Cardiology Flashcards
1
Q
What is Atherosclerosis
A
A degenerative condition of arteries characterised by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis.
2
Q
What are 7 risk factors for atherosclerosis
A
Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history
3
Q
What 4 components is an atherosclerotic plaque composed of
A
Lipid
Necrotic core
Connective tissue
Fibrous cap
4
Q
What are 4 major cell types involved in atherogenesis
A
endothelium, macrophages, smooth muscle cells and platelets.
5
Q
What are the 4 steps in the process of atherosclerosis
A
Fatty streaks
Intermediate lesions
Fibrous plaques of advanced lesions
Plaque rupture
6
Q
What are features of fatty streaks
A
Earliest lesion of atherosclerosis
Appears at a very early age (<10 years)
Consists of aggregations of lipid-laden macrophages (foam cells) and T lymphocytes within the intimal layer of the vessel wall
7
Q
What are intermediate lesions of atherosclerosis
A
Composed layers of vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall.
8
Q
What are features of fibrous plaques of advanced lesions
A
Impedes blood flow
Prone to rupture
Contains smooth muscle cells, macrophages and foam cells and T lymphocytes
9
Q
What is involved in plaque rapture of atherosclerosis
A
Fibrous cap has to be resorbed and redeposited in order to be maintained – if balance shifts, cap becomes weak and then the plaque ruptures
Thrombus formation and vessel occlusion
10
Q
What is involved in the initiation of atherosclerosis
A
Endothelial dysfunction and injury around sites of damage, with subsequent lipid accumulation at sites of impaired endothelial barrier.
Local cellular proliferation and incorporation of oxidised lipoproteins occurs.
Mural thrombi (thrombi adhered to vessel wall) heal the vessel and repeat of cycle.
11
Q
What is involved in the adaptation of an atherosclerotic plaque
A
As plaque progresses to 50% of lumen size, vessel can no longer compensate by re-modelling.
Becomes narrowed – drives cell turnover within the plaque.
New matrix surfaces and degradation of matrix.
May progress to unstable plaque
12
Q
What is involved in the clinical stage of atherosclerosis
A
Plaque continues to encroach upon the lumen and runs the risk of haemorrhage.
T cell accumulation is stimulated.
Inflammatory reaction against the plaque contents
13
Q
What is the clinical manifestation of atherosclerosis
A
Atherosclerosis is usually asymptomatic until the artery is so narrowed that the organs and tissues no longer receive an adequate blood supply.
14
Q
What is the clinical manifestation of atherosclerosis of the coronary arteries
A
chest pain/ pressure (angina)
15
Q
What is the clinical manifestation of atherosclerosis of the brain arteries
A
transient ischaemic attack (TIA): weak arms and legs, slurred speech, temporary vision loss, drooping face muscles.
16
Q
What is the clinical manifestation of atherosclerosis of the peripheral arteries
A
peripheral artery disease: leg pain when walking
17
Q
What is the clinical manifestation of atherosclerosis of the renal arteries
A
high blood pressure or kidney failure.
18
Q
What are 4 management options for atherosclerosis
A
Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel/ ticagrelor – inhibits the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
PCI – percutaneous coronary intervention
19
Q
What is restenosis and how to prevent it
A
a major limitation of treatment
The recurrence of abnormal narrowing of an artery or valve after corrective surgery.
Drug eluting stents improve duration of stents – anti-proliferative and inhibits healing.
20
Q
How are chest x-rays used to investigate heart disease
A
Provides just a snapshot of the heart and little detail but can be an important source of information.
An enlarged heart suggests congestive heart failure
Signs of pulmonary oedema suggested decompensated heart failure
A globular heart may indicate pericardial effusion
Metal wires and valves will show up, evidencing previous cardiothoracic surgery
21
Q
How is echocardiography used to investigate heart disease
A
Ultrasound is used to give real-time images of the moving heart. This can be transthoracic (TTC) or transoesophageal (TOE), at rest, during exercise or after infusion of a pharmacological stressor.
If the patient is too unwell to be moved, an echo machine can be brought to them and continuous TOE imaging may be used as a guide during surgery.
22
Q
How are cardiac CT scans used to investigate heart disease
A
This can provide detailed information about cardiac structure and function. CT angiography permits contrast-enhanced imaging of coronary arteries during a single breath hold with very low radiation doses.
It can diagnose significant stenosis in coronary artery disease with an accuracy of 89%.
CT coronary angiography has a negative predictive value of >99%, which makes it an effective non-invasive alternative to routine transcatheter coronary angiography to rule out CAD.
23
Q
How are cardiac MRIs used to investigate heart disease
A
A radiation-free method of characterising cardiac structure and function including viability myocardium.
By varying the settings, different defects can be found. MR is the first-choice imaging method to look at diseases that directly affect the myocardium.
24
Q
How is nuclear imaging used to investigate heart disease
A
Perfusion is assessed at rest and with exercise or pharmacologically-induced stress.
This test is particularly useful for assessing whether myocardium distal to a blockage is viable and so whether stenting or CABG will be of value.
25
What 4 abnormalities can ECGs identify
Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Electrolyte disturbances
26
What does the p-wave represent
atrial depolarisation
27
What does the QRS complex represent
ventricular depolarisation
28
What does the T-wave represent
ventricular repolarisation
29
What does the PR interval represent
atrial depolarisation and delay in AV junction (delay allows time for the atria to contract before the ventricles contract).
30
What is the standard calibration of an ECG
25 mm/s
0.1mV/mm
31
What are bipolar leads
leads with a positive and negative electrode
32
What are unipolar leads
only a positive electrode and a virtual reference point with zero electrical potential
33
how many electrodes are used in a 12 lead ECG
10
( 6 chest and 4 limb)
34
What is Einthovens triangle.
The map of limb lead placement
lead 1,2,3 are limb to limb
lead aVF,VL,VR are centre of the triangle to limb
35
What is the ECG appearance for right atrial enlargement
tall (>2.5mm) p- wave
(p pulmonale)
36
What is the ECG appearance for left atrial enlargement
notched (M-shaped) p- wave
(P mitrale)
37
What is the ECG appearance for first degree heart block
Long PR interval
38
What depth of S wave is considered pathological
30mm
39
What features of the Q wave are considered pathological
>2mm deep and >1mm wide
>25% amplitude of the subsequent R wave
40
What is the QRS axis
This represents the overall direction of the heart’s electrical activity, and abnormalities of the QRS axis hint at ventricular enlargement or conduction blocks.
41
What the normal appearance of the ST segment
flat (isoelectric)
42
What change in the ST segment is considered pathological
elevation or depression by 1mm or more can be pathological.
43
What is the normal amplitude of the T wave
Should be at least 1/8 but less than 2/3 of the amplitude of R
44
What features of the T wave can be considered pathological
Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted
Amplitude exceeding 10mm
45
What is the normal appearance of the QT interval
isoelectric
QT interval decreases when heart rate increases
Regular interval is 0.35-0.45s
46
What would be considered pathological about the QT interval
more than half of the interval between adjacent R wave
47
What are U waves
Small, round, symmetrical and positive in lead II, with amplitude <2mm (regular)
U wave should be same direction as T wave
48
How do you calculate heart rate for regular rhythms
count the number of small boxes between QRS complexes and divide by 1500 for BPM
49
How do you calculate heart rate for irregular rhythms
count the number of beats present over 10 seconds then multiply by 6
50
What is the quadrant approach for QRS axis
For the QRS complex in aVF and lead 1
positive+ positive = normal axis
positive + negative = right axis deviation
negative + positive = left axis deviation
negative + negative = indeterminate axis
51
What is the appearance of sinus tachycardia on ECG
All impulses are initiated in the sinoatrial node hence all QRSs are preceded by a normal P wave with a normal PR interval.
Tachycardia means rate >100bpm
52
What is sinus bradycardia
Sinus rhythm at a rate <60bpm
53
What are 8 causes of sinus bradycardia
Physical fitness
Vasovagal attacks
Sick sinus syndrome
Drugs (β-blockers, digoxin, amiodarone)
Hypothyroidism
Hypothermia
Raised intracranial pressure
Cholestasis
54
What are 6 causes of Atrial fibrilation
IHD, thyrotoxicosis, hypertension, obesity, heart failure, alcohol
55
What are 5 conditions that cause ST elavation
Normal variant, acute MI, Prinzmetal’s angina, acute pericarditis, left ventricular aneurysm
56
What are 6 conditions that cause ST depression
Normal variant, digitoxin toxicity, ischaemic, angina, NSTEMI, acute posterior MI
57
What 3 things could cause T inversion in leads v1-v3
normal, right bundle branch block, RV strain
58
What 4 things could cause T inversion in leads V2-V5
anterior ischaemia, HCM, subarachnoid haemorrhage, lithium
59
What 3 conditions could cause T inversion in leads V4-V6 and aVL
lateral ischaemia, LVH, left bundle branch block
60
What is the ECG presentation of Myocardial infarction in the first hours
the T wave may become peaked and ST segments may begin to rise
61
What is the ECG presentation for Myocardial infarction within 24 hours
T wave inverts. ST elevation rarely persists, unless a left ventricular aneurysm develops. T-wave inversion may or may not persist.
