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CARDIOVASCULAR Flashcards

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1
Q

what are the risk factors associated with the development of AAA?

A
  • Increasing age (typical onset is 65 - 75 years).
  • Male gender (incidence of 5% of men over 60 years).
  • Hypertension.
  • Hyperlipidaemia.
  • Smoking.
  • COPD.
  • Family history of abdominal aortic aneurysm.
  • Coronary, cerebrovascular or peripheral arterial disease.
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2
Q

what are the clinical features of AAA?

A
  • Typically asymptomatic and are found on routine examination or imaging.
  • Non-specific back pain.
  • Expansile and pulsatile abdominal mass may be felt.
  • Dusty discolouration of the digits secondary to emboli.
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3
Q

what are the clinical features of rapid expansion or rupture of AAA?

A
  • Severe epigastric pain radiating to the back
  • Signs of cardiovascular collapse e.g. hypotension and tachycardia
  • Sudden death
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4
Q

How is AAA <5.5cm treated?

A
  • Encourage smoking cessation.
  • Optimisation hypertension medication.
  • Offer a lifelong statin.
  • Offer clopidogrel.
  • Offer regular ultrasound surveillance.
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5
Q

how is AAA of 5.5cm or larger, symptomatic or rapidly enlarging managed?

A
  • Offer open surgical repair with insertion of a Dacron graft if there is no co-pathology, anaesthetic risks, or co-morbidities.
  • Offer a non-surgical endovascular aneurysmal repair (EVAR) with insertion of a stent via the femoral artery, if there is co-pathology, anaesthetic risks, or co-morbidities.
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6
Q

how is ruptured AAA managed?

A
  • Offer open surgical repair in men under 70.

- Offer endovascular aneurysmal repair for men over 70 and women of any age.

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7
Q

what are the risk factors for ACS?

A
  • Smoking
  • Hypertension.
  • Diabetes.
  • Obesity.
  • Hypercholesterolaemia / hyperlipidaemia.
  • Male gender.
  • Previous surgery.
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8
Q

what are the clinical features of ACS?

A
  • Rapid onset pain and lasts longer than 20 minutes.
  • Severe, constricting, and heavy in nature.
  • Referred to the arms, back or jaw.
  • Of new onset or is the result of abrupt deterioration of stable angina with pain occurring frequently with little or no exertion.
  • Dyspnoea due to pulmonary oedema is a sign of complication.
  • Autonomic features including sweating, nausea, vomiting and pallor.
  • Haemodynamic instability, including a systolic blood pressure less than 90 mmHg
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9
Q

how does a STEMIs appearance on ECG change over time?

A
  • ST elevation is the first ECG change.
  • After the first few minutes the T waves become tall, pointed and upright.
  • After the first few hours there is T wave inversion and Q wave development.
  • After a few days, the ST segment returns to normal.
  • After a few weeks the T wave may return upright but the Q wave remains.
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10
Q

what are the ECG features of an anterior wall MI and which artery is affected ?

A
  • ST elevation in leads V2-V4.

- LAD

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11
Q

what are the ECG features of a lateral wall MI and which artery is affected?

A
  • ST elevation in leads I, aVL and V5-V6.

- Circumflex

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12
Q

what are the ECG features of an inferior wall MI and which artery is affected?

A
  • ST elevation in leads II, III and aVF.

- Right coronary artery

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13
Q

what are the ECG features of a posterior wall MI and which artery is affected?

A
  • ST depression in leads V2-V4
  • a tall R wave in V1
  • ST elevation in leads V5-V6
  • Posterior descending .
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14
Q

How should a STEMI be managed initially?

A
  • Oxygen
  • aspirin with ticagrelor (no previous intracerebral haemorrhage or liver disease) or clopidogrel
  • morphine and metoclopramise IV
  • Sublingual GTN followed by IV GTN
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15
Q

which medication should be given to patients undergoing PCI or coronary angiography?

A

-Unfractionated or LMWH

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16
Q

what is the long term management post-MI?

A
  • aspirin 75mg indefinitely, combined with ticagrelor for 12 months
  • ACE inhibitor/ARB
  • Beta-blocker
  • Spironolactone
  • Statin
  • Lifestyle advice and cardiac rehab
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17
Q

what is seen on ECG in NSTEMI?

A
  • T wave inversion of greater than 1 mm in at least two leads corresponding to the site of myocardial damage.
  • There is no ST segment elevation and Q waves do not develop.
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18
Q

what is seen on ECG in unstable angina?

A
  • ST segment depression while the patient has pain

- once the pain has resolved the ECG returns to normal.

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19
Q

how is NSTEMI/unstable angina managed?

A
  • aspirin or ticagrelor
  • unfractionated heparin if coronary angiography to be done within 24 hours of admission
  • if >24 hours, give fondaparinux
  • given oxygen and nitrates
  • Diamorphine and metoclopramide
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20
Q

what is variant angina?

A
  • Prinzmetal angina and vasospastic angina
  • occurs at rest
  • caused by vasospasm of the coronary arteries, rather than an atherosclerotic plaque.
  • It occurs more frequently in women.
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21
Q

what is microvascular angina?

A
  • cardiac syndrome X
  • caused by normal coronary arterial perfusion, but poor perfusion of the microvasculature of cardiac muscles
  • It occurs more frequently in women.
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22
Q

what are the risk factors for angina?

A
  • Smoking.
  • Hypertension.
  • Diabetes.
  • Obesity.
  • Hypercholesterolaemia / hyperlipidaemia.
  • Male gender.
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23
Q

what are the clinical features of angina?

A
  • Constricting and heavy chest pain, or pain in the neck, shoulders, jaws or arms.
  • The pain is precipitated by physical exertion.
  • The pain is relieved by rest or GTN spray within about 5 minutes.
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24
Q

what is seen on ECG in angina?

