Cardiology Flashcards

(179 cards)

1
Q

Non Modifiable CVD risk factors

A

Older age
Family history
Male

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2
Q

Modifiable CVD risk factors

A

Raised cholesterol
Smoking
Alcohol
Poor diet
Lack of exercise
Obesity
Poor sleep
Stress

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3
Q

Which Co-morbidities increase the risk of CVD

A

Diabetes
HTN
CKD
Inflammatory conditions (e.g RA)
Pscyhosis (atypical antipsychotics)

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4
Q

What are the consequences of atherosclerosis

A

Angina
MI
TIA
Strokes
PAD
Mesenteric ischaemia

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5
Q

What is QRISK3?

A

Scoring system for primary prevention of CVD. It determines the risk of stroke or MI in next 10 years.

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6
Q

What is the main primary prevention strategy for CVD?

A

Atorvostatin 20mg at night for pts with CKD, T1DM or with a QRISK score >10%

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7
Q

Significant side effects of statins

A

Myopathy
Rhabdomyloysis
T2DM
Haemorrhagic strokes

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8
Q

Which drugs interact with statins?

A

Macrolide antibiotics - pts should stop statins temporarily when prescribed clarithromycin or erythromycin

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9
Q

Secondary prevention of CVD

A
  1. Antiplatelet medications (e.g aspirin, clopidogrel, ticagrelor)
  2. Atorvostatin 80mg
  3. Atenolol (or bisoprolol)
  4. ACEi (ramipril)
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10
Q

What is dual antiplatelet therapy

A

Aspirin 75mg daily (forever) + Clopidogrel/Ticagrelor (for 12 months)

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11
Q

What is Familial Hypercholesterolemia

A

Autosomal dominant genetic condition causing high cholesterol.

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12
Q

Features of familial hypercholesterolemia

A
  1. FHx of premature CVD (e.g MI <60yrs in first-degree relative)
  2. Very high cholesterol (>7.5mmol/L)
  3. Tendon xanthomata (hard nodules in tendons, often on back of hand or achilles)
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13
Q

Management of Familial hypercholesterolemia

A

Statins

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14
Q

What is angina

A

Narrowing of the coronary arteries leading to reduced blood flow to the myocardium.

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15
Q

Stable vs Unstable Angina

A

Stable = when symptoms are relieved by rest or GTN
Unstable = When symptoms occur randomly or at rest (considered an ACS)

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16
Q

Gold standard investigation for Angina

A

CT Coronary angiogram

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17
Q

What are the 4 principles to the management of Angina

A

RAMP;
Refer to cardiology (urgently if unstable angina)
Advise them about diagnosis, management and when to call ambulance
Medical treatment
Procedural or surgical interventions

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18
Q

Immediate management/Symptomatic relief for Angina

A

GTN - immediate symptom relief. Take GTN when symptoms occur, can repeat after 5 mins but if pain persists, call an ambulance.
+ Aspirin + Statin

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19
Q

Long-term medical management for angina

A

1st line = Beta-blocker +/Or Calcium channel blocker (Use Dihydropyridine e.g amlodipine if with beta-blocker or just Verapamil if not. Verapamil can’t be used with beta-blocker as causes complete heart block)

2nd line = Long acting nitrate e.g Isosorbide Mononitrate OR Ivabridine / Nicorandil / Ranolazine)
- Isosorbide mononitrate should be given as asymmetric dosing intervals to maintain a daily nitrate free time of 10-14hrs to minimise tolerance.

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20
Q

Surgical interventions for Angina and their indications

A
  1. PCI + Coronary angioplasty = this dilates a blood vessel using a balloon/stent. Indication = “proximal or extensive disease” on angiogram and Age <65
  2. CABG - Indications = Severe stenosis and Age >65
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21
Q

Why is PCI + Coronary angioplasty preferred over CABG

A

CABG has a slower recovery and higher complication rate

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22
Q

What is Prinzmetal’s angina

A

Coronary artery spasm typically occuring at rest without evidence of underlying cardiac disease (hence different to unstable angina). May cause ST elevation.
RF = Female,

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23
Q

What is cardiac syndrome X?

A

Angina + Positive exercise test despite normal angiography with no evidence of underlying cardiovascular disease. Commonly occurs in peri/post menopausal women. Difficult to treat.