62
What are 3 potential ECG findings for pulmonary embolism
sinus tachycardia, RBBB, right ventricular strain pattern
63
What is Echocardiography
A non-invasive technique that uses the differing ability of various structures within the heart to reflect ultrasound waves.
64
What is M-mode echocardiography
(motion mode): a single-dimension image
65
What is two-dimensional echocardiography
(real time): a 2D, fan-shaped image of a segment of the heart is produced on the screen. It is good for visualising conditions such as congenital heart disease, LV aneurysm, mural thrombus, LA myxoma, septal defects.
66
What is colour flow echocardiography
different coloured jets illustrate flow and gradients across valves and septal defects.
67
What is tissue doppler imaging
this employs Doppler ultrasound to measure the velocity of myocardial segments over the cardiac cycle. Particularly useful for assessing longitudinal motion, helping the diagnosis of systolic and diastolic heart failure.
68
What is transoesophageal echocardiography
more sensitive than transthoracic echocardiography as the transducer is nearer to the heart. Useful for diagnosing aortic dissections, assessing prosthetic valves, finding cardiac source of emboli.
69
What is stress echocardiography
evaluates ventricular function, ejection fraction, myocardial thickening, and to characterise valvular lesions.
70
What are 7 uses of echocardiography
Quantification of global LV function
Estimating right heart haemodynamics
Valve disease
Congenital heart disease
Endocarditis
Pericardial effusion
Hypertrophic cardiomyopathy
71
What is white coat hypertension
an elevated clinic pressure, but normal Ambulatory Blood Pressure Monitoring (ABPM)
72
What is hypertension
Chronic elevation of blood pressure in the arteries. WHO classification: >140/90mmHg.
73
What is the threshold for malignant hypertension
>160/110mmHg
74
Why is hypertension important to diagnose and manage
Hypertension is the chief risk factor for cardiovascular mortality, causing 50% of all vascular deaths.
75
What is the pathophysiology behind hypertension
Altered renin-angiotensin system elevates BP by impairing sympathetic output, increasing mineralocorticoid secretion and direct vaso-constriction.
This is balanced by atrial natriuretic factor.
Changes to auto-regulation produce an increase in peripheral resistance, which would normally allow increased BP, diuresis and restoration of normal pressure and volume
Hypertension alters blood vessel walls whereby the lumen size is decreased as the wall thickness increases.
76
What is malignant hypertension
a rapid rise in BP leading to vascular damage. Pathological hallmark is fibrinoid necrosis.
77
What is primary hypertension
90% of cases of hypertension are primary, and aetiology is unknown.
78
What are 4 causes of secondary hypertension
Endocrine disease
Renal disease
Exogenous agents (drugs)
Lifestyle
79
What are the signs and symptoms of hypertension
Usually asymptomatic
Malignant hypertension;
Bilateral renal haemorrhages
Papilledema
Headache and visual disturbance
Look for end-organ damage e.g. retinopathy
80
What are the tests for hypertension
First line= clinical BP
stage 1= >140/90
Stage 2= >160/90
stage 3= >180/120
gold standard= Ambulatory BP
81
What is cor pulmonale
Right ventricular hypertrophy and dilatation due to pulmonary hypertension.
82
What is cor pulmonale caused by
Caused by primary pulmonary hypertension
Can also be caused by emboli, cystic fibrosis or chronic bronchitis
83
What is the threshold and treatment goal for hypertension
Treat all patients with a BP 160/100mmHg
Treatment goal <140/90mmHg – reduce blood pressure SLOWLY
84
What are the lifestyle changes for hypertension
Stop smoking
Low-fat diet
Reduce alcohol and salt intake
Increase exercise
Reduce weight if obese
85
What is the drug therapy for hypertension
Monotherapy = Ca2+ channel antagonist
Combination Rx = ACE-I (or ARB) + Ca2+ channel antagonist or diuretic.
86
What is the group name and action of calcium antagonists
dihydropidines - inhibit the opening of voltage-gated calcium channels in vascular smooth muscle, reduced calcium entry and thereby calcium available for muscle contraction.
87
What is the action of ACE inhibitors and 2 examples
prevent generation of angiotensin II from angiotensin I.
Ramipril and captopril
88
What is the action of angiotensin receptor blockers and 2 examples
block the action of angiotensin II at peripheral angiotensin II receptors. Used if ACEi intolerant.
Losartan, Azilsartan
89
What is the action of thiazide diuretics and an example
inhibit sodium reabsorption by the DCT, reducing the ECF volume, which is elevated in hypertension.
Bendroflumethiazide
90
What is Angina pectoris
Recurrent transient episodes of chest pain due to myocardial ischaemia
91
What are 4 types of angina
Stable angina: induced by effort, relieved by rest. Good prognosis.
Unstable angina: angina of increasing frequency or severity – occurs on minimal exertion or at rest. Associated with high risk of MI.
Decubitus angina: precipitated by lying flat.
Prinzmetal angina: caused by coronary artery spasm (rare).
92
What is the pathology of angina
Myocardial ischaemia occurs whenever myocardial oxygen demand outstrips supply
A significant fixed stenosis of a coronary artery impairs coronary blood flow when myocardial oxygen demand increases e.g. during exercise
93
4 causes of angina
Atheroma!!!
Rarer;
Anaemia
Coronary artery spasm
Tachyarrhythmias
94
What are 10 risk factors for angina
Gender
Family history
Personal history
Age
Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Sedentary lifestyle
Stress
95
what are the 3 angina clinical presentations
Constricting/heavy discomfort to the chest, jaw, neck, shoulders or arms
Symptoms brought on by exertion
Symptoms relieved within 5min by rest or GTN spray.
96
What are 5 symptoms of angina
Dyspnoea
Nausea
Sweatiness
Faintness
Crushing chest pain
97
What are 7 differential diagnoses for angina
Pericarditis/ myocarditis
Pulmonary embolism
Chest infection
Dissection of the aorta
Gastro-oesophageal reflux/spasm/ulceration
Psychological
Musculo-skeletal
98
What is the ECG presentation for angina
Often normal – there are no direct markers of angina
Signs of IHD – T-wave inversion, BBB
99
What is the management for angina
Address exacerbating factors: anaemia, tachycardia, thyrotoxicosis.
Symptom relief: glyceryl trinitrate (GTN) spray. Ambulance required if pain doesn’t subside 5 minutes after second dose.
100
What is the primary prevention for angina
Reducing the risk of CAD and complications
Risk factor modification
101
What are 4 lifestyle changes for angina
Stop smoking
Exercise
Dietary advice
Optimise hypertension and diabetes control
102
What are 3 pharmacological interventions for angina
75mg aspirin daily
Consider ACE inhibitors (if diabetic)
Address hyperlipidaemia (high cholesterol)
103
What are the physical interventions used for angina
Percutaneous Coronary Intervention (PCI) and sometimes surgery
104
What is the action of beta blockers in angina and an example
antagonise sympathetic nervous activation and therefore reduce work of heart and O2 demand. bisoprolol
105
What is the action of nitrates in angina and an example
dilate systemic veins (venodilators) to reduce preload on the heart: Frank-S mechanism ‘reduce work of heart and O2 demand’.
Isosorbide mononitrate
106
What is the action of calcium channel antagonists in angina and an example
dilate systemic arteries (arterodilators) to reduce afterload on the heart. Reduced energy then required to produce same CO. Amlodipine
107
What is the action of statins for angina
reduce anginal events, reduce LDL-cholesterol.
108
What is the method of Percutaneous coronary intervention (PCI-stenting)
A balloon is inflated inside the stenosed vessel, opening the lumen. A stent is then inserted to reduce the risk of re-stenosis.
109
What is CABG surgery
Coronary artery bypass graft
110
What are Acute coronary syndromes
Acute coronary syndromes include unstable angina and myocardial infarctions. These share a common underlying pathology – plaque rupture, thrombosis, and inflammation.