A
  • can be normal
  • There may be ST depression in stable angina or unstable angina.
  • There may be ST elevation in variant angina.
  • ST elevation, T wave abnormalities, Q waves, and LBBB are suggestive of ischaemia or previous infarction.
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25
what lifestyle advice should be given to patients with angina?
- Smoking cessation. - Cardioprotective diet. - Increase in physical activity. - Limitation of alcohol consumption. - Maintenance of a healthy diet. - Avoidance of provoking factors such as exertion, stress, or cold exposure.
26
what symptomatic relief can be given to patients with angina?
- Offer a short-acting nitrate (GTN spray) to use for relief of symptoms while they are waiting for specialist referral. - Patients should repeat the dose after 5 minutes if the pain has not gone. - Patients should call an ambulance if the pain has not gone 5 minutes after taking a second dose.
27
what is the long term drug treatment for angina?
- betablocker, verapamil or diltiazem - combine beta blocker and nifedipine if poor response - Consider dual therapy with a second anti-anginal drug (isosorbide mononitrate, mivabradine, nicorandil, ranolazine) if there is a poor response to initial therapies.. - Consider triple therapy with a third anti-anginal drug if there is a poor response to dual therapy.
28
what secondary prevention should be given in angina?
- aspirin 75 mg daily. - ACE inhibitors (ramipril) for patients with diabetes. - statin (atorvastatin 80 mg).
29
which patients with angina should be offered revascularisation?
- Whose symptoms are not satisfactorily controlled in patients with optimal medical treatment. - In whom angiography has demonstrated left main stem (left anterior descending artery) disease or proximal three-vessel disease.
30
what are the causes of aortic regurgitation?
- idiopathic - ageing - syphilis - Marfan's syndrome - osteogenesis imperfecta - infective endocarditis - rheumatic fever
31
what are the symptoms of aortic regurgitation?
- Dyspnoea. - Fatigue. - Orthopnoea. - Paroxysmal nocturnal dyspnoea
32
what murmur is heard in aortic regurgitation?
- High pitched early diastolic murmur, best heard at the left sternal edge in the fourth intercostal space with the patient leaning forward and breath held in expiration - mid-diastolic Austin flint murmur
33
how does the pulse appear in aortic regurgitation?
- wide pulse pressure | - collapsing or bounding
34
which unique signs are seen in aortic regurgitation?
- Quincke’s sign (nail-bed pulsation). - De Musset’s sign (head nodding with each heart beat). - Duroziez’s sign (murmur heard over the femorals when compressed). - Pistol-shot femorals (bang heard on auscultation over femorals).
35
what is seen on chest x-ray in aortic regurgitation?
- Left ventricular dilatation. - Aortic root dilatation. - Features of left heart failure.
36
what is seen on ECG in aortic regurgitation?
-Tall R waves in lead V6 and deep S waves in V1 due to left ventricular hypertrophy.
37
how is aortic regurgitation managed?
- Perform regular review and assessment of asymptomatic aortic stenosis who are unsuitable for surgery. - Offer a calcium channel blocker (nifedipine) for symptomatic patients to reduce afterload and degree of regurgitation. - Offer an inotrope (dopamine) and a vasodilator (nitroprusside) for an acute exacerbation of aortic regurgitation.
38
in which patients with aortic regurgitation should valve replacement be offered?
- Symptomatic aortic regurgitation (including an acute exacerbation). - Asymptomatic aortic regurgitation with an ejection fraction < 50% or left ventricular dilation.
39
what are the causes of aortic stenosis?
- age/calcific aortic valve disease | - bicuspid aortic valve
40
what are the clinical features of aortic stenosis?
- Syncope. - Angina. - Dyspnoea
41
what murmur is associated with aortic stenosis?
- Harsh crescendo-decrescendo ejection systolic murmur that radiates into the carotids - with soft or inaudible second heart sound
42
how does the pulse appear in aortic stenosis?
- Slow rising carotid pulse with decreased pulse amplitude | - Narrow pulse pressure.
43
what is seen on ECG in aortic stenosis?
- Left ventricular hypertrophy (Deep S waves in V1 and tall R waves in V6). - Left atrial delay (prolonged P wave in lead II) - left ventricular strain (depressed ST segment and T wave inversion in lead I, AVL, V5 and V6).
44
what is seen on chest x-ray in aortic stenosis?
- Small heart - Prominent, dilated ascending aorta - Calcified aortic valve
45
how is aortic stenosis managed?
- Observation is recommended for asymptomatic patients. - Perform aortic valve replacement for symptomatic patients or those with a valvular gradient greater than 40 mmHg: - Offer long term anticoagulation for patients who have had aortic valve replacement using prosthetic mechanical valves.
46
what are the risk factors for mitral regurgitation?
- Mitral valve prolapse. - History of rheumatic heart disease. - Infective endocarditis. - history of MI
47
what are the symptoms of mitral regurgitation?
- Dyspnoea and orthopnoea. - Fatigue. - Palpitations. - Oedema and ascites.
48
what murmur is associated with mitral regurgitation?
-Pan-systolic murmur heard over the apex and radiating to the axilla.
49
what is seen on chest x-ray in mitral regurgitation?
- A large left atrium | - A large left ventricle.
50
what is seen on ECG in mitral regurgitation?
- Bifid P waves due to delayed left atrial activation. | - Tall R waves in lead V6 and deep S waves in V1 due to left ventricular hypertrophy.
51
how is mitral regurgitation managed?
-Offer an ACE inhibitor (ramipril) and a beta blocker (atenolol) for patients with minor symptoms and who are not appropriate for surgical intervention to reduce afterload and degree of regurgitation. - For patients with atrial fibrillation: - --Offer anticoagulants (warfarin) if atrial fibrillation is present, to reduce the risk of systemic embolism. - --Offer atenolol, diltiazem or digoxin for ventricular rate control in atrial fibrillation.
52
which patients with mitral regurgitation should have valve repair or replacement?
- With symptomatic severe mitral regurgitation. - Left ventricular ejection fraction less than 30%. - Asymptomatic severe mitral regurgitation with preserved left ventricular function and atrial fibrillation or pulmonary hypertension.
53
what are the causes of mitral stenosis?
-rheumatic heart disease
54
what are the clinical features of mitral stenosis?
- Progressive dyspnoea. - Peripheral oedema. - Palpitations.
55
which murmur is associated with mitral stenosis?
-Low-pitched, rumbling mid-diastolic murmur heard best in expiration with the bell of the stethoscope held lightly at the apex and the patient lying on their left side
56
what is seen on chest x-ray in mitral stenosis?
- A large left atrium - Distended pulmonary veins - Pulmonary oedema
57
what is seen on ECG in mitral stenosis?
- Bifid P wave due to delayed left atrial activation. - Absent P waves, rapid and irregular timing of QRS complexes due to atrial fibrillation - Tall R waves in V1 (right axis deviation) due to right ventricular hypertrophy.
58
how is mitral stenosis managed in patients with minor symptoms?
-Offer a loop diuretic (furosemide) to control pulmonary congestion
59
when should mitral balloon valvotomy be offered in mitral stenosis?
- Severe mitral stenosis with no mitral regurgitation - Non-calcified valve on echocardiography. - No left atrial thrombus on echocardiography
60
when should mitral valve replacement be offered in mitral stenosis?
- Severe mitral stenosis and mitral regurgitation. - Calcified valve on echocardiography. - Left atrial thrombus on echocardiography.
61
which murmur is associated with pulmonary regurgitation?
-High pitched early diastolic decrescendo murmur at the left sternal edge
62
what are the causes of pulmonary stenosis?
- carcinoid syndrome - rheumatic heart disease - fallot's tetralogy
63
which murmur is associated with pulmonary stenosis?
-Harsh mid-systolic ejection murmur, best heard on inspiration, to the left of the sternum in the second intercostal space.
64
what is seen on chest x-ray in pulmonary stenosis?
-Post-stenotic dilatation of the pulmonary trunk.
65
what is seen on ECG in pulmonary stenosis?
-Tall R waves in V1 due to right ventricular hypertrophy.
66
what are the clinical features of tricuspid stenosis?
- Abdominal pain due to hepatomegaly. - Swelling due to ascites. - Peripheral oedema.
67
which murmur is associated with tricuspid stenosis?
-Rumbling mid-diastolic murmur heard over the left sternal edge during inspiration.
68
what is seen on chest x-ray in tricuspid stenosis?
-prominent right atrial enlargement.
69
what is seen on ECG in tricuspid stenosis?
-Tall P waves in lead II due to right atrial enlargement
70
how is tricuspid stenosis managed?
- Offer diuretic therapy. - Encourage salt restriction. - Offer tricuspid valve replacement where diuretic therapy and salt restriction do not improve the condition.
71
what murmur is heard in tricuspid regurgitation?
-Blowing pansystolic murmur over the left sternal edge on inspiration
72
how is tricuspid regurgitation managed?
- Offer diuretic and vasodilator therapy. - Offer tricuspid valve repair in patients undergoing mitral valve replacement who have tricuspid regurgitation. - Offer tricuspid valve replacement if rheumatic damage is severe, or in drug addicts with infective endocarditis.
73
what are the risk factors for atrial myxoma?
- Female sex. - Age 40 - 60 years. - Family history of atrial myxoma.
74
what are the symptoms of atrial myxoma?
- Dyspnoea that can be worse when lying on left side. - Syncope. - Dizziness. - Weight loss. - Fatigue. - Fever. - Pallor. - Arthralgia. - Raynaud’s phenomenon.
75
what are the signs of atrial myxoma?
- Loud first heart sound. - A tumour plop ‘loud third heart sound produced as the pedunculated tumour comes to an abrupt halt). - Mid-diastolic murmur.
76
how is atrial myxoma diagnosed?
-Dense space-occupying lesion.
77
how is atrial myxoma managed in surgical candidates?
- Perform myxoma resection (atriotomy). - Perform adjunct mitral valve repair or replacement. - post-op aspirin
78
how is atrial myxoma managed in non-surgical candidates?
-Offer beta blockers, ACE inhibitors and furosemide
79
what are the causes of AF?
- hypertension - coronary artery disease - MI - rheumatic heart disease - cardiomyopathy - WPW - myocarditis - pericarditis - thyrotoxicosis - electrolyte imbalance - alcohol abuse - obesity - smoking
80
what are the clinical features of AF?
