight and nutrition
139
What hormones does the heart produce?
ANP and BNP
140
What are the functions of ANP and BNP?
1. Increased renal excretion of Na+ and therefore water.
2. Vasodilators.
3. Inhibit aldosterone release.
141
What drugs can we use in the management of heart failure
```
Diuretics (mainly symptomatic relief of oedema, usually loop diuretics)
ACE-inhibitors
Beta-blockers
Aldoesterone antagonist
Digoxin
```
142
What would you give if patient is intolerant to ACE-i
ARB (angiotensin II Receptor Blocker)
143
How does digoxin work?
It inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves.
144
What are the main effects of digoxin?
1. Bradycardia.
2. Reduced atrioventricular conduction.
3. Increased force of contraction (positive inotrope).
145
Give 4 potential side effects of digoxin.
1. Nausea.
2. Vomiting.
3. Diarrhoea.
4. Confusion.
146
In what diseases is digoxin clinically indicated
Atrial fibrillation
| LVSD
147
what drug is used to treat heart failure with preserved ejection fraction
Spironolactone
148
Hypertension is a major risk factor for what three conditions
Stroke
MI
Heart failure
Chronic renal disease
149
hypertension symptoms
asymptomatic!
150
signs of hypertension
high blood pressure
retinopathy
end organ damage (e.g proteinuria)
151
What is clinical high blood pressure defined as?
140/90mmHg or higher
152
If patients have suspected hypertension (have a clinical blood pressure) what is next offered?
Ambulatory blood pressure monitoring
153
why are ABPM results slightly lower than clinical blood pressure readings
white coat hypertension
154
definitions of stage 1 hypertension
clinical BP : 140/90
| ABPM : 135/85
155
definition of stage 2 hypertension
clinical BP : 160/100
| ABPM: 150/95
156
what are the two forms of hypertension
primary and secondary hypertension
157
cause of primary hypertension
unknown
158
cause of secondary hypertension
renal disease
endocrine disorders
pregnancy
drugs
159
what would be your first line of treatment for an adult with diabetes and hypertension for the treatment of hypertension
ACE-i or ARB
160
what would be your first line treatment for an adult without DM, under the age of 55 from white family origin
ACE-i or ARB
161
what would be your first line of treatment in an adult who is aged 55 years or over or is from a Black African or African-Caribbean family origin?
Calcium channel blocker
162
How can hypertension be treated?
1. Lifestyle modification e.g. reduce salt intake.
| 2. Anti-hypertensive drugs.
163
Write an equation for BP.
BP = CO X TPR.
164
Name 2 systems that are targeted pharmacologically in the treatment of hypertension.
1. RAAS.
| 2. Sympathetic nervous system (NAd).
165
Give 4 functions of angiotensin 2.
1. Potent vasoconstrictor.
2. Activates sympathetic nervous system; increased NAd.
3. Activates aldosterone = Na+ retention.
4. Vascular growth, hyperplasia and hypertrophy.
166
Give 3 ways in which the sympathetic nervous system (NAd) lead to increased BP.
1. Noradrenaline is a vasoconstrictor = increased TPR.
2. NAd has positive chronotropic and inotropic effects.
3. It can cause increased renin release.
167
Lifestyle modification in the treatment of hypertension
```
reduce weight if obese
reduce alcohol intake
stop smoking
control cholesterol
reduce salt intake
low-fat diet
increase exercise
```
168
what are the criteria for starting antihypertensive drug treatment
stage 1 hypertension: under age of 80 who have organ damage, established CVS, renal disease or diabetes
Offer treatment to anyone with stage 2 hypertension
169
Name 3 ACE inhibitors
1. Ramapril.
2. Enalapril.
3. Perindopril.`
170
In what diseases are ACE inhibitors clinically indicated?
1. Hypertension.
2. Heart failure.
3. Diabetic nephropathy.
171
Give 4 potential side effects of ACE inhibitors.
1. Hypotension.
2. Hyperkalaemia.
3. Acute renal failure.
4. Teratogenic.
172
Why do ACE inhibitors lead to increased kinin production?
ACE also converts bradykinin to inactive peptides. Therefore ACE inhibitors lead to a build up of kinin.
173
ACE inhibitors: give 3 potential side effects that are due to increased kinin production.
1. Dry chronic cough.
2. Rash.
3. Anaphylactoid reaction.
174
You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?
ACE inhibitors lead to a build up of kinin. One of the side effects of this is a dry and chronic cough.
175
Name three angiotensin receptor blockers
Candesartan
Valsartan
Iosartan
Irbesartan
176
What are ARBs?
Angiotensin 2 receptor blockers.
177
At which receptor do ARB's work?
AT-1 receptor blocker
178
In what diseases are ARBs clinically indicated?