111
What is myocardial infarction and the two types
myocardial cell death, releasing troponin.
Non-ST-elevation myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)
112
What is ischaemia
a lack of blood supply (sometimes cell death)
113
What is the pathology of acute coronary syndromes
Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases. Uncommon causes include coronary vasospasm without plaque rupture, drug abuse, dissection of the coronary artery and thoracic aortic depression.
114
What are 5 features involved in the diagnosis of acute coronary syndromes
An increase in cardiac biomarkers (e.g. troponin)
Symptoms of ischaemia
ECG changes of new ischaemia
Development of pathological Q waves
New loss of myocardium
115
What are 5 symptoms of acute coronary syndromes
Acute central chest pain lasting >20min
Nausea
Sweatiness
Dyspnoea
Palpitations
116
What are silent acute coronary syndromes
ACS without chest pain – seen in elderly and diabetic patients.
May present with syncope, pulmonary oedema, epigastric pain an vomiting
117
What are 7 signs for Acute coronary syndromes
Distress
Anxiety
Pallor
Sweatiness
4th heart sound
Possibly signs of heart failure
Low grade fever
118
What are 5 differential diagnoses for Acute coronary syndromes
Stable angina
Pericarditis
Myocarditis
Takotsubo cardiomyopathy
Aortic dissection
119
What is the ECG appearance for STEMI
STEMI: tall T waves, ST elevation, or new LBBB occurs within hours. T wave inversion and pathological Q waves follow non-specific changes
120
What is the appearance on Chest X-ray for acute coronary syndrome
Cardiomegaly
Pulmonary oedema
Widened mediastinum
121
What is the use of troponins in investigating acute coronary syndromes
specific marker of myocardial necrosis
Serial troponins are required to differentiate non-ST elevated Mis from unstable angina (no troponin rise).
122
What is used for symptom control of ACS
Manage chest pain with PRN GTN and opiates.
123
What can be done to modify risk factors for ACS
Patients should be strongly advised and helped to stop smoking
Identify and treat diabetes mellitus, hypertension and hyperlipidaemia
Advise a diet high in oily fish, fruit, vegetables, fibre and low in saturated fats
Encourage daily exercise
Mental health – flag it up to a patient’s GP
124
Name 5 classes of cardioprotective medications
protective medications
Antiplatelets: aspirin and Clopidogrel. Clopidogrel is a P2Y12 inhibitor (dual antiplatelet therapy)
Anticoagulants e.g. fondaparinux
Inhibit both fibrin formation and platelet activation
Beta-blockade reduces myocardial oxygen demand
ACEi – patients with LV dysfunction, hypertension or diabetes
High dose statin e.g. atorvastatin
125
Which patients should be considered for revascularisation in ACS
STEMI patients and very high-risk NSTEMI should receive immediate angiography. Patients with multivessel disease may be considered for CABG instead of PCI.
126
What is unstable angina
Severe acute myocardial ischaemia without myocardial necrosis.
Almost always due to coronary artery atherosclerosis.
127
What is the pathology of unstable angina
Erosion of the surface of an unstable atherosclerotic plaque stimulates platelets to aggregate over the plaque
Platelet fragments may also break off and embolise down the artery
The reduction in coronary blood flow causes acute ischaemia of the affected myocardium, but not myocardial necrosis.
128
What is the presentation of unstable angina
Acute coronary syndrome with sudden onset of prolonged ischaemic cardiac chest pain at rest or on minimal exertion.
The ECG shows ischaemic changes, but not ST-elevation
129
What is the clinical classification of unstable angina
Cardiac chest pain at rest
Cardiac chest pain with crescendo pattern
New onset angina
No significant rise in troponin levels.
130
What is the difference between unstable angina and NSTEMI
NSTEMI involves enough occlusion to cause myocardial damage and elevation in serum troponin and creatine kinase. Unstable angina does not cause myocardial damage.
131
What is Myocardial infarction
Full-thickness necrosis of an area of myocardium.
132
What is the chest pain associated with MI
Unremitting
Usually severe
Occurs at rest
Associated with sweating, breathlessness, nausea/vomiting
133
What is Subendocardial/ patchy infarction
involves the innermost layer and some middle parts of the myocardium, but not the epicardium. NSTEMI
134
What is transmural infarction
infarction of the full thickness of the myocardium
135
What is the pathology of MI
Results from rupture of an unstable coronary artery atherosclerotic plaque stimulates the formation of an occlusive fibrin-rich thrombus over the plaque
Complete occlusion of the coronary artery leads to full-thickness necrosis of the area of myocardium supplied by that artery.
136
What is the difference between STEMI and NSTEMI
NSTEMI is a retrospective diagnosis made after troponin results.
ST elevation MI and MI associated with LBBB are associated with larger infarcts unless effectively treated.
137
What is the difference between MIs and unstable angina
MIs have troponin rises, unstable angina does not.
138
What are the 6 steps to initial management of STEMI
Attach ECG monitor and record a 12-lead ECG
IV access. Bloods for FBC, U&E, glucose, lipids, troponin
History of cardiovascular disease; risk factors for IHD
Aspirin 300mg and ticagrelor 180mg
Morphine 5-10mg IV +anti-emetic
STEMI on ECG = primary PCI
139
What is the treatment of STEMI
Aspirin – inhibits platelet function
LMW heparin
Thrombolytic therapy
140
What are 13 complications of MI
Cardiac arrest
Cardiogenic shock
Left ventricular failure
Bradyarrhythmia
Tachyarrhythmia
Right ventricular failure
Pericarditis
Systemic embolism
Cardiac tamponade
Mitral regurgitation
Ventricular septal defect
Dressler’s syndrome
Left ventricular aneurysm
141
What are 2 features of right ventricular failure
Presents with low cardiac output
Fluid is key – avoid vasodilators and diuretics.
142
What are 2 features of pericarditis and its treatment
Central chest pain, relieved by sitting forwards
ECG: saddle-shaped ST elevation
Treatment: NSAIDs
143
What is the potential cause and therapy for systemic embolism
May arise from LV mural thrombus
After large anterior MI, consider anticoagulation with warfarin for 3 months
144
What is the presentation, investigation and treatment for cardiac tamponade
Presents with low cardiac output, pulsus paradoxus, muffled heart sounds
Diagnosis: echocardiogram
Treatment: pericardial aspiration, surgery
145
What is the presentation and treatment for mitral regurgitation
Presentation: pulmonary oedema
Treatment: consider valve replacement
146
What is Dressler's syndrome and its treatment
Recurrent pericarditis, pleural effusions, fever, anaemia
Treatment: NSAIDs if severe
147
What is Cardiac failure
Inability of the heart to keep up with the demands on it, and the failure of the heart to pump blood with normal efficiency = cardiac output is inadequate for the body’s requirements.
148
What causes the diminishing of cardiac contraction force
exceeding stretch capability of sarcomeres
149
What triggers the hypertrophic response to cardiac failure
Angiotensin 2
ET-1 and insulin-like growth factor 1
TGF-beta
150
What is systolic failure
inability of the ventricle to contract normally, resulting in low cardiac output. Ejection fraction <40%.
151
What are 3 causes of systolic failure
IHD
MI
Cardiomyopathy
152
What is diastolic failure
inability of the ventricle to relax and fill normally, causing increased filling pressures. (stiff heart = left ventricle can’t fill properly with blood during diastolic phase, reducing the amount of blood pumped out to the body). Typically, ejection fraction is >50% (termed heart failure with preserved EF).
153
What are 5 causes for diastolic failure
Ventricular hypertrophy
Constrictive pericarditis
Tamponade
Restrictive cardiomyopathy
Obesity
154
What is the outcome of left ventricular failure
pulmonary congestion (heart is not able to pump efficiently so blood backs up in the veins that take blood through the lungs. Pressure in these vessels increases and fluid is pushed into the alveoli) and then overload of right side.
155
What are 9 symptoms of left ventricular failure
Dyspnoea
Poor exercise tolerance
Fatigue
Orthopnoea (SOB when lying flat)
Paroxysmal nocturnal dyspnoea (SOB at night, awakening from sleep)
Nocturnal cough
Wheeze
Cold peripheries
Weight loss
156
What is the outcome of right ventricular failure
venous hypertension (high pressure in the veins of the legs, caused by venous insufficiency where blood leaks downwards due to the effect of gravity through leaky valves) and congestion.