- Irregular pulse. - Breathlessness. - Palpitations. - Syncope / dizziness. - Chest discomfort. - Stroke / TIA.
81
what is seen on ECG in AF?
- Absent P waves - F waves - Irregularly irregular QRS rhythm - Normal QRS complexes.
82
how is acute AF with haemodynamic instability treated?
-emergency electrical cardioversion
83
how is acute AF in stable patients managed?
- Offer rate control with rhythm control if the onset of AF is less than 48 hours, or rate control if the onset if more than 48 hours or uncertain - Offer electrical cardioversion: immediately if the symptoms have occurred for less than 48 hours, the patient start LMWH prior to this OR - After 3 weeks if the symptoms have persisted for longer than 48 hours and the patient is being considered for long term rhythm control. The patient should be fully anticoagulated for 3 weeks and offer rate control as appropriate - Offer pharmacological cardioversion (amiodarone or flecainide) as an alternative to electrical cardioversion. Flecainide should be avoided if there is underlying structural or ischaemic heart disease.
84
how is long term rate control achieved in AF?
- beta blocker or diltiazem - digoxin monotherapy - combine
85
how is long term rhythm control achieved in AF?
- pill-in-the-pocket strategy using flecainide or propafenone - beta blocker or diltiazem - dronderone - left atrial catheter ablation
86
what is seen on ECG in atrial ectopics?
- abnormally shaped P wave | - an early QRS complex.
87
what is seen on ECG in atrial tachycardia?
- some absent P waves | - a rate of 150 bpm
88
what is seen on ECG in atrial flutter?
- sawtooth F wave rate of 300/min - narrow QRS complexes - QRS rate is 150, 100 or 75 bpm if there is 2:1, 3:1 or 4:1 heart block.
89
how are atrial ectopic beats managed?
-treatment is not normally required unless the ectopic beats provoke more significant arrhythmia, when beta blockers are effective.
90
how is atrial flutter managed?
- Perform emergency electrical cardioversion when there are signs of haemodynamic compromise, such as a systolic blood pressure less than 90 mmHg or a pulse greater than 150 bpm. - Provide a beta-blocker (atenolol), diltiazem or verapamil for rate control. - Provide cardioversion for conversion to sinus rhythm, the patient should receive oral anticoagulation for at least 3 weeks prior to cardioversion. - Provide catheter ablation for treatment of recurrent atrial flutter.
91
how is atrial tachycardia managed?
- cardioversion - beta blockers - calcium channel blockers - catheter ablation.
92
define sinus bradycardia
pulse rate of less than 50 bpm.
93
what are the intrinsic causes of bradycardia?
- Acute ischaemia and infarction of the sinus node, as a complication of acute myocardial infarction. - Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick sinus syndrome, an idiopathic fibrosis of the sinus node).
94
what are the extrinsic causes of bradycardia?
- Hypothermia, hypothyroidism, cholestatic jaundice, and raised intracranial pressure. - Drug therapy with beta blockers, digitalis and other anti arrhythmic drugs. - Neurally mediated syndromes including: - --Carotid sinus syndrome. - --Vasovagal syncope. - --Postural orthostatic tachycardia syndrome (POTS)
95
what are the clinical features of bradycardia?
- Pulse rate < 50 bpm. - Syncope. - Fatigue. - Exercise intolerance. - Shortness of breath. - Cannon a-waves in JBP. - Jugular venous distension. - Increased intracranial pressure.
96
how is bradycardia managed?
- Administer atropine for haemodynamically unstable patients. - Offer permanent pacing for carotid sinus syndrome and sick sinus syndrome. - Offer fludrocortisone or midodrine for vasovagal syncope.
97
what are the reversible causes of cardiac arrest?
- hypoxia - hypovolaemia - hypo/hyperkalaemia - hypothermia - acidosis - thrombosis - toxins - tension pneumothorax - cardiac tamponade.
98
what are the risk factors for cardiac arrest?
- Coronary artery disease - Left ventricular dysfunction - Hypertrophic cardiomyopathy - Arrhythmogenic right ventricular dysplasia - Long QT syndrome - Medical or surgical emergency such as pulmonary embolism or tension pneumothorax
99
how should cardiac arrest with a shockable rhythm be managed?
- Use 150 J for the first shock and immediately resume CPR for 2 minutes with a ratio of 30:2. - If VF or VT persists, repeat this process twice more, for a total of three shocks. - Give adrenaline 1 mg IV and amiodarone 300 mg IV and immediately resume CPR with a ratio of 30:2 for 2 minutes. - Repeat the sequence and further adrenaline. - Start post-resuscitation care if there are signs of return of spontaneous circulation. - If there is shockable rhythm in a monitored patient (coronary care unit) give up to three quick successive stacked shocks rather than 1 shock followed by CPR.
100
how is cardiac arrest with a non-shockable rhythm managed?
- Give adrenaline 1 mg IV and and immediately resume CPR with a ratio of 30:2. - Use a laryngeal mask airway (LMA) to secure the patient’s airway. Ventilate the lungs at a rate of 10 breaths per minute and continue chest compressions without pausing ventilation. - Continue CPR and give adrenaline 1 mg IV after revert to alternative sequence of CPR. - Manage as shockable rhythm if ECG shows signs of VF or VT.
101
what are the clinical features of hypertrophic cardiomyopathy?
- Many patients are asymptomatic and the condition is detected through family screening. - Exertional syncope, angina, and dyspnoea (similar to aortic stenosis). - Sudden death.
102
what are the signs of hypertrophic cardiomyopathy?
- A jerky carotid pulse, which can distinguish it from aortic stenosis. - Double apical pulsation. - Ejection systolic murmur due to left ventricular outflow obstruction. - Pansystolic murmur due to mitral regurgitation secondary to systolic anterior motion. - 4th Heart sound if not in AF
103
what is seen on echo in hypertrophic cardiomyopathy?
-asymmetric left ventricular hypertrophy involving the septum
104
which patients with hypertrophic cardiomyopathy should have an ICD?
- Massive left ventricular hypertrophy greater than 30 mm on echocardiography. - Family history of sudden cardiac death below 50 years of age. - History of previous cardiac arrest or sustained ventricular tachycardia. - Ventricular tachycardia on ambulatory ECG monitoring. - Recurrent syncope. - Exercise induced hypotension.
105
how is chest pain and dyspnoea managed in hypertrophic cardiomyopathy?
- beta-blockers and or calcium channel blockers | - Offer disopyramide as an alternative for patients with left ventricular outflow obstruction.
106
what are the causes of acquired dilated cardiomyopathy?
- myocarditis secondary to Chagas's disease - toxins e.g. alcohol and chemotherapy - pregnancy
107
what are the clinical features of dilated cardiomyopathy?
- Signs and symptoms of heart failure e.g. breathlessness, fluid retention, fatigue, third or fourth heart sounds, raised JVP, hepatomegaly. - Palpitations due to arrhythmia. - Sudden death.
108
what is seen on echo in dilated cardiomyopathy?
- Dilatation of the left and right ventricles | - with poor global contraction.
109
how is dilated cardiomyopathy managed?
- Pharmacological management of heart failure e.g. an ACE inhibitor, a beta blocker, and spironolactone. - Offer an ICD in patients with NYHA3/4 grading. - Cardiac transplantation for certain patients.
110
what are the clinical features of arrhythmogenic RV cardiomyopathy?
- Most patients are asymptomatic. - Palpitations due to ventricular arrhythmias. - Syncope due to reduced cardiac output. - Sudden death. - Features of right heart failure including peripheral oedema, raised JVP, hepatomegaly, ascites
111
what are the task force criteria for the diagnosis of arrhythmogenic RV cardiomyopathy?
- Perform cardiac MRI to assess structural abnormalities of the right ventricle . - Perform tissue biopsy to demonstrate fibro-fatty replacement of myocytes. - Perform ECG shows T wave inversion in V1-V3 and RBBB. - Perform ambulatory blood pressure monitoring (ABPM) to demonstrate ventricular tachycardia or ventricular extrasystoles. - A family history of ARVC or sudden death.
112
how is arrhythmogenic RV cardiomyopathy managed?
- Offer a beta blocker for non-life threatening arrhythmias. - Offer amiodarone or sotalol for symptomatic arrhythmia. - Offer an ICD for life-threatening arrhythmias. - Cardiac transplantation is indicated for either intractable arrhythmia or cardiac failure.
113
what are the clinical features of restrictive cardiomyopathy?
- Dyspnoea and fatigue owing to heart failure. - Hepatic enlargement, ascites and oedema owing to heart failure. - On examination of the JVP: - --Elevated JVP with diastolic collapse (Friedreich’s sign) - --Elevation of venous pressure with inspiration (Kussmaul’s sign). - --Third and fourth heart sounds.
114
what is seen on echo in restrictive cardiomyopathy?
Impaired ventricular filling - tram-lines - speckled myocardium in amyloid patients.
115
how is restrictive cardiomyopathy managed?
- Offer pharmacological management of heart failure e.g. an ACE inhibitor, a beta blocker, and spironolactone. - Offer melphalan with prednisolone for primary amyloidosis. - Consider liver transplantation in familial amyloidosis. - Consider cardiac transplantation in severe cases, usually of idiopathic origin, as there is recurrence after transplantation with amyloidosis
116
what are the clinical features of coarctation of the aorta?
- Hypertension presenting at young age or resistant to treatment. - Diminished lower extremity pulses. - Differential upper and lower extremity blood pressure. - Ejection systolic murmur at upper sternal edge. - Radio-femoral delay, due to blood bypassing the obstruction via collateral walls. - Headaches and nosebleeds due to hypertension. - Claudication due to poor lower limb perfusion.
117
what is seen on chest x-ray in coarctation of the aorta?
- Rib notching due to development of enlarged collateral intercostal arteries - A ‘3’ sign at the site of coarctation.
118
what are the clinical features of critical coarctation of the aorta?
- Examination on the first day of life is usually normal. - The neonates usually present with acute circulatory collapse at 2 days of age when the duct closes. - A sick baby, with severe heart failure - Absent femoral pulses - Severe metabolic acidosis.
119
how is critical coarctation of the aorta managed?
- Give a prostaglandin (alprostadil) and oxygen to maintain ductal patency - followed by surgical repair.
120
what is a hypertensive emergency?
- a severely elevated blood pressure (greater than 180/120 mmHg) - with new or progressive target organ dysfunction.
121