1. Hypertension.
2. Heart failure.
3. Diabetic nephropathy.
179
When would you prescribe an ARB
If an ACE-i is contraindicated
| Have developed a chronic dry cough from ACE-i
180
When are ARBs contraindicated
pregnancy
181
Give 4 potential side effects of ARBs.
1. Hypotension.
2. Hyperkalaemia.
3. Renal dysfunction.
4. Rash.
182
Name 3 calcium channel blockers
1. Amlodipine
2. Nifedipine
3. Felodipine
4. Lacidipine
5. Verapamil
6. Diltiazem
183
Clinical indications for CCB
Hypertension.
2. IHD.
3. Arrhythmia.
184
Name 2 dihydropyridines and briefly explain how they work.
Dihydropyridines are a class of calcium channel blockers. Amlodipine and felodipine are examples of dihydropyridines. They are arterial vasodilators.
185
Name a calcium channel blocker that acts primarily on the heart (phenylalkylamines)
Verapamil – it is negatively chronotropic and inotropic.
186
Name a calcium channel blocker that acts on the heart and on blood vessels.
Diltiazem – acts on the heart and the vasculature.
187
On what channels do calcium channel blockers work?
L type Ca2+ channels.
188
Give 3 potential side effects that are due to the vasodilatory ability of calcium channel blockers.
Flushing.
2. Headache.
3. Oedema.
189
Give a potential side effect that is due to the negatively inotropic ability of calcium channel blockers.
Worsening cardiac failure
190
what is normal heart rate
60-100bpm
191
what is bradycardia?
slow heart rate (less than 60bpm)
192
Give three potential consequences of arrhythmias
1. Sudden death.
2. Syncope.
3. Dizziness.
4. Palpitations.
5. Can also be asymptomatic.
193
Define tachycardia
Heart rate that is over 100bpm
194
what type of nervous system simulation leads to bradycardia
increased parasympathetic tone
| decreased sympathetic tone
195
what are the two broad categories of tachycardia
1. Supra-ventricular tachycardia's.
| 2. Ventricular tachycardia's.
196
Where do supra-ventricular tachycardia's arise from?
They arise from the atria or atrio-ventricular junction.
197
Do supra-ventricular tachycardia's have narrow or broad QRS complexes?
Supraventricular tachycardias are often associated with narrow complexes.
198
Name 3 examples of supra-ventricular tachycardias?
Atrial fibrillation
Atrial flutter
Atrioventricular junctional tachycardias
199
Where do ventricular tachycardia's arise from?
The ventricles.
200
Do ventricular tachycardia's have narrow or broad QRS complexes?
Ventricular tachycardias are often associated with broad complexes.
201
what type of nervous system stimulation can lead to tachycardias
Decreased parasympathetic tone or an increased sympathetic tone
202
Pathology of atrial fibrillation>
There is a loss of atrial mechanical contraction.
Multiple waves of electrical activity bombard the AV node. The atria respond electrically by contracting but there is no coordinated mechanical action and only a proportion of the impulses are conducted to the ventricles. Leads to a state of atrial spasm.
203
what is the main risk associated with atrial fibrillation?
embolic stroke
204
Aetiology of AF? (name three causes)
```
Idiopathic
Hypertension
Heart failure
Coronary artery disease
Valvular heart disease (especially mitral stenosis)
```
205
Name three risk factors which increase your likelihood of developing AF?
```
Older than 60
Diabetes
Hypertension
Coronary artery disease
Prior MI
Structural heart disease
```
206
What are the symptoms of AF?
Palpitations
Dyspnoea
Chest pains
Fatigue
207
Name 2 signs in AF?
Irregularly irregular pulse
| S1 heart sounds
208
What investigation would you do in a patient with AF? And what does it show?
ECG
- No p waves
- Irregular and rapid QRS complex
- fine oscillation over the baseline
209
What is used to calculate stroke risk and need for anticoagulation in AF patients?
```
Use the CHA2DS2-VASc score to calculate stroke risk at the need for anticoagulation
Congestive HF (1)
Hypertension (1)
Age greater or equal to 75 (2)
Diabetes (1)
Stroke (2)
Vascular disease (1)
Age 65-75 (1)
Sex: female (1)
```
If the score is 2 or more need anticoagulation
210
What is the management in a patient with acute AF + adverse signs
ABCDE
Electrical cardioversion by DC shock + amiodarone if unsuccessful
Heparin
211
What is the management in a stable patient with acute AF that started less than 48 hours ago?
- Electrical cardioversion with DC shock
- If this failed can give it medically via IV infusion of flecainide or amiodarone
- Enoxaparin to minimize risk of thromboembolism
212
What is the management in a stable patient with acute AF that started more than 48 hours ago?
Ventricular rate control, use either
Calcium Channel Blocker e.g Diltiazem or Verapamil
Beta blocker e.g bisoprolol
213
What are the two strategies use to manage chronic AF?
Rate control
| Rhythm control
214
Outline the rate control strategy used to manage chronic AF?