157
What are 3 causes of right ventricular failure
LVF
Pulmonary stenosis
Lung disease
158
What are 6 symptoms of right ventricular failure
Peripheral oedema
Ascites
Nausea
Anorexia
Facial engorgement
Epistaxis
159
What is acute heart failure
new-onset acute or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with/without signs of peripheral hypoperfusion.
160
What is chronic heart failure
develops or progresses slowly. Venous congestion is common but arterial pressure is well maintained until very late.
161
What is low-output heart failure
cardiac output is low and fails to increase normally with exertion.
162
What are 3 causes of Low-output heart failure
Excessive preload: mitral regurgitation or fluid overload (e.g. from renal overload)
Pump failure: decreased heart rate, negatively inotropic drugs
Chronic excessive afterload: e.g. aortic stenosis, hypertension.
163
What is high-output heart failure
output is normally increased in the face of extremely increased needs. Failure occurs when cardiac output fails to meet these needs.
164
What are 4 causes of High-output heart failure
Anaemia
Pregnancy
Hyperthyroidism
Paget’s disease
165
What are the tests for heart failure
FBC – U&E
CXR
ECG – may indicate cause (MI, ischaemia, ventricular hypertrophy)
Echocardiography – indicates the cause and can confirm the presence or absence of LV dysfunction.
Objective evidence of cardiac dysfunction at rest
166
What are the signs of heart failure
Cyanosis
Decreased BP
Narrow pulse pressure
Pulsus alternans
Displaced apex (LV dilatation)
Pulmonary hypertension
Pink frothy sputum
Signs of valve diseases
167
What are the 5 differential diagnoses for heart failure
COPD
Emphysema
Myocardial infarction
Pulmonary embolism
Pneumonia
168
What are the 9 steps in management of acute cardiac failure
Sit the patient upright
High flow oxygen if low peripheral capillary oxygen saturation
Treat any arrhythmias
Investigations whilst continuing treatment
Diamorphine 1.25-5mg IV slowly (caution in liver failure and COPD)
Furosemide 40-80mg IV slowly (larger doses required in renal failure)
GTN spray 2 SL puffs
If systolic BP 100mmHg, start a nitrate transfusion
If systolic BP is <100mmHg, treat as cardiogenic shock and refer to ICU
169
What is 6 management options in chronic heart failure
Stop smoking, stop drinking alcohol, eat less salt, optimise weight and nutrition.
Treat the cause
Treat exacerbating factors e.g. anaemia, infection
Avoid exacerbating factors e.g. NSAIDs (fluid retention)
Annual flu vaccine, one-off pneumococcal vaccine
medications
170
What 7 medications can be used for heart failure
Diuretics
ACE inhibitors
ARB
β-blockers
Mineralocorticoid receptor antagonists
Digoxin
Vasodilators
171
What is intractable heart failure and its management
failure that is resistant to further treatment -> palliative care.
172
What is Valvular heart disease
Any disease process involving one or more of the four valves of the heart.
173
What are 2 congenital valvular heart diseases
Congenital aortic stenosis
Congenital bicuspid valve
174
What are 3 acquired Valvular heart disease
Degenerative calcification
Rheumatic heart disease
Rare causes
175
What is mitral regurgitation
Backflow through the mitral valve during systole.
176
Whats are the different outcomes of acute vs chronic mitral regurgitation
Acute – back up into the lungs
Chronic – LA dilation as it has had time to adjust
177
What is the pathophysiology of mitral regurgitation
Pure volume overload
Compensatory mechanisms: left atrial enlargement, LVH and increased contractility
Progressive LA dilation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilatation and progressive HF
178
6 Causes of mitral regurgitation
Rheumatic fever
Infective endocarditis
Mitral valve prolapse
Ruptured chordae tendinea
Papillary muscle dysfunction
Cardiomyopathy
179
What are 4 symptoms of mitral regurgitation
Dyspnoea (exertion)
Pulmonary oedema
Fatigue
Palpitations
180
What are 3 signs of mitral regurgitation
AF – displaced, hyperdynamic apex
Pansystolic murmur at apex radiating to axilla
Severity: the more severe, the larger the left ventricle
181
What are 4 tests for mitral regurgitation
ECG; AF, P-mitrale if in sinus rhythm, LA enlargement, LV hypertrophy
CXR – large LA and LV
Mitral valve calcification
Echocardiogram
182
What are 5 management options for mitral regurgitation
Control heart rate if fast AF (beta blockers)
Anticoagulate if there is a history of AF, embolism, prosthetic valve or additional mitral stenosis
Vasodilators – hydralazine (calcium channel blockers)
Diuretics (for fluid overload) improve symptoms
Surgery – repair/replace valve.
183
What is mitral valve prolapse
The most common valvular abnormality. It is a condition in which the two valve flaps of the mitral valve do not close smoothly or evenly, but instead bulge upwards into the left atrium.
184
What are the symptoms of mitral valve prolapse
Usually asymptomatic
May develop atypical chest pain, palpitations, and autonomic dysfunction symptoms
185
What are the 2 signs of mitral valve prolapse
Mid-systolic click and/or late systolic murmur
186
What are 4 complications of mitral valve prolapse
Mitral Regurgitation (MR)
Cerebral emboli
Arrhythmias
Sudden death
187
What are 2 tests for mitral valve prolapse
Echocardiogram is diagnostic
ECG may show inferior T-wave inversion
188
What is the treatment for mitral valve prolapse
β-blockers may help palpitations and chest pain. Surgery if severe MR.
189
Define Mitral stenosis
Obstruction of LV inflow that prevents proper filling during diastole.
Normal mitral valve area 4-6cm2. Symptoms begin at areas less than 2cm2.
190
Mitral stenosis key symptoms
Dyspnoea, orthopnoea, haemoptysis, RHF symptoms, palpitations
191
What are 4 causes of mitral stenosis
Rheumatic fever
Congenital
Infective endocarditis
Malignant carcinoid
192
What is 7 clinical presentations for mitral stenosis
Pulmonary hypertension causes dyspnoea, haemoptysis
Pressure from large left atrium on local structures causes hoarseness (recurrent laryngeal nerve)
Dysphagia
Bronchial obstruction
Fatigue
Palpitations
Chest pain
193
What are 6 signs for mitral stenosis
Prominent ‘a’ wave in jugular venous pulsations: due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure
Mitral facies – severe MS leads to vasoconstriction: pink patches on cheeks
Malar flush on cheeks
Low-volume pulse
Low pitch rumbling at apex
194
What are 3 investigations for mitral stenosis
ECG – may show AF and LA enlargement
CXR – LA enlargement and pulmonary congestion
Echo – assess mitral valve mobility, gradient and mitral valve area
195
What are the management options for mitral stenosis
Atrial fibrillation – rate control is crucial
Medications
Serial echocardiography
Mitral balloon valvotomy
Mitral valve replacement
196
What are the medications used in mitral stenosis management
Anticoagulate with warfarin
β-blockers, CCBs, digoxin – control heart rate, prolong diastole (improved diastolic filling)
Diuretics – reduce fluid overload
197
What is Aortic stenosis
Narrowing of the aortic valve opening that restricts blood flow from the left ventricle to the aorta.
Normal aortic valve is 3-4cm2. Symptoms occur when valve area is ¼ of normal.
198
What are the 3 types of Aortic stenosis
Supravalvular
Subvalvular
Valvular
199
What is the pathophysiology of Aortic stenosis
A pressure gradient develops between the left ventricle and the aorta (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines
200
What are 3 causes for aortic stenosis
Senile calcification (most common)
Congenital (bicuspid valve, Williams syndrome)
Rheumatic heart disease
201
What are 6 clinical presentations for aortic stenosis
Angina (Chest pain)
Syncope
Breathlessness
Exertional dyspnoea
Dizziness, faints
Systemic emboli (if infective endocarditis)
202
What are 3 signs for aortic stenosis
Slow rising carotid pulse with narrow pulse pressure
Heaving, non-displaced apex beat
Ejection systolic murmur – crescendo-decrescendo character
203
What are the 5 investigations for aortic stenosis
Echocardiography
LVH, dilation, ejection fraction
Doppler derived gradient and valve area
Cardiac catheter can access valve gradient, LV function, CAD.
Pulsus parvus et tardus – weak and late pulse
204
What are 2 differential diagnoses for aortic stenosis
Hypertrophic cardiomyopathy
Aortic sclerosis
205
What are 4 management options for aortic stenosis
Poor prognosis without surgery for symptomatic patients
Valve replacement – definitive treatment
Percutaneous valvuloplasty/ replacement
TAVI – transcatheter aortic valve implantation
206
What is aortic sclerosis
Senile degeneration of the valve. There is an ejection systolic murmur; but no carotid radiation, and normal pulse and S2 heart sound.