what are the complications of malignant hypertension?
- Cardiac failure with left ventricular hypertrophy and dilatation. - Blurred vision due to papilloedema and retinal haemorrhages. - Haematuria and renal failure due to fibrinoid necrosis of glomeruli. - Severe headache and cerebral haemorrhage.
122
what are the risk factors for a hypertensive emergency?
- Inadequately treated hypertension. - Chronic kidney disease. - Renal artery stenosis. - Renal transplant. - Pregnancy.
123
what are the clinical features of a hypertensive emergency?
- Neurological features include vision changes, dizziness, and headaches. - Cardiopulmonary features include shortness of breath, chest pain, raised JVP, third heart sound, peripheral oedema. - Haematuria. - Oliguria. - Nosebleeds.
124
what is seen on fundoscopy in malignant hypertension?
- Cotton wool spots - Hard exudates - Papilloedema - Engorged veins
125
how is a hypertensive emergency managed?
- Administer intravenous labetalol if there is malignant hypertension or pre-eclampsia. - Administer intravenous glyceryl trinitrate if there is left ventricular failure or pulmonary oedema, or myocardial ischaemia or infarction. - Administer intravenous fenoldapam for patients with acute kidney injury. - For a hyperadrenergic state: - --Offer a benzodiazepine (lorazepam) if there is evidence of sympathomimetic drug use including cocaine and amphetamines. - --Offer an alpha blocker (phentolamine) for phaeochromocytoma.
126
which drugs cause long QT syndrome?
- amiodarone - sotalol - tricyclic antidepressants - SSRIs - erythromycin - haloperidol - ondansetron.
127
what are the clinical features of LQT1?
Syncope during exercise, particularly swimming
128
what are the clinical features of LQT2?
- Syncope when startled by auditory stimuli, as by a telephone or alarm clock - Syncope postpartum.
129
what are the clinical features of LQT3?
-Syncope with rest and bradycardia (typically at night).
130
How is acquired long QT syndrome managed?
- Stop causative drugs in acquired LQTS. - Correct electrolyte abnormalities. - The heart rate is maintained with atrial or ventricular pacing - Magnesium sulphate 8 mmol (Mg2+) over 10–15 min for acquired long QT - Intravenous isoprenaline may be effective when QT prolongation is acquired
131
how is congenital long QT managed?
- Recommend lifestyle modification including limiting certain sports such as swimming. - Offer a beta blocker (nadolol) for low risk patients (QTc < 500 ms and no previous cardiac arrest. - Offer an implantable cardioverter defibrillator (ICD) for high risk patients (QTc > 500 ms or previous cardiac arrest), or if beta-blockers are contra-indicated.
132
how is Marfan's syndrome inherited?
-autosomal dominant
133
describe the Marfan's phenotype
- Tall stature. - Wide arm span. - High arched palate. - Arachnodactyly. - Pectus excavatum. - Pectus carinatum. - Scoliosis. - Flat feet. - Joint hyper-mobility.
134
what visual system abnormalities are associated with Marfan's?
- Dislocated eye lens. - Myopia or astigmatism. - Retinal abnormalities. - Glaucoma
135
what cardiovascular system abnormalities are associated with Marfan's?
- Aortic valve murmur. - Mitral valve murmur. - History of spontaneous pneumothorax.
136
how is aortic root dilation slowed in marfan's syndrome?
- Offer beta-blocker therapy to slow down the rate of aortic root dilatation. - Offer an ACE inhibitor which inhibits TNF-β, which is upregulated in Marfan’s syndrome.
137
which patients should be offered aortic root replacement in Marfan's?
- yearly echocardiogram reveals an aortic root diameter measures more than 4.5 to 5 cm. - In women of child-bearing age who wish to become pregnant.
138
what are the causes of myocarditis?
- viral - parasitic - bacterial - fungal - Drugs, including alcohol, doxorubicin, methyldopa, penicillins, sulfonamides. - Autoimmune conditions, such as systemic lupus erythematosus and rheumatoid arthritis. - Complication of infective endocarditis. - Drugs causing hypersensitivity, including methyldopa, penicillin and sulfonamides.
139
what are the clinical features of myocarditis?
- May be asymptomatic. - Fever, especially when infectious. - Chest pain that is stabbing in nature. - Palpitations due to arrhythmia. - Dyspnoea and oedema due to congestive cardiac failure. - Sudden death. - Tachycardia.
140
what is found on auscultation in myocarditis?
- Soft heart sounds. - Prominent third heart sounds. - Pericardial friction rub.
141
how is myocarditis managed?
- Recommend bed rest. - Recommend avoidance of athletic activity for 6 months. - Offer antibiotics for bacterial causes. - Offer γ-interferon for viral causes. - Offer ACE inhibitors, beta blockers, spironolactone if evidence of congestive cardiac failure. - Offer corticosteroids in giant cell or eosinophilic myocarditis. - Offer nifurtimox and benznidazole in Chagas’ disease.
142
what are the clinical features of acute pericarditis?
- Sharp, constant retrosternal pain that is relieved by sitting forward and worsened by lying down. It may be referred to left shoulder. - Pericardiac friction rub, a high pitched stretching sound heard over the left sternal border during expiration. - Fever - Arthralgia
143
what are the clinical features of chronic pericarditis?
- Kussmaul's sign (a paradoxical rise in JVP during inspiration). - Ascites, hepatomegaly and peripheral oedema. - Dyspnoea, cough, and orthopnoea - Fatigue, hypotension, and tachycardia.
144
what is seen on ECG in pericarditis?
- Global saddle shaped ST elevation in acute pericarditis | - Low voltage QRS complexes and flat T waves in chronic pericarditis.
145
how is pericarditis managed?
- Offer an NSAID (ibuprofen) plus colchicine as the first line treatment. - Perform pericardiocentesis with systemic antibiotics (vancomycin and gentamicin) for patients with purulent pericarditis.
146
what are the clinical features of cardiac tamponade?
- Beck’s triad - hypotension, muffled heart sounds, and distended jugular veins. - Pulsus paradoxus, a drop in blood pressure during inspiration. - Dyspnoea. - Tachycardia.
147
what is seen on ECG in cardiac tamponade?
- Low voltage QRS complexes | - Electrical alternans (alteration of QRS amplitude between beats).
148
how is cardiac tamponade managed?
- Perform pericardiocentesis if there is no haemorrhage, trauma, neoplasm or purulence. - Perform surgical drainage (pericardial window) for haemopericardium, trauma, purulent effusion, or neoplastic disease.
149
what is intermittent claudication?
ischaemic leg pain upon walking and relieved by rest.
150
what is critical limb ischaemia?
ischaemic pain at rest, associated with ulceration and gangrene, that may be complicated by sepsis.
151
what are the risk factors for peripheral arterial disease?
- Smoking. - Diabetes. - Advancing age. - Hypertension. - Hypercholesterolaemia. - Existing atherosclerotic disease. - Chronic kidney disease.
152
what are the clinical features of acute limb ischaemia?
- Pain. - Pulselessness. - Pallor. - Paralysis. - Paraesthesia. - Perishingly cold limb. - If due to embolus the onset is acute, the limb appears white. - If due to thrombosis the onset is more gradual, the leg may not be white.
153
how is peripheral arterial disease diagnosed using ABPI?
- An ABPI of less than 0.9 indicates peripheral arterial disease. - An ABPI of less than 0.5 is associated with severe peripheral arterial disease - An ABPI of 0.9 - 1.2 is a normal finding. - An ABPI of > 1.2 indicates renal or diabetic disease because the arteries are heavily calcified and incompressible.
154
how is acute limb ischaemia managed?
- Administer anti-platelet therapy (aspirin 300 mg). - Administer intravenous heparin for a target APTT of 2.0 - 3.0. - Perform endovascular revascularisation (balloon angioplasty) and intra-arterial thrombolysis (urokinase) if the limb is viable (no significant tissue loss, never damage, or sensory loss). - Perform amputation if the limb is not viable (significant tissue loss, never damage, or sensory loss).
155
how is chronic limb ischaemia managed?
- Administer anti-platelet therapy (aspirin 300 mg). - Perform endovascular revascularisation (balloon angioplasty) for revascularisation candidates (patient can walk, have a life expectancy of greater than 1 year). - Perform amputation if the patient is not a candidate for revascularisation (patient cannot walk, has a life expectancy of less than 1 year).
156
how is intermittent claudication managed?
- Offer anti-platelet therapy (aspirin 300 mg). - Offer a supervised exercise programme which involves 2 hours of supervised exercise a week for a 3‐month period, encourage exercise to the point of maximal pain. - Refer for consideration of angioplasty when risk modification has been offered and supervised exercise has failed to improve symptoms. - Offer naftidrofuryl oxalate or cilostazol where a supervised exercise programme has failed and the patient does not wish to be referred for surgery.
157
what are the causes of postural hypotension?
- Alpha blockers. - Diuretics. - Diabetes mellitus due to autonomic neuropathy. - Tricyclic antidepressants. - Hypovolaemia. - Amyloidosis. - Parkinson’s disease.
158
what are the clinical features of postural hypotension?
- Light-headedness. - Syncope. - Visual changes. - Weakness. - Fatigue. - Dyspnoea.
159
how is postural hypotension diagnosed?
-Systolic blood pressure falls 20 mmHg within three minutes of standing.
160
how is postural hypotension managed?
- Stop causative drugs if appropriate. - Offer a mineralocorticoid (fludrocortisone) if the patient has an inadequate response to simple non-pharmacological measures. - Offer a short-acting pressor (midodrine) if there is an inadequate reposes to mineralocorticoid therapy.
161
what are the complications associated with occlusion of the aortic branches in aortic dissection?
- Myocardial ischaemia and infarction due to occlusion of the coronary arteries. - Stroke due to occlusion of the carotid arteries. - Paraplegia due to occlusion of the spinal arteries. - Mesenteric infarction with an acute abdomen due to occlusion of the coeliac and superior mesenteric arteries. - Acute (typically lower) limb ischaemia due to occlusion of the femoral arteries.
162
what are the risk factors for aortic dissection?
- Hypertension (80% of cases) - Aortic atherosclerosis - Non-specific aortic aneurysm - Aortic coarctation. - Collagen disorders (Marfan’s syndrome, Ehler’s Danlors syndrome) - Previous aortic surgery - Pregnancy (usually third trimester) - Trauma. - Iatrogenic (cardiac catheterisation) - Male gender and increasing age
163
what are the clinical features of aortic dissection?