First line = beta blocker or CCB monotherapy
Plus digoxin if doesn’t work
Then consider amiodarone
215
What patients do you use rhythm control strategy to control chronic AF?
younger
symptomatic
active
216
outline the rhythm control strategy to control chronic AF?
Either so elective DC cardioversion (electric shock) or elective pharmacological cardioversion (IV flecainide is first line, then IV amiodarone)
217
What treatment can you give to patients that have infrequent, symptomatic AF?
Flecainide PRN tablets
218
what other medication should some AF patients be on? Why?
Anticoagulation
- Warfarin
- DOACS (Rivaroxaban, apixaban, edoxaban)
To reduce the risk of embolic stroke
219
What is atrial flutter?
What is the pathological mechanism behind it?
Fast but organised atrial rhythm with an atrial rate between 250-300bpm. Regular response of the ventricles
The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.
220
Name one risk factor that increases likelihood of developing atrial flutter?
Atrial fibrillation
221
Aetiology of atrial flutter?
```
Idiopathic
Coronary heart disease
Obesity
Hypertension
Heart failure
COPD
Pericarditis
Acute excess alcohol intoxication
```
222
Symptoms of atrial flutter
```
Palpitations
Breathlessness
Chest pain
Syncope
Fatigue
Dizziness
```
223
Investigation in atrial flutter and what does it show?
ECG
| Regular sawtooth like atrial flutter waves between QRS complexes due to continuous atrial depolarisation
224
What is a regular sawtooth like pattern on an ECG suggestive of?
Atrial flutter
225
Treatment of atrial flutter
Acute : electrical cardioversion but anticoagulate before with enoxaparin
Catheter ablation (creating a conduction block to try and restore rhythm and block offending re-rentrant wave)
Iv amiodarone to restore sinus rhythm and use a beta blocker to suppress any further arrhythmias
226
What is the pathology of AV re-entrant tachycardia Wolff-Parkinson White Syndrome?
Type of AV reentrant tachycardia
Normal AV circuit and accessory circuit can transmit impulses from the atria to ventricles.
The accessory circuit can transmit impulses from the atria to the ventricle or from the ventricle to the atria. This can set up a re-entrant circuit and the electrical signal goes around this accessory circuit stimulating the atria and ventricles to contract causing tachycardia
227
Aetiology of Wolff-Parkinson-White syndrome?
Accessory pathway results from the incomplete separation of the atria and ventricles during fetal development
228
Symptoms of Wolff-Parkinson-White Syndrome?
Palpitations
Severe dizziness
Dyspnoea
Syncope
229
Investigation in Wolff-Parkinson -White syndrome? What does it show?
ECG
Short PR interval
Wide QRS complex with a delta wave (start of the complex is sloped)
230
What syndrome is suggestive of a delta wave on an ECG ad short PR interval?
Wolff-Parkinson-White Syndrome
231
Treatment of Wolff-Parkinson-White Syndrome?
Patients that present with haemodynamic instability (hypotension and pulmonary oedema) require emergency cardioversion.
If the patient is stable can use vagal manoeuvres
Breath-holding
Carotid massage
Valsalve manoeuvre - abrupt voluntary increase in intra-abdominal pressure and intra thoracic pressure by straining
If unsuccessful : IV adenosine
Surgery: catheter ablation of the accessory pathway
232
what is the pathology behind AVNRT?
There are slow and fast pathways. Signals from the SAN can be carried by the slow pathway and transmitted to the ventricles and then travel back up the fast pathway setting up a reentrant loop at the AV node
233
Risk factors for developing an AVNRT syndrome?
```
Exertion
Emotional Stress
Coffee
Tea
Alcohol
```
234
Symptoms of AVNRT syndromes?
Rapid regular palpitations with abrupt onset and sudden termination
Chest pain
Breathlessness
Neck pulsations
235
Investigation in AVNRT syndrome and what does it show?
ECG
- QRS complexes will show typical BBB sometimes
- Narrow complex tachycardia
- P waves are either not visible (hidden by QRS) or appear both before and after the QRS complex
236
Treatment for AVNRT?
Catheter ablation
237
What is the difference between AV Heart Block and Bundle Branch Block
AV Block : block in the AV node or Bundle of His
| BBB: Block lower down in the conduction system
238
define first degree heart block
Every atrial depolarisation is followed by conduction to the ventricles but with delay
239
Aetiology of first degree heart block
Hyperkalaemia
Myocarditis
Inferior MI
AVN blocking drugs (Beta blockers, CCB or digoxin)
240
What does an ECG show in first degree heart block?
Prolongation of the PR interval to greater than 0.22 seconds
241
What are the subtypes of AV node blocks?
First degree
Second degree
Third degree
242
Pathology of first degree AV block?
Every atrial depolarisation is followed by conduction to the ventricles but with delay
243
Aetiology of First degree heart block?