207
What is aortic regurgitation
Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.
208
What are 3 causes of acute aortic regurgitation
infective endocarditis, ascending aortic dissection, chest trauma.
209
What are 5 causes for aortic regurgitation
congenital, connective tissue disorders (Marfan’s syndrome), rheumatic fever, Takayasu arteritis, rheumatoid arthritis.
210
What is the pathophysiology of aortic regurgitation
Combined pressure and volume overload
Compensatory mechanisms: LV dilation, LH, progressive dilation leads to heart failure
211
What are 4 clinical presentations of aortic regurgitation
Breathlessness
Orthopnoea (breathless lying down)
Palpitations
Diastolic blowing murmur
212
What are 3 investigations for aortic regurgitation
CXR – enlarged cardiac silhouette and aortic root enlargement
Echo – evaluation of the AV and aortic root with measurements of LV dimensions and function
Cardiac catheterisation to assess severity of lesion, anatomy of aortic root
213
What are 3 management options for aortic regurgitation
Medical: vasodilators
Serial echocardiograms to monitor progression
Surgical treatment: definitive
214
What is rheumatic fever caused by
Pharyngeal infection with Lancefield group Aβ-haemolytic streptococci (s.pyogenes) triggers rheumatic fever 2-4weeks later.
215
What is the pathology of rheumatic fever
An antibody to the carbohydrate cell wall of the streptococcus cross-reacts with valve tissue and may cause permanent damage to the heart valves.
216
What are 4 pieces of evidence of group A β-haemolytic streptococcal infection
Positive throat culture
Rapid streptococcal antigen test +ve
Elevated or rising streptococcal antibody titre
Recent scarlet fever
217
What is the dukes modified criteria
Evidence of a recent group A β-haemolytic streptococcal infection
plus 2 major criteria or 1 major+ 2 minor
218
What are the 4 major criteria for rheumatic fever
Carditis – tachycardia, murmurs etc.
Arthritis
Subcutaneous nodules
Erythema marginatum
219
What are the 3 minor criteria for rheumatic fever
Fever
Raised ESR/ CRP
Arthralgia
220
What are the 4 management options for rheumatic fever
Bed rest until CRP normal for 2 weeks
Benzylpenicllin
Analgesia for carditis/ arthritis
Immobilise joints in severe arthritis
221
What is infective endocarditis
Infection of the heart valve/s or other endocardial lined structures within the heart e.g. septal defects, surgical patches.
It is a really bad infection that showers infectious material all around the bloodstream.
222
What are 5 types of Infective endocarditis
Left sided native IE (mitral or aortic)
Left sided prosthetic IE
Right sided IE
Device related IE (pacemakers/ defibrillators)
Prosthetic heart
223
What are 3 causes of endocarditis
Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected
Introduce infectious material into the blood stream or directly onto the heart during surgery (bacteria e.g. Strep.viridans, Staph. Aureus)
Have had IE previously
224
What is the pathology of IE by S.aueus
S. aureus usually gains access to the blood from the skin via indwelling vascular lines or via intravenous drug abuse
225
What is the pathology of IE by S. viridans
S. viridans gains access to the blood from the oropharynx following tooth brushing or dentistry
226
What is the mechanism of infection in IE by enterococci
enterococci gain access to the bloodstream following instrumentation of the bowel or bladder
227
What are the clinical presentations for IE
Depends on site and organism
Left-sided: fever and signs of valve damage
Right-sided: fevers, chills and prominent pulmonary symptoms due to numerous septic emboli in the lungs
Signs of systemic infection e.g. fever, sweats
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, MI
Valve dysfunction – HF, arrhythmia
228
What visible clinical presentations are there for IE
Petechiae (skin lesions)
Splinter haemorrhages (bruised nails)
Osler’s nodes (small, tender, purple nodules on the pulp of the digits)
Janeway lesions (non-tender lesions on the fingers, palm or sole)
Roth spots on fundoscopy
229
What are the 2 major Duke criteria for IE
Bugs grown from blood cultures
Evidence of endocarditis on echo, or new valve leak
230
What are the 5 minor Duke criteria for IE
Predisposing factors e.g. IV drug abuse
Fever
Vascular phenomena e.g. Janeway lesions
Immune phenomena e.g. Osler’s nodes
Equivocal blood cultures
231
What is the Modified Duke criteria for definitive IE
2 major/ 1 major + 3 minor / 5 minor
232
What investigations are used for IE
CXR – cardiomegaly, pulmonary oedema
Regular ECGs – to look for heart block
CT – to look for emboli
Raised CRP
ECG
Echo - TOE (transoesophageal echo) – improved rate of detection of vegetations
A negative result doesn’t eliminate IE
Many blood tests require long incubation periods for the organisms to grow, so they provide very slow results
233
What are the treatment options for IE
Antimicrobials; IV for 6 weeks
Treat complications
Surgery
234
What are 5 complications of IE
arrhythmia, HF, heart block, embolisation, stroke rehab
235
What are the surgical options for IE
Indications: cannot be cured with antibiotics, severe valve damage, to remove infected devices, to replace valve after infection cured, to remove large vegetations before they embolise.
236
What is Congenital heart disease
a general term for a range of birth defects that affect the normal way the heart works.
237
What are 7 structural heart defects
Ventricular septal defect
Atrio-ventricular septal defects
Patent ductus arteriosus
Coarctaction of the aorta
Bicuspid aortic valve and aortopathy
Pulmonary stenosis
Eisenmenger syndrome
238
What is Eisenmenger syndrome
any untreated congenital cardiac defect with intracardiac communication that leads to pulmonary hypertension, cyanosis, reversal of flow
239
What are the investigations for structural heart defects
Echocardiography is first line
CT and MR are used to provide precise anatomical and functional information
Exercise testing assesses functional capacity
240
What is the pathophysiology of VSD
High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber (so, not blue)
Increased blood flow through the lungs
241
What are the 2 causes of VSD
Congenital
Acquired: post-MI
242
What is VSD
ventricular septal defect, Abnormal connection between the 2 ventricles (a hole)
243
What are 5 symptoms of VSD
Severe heart failure in infancy
Very high pulmonary blood flow in infancy
Breathless
Poor feeding
Failure to thrive
244
What are 6 signs for VSD
Small, breathless, skinny baby
Increased respiratory rate
Tachycardia
Big heart on chest X-ray
Murmur varies in intensity
Harsh pansystolic murmur heard at left sternal edge (small holes give louder murmurs)
245
What are 3 complications for VSD
Pulmonary hypertension
Eisenmenger’s complex
Heart failure from volume overload
246
What are the 7 steps to eisenmengers syndrome
Pulmonary hypertension from initial left to right shunt
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
De-oxygenated blood enters systemic circulation
The patient becomes blue
247
What are the investigations for VSD
ECG: normal
CXR: normal heart size, large pulmonary arteries
Cardiac catheter: step up in O2 saturation in right ventricle
248
What are the treatment options for VSD
Many close spontaneously
Indications for surgical closure;
Failed medical therapy
Symptomatic VSD
Shunt >3:1
249
What is an ASD
Atrial septal defect
Abnormal connection between the two atria (a hole).
250
What is the pathophysiology of an ASD
Slightly higher pressure in the LA than the RA
Shunt is left to right (therefore not blue)
Increased flow into right heart and lungs
251
What are 6 symptoms of ASD
Significant increased flow through the right heart and lungs in childhood
Right heart dilatation
Shortness of breath on exertion
Increased chest infections
Chest pain
Palpitations
252
What are 4 signs of ASD
Pulmonary flow murmur
Fixed split-second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X-ray
253
What are 2 complications of atrial septal defect
Eisenmenger’s complex
Paradoxical emboli
254
What are paradoxical emboli
embolisms that cross an intracardiac shunt to the other side of the circulation
255
What are the treatment options for ASD
May close spontaneously
Close if symptomatic
Transcatheter closure is more common than surgical
256
What are atrio-ventricular septal defects (AVSD)
A hole in the very centre of the heart.
Involves the ventricular septum, atrial septum, mitral and tricuspid valves
Can be complete or partial
AV valves – instead of two separate valves, there is one big malformed one
257
What are the consequences of a complete AVSD
Poor feeding, poor weight gain
Torrential pulmonary blood flow
Breathless as neonate
Needs repair or PA band in infancy
258
What are the features of a partial AVSD
Presents like a small VSD/ASD
Can present in late adulthood
May be left alone if there is no right heart dilatation
259
What is a patent ductus arteriosus
The ductus arteriosus fails to close after birth, leaving a vessel connecting the aorta and pulmonary artery.