- Chest pain that is sharp and tearing in nature, that radiates to the back, classically between the shoulder blades. - Hypertension. - Difference in blood pressure between the 2 arms. - Pulse deficit (reduction or absence of upper limb pulses) in type A dissection. - Diastolic murmur in type A dissection. - Hypotension suggests acute pericardial tamponade and is a grave prognostic indicator.
164
how is aortic dissection diagnosed?
- CT angiography | - Transoesophageal echocardiography
165
how is type A aortic dissection managed?
- Give intravenous labetalol to reduce blood pressure to under 120 mmHg. - Perform open surgery (arch replacement).
166
how is type B aortic dissection managed?
- Give intravenous labetalol. - Perform open surgery (endovascular stent-graft repair) if there is evidence of complications including vital organ or limb ischaemia. For patients with Type B dissection in whom surgery is not indicated, offer medical management only. - Consider verapamil or diltiazem where beta-blockers are contra-indicated. - Consider sodium nitroprusside where beta blockers fail to control blood pressure adequately.
167
what are the risk factors for WPW?
- Ebstein’s anomaly. - Hypertrophic cardiomyopathy. - Mitral valve prolapse. - Atrial septal defect.
168
what are the clinical features of WPW?
- Palpitations. - Dizziness. - Shortness of breath. - Chest pain. - Atrial fibrillation.
169
What is seen on ECG in WPW?
- Short PR interval - Type A WPW: Positive delta wave in all precordial leads with R/S >1 in V1 - Type B WPW: Negative delta wave in leads V1 and V2 - Secondary ST-T Wave changes - Right axis deviation if left (lead 1 is negative and lead 3 is positive).
170
how is WPW managed?
- Offer accessory pathway catheter ablation as the definitive management. - Offer an anti-arrhythmic such as flecainide or propafenone for patients who refuse ablation/are unsuitable for ablation if they have structural or coronary heart disease - In patients with structural heart disease, give dofetilide or sotalol - Perform DC cardioversion in unstable patients with a systolic blood pressure of less than 90 mmHg.
171
define stage 1 hypertension
140/90 mmHg to 159/99 mmHg.
172
define stage 2 hypertension
160/100 mmHg to 179/119 mmHg.
173
define stage 3 hypertension
180/120 mmHg or higher
174
what are the risk factors for developing hypertension?
- Increasing age. - Male gender. - Black African and Black Caribbean origin. - Social deprivation. - Smoking. - Excess alcohol consumption. - Excess dietary salt. - Obesity and lack of physical exercise. - Anxiety and emotional stress.
175
what are the complications associated with essential hypertension?
- Heart failure. - Coronary artery disease. - Peripheral arterial disease. - Chronic kidney disease. - Intracerebral haemorrhage. - Vascular dementia. - stroke - MI
176
how is essential hypertension diagnosed?
- clinic BP measured in both arms - repeat if>140/90 - ABPM or HBPM - Confirm a diagnosis of hypertension in people with a clinic blood pressure of 140/90 mmHg or higher and a ABPM or HBPM daytime average of 135/85 mmHg or higher
177
in which patients with hypertension should anti-hypertensive medication be started?
- Patients with stage 2 hypertension. - Patients with stage 1 hypertension with target organ damage, established cardiovascular disease, renal disease, diabetes or a QRISK score > 10%.
178
what is the first step of hypertension management?
- Offer an ACE inhibitor (ramipril) to patients under 55, or who have diabetes or who are not of African or Caribbean origin. - Offer a calcium channel blocker (amlodipine) to patients over 55 and people of African or Caribbean origin.
179
what is the second step management of hypertension?
- Add a calcium channel blocker in patients under 55 or who have diabetes or who are not of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg). - Add an ACE inhibitor in patients over 55 who are not of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg). - Add an ARB (losartan) in patients over 55 who are of Afro-Caribbean origin with poorly controlled hypertension (their blood pressure is above 140/90 mmHg).
180
what is step 3 of hypertension management?
-Offer an ACE inhibitor, calcium channel blocker and a thiazide-like diuretic (indapamide) for all patients in whom hypertension is not controlled by step 2 treatment.
181
how is resistant hypertension managed?
- Offer a mineralocorticoid receptor antagonist (spironolactone) in addition to step 3 treatment to patients with resistant hypertension with a blood potassium level of 4.5 mmol/L or less. - Offer an alpha blocker (doxazosin) or a beta blocker (atenolol) in addition to step 3 treatment to patients with resistant hypertension with a blood potassium level of more than 4.5 mmol/L.
182
what is the target blood pressure for patients under 80?
- clinic blood pressure below 140/90 mmHg | - home blood pressure below 135/85 mmHg.
183
what is the target blood pressure for patients over 80?
- clinic blood pressure below 150/90 mmHg. | - home blood pressure below 145/85 mmHg
184
what is first degree AV block?
simple prolongation of the PR interval to > 0.22 seconds
185
what is mobitz 1 AV block?
progressive PR prolongation until a P wave fails to conduct.
186
what is mobitz 2 AV block?
- AV block Mobitz II occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation - Wide QRS
187
what is third degree AV block?
all atrial activity fails to conduct to the ventricles.
188
what are the clinical features of AV block?
- Typically asymptomatic. - Syncope (Stokes-Adams attacks) - Heart rate < 40 bpm. - Fatigue. - Dyspnoea. - Angina. - High blood pressure. - Cannon A waves (complete heart block)
189
how are 1st degree and mobitz 1 AV block managed?
- Monitoring if asymptomatic. - Discontinuation of AV-nodal blocking medications if symptomatic. - Dual chamber pacing (1 right atrial and 1 right ventricular lead) with or without an implantable cardioverter-defibrillator (ICD) if severe.
190
how are Mobitz II and third degree AV block managed?
- Digoxin immune Fab if digitalis toxicity. - Glucagon if beta-blocker toxicity. - Calcium chloride if calcium channel blocker toxicity. - Dual chamber pacing with or without an implantable cardioverter-defibrillator (ICD) if severe.
191
what are the causes of RBBB?
- right ventricular hypertrophy - coronary artery disease - congenital heart disease.
192
what are the causes of LBBB?
- coronary artery disease - hypertension - aortic valve disease - cardiomyopathy.
193
what is heard on auscultation in RBBB?
-Wide splitting of the 2nd heart sound
194
what is heard on auscultation in LBBB?
-reverse splitting of the second heart sound
195
what is seen on ECG in RBBB?
- tall R waves in V1 | - deep S waves in leads V6 and I.
196
what is seen on ECG in LBBB?
- deep S waves in V1 | - tall R waves in leads V6 and I.
197
what is seen on ECG in left anterior hemiblock?
-left axis deviation (negative QRS deflections in leads II and III)
198
what is seen on ECG in bifascicular block?
- tall R waves in V1 and deep S waves in leads V6 and I | - negative QRS deflections in leads II and III.
199
what is seen on ECG in trifascicular block?
- tall R waves in V1 - deep S waves in leads V6 and I - negative QRS deflections in leads II and III - first (incomplete) or third degree (complete) heart block
200
how does left sided heart failure present?
- salt and water retention | - pulmonary congestion and oedema, pleural effusions, and cardiomegaly.
201
how does right sided heart failure present?
- increase in right atrial pressure - compounded by salt and water retention - causes peripheral oedema - hepatomegaly - ascites.
202
what are the complications associated with heart failure?
- renal failure - impaired liver function - hypokalaemia - hyponatraemia - arrhythmia - thromboembolism
203
what are the symptoms of heart failure?
- Dyspnoea on exertion. - Dyspnoea at rest. - Dyspnoea lying flat (orthopnoea). - Nocturnal cough, waking from sleep (paroxysmal nocturnal dyspnoea). - Coughing up pink frothy sputum with pulmonary oedema. - Fatigue and decreased exercise tolerance. - Light headedness or history of syncope.
204
what are the signs of heart failure?
- Signs of fluid retention such as ankle swelling, abdominal swelling. - Tachycardia. - Third heart sound. - Displaced apex beat. - Murmurs on auscultation. - Hepatomegaly. - Raised JVP. - Tachypnoea. - Basal crepitations. - Pleural effusions.
205
what is class 1 of the NYHA?
- No symptoms | - Ordinary physical exercise does not cause limitation.
206
what is class 2 of the NYHA?
- Mild symptoms | - Slight Limitation of ordinary physical activity.
207
what is class 3 of the NYHA?
- Moderate symptoms | - Marked limitation on ordinary physical activity
208
what is class 4 of the NYHA?
- Severe symptoms | - Limitation at rest.
209
when should patients with suspected heart failure be referred for echo with respect to NT-proBNP?
- Urgently refer for specialist assessment and echocardiography within 2 weeks for levels above 2,000 ng/l. - Refer for specialist assessment and echocardiography within 6 weeks for levels between 400 and 2,000 ng/l.
210
what factors reduce NT-proBNP levels?
- obesity - heart failure medications - afro-caribbean
211
what factors increase NT-proBNP levels?
- >70 years old - pulmonary hypertension - PE - Diabetes mellitus - CKD
212
what is seen on chest x-ray in heart failure?
- Alveolar batwing oedema - Kerley B lines - Cardiomegaly - Dilated pulmonary vessels - Pleural effusions.
213
how are congestive symptoms treated in chronic heart failure?
-furosemide 80mg
214
what is the first line treatment for heart failure with REF?
- ACE inhibitor (ramipril) | - beta blocker (bisoprolol or carvedilol)
215
what is the second line treatment for heart failure with REF?
- an aldosterone antagonist | - with an ACEi and beta-blocker
216
what are the 3rd line treatments for heart failure with REF by a specialist?
- ivabradine or sacubitril valsartan - hydralazine and nitrate for afro-caribbean patients - digoxin with AF - Cardiac resynchronisation, ICD or heart transplant
217
how is acute heart failure managed?
- Administer high flow oxygen in patients with a capillary oxygen saturation of less than 90%. - Administer an intravenous loop diuretic (furosemide) for acute pulmonary oedema. - Administer a vasodilator (glyceryl trinitrate IV) for patients with a systolic blood pressure greater than 90 mmHg. - Administer an inotrope (dobutamine IV) followed by a vasopressor (noradrenaline IV) for patients with a systolic blood pressure less than 90 mmHg. - Consider ultrafiltration in patients with confirmed diuretic resistance. - Consider left ventricular assist device (LVAD) for advanced heart failure resistant and refractory to maximal medical therapy.