Hyperkalaemia
Myocarditis
Inferior MI
AVN blocking drugs (Beta blockers, CCB or digoxin)
244
What does an ECG show of a patient with first degree heart block
Prolongation of the PR interval to greater than 0.22 seconds
245
How is Second degree heart block classified?
Mobitz I
| Mobitz II
246
What is the difference in presentation between Mobitz I and Mobitz II second degree heart block?
Mobitz I: Light headedness, dizziness, syncope
Mobitz II: SOB, postural hypotension and chest pain
247
Aetiology of Mobitz I heart block?
AVN blocking drugs, inferior MI
248
Aetiology of Mobitz II heart block?
Anterior MI, mitral valve surgery, SLE, Rheumatic fever
249
What would the ECG of a patient with Mobitz I heart block show?
longer PR interval until no QRS complex and resets
250
What would the ECG of a patient with Mobitz II heart block show?
QRS complex is dropped after every other p wave
251
What is the treatment for Mobitz II heart block? Why?
Pacemaker - high risk of developing sudden complete AV block
252
What is AV Third Degree Heart Block?
Complete heart block.
| All electrical activity fails to conduct to the ventricles.
253
How come ventricular contractions are sustained in AV Third Degree Heart Block?
sustained by spontaneous escape rhythm which originates below the block
254
What are the causes of AV Third degree heart block?
Structural heart disease
Ischaemic heart disease (acute MI)
Hypertension
Endocarditis
255
What are the symptoms of third degree heart block
```
Light headedness
Dizziness
Syncope
Fatigue
Chest pain
Bradycardia
```
256
What investigations do you do in third degree heart block?
ECG
257
What may the ECG show in a patient with third degree heart block?
P waves are completely independent of the QRS complex
Can have either a narrow complex escape rhythm or broad complex escape rhythm
258
What is the difference between a narrow and broad complex escape rhythm?
Narrow complex escape rhythm
QRS complex less than 0.12 seconds
Block originates in the His bundle (more proximal to AV node)
Broad complex escape rhythm
B = below His
QRS complex is greater than 0.12 seconds
259
What is the treatment for narrow complex escape rhythm third degree heart block?
Acute may respond to IV atropine
Chronic : permanent pacemaker `
260
What is the treatment for broad complex escape rhythm third degree heart block?
Permanent pacemaker
261
What is right bundle branch block?
Right bundle no longer conducts so ventricles do not contract together.
Late activation of the right ventricle
262
Name 2 causes of right bundle branch block?
Pulmonary embolism
Ischaemic Heart Disease
Atrial/ventricular septal defect
263
What does the ECG show in a patient with right bundle branch block?
MaRRoW
QRS complex looks like an M in lead VI
QRS complex looks like a W in V5 and V6
Splitting of the second heart sound
264
What is left bundle branch block?
Late activation of the left ventricle
265
Name a cause of left bundle branch block?
IHD
| Aortic valve disease
266
What does the ECG show in a patient with left bundle branch block?
WiLLiaM
QRS complex looks like a W in leads VI and V2
QRS complex looks like a M in leads V4, V5 and V6
Splitting of the second heart sound
267
What is the pathology of prolonged QT syndrome?
Cardiac channelopathy.
Function of the cardiac ion channels lead to prolongation of ventricular action potential, lengthening the QT interval.
268
Name 1 congenital cause and 2 acquired causes of prolonged QT syndrome?
Congenital :
Autosomal dominant condition Romano-Ward syndrome
```
Acquired
Hypokalaemia
Hypocalcaemia
Drugs ; amiodarone, tricyclic antidepressants
Bradycardia
Acute MI
```
269
What symptoms may a patient with prolonged QT syndrome have?
Some people are asymptomatic and may only become aware of their condition after having an ECG
Syncope
Seizures
Palpitations
Can lead to cardiac arrest and death.
270
What does the ECG show of a patient with prolonged QT syndrome?
Prolonged QT interval
| longer than 440ms at a HR of 60bpm
271
Treatment of prolonged QT syndrome?
Treat the underlying cause
IV isoprenaline
272
What is a ventricular ectopic?
A premature beat that arises from an abnormal (ectopic) site in the ventricular myocardium.
273
Aetiology of a ventricular ectopic beat?
Most common post MI arrhythmia
Can also occur in healthy patients and are relatively common
Hypokalaemia
274
What are the symptoms of a ventricular ectopic beat
Usually asymptomatic, patients may be uncomfortable especially if it is happening frequently.
Pulse is irregular
Can feel faint or dizzy
275
What complication can arise from a ventricular ectopic beat?
High burden ventricular ectopic can cause heart failure
276
What is the pathology of ventricular tachycardia?
Rapid ventricular beating that results in inadequate blood filling of the ventricles. This results in a decreased cardiac output leading to a decrease in the amount of oxygenated blood that is circulated by the body.
277
Aetiology of ventricular tachycardia?
Commonly idiopathic
278
Symptoms of ventricular tachycardia?