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24
Q

Definition of Hypertension

A

Persistently raised arterial BP >140/90 in clinic or >135/85 at home

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25
What is considered 'pre-hypertension'
130/85 - 139/89
26
What is malignant hypertension
Acutely, severely elevated BP with new or progressive organ dysfunction. It is a medical emergency. Generally a BP >180/120
27
British Hypertension Society Grading Criteria
Grade 1 (mild) = 140/90 to 159/99 Grade 2 (Moderate) = 160/100 to 179/109 Grade 3 (Severe) = >180/110
28
Risk Factors of essential HTN
FHx Obesity High alcohol consumption High sodium consumption Stress Insulin resistance Low foetal birth weight Age Being male (age <65) or Female (65-74yrs) Black Afrocarribean ethnicity Poor lifestyle
29
Causes of Secondary Hypertension (ROPE)
Renal disease - main cause of HTN. if BP does not respond to treatment, consider renal artery stenosis (also causes hypokalemia) Obesity Pre-eclampsia Endocrine - mainly Conn's syndrome (primary hyperaldosteronism)
30
1st line investigation for Conn's syndrome
Renin:aldosterone ratio blood test - this would show high aldosterone but low renin levels (due to negative feedback)
31
Clinical presentation of HTN
Usually asymptomatic unless very high. Headaches Visual disturbances Seizures Epistaxis
32
Gold standard investigation for diagnosis of HTN
24hr ABPM or home blood pressure monitoring
33
Investigations for new onset HTN (NICE guidance)
Fundoscopy Blood tests (HbA1C, Renal function, Lipid profile, U&Es) ECG Urine ACR + Dipstick (for hypertensive nephropathy)
34
Keith-Wagener classification (Hypertensive Retinopathy)
Stage 1 = Mild narrowing of arterioles + Silver wiring Stage 2 = AV nipping (due to sclerosis of arterioles causing compression of veins where they cross) Stage 3 = Cotton-wool patches, exudates and flame haemorrhages Stage 4 = Papilledema Stage 3 + 4 indicate malignant hypertension!!!!
35
Pharmacological management of HTN
1st line = ACEi / ARB - ARBs should be used when ACEi can't be tolerated due to cough - ACEi should be used as preference in pts with diabetes regardless of age - In pts >55yrs or AfroCarribean descent a CCB should be used 1st line 2nd line = ACEi/ARB + CCB OR ACEi/ARB + Thiazide-like diuretic (indapamide) - Pts >55yrs or Afro-Carribean should try CCB + ARB - Avoid thiazide diuretics in diabetes as worsenes glucose tolerance - CCBs prefered in pts with gout. 3rd line = ACEi/ARB + CCB + Thiazide Diuretic 4th line = Consider adding either Spironolactone (If K+ <4.5) or Alpha/Beta-blocker (K+ >4.5). If no response then refer for specialist input.
36
What is the BP target for adults age <80 with HTN +/- T2DM
<140/90 or ABPM <135/85
37
What is the BP target for adults age >80yrs with HTN
<150/90mmHg (or ABPM <145/95)
38
What is the BP target for pts with CVD + HTN
<130/90mmHg
39
Complications of Hypertension
IHD Cerebrovascular event Hypertensive retinopathy Hypertensive nephropathy HF
40
What monitoring should pts recieving HTN treatment
U&Es - as spirinolactone and ACEi both increase the risk of Hyperkalemia and Thiazide diuretics can cause electrolyte disturbances
41
ACE inhibitors
Rampiril, Lisinopril MOA = inhibits the conversion of angiotensin 1 to angiotensin 2 Side effects = Cough, Angiodema, Hyperkalemia Monitoring = Renal function before starting + after 2wks
42
ARBs
Losartan, Candesartan MOA = Inhibits angiotensin II at the AT1 receptor Side effects = Hyperkalemia
43
Calcium channel blockers
Amlodipine, Felodipine, Diltiazem MOA = Inhibits voltage-gated calcium channels + causes smooth muscle relaxation + reduced force of myocardial contraction Side effects = Flushing, Ankle Oedema, Headaches
44
Thiazide Diuretics
Bendroflumethiazide, Indapamide MOA = Inhibits sodium absorption at the beginning of the DCT Side effects = Hyponatremia, Hypokalemia, Dehydration Monitoring = monitor serum electrolytes
45
Potassium-sparing Diuretics
Spirinolactone, Eplerenone MOA = inhibits aldosterone in the kidneys, causing sodium excretion + potassium reabsorption Side effects = Hyperkalemia *useful if thiazide diuretics are causing hypokalaemia
46
Preload
End diastolic volume. The maximal volume of blood held in the ventricles after atrial systole. (Normal = 130ml)
47
Afterload
Resistance to blood flow - created by the vascular system
48
Risk Factors of HF
Old age Female Obesity Diabetes CKD
49
Causes of HF
IHD Dilated cardiomyopathy Hypertension Valvular heart disease Others = Congenital heart disease, alcohol, drugs, tricuspid imcompetence, pericardial disease, arrythmias
50
Types of HF
Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN. Further divided into; 1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation. 2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS. Right sided;
50
Types of HF