260
What are 3 clinical signs of patent ductus arteriosus
Continuous murmur
If large – big heart, breathless
Eisenmenger’s syndrome – cyanosis
261
What is the pathophsysiology of a patent ductus arteriosus
Breathless, poor feeding, failure to thrive
Torrential flow from the aorta to the pulmonary arteries in infancy
262
What is the treatment plan for ductus arteriosus
Closure is usually done surgically, under local anaesthetic. There is a low risk of complications.
263
What is coarctation of the aorta
Congenital narrowing of the descending aorta (usually occurs just distal to the origin of the left subclavian artery – the site of insertion of the ductus arteriosus).
264
What other conditions is Coarctation of the aorta
associated with
down's syndrome, bicuspid aortic valve and Turner’s syndrome.
265
What are 5 signs and symptoms of coarctation of the aorta
Radiofemoral delay
Weak femoral pulse
High blood pressure
Cold feet
Scapular bruit (buzzes over the scapulae from collateral vessels)
266
What are the treatment options for coarctation of the aorta
Surgery
Balloon dilatation
267
What is tetralogy of fallot
A congenital heart condition involving 4 abnormalities occurring together
268
What 4 abnormalities are involved in Tetralogy of Fallot
Ventricular septal defect (VSD)
Pulmonary stenosis
Right ventricular hypertrophy
The aorta overrides the VSD, accepting right heart blood
269
What is the pathophysiology of tetralogy of fallot
The stenosis of the RV outflow leads to the RV being at a higher pressure than the left
Therefore (blue) blood passes from the RV to the LV
270
What is the presentation for tetralogy of fallot
Severity depends on degree of pulmonary stenosis
Cyanotic due to decreasing blood flow to the lungs
Hypoxic spell – child becomes restless and agitated
271
What are the investigations for tetralogy of fallot
ECG: RV hypertrophy with RBBB.
CXR may be normal or show a boot shaped heart (hallmark of TOF)
Echo: can show the anatomy and degree of stenosis
272
What is the management for tetralogy of fallot
Surgery is usually done before age of 1 – closure of VSD and correction of pulmonary stenosis.
273
What is a cardiomyopathy
Refers to primary heart muscle disease – often genetic. All cardiomyopathies carry an arrhythmic risk. The heart doesn’t pump as well as it should.
274
What is acute myocarditis
Inflammation of the myocardium - often associated with pericardial inflammation.
275
What are 6 causes of acute myocarditis
Idiopathic (unknown)
Viral, bacterial, protozoan
Spirochaetes (Lyme disease/ syphilis)
Drugs e.g. penicillin
Toxins e.g. cocaine, lithium, alcohol, lead, arsenic
Immunological e.g. heart transplant rejection
276
What are 4 symptoms and signs of acute myocarditis
ACS-like symptoms
Heart failure symptoms
Palpitations
Tachycardia
277
What are the 3 treatment options for acute myocarditis
Supportive
Treat underlying cause
Treat arrhythmias and heart failure.
278
What is dilated cardiomyopathy
A dilated, flabby heart of unknown cause.
279
What are the potential causes for dilated cardiomyopathy (DCM)
Congenital
Most autosomal dominant, but some recessive and X-linked. Mutations in several genes are recognised – dystrophin, troponin T
280
What is the pathology of DCM
Poorly generated contractile force leads to progressive dilation of the heart with some diffuse interstitial tissue
281
What are 6 conditions associated with DCM
alcohol, high BP, chemotherapeutics, viral infection, autoimmune.
282
What are 5 clinical presentations of DCM
Fatigue
Dyspnoea
Pulmonary oedema
RVF
Emboli
283
What are 4 signs of DCM
High pulse
Low blood pressure
Hepatomegaly
Mitral or tricuspid regurgitation
284
What are 4 investigations for DCM
Bloods: low sodium indicates a poor prognosis
CXR: cardiomegaly, pulmonary oedema
ECG: tachycardia, non-specific T-wave changes
Echo: low ejection fraction
285
What are the 5 management options for DCM
Bed rest
Diuretics
β-blockers
Anticoagulation
Transplantation
286
What is hypertrophic cardiomyopathy (HCM)
LV outflow tract obstruction from asymmetrical septal hypertrophy.
287
What causes HCM
Caused by sarcomeric protein gene mutations – many recognised involving beta-myosin binding protein C, troponin T, titin.
288
What are 7 signs and symptoms of HCM
Sudden death (troponin T)
Cardiac hypertrophy and dysrhythmia (beta-myosin)
Angina
Dypsnoea
Palpitations
Dizziness
Syncope
289
What are 2 investigations for HCM
Echo: shows asymmetrical septal hypertrophy, small LV cavity, dilated left atrium and systolic anterior motion of the mitral valve.
ECG: progressive T-wave inversion, deep Q waves
290
What are the 3 treatment methods for HCM
β-blockers for symptoms
Amiodarone for arrhythmias
Anticoagulate for systemic emboli.
291
What is restrictive cardiomyopathy
Restrictive filling of the ventricles. A group of diseases in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body.
292
what are 3 causes of restrictive cardiomyopathy
Idiopathic
Amyloidosis
Endomyocardial fibrosis
293
What is 2 clinical presentations of restrictive cardiomyopathy
Like constrictive pericarditis
Features of RVF – hepatomegaly, oedema, ascites
294
right ventricular cardiomyopathy
A degenerative condition with progressive dilation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement.
295
What is the cause of Arrhythmia right ventricular cardiomyopathy
Often caused by desmosome gene mutations
296
What is a channelopathy
Inherited arrhythmia caused by ion channel protein gene mutations.
297
What are the features of channelopathies
Usually relate to potassium, sodium or calcium channels
Channelopathies include long QT, short QT, and Brugada syndrome (abnormal electrical activity of the heart)
Structurally normal heart
May present with recurrent syncope
Be aware of QT prolonging drugs – they can kill people with long QT syndrome
298
What is Familial hypercholesteremia (FH)
An inherited abnormality of cholesterol metabolism (abnormal LDL protein)
299
What are 6 features of Familial hypercholesteraemia
Leads to serious premature coronary and other vascular disease
Aortic aneurysm or dissection is often inherited
Aortovascular syndromes include Marfan, Loeys-Dietz, vascular Ehler Danlos (EDS)
Inherited Cardiovascular Conditions are usually dominantly inherited – offspring have 50% risk of inheritance
Family evaluation is essential and not in question
Genetic testing is available for many of these conditions
300
What is Pericarditis
Inflammation of the pericardium.
301
What is the aetiology of pericarditis
Infections are a common cause, and these may be viral, bacterial or fungal
Full-thickness acute myocardial infarction causes pericarditis overlying the infarct
Other miscellaneous causes include severe renal failure, hypothyroidism, multisystem autoimmune diseases, cardiac surgery, radiotherapy, malignant infiltration, and some drugs
302
What is the presentation of pericarditis
Central chest pain which is worse on inspiration or lying flat and relieved by sitting forward.
A superimposed large pericardial effusion may cause breathlessness
303
What are the investigations for pericarditis
ECG shows concave (saddle-shaped) ST segment elevation and PR depression
Blood tests: FBC, ESR, cardiac enzymes, tests related to aetiologies
Cardiomegaly on CXR may indicate pericardial effusion
CMR and CT may show localised inflammation
304
What is the treatment for pericarditis
NSAIDs or aspirin with gastric protection
305
What is constrictive pericarditis
The heart is encased in a rigid pericardium.
306
What are 5 potential causes for constrictive pericarditis
pericarditis, myocardial rupture, aortic dissection, pericardium filling with pus, malignancy
307
What are the clinical features of costrictive pericarditis
Dyspnoea, chest pain, signs of local structures being compressed
Nausea
Bronchial breathing
308
What are the investigations for constrictive pericarditis
CXR shows an enlarged, globular heart if effusion >300mL
ECG shows low-voltage QRS complexes
Echo: an echo-free zone surrounding the heart
309
What are the 3 management steps for constrictive pericarditis
Treat the cause
Pericardiocentesis- draining
Send pericardial fluid for culture and cytology
310
What are 6 cardiac causes of arrythmias
: ischaemic heart disease; structural changes e.g. left atrial dilatation secondary to mitral regurgitation; cardiomyopathy; pericarditis; myocarditis; aberrant conduction pathways.
311
What are 6 non-cardiac causes of arrythmias
caffeine, smoking, alcohol, pneumonia, drugs, metabolic imbalance.