Breathlessness
Chest pain
Palpitations
Light headed or dizzy
279
What would the ECG show in a patient who had sustained ventricular tachycardia?
ECG shows rapid ventricular rhythm and a broad and abnormal QRS complex (greater than 0.14s)
280
Treatment for ventricular tachycardia?
Treatment if sustained and unstable/stable?
Beta-blockers
If sustained
```
1. Hemodynamically unstable
Emergency electrical cardioversion
2. Stable
IV beta-blocker
IV amiodarone
```
281
What is ventricular fibrillation?
Very rapid and irregular ventricular activation with no mechanical effect (no cardiac output, no meaningful contraction)
282
Aetiology of ventricular fibrillation?
Usually caused by a ventricular ectopic beat
283
signs of ventricular fibrillation?
Patient is in cardiac arrest.
Pulseless
Unconscious
Respiration ceases
284
What does the ECG show of a patient in ventricular fibrillation?
Shapeless, rapid oscillations
| No hint of organised complexes
285
Treatment for ventricular fibrullation?
Electrical defibrillation
Survivors are at an increased risk of sudden death so long term, implantable cardioverter - defibrillators are the first line therapy
286
What is sinus tachycardia?
Conduction occurs as normal but impulses are initiated at a higher frequency
287
What can cause sinus tachycardia?
```
Anaemia
Anxiety
Exercise
Pain
Heart failure
Pulmonary embolism
```
288
What number of bpm = tachycardia?
Over 100bpm
289
What are the symptoms of sinus tachycardia?
Fast heart rate
Difficulty breathing
Fainting
Dizziness
290
What is an aortic aneurysm?
An artery with a dilatation of over 50% of its original diameter.
291
What is the difference between true and false aneurysms?
True aneurysms : abnormal dilatations that involve ALL layers of the arterial wall
False aneurysms : involve a collection of blood in the outer layer only (adventitia)
292
What is the pathology of aortic aneurysms?
Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss.
293
Where are aortic aneurysms most commonly found?
infrarenal abdominal aorta
294
What are aortic aneurysms associated with?
```
Smoking
Hypertension
Family History
Marfan’s Syndrome
Ehlers-Danlos syndrome
Trauma
Arteriomegaly (familial)
```
295
What are the three ways that an abdominal aortic aneurysm can present
Asymptomatic
Symptomatic
Ruptured
296
What are the symptoms/signs of an abdominal aortic aneurysm?
Central abdominal pain
Back pain
Distal embolic events
Pulsatile abdominal swelling
297
How does a ruptured abdominal aortic aneurysm present?
```
Severe and sudden onset epigastric pain
Sudden unexplained hypotension
Unexplained collapse
Sweating associated with pulsatile abdominal mass
Tachycardia
Profound anaemia
Sudden death
```
298
What investigations happen if an AAA is detected?
If an aneurysm is detected then patient should be monitored with 6monthly abdominal US scans until the AAA reaches a diameter greater than 5.0cm.
Then CT angiogram
299
What is the management for an AAA
Patient should be monitored with regular US scans until it reaches a diameter greater than 5.0cm.
Modify risk factors : stop smoking, healthy diet, control blood pressure, lower lipid
300
Once an AAA reaches a diameter greater than 5.0cm what are the two surgical options for repair?
Endovascular aneurysm repair : placing a stent graft inside the aneurysm
Open repair: replace the aneurysmal section of the aorta with a new prosthetic graft.
301
What is the emergency management of a ruptured AA?
```
ECG
Take blood for amylase, Hb and cross match
Catheterize bladder
IV access with 2x large bore cannulae
Treat shock with O-ve blood
Prophylactic antibiotics
Emergency repair
```
302
Define a thoracic aortic aneurysm?
focal dilatation of the thoracic aorta to more than 1.5 times its normal diameter
303
What is associated with thoracic aortic aneurysms?
Strong genetic link
Connective tissue disorders such as Marfan’s syndrome, Ehlers-Danlos syndrome
Weight lifting, cocaine and amphetamine use
304
What are the symptoms of thoracic aortic aneurysms?
Most TAAs are asymptomatic
Pain/pressure in chest
Thoracic back pain
Aortic regurgitation
Difficulting swallowing (due to compression of the oesophagus)
Acute pain
Collapse, shock and sudden death if ruptures
305
What investigations do you do with somebody who has a TAA?
CT chest with contrast
MRI chest
Transoesophageal echocardiography can be useful for identifying aortic dissection
Ultrasound
306
What is the treatment for a TAA?
Regular monitoring for asymptomatic TAAs every 6 months by CT
Surgery : endovascular stent grafting repair or open repair
Surgery is needed for ruptured TAA or a symptomatic TAA
Reduce cardiovascular risk factors
307
What is the pathology of an aortic dissection?
Tear in the intimal lining of the aorta which allows a column of blood under pressure to enter the aortic wall forming a haematoma which separates the intima from the adventitia. This forcing of the layers of the vessel apart results in dissection
308
What are the majority of aortic dissections?