218
what are the clinical features of infective endocarditis?
- Malaise. - Pyrexia. - New systolic murmur. - Haematuria. - Petechia. - Heart failure. - Splenomegaly. - Arthralgia. - Osler’s nodes - Splinter haemorrhages. - Janeway lesions.
219
what are the major modified Duke criteria for infective endocarditis?
- Positive blood cultures from two samples taken 12 hours apart. - Positive echocardiogram. - New valvular regurgitation.
220
what are the minor modified Duke criteria for infective endocarditis?
- Predisposing heart condition or intravenous drug use. - Fever greater than 38 degrees Celsius. - Vasculitic phenomenon including conjunctival haemorrhages, Janeway’s lesions. - Immunological phenomena including glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor. - Microbiolgoical evidence including a positive culture or serological test that does not meet major criteria. - Echocardiographic evidence that does not meet major criteria.
221
when should urgent surgical valve replacement be performed in infective endocarditis?
- Heart failure due to valve damage. - Persistent or uncontrolled infection despite antibiotic therapy. - Recurrent embolic episodes despite antibiotic therapy. - Pregnancy.
222
how should suspected endocarditis be treated while awaiting culture results be treated?
- amoxicillin | - gentamicin.
223
how should staphylococci endocarditis be treated?
- Offer flucloxacillin + gentamicin for 4 weeks for patients with native valves. - Offer flucloxacillin + gentamicin + rifampicin for 6 weeks for patients with prosthetic valves
224
how should streptococcal endocarditis be treated?
- Offer benzylpenicillin for 4 - 6 weeks if fully sensitive. | - Offer benzylpenicillin + rifampicin for 4 - 6 weeks if less sensitive.
225
how should enterococcal endocarditis be treated?
-Offer amoxicillin + gentamicin for 4 - 6 weeks.
226
how should HACEK endocarditis be treated?
-amoxicillin + gentamicin for 4 - 6 weeks
227
what are the clinical features of an ASD?
- Asymptomatic - Recurrent chest infections/wheeze - Arrhythmias
228
what is found on examination in ASD?
- An ejection systolic murmur best heard at the upper left sternal edge. - A fixed and widely split second heart sound. - An apical pansystolic murmur from atrioventricular valve regurgitation with a partial AVSD.
229
what is seen on ECG in secundum ASD?
- right axis deviation | - RBBB.
230
what is seen on ECG in partial AVSD?
-superior QRS axis (where QRS axis is negative in AVF)
231
what are the clinical features of a large VSD?
- Failure to thrive. - Dyspnoea and heart failure - Recurrent pulmonary infections.
232
what are the signs of a large VSD?
- Tachypnoea - Tachycardia - Soft pansystolic murmur or no murmur - Apical mid diastolic murmur from increased flow across the mitral valve - Loud pulmonary second sound
233
what are the signs of a small VSD?
- loud pansystolic murmur at the lower left sternal edge | - quiet pulmonary second sound
234
what are the clinical features of PDA?
- Tachypnoea and reduced exercise tolerance. - Failure to thrive. - Apnoea.
235
what are the signs of PDA?
- A continuous machinery/Gibson murmur beneath the left clavicle - collapsing or bounding pulse
236
how is a PDA managed?
- prostaglandin inhibitor (indomethacin) in premature very low birth weight infants. - Perform percutaneous catheter device closure in small-to-moderate sized ducts in term infants and children and adults. - Perform surgical ligation in large ducts or symptomatic infants too small for device closure.
237
what are the signs of an innocent ejection murmur?
- Soft blowing murmur - systolic murmur only, not diastolic - Left Sternal edge. - Normal heart sounds with no added sounds - No parasternal thrill - No radiation. - During a febrile illness or anaemia, innocent or flow murmurs are often heard because of increased cardiac output.
238
what are the clinical features of hypoplastic left heart syndrome?
- detected antenatally - duct-dependent systemic circulation - profound acidosis - cardiovascular collapse - weakness or absence of all peripheral pulses
239
what are the 4 cardinal features of tetralogy of fallot?
- Ventricular septal defect. - An enlarged aorta that overrides the defects and receives blood from both the right and left ventricles. - Pulmonary valve stenosis. - Right ventricular hypertrophy.
240
what are the clinical features of tetralogy of fallot?
- Severe cyanosis. - Hyper-cyanotic episodes. The baby is typically crying, and squatting on exertion. - Tachypnoea. - Clubbing.
241
what murmur can be heard in tetralogy of fallot?
harsh ejection systolic murmur at the left sternal edge.
242
what is seen on chest x-ray in tetralogy of fallot?
- Boot-shaped heart | - Right-sided aortic arch
243
how are hyper-cyanotic spells in tetralogy of ballot managed?
- Keeping the infant calm, hold in the parents arms with the knees to the chest. - Offer supportive therapy such as oxygen and volume administration. - Second line treatment involves administration of an intravenous beta blocker (esmolol or propranolol) which works by decreasing heart rate and prolonging diastolic filling. - Third line treatment involves administration of intravenous phenylephrine.
244
what are the clinical features of transposition of the great arteries?
- Profound cyanosis. - Presentation is usually on day 2 of life when ductal closure leads to a marked reduction in mixing of the desaturated and saturated blood. - Cyanosis will be less severe and presentation delayed if there is more mixing of blood from associated anomalies, e.g. an ASD. - Second heart sound is often loud and single.
245
what is seen on chest x-ray in transposition of the great arteries?
-‘egg on one side’ appearance of the cardiac shadow
246
how is transposition of the great arteries managed?
- prostaglandin infusion to maintain the latency of the ductus arteriosus. - balloon atrial septostomy - arterial switch procedure
247
what are the clinical features of supraventricular tachycardias?
- Palpitations which are typically regular and fast, with a sudden onset with a ‘jump’. - Polyuria - Chest pain. - Dyspnoea. - Syncope.
248
what is seen on 12 lead ECG in AVNRT?
- no visible P wave | - an inverted P wave immediately before or after a QRS complex.
249
what is seen on 12 lead ECG in AVRT?
P wave between the QRS and T wave.
250
how are acute episodes of supraventricular tachycardia managed?
- Perform emergency cardioversion in patients with haemodynamic instability - Perform the vagal manoeuvres (Valsava manoeuvre or carotid sinus massage) if the patient is haemodynamically stable - Give intravenous adenosine (6 mg) - Give an additional 2 doses of intravenous adenosine (12 mg) if there is no response to the 6 mg dose of adenosine, and before considering cardioversion. - Give intravenous diltiazem as an alternative treatment to intravenous adenosine in whom it is contraindicated (e.g. asthma). - Perform cardioversion in haemodynamically stable patients who respond to neither intravenous adenosine (3 doses) or verapamil.
251
how are recurrent episodes of supraventricular tachycardia prevented?
- Offer a class I anti-arrhythmic agent (flecainide or propafenone) for patients with no additional cardiac disease. - Offer a class III anti-arrhythmic agent (sotalol or amiodarone) for patients with coronary artery disease or structural heart disease - Catheter ablation.
252
what are the clinical features of ventricular tachyarrhythmias?
- Palpitations - Regular fast palpitations in ventricular tachycardia. - Dropped or missed beats in ventricular ectopics. - Chest pain. - Dyspnoea and syncope. - Pulseless and unconscious patient in VF
253
what is seen on ECG in ventricular ectopics?
- Absent P wave - Early wide QRS complex - an abnormal T wave.
254
what is seen on ECG in ventricular tachycardia?
- No P wave | - Broad QRS complex and a rate greater than 160 bpm.
255
what is seen on ECG in brugada syndrome?
- administer flecainide or ajmaline to provoke the classic ECG changes - RBBB - ST elevation in V1 and V2.
256
what is seen on ECG in torasdes des pointes?
QRS complexes alternate in direction.
257
what is seen on ECG in ventricular fibrillation?
totally unorganised ECG with no QRS complex.
258
how are ventricular ectopics managed?
-beta blockers
259
how are haemodynamically stable patients with ventricular tachycardia managed?
IV amiodarone
260
how is pulseless VT or VF managed?
- Perform emergency cardioversion when there are signs of haemodynamic compromise - Administer amiodarone for patients who are haemodynamically stable. - Refer to a specialist who may provide an implantable cardioverter defibrillator (ICD), in addition to a sotalol or amiodarone in combination with a standard beta-blocker.
261
how is torsades de pointes managed?
magnesium sulphate
262
how is brugada syndrome managed?
implantable cardioverter defibrillator
263
what are the major manifestations of rheumatic fever according to the revised Jones criteria?
- Carditis e.g. murmurs, cardiomegaly, cardiac failure, pericarditis, myocarditis. - Polyarthritis: that is fleeting and affecting large joints - Chorea - Erythema marginatum - Subcutaneous nodules
264
what are the minor manifestations of rheumatic fever according to the revised Jones criteria?
- Fever - Arthralgia - Raised CRP - Leucocytosis - First degree AV block - Previous rheumatic fever
265
how is rheumatic fever managed?
- Offer oral phenoxymethylpenicillin 500 mg four times daily for 1 week. - Erythromycin or clarithromycin is used if the patient is allergic to penicillin
266
what are the risk factors for developing varicose veins?
- Female gender - Pregnancy - Previous DVT - Obesity - Family history - Occupation with prolonged standing
267
how are varicose veins diagnosed?
- assesses for reversed flow - roughly, valve closure time >0.5 second is indicative of reflux, while valve closure time >1.0 second is indicative of reflux in the deep system
268
how are varicose veins managed?
- Offer endothermal ablation and endovenous laser treatment of the long saphenous vein - If endothermal ablation is unsuitable, offer ultrasound guided foam scleropathy - If ultrasound guided foam scleropathy is unsuitable, offer surgery
269
what are the clinical features of superficial thrombophlebitis?
- painful - tender - cord-like structure - associated redness and swelling.
270
what are the causes of distributive shock?
- sepsis - anaphylaxis -brainstem or spinal injury
271
what are the causes of cariogenic shock?