312
What are 6 clinical presentations of Cardiac arrhythmias
Palpitations
Chest pain
Presyncope
Syncope
Hypotension
Pulmonary oedema
313
What are 5 investigations for arrhythmias
FBC, U&E, glucose, Ca2+, Mg2+
ECG: look for signs of IHD, AF, short PR interval, long QT interval, U waves
24h ECG monitoring
Echo: look for structural heart disease e.g. mitral stenosis
Provocation tests: exercise ECG, cardiac catheterisation
314
What are the 3 types of management for arrhythmias
Conservatively – reducing alcohol intake
Medical management – regular tablets
Interventional management – pacemakers, ablation, implantable cardioverter defibrillators
315
What is sinus tachycardia and its causes
conduction impulses are initiated at high frequency. Causes include infection, pain, exercise, anxiety, dehydration.
316
What is focal atrial tachycardia
a group of atrial cells act as a pacemaker, out-pacing the SAN. P-wave morphology is different to sinus.
317
What is atrial flutter
electrical activity circles the atria 300 times per minute, giving a sawtooth baseline. The AVN passes some of these impulses on, resulting in ventricular rates that are factors of 300.
318
What is Atrioventricular re-entry tachycardia
an accessory pathway that allows electrical activity from the ventricles to pass to the resting atrial myocytes, creating a circuit; atria-AVN-ventricles-accessory pathway-atria.
319
What is Atrioventricular nodal re-entry tachycardia
circuits form within the AVN, causing narrow complex tachycardias.
320
What is Junctional tachycardia
cells in the AVN become the pacemaker, giving narrow QRS complexes as impulses reach the ventricles through the normal routes; P waves may be inverted and late.
321
What is bundle branch block
a delay or blockage along the pathway that electrical impulses travel to make your ventricle contract
322
What is Ventricular tachycardia
this can result from circuits, similar to atrial flutter. The QRS is broad. When a circuit is in action and its plane rotates, the ECG shows broad complex tachycardia with regularly increasing and decreasing amplitudes; this is called torsades de pointes.
323
What is narrow complec tachycardia
ECG shows rate of >100bpm and QRS complex duration of <120ms. Narrow QRS complexes occur when the ventricles are depolarised via the normal conduction pathways.
324
What is the management of narrow complex tachycardias
Identify and treat underlying rhythm e.g. treating sinus tachycardia secondary to dehydration with IV fluids.
325
What is broad complex tachycardia
ECG shows rate of >100bpm and QRS complexes >120ms. If no clear QRS complexes, is it VF or asystole.
326
What are the differential diagnoses for broad complex tachycardia
Ventricular fibrillation
Ventricular tachycardia
327
What is the management for broad complex tachycardia
Correct electrolyte problems – low potassium, magnesium, calcium
328
What are ventricular extrasystoles
Patients describe palpitations, a thumping sensation, or their heart missing a beat. The pulse may feel irregular if there are frequent ectopics.
The ectopics are broad QRS on ECG
329
What are the 5 patterns of ectopic beats
single
Bigeminy – ectopic every other beat
Trigeminy – every third beat is an ectopic
Couplet – two ectopics together
Triplet – three ectopics together
330
What is atrial fibrillation
A chaotic, irregular atrial rhythm at 300-600bpm. The AVN responds intermittently, hence an irregular ventricular rhythm.
331
What are 7 causes of atrial fibrillation
Heart failure
Hypertension
IHD
PE
Mitral valve disease
Pneumonia
Hyperthyroidism – thyrotoxicosis
332
What are 5 symptoms of atrial fibrillation
Asymptomatic
Chest pains
Palpitations
Dyspnoea
Faintness
333
What are 2 signs of atrial fibrillation
Irregularly irregular pulse – the apical pulse rate is greater than the radial rate, and the 1st heart sound is of variable intensity.
Signs of LVF
334
What are 3 investigations for AF
ECG: absent P waves, irregular rapid QRS complexes
Blood tests: U&E, cardiac enzymes, thyroid function tests
Echo: left atrial enlargement, mitral valve disease, poor LV function, other structural abnormalities.
335
What is the management for acute AF
If the patient is stable and AF started <48h ago: rate or rhythm control may be tried: amiodarone.
if the patient is stable and AF started >48h ago: rate control with bisoprolol.
Correct electrolyte imbalances, treat associated illnesses.
336
What is the management for chronic AF
Rate control: β-blocker or rate-limiting Ca2+ blockers are 1st choice – if this fails, add digoxin.
Rhythm control: elective DC conversion
337
What is Atrial flutter
Organised atrial rhythm, rate 250-350bpm.
Similar to AF regarding rate and rhythm control and the need for anticoagulation.
338
What is the treatment for atrial flutter
DC cardioversion is preferred to pharmacological cardioversion. IV amiodarone may be need if rate control is proving difficult.
339
What are the 5 causes for atrial flutter
Obesity
Hypertension
Excess alcohol
COPD
Heart failure/ CHD
340
What are 4 symptoms of atrial flutter
Palpitations
Breathlessness
Dizziness
Chest pain
341
What is the investigation for atrial flutter
ECG: narrow QRS complex, F waves (no P wave)
2:1 to QRS
342
What is the management of Atrial flutter
Amiodarone – anti-arrhythmic drug
Beta blockers - Bisoprolol
LMW Heparin
Catheter ablation
343
What is heart block
Disrupted passage of electrical impulse through the AV node.
344
What is 1st degree heart block
the PR interval is prolonged and unchanging; no missed beats
345
What is Mobitz I 2nd degree HB
the PR interval becomes longer and longer until a QRS is missed, the pattern then resets. This is Wenckebach phenomenon
346
What is Mobitz II 2nd degree HB
QRSs are regularly missed e.g. after every second p wave
This is a danger rhythm as it may progress to complete heart block
347
What is are 6 causes of 1st and 2nd degree heart block
normal variant, athletes, sick sinus syndrome, IDH, acute myocarditis, drugs (digoxin, β-blockers)
348
What is 3rd degree heart block
no impulses are passed from atria to ventricles so P waves and QRSs appear independently of each other
349
What is the pathophysiology of 3rd degree heart block
As tissue distal to the AVN paces slowly, the patient becomes very bradycardic, and may develop haemodynamic compromise.
350
What are 7 causes of 3rd degree heart block
IHD, idiopathic, congenital, aortic valve calcification, cardiac surgery/trauma, digoxin toxicity, infiltration
351
What is the treatment of heart block
IV atropine
Permanent pacemaker
352
what are features of prolonged QT syndrome
Can be congenital – romano-ward syndrome
Ventricular repolarisation grossly prolonged
Causes: low K+, Ca2+, acute MI, diabetes, amiodarone, amitriptyline
Signs: syncope, palpitations
If acquired give IV isoprenaline
353
What are features of wolff-parkinson-white syndrome
An extra electrical pathway in the heart, leading to periods of tachycardia.
Due to congenital accessory conduction pathway between atria and ventricles
Resting ECG – short PR interval, wide QRS complex (due to slurred upstroke/ delta wave) and ST-T changes
Patients present with SVT
It’s a type of atrioventricular reciprocating tachycardia (AVRT)
Patients will be prone to AF (and VF)
354
What is an Aortic aneurysm
An aortic aneurysm is an abnormal bulge that occurs in the wall of the aorta. An artery with a dilatation >50% of its original diameter has an aneurysm.
355
What are true aneurysms
abnormal dilatations that involve all layers of arterial wall.
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What are false aneurysms
involve a collection of blood outside the vessel, held to the vessel by surrounding tissues
357
What is the pathology of aneurysms
Aneurysms are dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels. Incidence rises with age, described as fusiform, saccular, dissecting and arterio-venous.
358
What are 5 causes of aneurysms
Atheroma
Trauma
Infection
Connective tissue disorders
Inflammatory
359
What are the clinical presentations of a Ruptured abdominal aortic aneurysm
Abdominal pain
Collapse
Shock
360
What are the symptoms of unruptured AAAs
Often none
Abdominal/ back pain
361
What are 5 complications with aneuryms
Rupture
Thrombosis
Embolism
Fistulae
Pressure on other structures
362
What is the management for aneurysms
Annual check-ups and monitoring with regular ultrasound scans
Surgery
Endovascular: the graft is inserted into a blood vessel in your groin and then carefully passed up into the aorta
Open – the graft is placed in the aorta through a cut in your stomach
363
What is aortic dissection
A tear in the wall of the aorta. Blood can flow in between the layers of the blood vessel wall (dissection). This can lead to aortic rupture or decreased blood flow to organs.