Type A dissections (ascending aorta)
309
Name 3 causes of an aortic dissection
Inherited
Familial thoracic aortic aneurysm type 1 and 2
Marfan’s syndrome
Ehlers-Danlos syndrome
Degenerative
Atherosclerosis
Inflammatory
Trauma: shearing stresses in a RTA
310
What are the symptoms of aortic dissection?
Sudden onset of severe chest pain, classically described as tearing pain
Other symptoms may occur which are a direct result of occlusion of smaller arteries by the dissecting process
- Angina
- Paraplegia
- Limb ischaemia
- Pulse deficit
311
What are the signs of aortic dissection?
- Hypertension
- Pain is abrupt in onset and maximal at the time of onset
- Pain migrates as the dissection progresses
- Sharp/tearing pain
- Patients may be shocked and may have neurological symptoms secondary to loss of blood supply to the spinal cord
312
What investigations are done in an aortic dissection?
ECG
To distinguish from an MI
May be evidence of acute MI or acute ischaemia
MRI confirms a diagnosis
Transthoracic / transesophageal ultrasound will give an indication of site and extent of dissection
313
What is the treatment for aortic dissection?
Urgent antihypertensive medication
- IV labetalol or esmolol
- CCB can be used if beta blocker is contraindicated
Morphine
Surgery
Endovascular intervention with stents
Open repair
314
What is the pathology of intermittent claudication?
Partial blockage of leg/peripheral vessels by an atherosclerotic plaque/thrombus resulting in insufficient perfusion of the lower limb leading to lower limb ischaemia when exercising.
315
what is the cause of intermittent claudication?
Atherosclerosis.
316
what are the symptoms of intermittent claudication?
Cramping pain in the calf, thigh or buttock after walking for a given distance (claudication distance)
Pain is relieved by rest
Male impotence
317
A patient experiences intermittent claudication pain in the calf. Where is the likely blockage?
Femoral artery disease
318
A patient experiences intermittent claudication pain in the buttock. Where is the likely partial blockage?
iliac disease
319
What are the signs of intermittent claudication?
```
Pale
Cold leg with hair loss
May be poorly healing wounds of the extremities
Pulseless
Paraesthesia
```
320
What investigations do you do for intermittent claudication?
Blood tests
ECG
Ankle brachial pressure index
Imaging
321
What blood tests do you do for intermittent claudication and critical ischaemia?
```
HbA1c - exclude diabetes
ESR and CRP - exclude arthritis
FBC - anaemia, polycythaemia
U&Es
Lipids
```
322
What is is Ankle brachial pressure index (ABPI) ? What value defines intermittent claudication?
What value defines critical ischaemia?
Measurement of the cuff pressure at which blood flow is detectable by Doppler in the posterior tibial arteries compared to the brachial artery
Normal : 1-1.2
Intermittent claudication: 0.5-0.9
Critical Ischaemia: less than 0.5
323
What imaging do you do in a patient with intermittent claudication/critical ischaemia?
Colour duplex ultrasound
If considering intervention MR/CT angiography is used to identify the extent and location of stenoses and quality of distal vessels
324
What is the management of intermittent claudication?
Risk factor modification
Stop smoking
Treat hypertension, hyperlipidemia, diabetes
Clopidogrel to prevent progression and minimise risk
Exercise and weight loss
Supervised exercise programmes to reduce symptoms by improving collateral blood flow
Vasoactive drugs e.g naftidrofuryl oxalate
325
What is critical ischaemia?
Partial blockage of leg/peripheral vessels by an atherosclerotic plaque/thrombus resulting in insufficient perfusion of the lower limb leading to lower limb ischaemia when exercising and at rest.
326
Cause of critical ischaemia?
Atherosclerosis.
327
What are the symptoms of critical ischaemia?
Severe unremitting pain in the foot, particularly at night
| Pain can be partially relieved by hanging the foot out of the bed (gravity)
328
Signs of critical ischaemia?
```
Pallor
Perishingly cold
Pain
Pulseless
Paresthesia
Paralysis
Ulceration
Gangrene
```
329
Treatment of critical ischaemia?
Risk factor modification
Stop smoking
Treat hypertension, hyperlipidemia, diabetes
Clopidogrel to prevent progression and minimise risk
Exercise and weight loss
Supervised exercise programmes to reduce symptoms by improving collateral blood flow
Revascularisation
Percutaneous transluminal angioplasty
Surgical reconstruction with a bypass graft
Amputation if severe, may relieve intractable pain and death from sepsis and gangrene.
330
What is pericarditis?
An inflammatory pericardial syndrome with or without pericardial effusion
331
What is the most common cause of pericarditis?
Viral infection
| enteroviruses, herpesviruses
332
aside from infectious causes, what other causes of pericarditis are there?