- myocardial infarction - tachyarrhythmias - bradyarrhythmias - toxic substances - non-adherence with salt/fluid intake or medications - excessive rise in blood pressure - infection - acute mechanical causes
272
what are the causes of hypovolaemic shock?
- haemorrhagic causes include gastrointestinal bleeding and trauma - Non-haemorrhagic causes include burns and diabetic ketoacidosis.
273
what are the causes of obstructive shock?
- pulmonary embolism - cardiac tamponade - tension pneumothorax
274
how should suspected shock be assessed initially?
- urgent ABCDE assessment - ABG - Fluid rests immediately - measure temp - measure blood glucose
275
what are the diagnostic features of shock?
- hypotension - tachycardia - poor peripheral perfusion - oliguria - mental state change - fever - chest pain - dyspnoea - hypoxaemia - hypothermia
276
what is seen on ABG in shock?
- metabolic acidosis with negative base excess | - raised lactate
277
how should all shock be managed initially?
- airway management - give oxygen as required - IV fluids e.g. normal saline or hartmann's - give blood products if haemorrhage shock - give vasopressor or inotrope if not responding to fluids - manage underlying causes
278
how should cardiogenic shock be managed?
- cautious fluid resus - IV furosemide - vasodilator (GTN) - vasopressor and inotrope
279
how should haemorrhagic shock be managed?
- MHP - use blood products - reverse anti-coagulation - IV TXA - vasopressor
280
how should obstructive, non-haemorrhagic hypovolaemic or distributive shock be managed?
- treat cause - give crystalloids - give vasopressors and inotropes
281
what are the causes of acute digoxin toxicity?
- Overdose after suicide attempt - Medication dosing error - Malicious intent (homicidal poisoning).
282
what are the causes of chronic digoxin toxicity?
- Chronic digoxin over-medication - Increased gastrointestinal absorption - Decreased renal clearance due to renal insufficiency or drugs - Displacement of digoxin from protein-binding sites - Conditions that increase susceptibility to digoxin - drugs
283
what are the risk factors for developing digoxin toxicity?
- Age >55 - Decreased renal clearance - Hyper/hypokalaemia - Hypomagnesaemia - Hypercalcaemia - Hypothyroidism - Use of other drugs e.g. amiodarone, clarithromycin, ciclosporin, itraconazole, propafenone, quinidine, spironolactone, verapamil, diltiazem, ketoconazole, vinblastine, doxorubicin, reserpine and erythromycin
284
what are the clinical features of digoxin toxicity?
- Presence of risk factors - Digoxin exposure - Nausea, vomiting and diarrhoea - Abdominal pain - Anorexia - Lethargy and weakness - Confusion - Disturbances of colour vision: tendency to perceive yellow halos (xanthopsia) around objects - Blurred vision and diplopia - Palpitations - Syncope and dyspnoea - Arrhythmias
285
how is acute digoxin ingestion with low to moderate toxicity managed?
- 1mg/kg activated charcoal, to a maximum of 4 doses, to be given within 6-8 hours of ingestion - Supportive care
286
how is chronic digoxin ingestion with low to moderate toxicity managed?
-supportive care
287
when should digoxin immune Fab be given?
- symptomatic bradyarrhythmias - ventricular dysrhythmias - any patient with digoxin overdose and potassium concentrations >5.0 millimol/L (>5.0 mEq/L - acute ingestion of >4 mg in a healthy child (or 0.1 mg/kg) - acute ingestion of >10 mg in a healthy adult - serum concentration of ≥12.8 nanomol/L ( ≥10 nanograms/mL) 4-6 hours after ingestion (steady state) - serum concentration of ≥19.2 nanomol/L (≥15 nanograms/mL) at any time.
288
what are the adverse effects of ACEi?
- Hypotension - Persistent dry cough - Hyperkalaemia - Renal Failure - Angiodema (more common in Afro-Caribbean patients) - Anaphylactoid reactions.
289
in which patients should ACEi be used cautiously?
- Avoid in renal artery stenosis - Avoid in acute kidney injury - Caution in pregnancy and breastfeeding - Caution in chronic kidney disease.
290
with which other drugs do ACEi interact?
- Increased risk of hyperkalaemia with potassium supplements and potassium sparing diuretics - Increased risk of renal failure with NSAIDs
291
what are the adverse effects of ARBs?
- Hypotension - Hyperkaleamia - Acute renal failure.
292
in which patients should ARBs be used cautiously?
- Avoid in renal artery stenosis - Avoid in acute kidney injury - Caution in pregnancy and breastfeeding - Caution in chronic kidney disease.
293
with which other drugs do ARBs interact?
- Increased risk of hyperkalaemia with potassium supplements and potassium sparing diuretics - Increased risk of renal failure with NSAIDs
294
what are the adverse effects of dihydropyridine CCB?
- Ankle swelling - Flushing - Headache - Palpitations.
295
in which patients should dihydropyridine CCBs be used cautiously?
- Avoid in unstable angina | - Avoid in severe aortic stenosis.
296
with which other drugs do dihydropyridine CCBs interact?
- Antihypertensives - Statins - Antiepileptics - Digoxin - Theophylline.
297
what are the adverse effects of beta-blockers?
- Fatigue - Cold extremities - Headache - GI disturbances - Sleep disturbance and nightmares - Impotence in males
298
in which patients should beta-blockers be used cautiously?
- Avoid in asthma due to bronchospasm - Avoid in heart block - Caution in heart failure - Caution in haemodynamic instability - Caution in hepatic failure.
299
with which other drugs do beta-blockers interact?
Verapamil and diltiazem
300
what are the adverse effects of alpha-adrenoreceptor blockers?
- Postural hypotension - Dizziness - Syncope.
301
in which patients should alpha-blockers be used cautiously?
-Avoid in patients with postural hypotension.
302
with which other drugs do alpha-blockers interact?
- Antihypertensives | - Phosphodiesterase-5 inhibitors.
303
what are the adverse effects of hydralazine?
- Lupus-like syndrome - Angina pectoris - Headache and flushing, - Gastrointestinal disturbances.
304
in which patients should hydralazine be used cautiously?
- Avoid with acute porphyrias - Avoid with systemic lupus erythematous - Avoid with dissecting aortic aneurysm - Caution with cerebrovascular disease - Caution with coronary artery disease.
305
what are the adverse effects of loop diuretics?
- Dehydration - Hypotension - Low electrolyte state - Hearing loss and tinnitus as it blocks a Na+K+2Cl- transporter that regulates endolymph composition in the inner ear.
306
where in the nephron do loop diuretics act?
-thick ascending limb of the loop of henle
307
in which patients should loop diuretics be used cautiously?
- Avoid in patients with severe hypovolaemia or dehydration - Caution in patients with hepatic encephalopathy where hypokalaemia can worsen coma - Caution in patients with hypokalaemia and/or hyponatraemia - Caution in patients with gout as they inhibit uric acid excretion.
308
with which other drugs do loop diuretics interact?
- Reduced urinary excretion of lithium - Reduce urinary excretion of digoxin with increased risk of digoxin toxicity - Reduce urinary excretion of aminoglycosides with increased risk of ototoxicity or nephrotoxicity of aminoglycosides.
309
where in the nephron do thiazide diuretics act?
-distal convoluted tubule
310
what are the adverse effects of thiazide diuretics?
- Hyponatraemia - Hypokalaemia - Erectile dysfunction - Rarely agranulocytosis - Rarely pancreatitis.
311
in which patients should thiazide diuretics be used cautiously?
- Avoid in patient with hypokalaemia and hyponatraemia - Avoid in patients with hypercalcaemia - Avoid in patients with Addison’s disease - Caution in patients with gout due to reduced uric acid excretion.
312
with which other drugs do thiazide diuretics interact?
- Diuretics | - Reduced efficacy by NSAIDs.
313
what are the adverse effects of potassium sparing diuretics?
- GI upset - Hypotension - Urinary symptoms - Electrolyte disturbances.
314
in which patients should potassium sparing diuretics be used cautiously?
- Avoid in severe renal impairment - Avoid in hyperkalaemia - Avoid in hypovolaemia.
315
with which other drugs do potassium sparing diuretics interact?
- Potassium supplements - Aldosterone antagonists - Altered renal clearance of digoxin and lithium.
316
what are the adverse effects of adolesterone antagonists?
- Hyperkalaemia, leading to muscle weakness, arrhythmias and cardiac arrest - Gynaecomastia as it acts on progesterone and oestrogen receptors - Stevens-Johnson syndrome (bullous skin eruption).
317
in which patients should aldosterone antagonists be used cautiously?
- Avoid in patients with renal impairment - Avoid in patients with hyperkalaemia - Avoid in patients with Addison’s disease (who are aldosterone deficient) - Avoid in pregnancy or lactating women as it can cross the placenta.
318
with which other drugs do aldosterone antagonists interact?
- Increased risk of hyperkalaemia with potassium-elevating drugs - Increased risk of hyperkalaemia with potassium supplements.
319
what are the adverse effects of calcium gluconate?
- Cardiovascular collapse if administered too fast | - Local tissue damage if given into subcutaneous tissue.
320
what are the adverse effects of nitrates?
- Flushing - Headaches - Light-headedness - Hypotension - Tolerance - Methaemoglobinaemia in overdose.
321
in which patients should nitrates be used cautiously?
- Avoid in patients with severe aortic stenosis due to risk of cardiovascular collapse - Avoid in patients with hypotension.
322
with which drugs do nitrates interact?
Phosphodiesterase 5 inhibitors.
323
what are the adverse effects of nicorandil?
- Flushing - Dizziness - Headache - Nausea and Vomiting - Hypotension - Ulceration of genitals, eyes and skin.
324
in which patients should nicorandil be used cautiously?
- Avoid in patients with poor left ventricular function - Avoid in patients with hypotension - Avoid in patients with pulmonary oedema.
325
with which drugs do nicorandil interact?
Enhanced hypotensive effects with phosphodiesterase 5 inhibitors.
326
what are the adverse effects of digoxin?
- Bradycardia - GI disturbance - Rash - Dizziness - Blurred or yellow vision - Digoxin toxicity causing a range of life threatening arrhythmia.
327
in which patients should digoxin be used cautiously?
- Avoid in heart block and arrhythmias due to worsening of conduction abnormalities - Caution in renal failure as digoxin is eliminated by kidneys - Caution in hypokalaemia, hypomagnesaemia and hypercalcaemia due to increased risk of digoxin toxicity.
328
with which drugs do digoxin interact?
- Loop and thiazide diuretics increase risk of digoxin toxicity due to hypokalaemia - Amiodarone, calcium channel blockers, spironolactone and quince all increase plasma concentration of digoxin and therefore increase toxicity.