Associated with aortic aneurysms.
364
What are 6 risk factors for aortic dissection
Ageing
Atherosclerosis
Blunt trauma to the chest
High blood pressure
Bicuspid aortic valve
Coarctation (narrowing) of the aorta
365
What are 7 clinical manifestations of aortic dissection
Chest Pain – sharp, stabbing, tearing or ripping which radiates to the back
Anxiety and feeling of doom
Fainting or dizziness
Heavy sweating (clammy skin)
Nausea and vomiting
Pale skin (pallor)
Rapid, weak pulse
366
What are 6 investigations for aortic dissection
Aortic angiography
Chest x-ray
Chest MRI
CT scan of chest
Echocardiogram
Transoesophageal echocardiogram (TEE)
367
What is peripheral vascular disease
Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors. Disease in which a build-up of fatty deposits in the arteries restricts blood supply to leg muscles.
368
What are 2 symptoms of peipheral vascular disease
Cramping pain in the calf, thigh, or buttock after walking for a given distance and relieved by rest
Ulceration, gangrene and foot pain at rest
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What are 5 signs of Peripheral vascular disease
Absent femoral, popliteal or foot pulses
Cold, white legs
Atrophic skin
Punched out ulcers
Buerger’s angle (angle that leg goes pale when raised off the couch).
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What are 4 investigations for Peripheral vascular disease
FBC – anaemia, polycythaemia
ECG – cardiac ischaemia
Ankle-brachial pressure index (ABPI)
Colour duplex USS – can show vessels and blood flow within them
371
What are 4 management options for peripheral vascular disease
Risk factor modification – quit smoking, treat hypertension and high cholesterol
Management of claudication – supervised exercise programmes reduce symptoms by improving collateral blood flow.
Surgical reconstruction – arterial reconstruction with a bypass graft.
Amputation
372
What is shock
Circulatory failure resulting in inadequate organ perfusion. Often defined by low BP – systolic <90mmHg, with evidence of tissue hypoperfusion.
373
What is cardiogenic shock
a state of inadequate tissue perfusion primarily due to cardiac dysfunction.
374
What are the causes of cardiogenic shock
Myocardial infarction
Arrhythmias
Pulmonary embolus
Tension pneumothorax
Cardiac tamponade
Myocarditis
Aortic dissection
375
What are 6 clinical manifestations of cardiogenic shock
Agitation
Pallor
Cool peripheries
Tachycardia
Slow capillary refill
Oliguria (abnormally small amounts of urine)
376
What are the 6 management steps for cardiogenic shock
Oxygen – titrate to maintain saturations of 94-98%
Diamorphine 1.25-5mg IV for pain and anxiety
Investigations and close monitoring
Correct arrhythmias, U&E abnormalities, or acid-base disturbance
Optimize filling pressure
Look for and treat any reversible cause
377
What is cardiac tamponade
Compression of the heart by an accumulation of fluid in the pericardial sac.
Pericardial fluid collects -> intrapericardial pressure rises -> heart cannot fill -> pumping stops.
378
What are 5 causes for cardiac tamponade
Trauma
Lung/breast cancer
Pericarditis
MI
Bacteria
379
What are 4 signs of cardiac tamponade
Low BP
Muffled heart sounds (Beck’s triad)
Echocardiography may be diagnostic
CXR: globular heart – left heart border convex
380
What are 3 management options for cardiac tamponade
Pericardiocentesis – quick relief
Give oxygen, monitor ECG, set up IV
Surgery may be required
381
What is the mechanism of syncope
A state of consciousness is maintained by adequate cerebral blood flow. Cerebral vascular autoregulation ensures that the cerebral blood flow is kept within a narrow range, independent of the underlying systemic blood pressure. If the blood pressure drops below this range, the lack of blood causes syncope
382
What are the signs that indicate a CNS cause of syncope
aura, headache, dysarthria and limb weakness
383
What are the signs that indicate a Cardiac cause of syncope
chest pain, palpitations and dyspnoea
384
What are 3 investigations for syncope
Blood pressure in supine and standing positions, on immediate standing, and after 3 minutes of standing.
Basic neurologic exam – checking for sensory, motor, speech and vision deficits
12-lead ECG
385
What are 5 red flag symptoms with syncope
Syncope with exercise
Chest pain
Palpitations
Back pain
Haematemesis- vomit blood
386
What is the management for syncope
Treat underlying cause
387
What are antiplatelet drugs used for
Used in low dose for secondary prevention following MI, TIA/stroke, and for patients with angina or peripheral vascular disease
388
What is the mechanism of aspirin
Aspirin irreversibly acetylates cyclo-oxygenase, preventing production of thromboxane A2, thereby inhibiting platelet aggregation
389
What are 2 types of DOAC
Xa inhibitors and direct thrombin inhibitors
390
What are anticoagulants used for
treatment of AF and clots.
391
Which anticoagulant is used for mechanical valves.
warfarin
392
What are 3 anticoagulant drugs used for acute coronary syndomes
LMWH, fondaparinux (Xa inhibitor) and bivalirudin (thrombin inhibitor)
393
What is the mechanism of beta blockers
Block β-adrenoreceptors, thus antagonising the sympathetic nervous system.
394
What is the action of blocking β1-receptors
negatively inotropic and chronotropic
395
What is the action of blocking β2-receptors
induces peripheral vasoconstriction and bronchoconstriction
396
What are β-blockers used for
angina, hypertension, antidysrhythmic, post MI, heart failure
397
What are 3 side effects of β-blockers
lethargy, ED, headache
398
What are ACE inhibitors used for
hypertension, heart failure and post MI
399
What are 2 side effects of ACE inhibitors
dry cough and urticaria
400
What are loop diuretics used for
heart failure, and inhibit the Na/2Cl/K co-transporter
401
What are side effects of loop diuretics
dehydration, low Na+, K+, Ca2+
402
What are Thiazides and thiazide-like diuretics used for
hypertension and heart failure
403
What are the side effects of Thiazides and thiazide-like diuretics
low K+, raised Ca2+, low Mg2+, increased urate, impotence
404
What is the action of potassium sparing diuretics
aldosterone antagonists directly block aldosterone receptors; amiloride blocks the epithelial sodium channel in the distal convoluted tubules
405
What are vasodilators used for
heart failure, IHD and hypertension
406
What is the action of nitrates
preferentially dilate veins and the large arteries, lower filling pressure (pre-load)
407
What is the action of hydralazine
primarily dilates the resistance vessels, thus lowering BP (after-load)
408
What is the action of calcium antagonists
Decrease cell entry of Ca2+ via voltage-sensitive channels in smooth muscle, thereby promoting coronary and peripheral vasodilation and reducing myocardial oxygen consumption.
409
Which channel do Calcium antagonists block
L-type Ca2+ channels
410
What are 4 side effects of calcium antagonists
flushes, headaches, ankle oedema, lowered LV function
411
What are the features of dihydropyrdines
Mainly peripheral vasodilators and cause a reflex tachycardia so are often used with a β-blocker.
Used mainly in hypertension and angina
e.g. amlodipine
412
What are the features of Non-dihydropyridines
Slow conduction at the AV and SA nodes
May be used to treat hypertension and angina and dysrhythmias
e.g. verapamil
413
What is the action of digoxin
Blocks the Na+/K+ pump
It is used to slow the pulse in fast AF
As it is a weak +ve inotrope, its role in heart failure in sinus rhythm may be best reserved if symptomatic despite optimal ACE-i therapy
414
What are 4 side effects of digoxin
nausea, decreased appetite, yellow vision, confusion
415
What is amiodarone
A class III anti-arrhythmic
416
What is the action of amiodarone
Prolongs the cardiac action potential, reducing the potential for tachyarrhythmias
417
What is amiodarone used for
Used in both supra-ventricular and ventricular tachycardias, including during cardiac arrest.
418
What are 3 side effects of amiodarone
thyroid disease, liver disease, pulmonary fibrosis
419
murmur for Aortic stenosis
systolic ejection murmur, crescendo-decrescendo. S4 sound
420
Aortic regurgitation murmur
diastolic decrescendo murmur, austin flint
421
mitral stenosis murmur
diastolic rumble murmur
422
mitral regurgitation murmur
pansystolic murmur, S3 sound
423
ECG presentation of RBBB
MARROW, m shaped QRS on v1, W shaped QRS on v6
424
ECG presentation of LBBB
WILLIAM, W shaped QRS on v1, M shaped QRS on v6