```
- Neoplastic (second most common cause!)
Metastatic tumours (lung, breast, cancer, lymphoma)
```
- Idiopathic
- Autoimmune (RA)
- Metabolic (anorexia nervosa)
333
Symptoms of pericarditis?
```
Chest pain
Severe
Central
Sharp and pleuritic in nature
Rapid onset
Radiates to arm
Relieved by sitting forward
Exacerbated by lying down
Dyspnoea
Cough
Hiccups (potential irritation to phrenic nerve)
```
Systemic disturbance : fever, headache, nausea, vomiting
334
What is a pathognomonic sign of pericarditis?
Pericardial friction rub
335
What does an ECG show in a patient with pericarditis?
Saddle ST elevation
PR depression
(Sinus tachycardia)
336
What investigations do you do in a patient with pericarditis?
ECG
Bloods: FBC
Increase in WCC
High ESR may suggest a cause
Troponin : elevations suggest myopericarditis
CXR : identify a cause
Cardiovascular MR/CT may show localised inflammation
337
Treatment of pericarditis?
Treat the cause !
NSAID
Ibuprofen
Aspirin
Gastric protection
Colchicine reduces recurrence but is not very well tolerated
338
What is infective endocarditis?
Infection of the heart valves or other endocardial lined structures within the heart (such as septal defects, pacemakers, surgical patches)
339
What is the most common type of infective endocarditis?
Left sided native
340
Name 2 bacterial causes of infective endocarditis?
Strep. Viridans
Staph. Aureus (commonly in acute, native valves)
Enterococci
Coxiella burnetii
341
Name one fungal cause of infective endocarditis? What patients do these more commonly present in?
Candida
Aspergillus
Histoplasma
Usually in IV drug abusers, immunocompromised
342
Name three risk factors that increase a person's likelihood of developing infective endocarditis?
```
Skin breaches
Renal failure
Immunosuppression
Diabetes
IV drug abusers
Anyone with a prosthetic heart valve
```
343
Name the signs of infective endocarditis?
New murmur
Vegetations (infected mass)
Petechiae
Splinter haemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules usually found on the pulp of the digits)
Janeway lesions (erythematous, macular, nontender lesions on the fingers, palm or sole of the feet)
Roth spots on fundoscopy (dark ring with a pale centre)
344
What complications can arise from infective endocarditis?
complication caused by a embolisation of collection of infective organism and their inflammatory mechanisms in organs: stroke, pulmonary embolism, bone infections, kidney dysfunction, MI
345
What investigations do you do in a patient with infective endocarditis?
Bloods, raised CR, cultures
ECG: ischaemia, infarction, new appearance of first degree or worse heart block
Echocardiography (Transthoracic or transesophageal to detect vegetation)
346
What is the first line treatment for infective endocarditis?
IV Antimicrobials for 6 weeks - choice is based on culture sensitivities
347
What surgical treatment is there for patients with infective endocarditis?
Infection cannot be cured with antibiotics
ALWAYS to remove infected devices
Replace valve after the infection is cured
Remove large vegetations before they embolise
348
what can cause aortic stenosis?
Congenital bicuspid valve which can progress to stenosis
Age related degenerative calcification
349
What are the signs of aortic stenosis?
Crescendo-decrescendo ejection systolic murmur
| Slow rising carotid pulse and decreased pulse amplitude
350
what are the symptoms of aortic stenosis?
Syncope on exertion
Angina
Dyspnoea
351
What investigation is diagnostic of aortic stenosis?
Echocardiography is diagnostic!
352
What investigations do you in a patient with aortic stenosis?
```
ECG
LVH
P-mitrale
Poor R wave progression
Complete AV block
```
CXR
LVH
Calcified aortic valve
353
What is the treatment for aortic stenosis ?
Surgical replacement using a mechanical or bioprosthetic valve.
Procedure: Transcatheter Aortic Valve Implantation
354
What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole.
355
What can mitral regurgitation lead to?
Leads to left atrial enlargement and then progressive left ventricular volume overload leads to dilatation and progressive heart failure.
356
Aetiology of mitral regurgitation?
- Annular calcification
- Mitral valve prolapse
- Ruptured Chord of Mitral Valve
- Dilated heart so there is a hole between the LA and LV and the leaflets will never close
- Ischaemic MR caused by coronary disease - rupture or weakening of mitral valve
- Infective endocarditis
357
Symptoms of mitral regurgitation?
Exertion dyspnoea
Heart failure which may coincide with increased haemodynamic burden
Fatigue
Palpitations
358
Signs of mitral regurgitation
Pansystolic murmur at the apex radiating to the axilla
| Displaced hyperdynamic apex beat
359
Investigations for mitral regurgitation?
ECG
CXR
Echo
360
Treatment for mitral regurgitation?
Vasodilator (ACE-i, hydralazine)
Rate control for AF
Anticoagulation in AF and atrial flutter
Diuretics for fluid overload
Serial echo
IE prophylaxis for patients with prosthetic valves or a history of IE for dental procedures
361
What is sepsis?