329
what are the adverse effects of class 1 antiarrhythmics?
- Disopyramide causes blurred vision, dry mouth, constipation and urinary retention - Lidocaine causes drowsiness, disorientation and convulsions.
330
in which patients should class 1 antiarrhythmics be used cautiously?
- Avoid in bundle branch block - Avoid in AV block - Avoid in long QT syndrome - Caution in atrial flutter - Caution in atrial tachycardia - Caution in heart failure - Caution in myasthenia gravis - Caution in prostatic enlargement.
331
what are the adverse effects of class 2 antiarrhythmics?
- Bronchoconstriction - Bradycardia - Hypotension - Hypoglycaemia.
332
in which patients should class 2 antiarrhythmics be used cautiously?
- Avoid in asthma - Avoid in heart block - Avoid in hypotension - Caution in heart failure - Caution in COPD - Caution in diabetes mellitus - Caution in portal hypertension.
333
with which drugs do class 2 antiarrhythmics interact?
- Adrenaline - Noradrenaline - Amiodarone - Diltiazem - Ergometrine - Flecainide - Lidocaine - Propafenone - Verapamil.
334
what are the adverse effects of amiodarone?
- Torsade de pointes - Hypotension - Optic neuritis - Pneumonitis - Hepatitis - Photosensitivity - Grey discolouration - Hyperthyroidism due to its iodine content.
335
in which patients should amiodarone be used cautiously?
- Avoid in patients with severe hypotension - Avoid in patients with heart block - Avoid in patients with active thyroid disease.
336
with which other drugs does amiodarone interact?
- Increases plasma concentration of digoxin - Increases plasma concentration of diltiazem and verapamil - Antipsychotics, which prolong QT interval, causing torsade de pointes.
337
what are the adverse effects of sotalol?
- Torsade de pointes - Bradycardia - Bronchospasm - Fatigue - Headaches - Hyperglycaemia.
338
in which patients should sotalol be used cautiously?
- Avoid in asthma - Avoid in cardiogenic shock - Avoid in hypotension - Avoid in bradycardia - Caution in diabetes - Caution in first degree AV block.
339
with which drugs does sotalol interact?
- Adrenaline | - Noradrenaline
340
what are the adverse effects of non-dihydropyridine CCBs?
- Constipation - Bradycardia - Heart block - Cardiac failure - Hot flushes - Headache - Ankle oedema.
341
in which patients should non-dihydropyridine CCBs be used cautiously?
- Avoid in patient with AV nodal conduction delay in whom they may provoke complete heart block - Avoid in patients with unstable angina as vasodilation causes increase in contractility and tachycardia which increase oxygen demand - Avoid in severe aortic stenosis as they may provoke collapse. - Caution in patients with poor left ventricular function as they can precipitate or worsen heart failure.
342
with which other drugs do non-dihydropyridine CCBs interact?
-beta blockers
343
what are the adverse effects of anti-muscarinincs?
- dry mouth - tachycardia - urinary retention - blurred vision - drowsiness - confusion.
344
in which patients should anti-muscarinics be used cautiously?
- angle-closure glaucoma | - Caution with arrhythmias
345
with which other drugs do anti-muscarinics interact?
-TCAs
346
what are the adverse effects of adenosine?
- Bradycardia and asystole - Sinking feeling in chest accompanied by breathlessness and a sense of impending doom - Bronchospasm
347
in which patients should adenosine be used cautiously?
- Avoid in hypotension - Avoid in coronary ischaemia - Avoid in decompensated heart failure - Avoid in asthma - Caution in COPD - Caution in patients who have had a heart transplant.
348
with which other drugs does adenosine interact?
- Dipyridamole blocks cellular uptake of adenosine which prolongs and potentiates its effect - Theophylline is a competitive antagonist of adenosine receptors and reduce its effect.
349
what are the adverse effects of statins?
- Headache - GI disturbances - Muscle ache - Myopathy - Rhabdomyolysis - Rise in ALT.
350
in which patients should statins be used cautiously?
- Caution in hepatic impairment - Caution in renal impairment - Avoid in pregnancy or with breastfeeding.
351
with which drugs do statins interact?
-Reduced metabolism by cytochrome P450 inhibitors such as amiodarone, diltiazem, fluconazole, macrolides.
352
what are the adverse effects of aspirin?
- GI irritation, ulceration and haemorrhage - Hypersensitivity reactions including bronchospasm due to overproduction of leukotrienes - Tinnitus
353
in which patients should aspirin be used cautiously?
- Avoid in children under 16 years due to risk of Reye’s syndrome - Avoid in aspirin hypersensitivity - Avoid in third trimester of pregnancy where prostaglandin inhibition may lead to premature closure of ductus arteriosus - Caution with peptic ulceration - Caution with gout.
354
with which drugs do aspirin interact?
Increased risk of bleeding with other anti platelets agents and anticoagulants.
355
what are the adverse effects of clopidogrel?
- Bleeding - GI upset including dyspepsia, pain and diarrhoea - Thrombocytopenia.
356
in which patients should clopidogrel be used cautiously?
- Avoid in active bleeding - Stop 7 days before elective surgery - Caution in patients with renal and hepatic impairment.
357
with which other drugs does clopidogrel interact?
- Reduced efficacy with P450 inhibitors including omeprazole, quinolones, erythromycin, antifungals, SSRIs - Increased risk of bleeding with anti platelets, anticoagulants or NSAIDs.
358
what are the adverse effects of dipyradimole?
- Headache - Flushing - Dizziness - GI symptoms - Increased risk of bleeding - Thrombocytopenia.
359
in which patients should dipyradimole be used cautiously?
- Caution in patients with ischaemic heart disease - Caution in aortic stenosis - Caution in heart failure.
360
with which drugs does dipyradimole interact?
- Increased risk of cardiac arrest with adenosine as it inhibits cellular uptake of adenosine - Increased risk of bleeding with anti-platelets and anticoagulants.
361
what are the adverse effects of LMWH?
- Bleeding - Injection site reactions - Thrombocytopenia.
362
in which patients should LMWH be used with caution?
- Caution with clotting disorders - Caution with severe uncontrolled hypertension and renal impairment - Caution after surgery or trauma
363
what are the adverse effects of warfarin?
- Bleeding especially in genetically susceptible individuals who have lower CYP2C9 activity - Skin necrosis - Blue-toe syndrome - Liver dysfunction.
364
in which patients should warfarin be used cautiously?
- Avoid in patients at immediate risk of haemorrhage - Avoid in pregnancy as it causes fetal malformations - Caution in liver disease where patients are less able to metabolise drug and are at risk of over-anticoagulation/bleeding.
365
which factors increase the effect of warfarin?
- drugs that inhibit hepatic drug metabolism (macrolides and azoles) - drugs that inhibit the reduction f vitamin K (cephalosporins) - drugs that suppress intestinal flora that synthesise vitamin K sulphonamides) - drugs that interfere with platelet function - liver disease
366
which factors lessen the effect of warfarin?
- drugs that induce hepatic metabolism (aminoglycosides) - vitamin K - drugs that reduce absorption (cholestyramine) - pregnancy
367
what are the adverse effects of factor 2a inhibitors?
- Abnormal hepatic function - Haemorrhage - Anaemia - Gastrointestinal disorders.
368
in which patients should factor 2a inhibitors be used cautiously?
- Avoid with active bleeding - Avoid with antiphospholipid syndrome - Avoid with prosthetic heart valves - Avoid with malignancy - Avoid with oesophageal varices - Avoid with recent surgery - Avoid with peptic ulcer.
369
with which drugs do factor 2a inhibitors interact?
- Carbamazepine - Dronaderone - Ritonavir - St John’s Wart - Triazole antifungals.
370
what are the adverse effects of factor Xa inhibitors?
- Haemorrhage - Anaemia - GI disturbances - Headache - Hypotension.
371
in which patients should factor Xa inhibitors be used cautiously?
- Avoid with active bleeding - Avoid with antiphospholipid syndrome - Avoid with prosthetic heart valves - Avoid with malignancy - Avoid with oesophageal varices - Avoid with recent surgery - Avoid with peptic ulcer.
372
with which drugs do factor Xa inhibitors interact?
- Carbamazepine - Dronaderone - Ritonavir - St John’s Wart - Triazole antifungals.
373
what are the adverse effects of fibrinolytic agents?
- Nausea and Vomiting - Bruising at injection site - Hypotension - Serious bleeding - Allergic reaction - Cardiogenic shock - Cardiac arrest - Cerebral oedema - Arrhythmias.
374
in which patients should fibrinolytic agents be used cautiously?
- Avoid with recent haemorrhage, trauma or surgery - Avoid streptokinase with previous streptokinase treatment as antibodies develop and block its action - Intracranial haemorrhage must be excluded with CT.
375
with which drugs do fibrinolytic agents interact?
- Increased risk of haemorrhage with anticoagulants and anti platelet agents - Increased risk of anaphylactoid reactions with ACE inhibitors.
376
what are the adverse effects of endothelin receptor antagonists?
- Headaches and flushing - Nausea and vomiting - Epistaxis and nasal congestion - Rarely hepatic disorders and sudden hearing loss.
377
in which patients should endothelin receptor antagonists be used cautiously?
- Avoid in idiopathic pulmonary fibrosis | - Caution in anaemia.
378
what are the adverse effects of adrenaline?
- Hypertension - Anxiety - Tremor - Headache - Palpitations - Angina - Myocardial infarction - Arrhythmias.
379
in which patients should adrenaline be given cautiously?
-Caution in patients with heart disease
380
with which drugs does adrenaline interact?
- Widespread vasoconstriction with a beta blocker because its vasoconstriction effect is not opposed by β2-mediated vasodilation - MAOIs such as phenelzine and tranylcypromine increase risk of hypertensive crisis.
381
what are the adverse effects of dopamine?
- Arrhythmia - Tachycardia - Anxiety - Angina pectoris - Tremor - Vasoconstriction - Vomiting.
382
in which patients should dopamine be used cautiously?
- Avoid with phaeochromocytoma - Avoid in with tachyarrhythmia - Caution with hypovolaemia - Caution with hypertension - Caution with hyperthyroidism.
383
what are the adverse of noradrenaline?
- Arrhythmia - Hypertension - Peripheral ischaemia - Dyspnoea - Extravastation necrosis - Headache - Peripheral ischaemia.
384
with which drugs does noradrenaline interact?
- Beta blocker - TCA - MAO inhibitors.

FINALS (18 decks)

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