Infection with any organism can cause acute vasodilation from inflammatory cytokines
Life threatening organ dysfunction
362
Name two organisms that commonly can cause sepsis?
coagulase-negative Staphylococcus and E. coli,
363
What are the red flags to look out for in sepsis?
```
Responds only to voice or pain/ unresponsive
Acute confusional state
Systolic BP < 90mmHg
Heart rate > 130 per minute
Respiratory rate > 25 per minute
Needs oxygen to keep SpO2 > 92%
Non-blanching rash, mottled/ashen/cyanotic
Not passed urine in the last 18hr
Lactate > 2mmol/L
```
364
What investigations do you do for sepsis ?
```
Blood gas for lactate
Observations
HR
BP
RR
O2 sats
Temperature
ECG
Urine dip
Urine output monitoring
```
```
Blood cultures
U&Es
CRP
FBC
LFT
Clotting screen
```
365
Management/treatment of sepsis?
Early recognition and treatment is key!
Administer Oxygen
Aim to keep above 94%
88-92% if ar risk of CO2 retention (COPD)
IV Antibiotics
Broad spectrum
Start within 1 hour
Consider allergies
IV Fluids
If hypotensive/lactate > 2mmol/L give 500mL
Manage acute complications
Critical care review
366
What type of reaction is anaphylaxis?
Type 1 IgE mediated hypersensitivity reaction.
367
What is the pathology of an anaphylactic shock?
When a person is first exposed - sensitisation
Allergen interacts with B cells (B cells create antibodies). Antibodies are created in response to the antigen - IgE.
IgE attaches to mast cells.
The next time a person is exposed to allergen, the allergen attaches to IgE on the mast cells.
This activates the mast cells
Mast cells release cytokines (causing WBC recruitment)
Activation of mast cells and immune cells causes release of histamine
368
What is the effect of histamine in anaphylaxis?
Histamine is a vasodilator
Causes large drop in blood pressure due to widespread vasodilation
The vessels also become leaky, which causes widespread oedema
369
Name some examples of common allergens which can cause anaphylaxis?
Foods: peanuts, brazil, cashews, shellfish, dairy products
Venoms: wasps, bee, hornets
Medications: antisera (tetanus, diphtheria), latex, penicillin, aspirin, NSAIDs
370
What are the signs and symptoms of anaphylaxis?
```
Swelling (facial and laryngeal oedema)
Bronchospasms
Hypotension
Rash - urticaria
Central cyanosis
Wheezing
Cardiac arrest
Tachycardia
Hypotension
```
371
What is the first line treatment for anaphylaxis?
0.5mg adrenaline IM and repeat every 5 minutes if shock persists
372
What is the management of anaphylaxis?
Administer IV antihistamine slowly
Administer 100mg intravenous hydrocortisone
If hypotension persists give 1-2L of IV fluid
If hypoxia is severe consider ventilation
373
What is the action of giving adrenaline in an anaphylactic shock?
Beta adrenergic receptor activity
B1: increase heart rate and contractility
B2: bronchodilation
Alpha adrenergic receptor activity
A1: vasoconstriction, thus increasing peripheral vascular resistance and increasing blood pressure
A2: reduces further release of substances from mast cells by increasing intracellular cAMP
374
What is the action of IV antihistamine in the treatment of an anaphylactic shock?
Inverse agonist of H1 receptor (so elicits the opposite response)
Blocks histamine so no…
- Vasodilation, hypotension, flushes, headaches, bradycardia, bronchoconstriction, increased vascular permeability
```
Weak antagonist of muscarinic ACh receptors
Inhibit parasympathetic effects
Increase heart rate
May induce smooth muscle contraction
Dry out secretions
```
375
Action of IV hydrocortisone? Anaphylaxis
Immunosuppressive effects
Inhibits the release of histamine from mast cells and increases body’s response to circulating catecholamines (so enhances effects of adrenaline)
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What are the mediators involved in the allergic response? What are their roles?
Preformed mediators
- Histamine and serotonin
* Bronchoconstriction
* Increased vascular permeability - capillary leak
- Neutrophil and eosinophilic chemotactic factors
* Induce inflammatory cell infiltration
Newly formed mediators
- Chemoattractants
- Prostaglandins and thromboxanes - platelet activating factor and prolonged airway hyperactivity. PAF levels correlate directly with severity of anaphylaxis
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What makes an allergen so powerful?
Many allergens are proteolytic, allowing them to cross skin and mucosal barriers. They are often aerodynamic particles which allow them to get in nasal and bronchial mucosa.
378
Name an antihistamine
Chlorphenamine
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What confirmatory blood test is needed to take to confirm anaphylaxis has occurred?
Mast Cell Tryptase
| Anaphylaxis causes an elevated serum mast cell tryptase.