Left-sided; Occurs due to decreased left ventricle function causing a decreased flow of blood out of pulmonary circulation, leading to pulmonary HTN. Further divided into; 1. LV-pEF (Diastolic) - impaired ventricular filling during diastole, E.g Aortic regurgitation. 2. LV-rEF (EF <50%) / Systolic - due to impaired myocardial contraction during systole E.g ventricular dilation or AS. Right sided; This is when decreased right ventricular function causes a systemic HTN leading to oedema. Typically occurs due to left-sided HF. Can be related to Pulmonary HTN, Tricuspid/pulmonary valve disease or Pericardial disease Congestive HF; When both occur
51
Symptoms of HF
Fatigue SOB Exertional dyspnoea Cough +/- pink frothy sputum if pulmonary oedema Orthopnoea PND
52
Signs of HF
1. Pulmonary oedema - Bibasal fine crackles + Pleural effusion + Tachypnoea + Hypoxia + Cyanosis 2. Systemic oedema - Peripheral pitting oedema + tender hepatomegaly + ascites + elevated JVP 3. May have signs of underlying heart disease
53
New York Heart Failure Classification:
Class I = no symptoms + no limitation in ordinary physical activity. Class II = Mild symptoms (SOB/Angina) + Slight limitation during ordinary activity Class III = Marked limitation in activity due to Sx in less than ordinary activity Class IV = Severe limitation. Sx at rest, mostly bedbound
54
Main diagnostic test for HF
pro-BNP (released by cardiomyocytes in response to excessive stretching)
55
Interpretation of Pro-BNP values;
If >2000 = Refer to cardiology urgently If 400-2000 = Refer to cardiology + Echocardiogram within 6 weeks If <400 = HF diagnosis is less likely. Consider alternative
56
Besides from HF, what other conditions cause raised BNP?
Tachycardia Sepsis PE Renal impairment COPD
57
What are the findings on CXR in HF?
Alveolar oedema Batwing opacities (Bilateral perihilar lung shadowing) + Kerley B lines Cardiomegaly Dilated prominent upper lobe vessels + upper lobe congestion Effusion (bilateral + transudative)
58
What lifestyle advice should you give to patients with HF?
Avoid large meals Exercise regularly (20-30 min walk 3-5times per week) If congestive heart failure 1-2 days bed rest per week Annual influenza vaccine + one-off pneumococcal vaccine
59
Medical therapy of Heart failure (in HF- rEF)
1st line = ACEi + Beta-blocker (Rampril + Bisoprolol/carvedilol) 2nd line = Aldosterone antagonist (e.g spirinolactone - must monitor U&Es for hyperkalemia) 3rd line = Consider use of SGLT-2 inhibitors if HF-rEF (dapagliflozin) 4th line = should be initiated by a specialist. options include; > If EF <35% give Ivabridine or Subcubitril-valsartan > If AF is present give Digoxin > If Afro-Carribean descent give Hydralazine + Nitrate > If widened QRS complex = Cardiac resynchronisation 5th line = Palliative. Consider ionotropes / cardiac transplant / hospice
60
Which diuretic is best for symptomatic relief of fluid overload (i.e if a patient has preserved EF)
Furosemide 20mg
61
What is Cor Pulmonale
Right sided HF caused by respiratory disease Most commonly due to COPD but also PE, Interstitial lung disease, CF, Primary pulmonary HTN
62
Pathophysiology of cor pulmonale
Existing pulmonary disease leads to an increased stiffness of pulmonary arteries resulting in pulmonary HTN. This causes an increased afterload in the right ventricle leading to right ventricular hypertrophy and therefore a reduced right ventricle ejection fraction. This leads to a back pressure of blood in the right atrium, vena cava and systemic system (leading to systemic HTN)
63
Clinical features of Cor Pulmonale
Often asymptomatic in early stages. 1. Signs of lung disease = SOB + Exertional dyspnoea + Hypoxia + Cyanosis 2. Signs of R sided HF = Peripheral oedema, Syncope, Raised JVP, S3 gallop, Pan-systolic murmur (tricuspid regurg / Pulmonary HTN) + Hepatomegaly + Ascites.
64
Management of Cor Pulmonale
Treat underlying cause Alleviate hypoxia - with long term oxygen therapy Medical management as for HF
65
Aortic stenosis murmur
Ejection systolic, high-pitched murmur with a cresendo-decresendo pattern heard best over the aortic area with radiation to the carotids. *May have reduced/absent S2 in moderate/severe disease
66
Pulse characteristics in Aortic Stenosis
Slow rising pulse + Narrow pulse pressure (pulse pressure <25% of SBP)
67
Symptoms of Aortic stenosis
Exertional syncope due to difficulty maintaining good blood flow to brain Chest pain SOB
68
Causes of Aortic stenosis
Age related calcification (most common) Bicuspid aortic valve (most common congenital heart disease 1-2%, most common cause in <65yrs) Rheumatic heart disease William's syndrome (supravalvular AS) HOCM (subvalvular)
69
Complications of Aortic stenosis
Left bundle branch block (usually present on ECG)
70
Aortic sclerosis
Thickening / Calcification of the aortic valve without obstruction of blood flow. Consider this when Ejection systolic murmur + No ECG changes + No carotid radiation
71
Mitral stenosis murmur
Mid-diastoic low pitched rubmling murmur, best heard on expiration with pt in the left lateral decubitus position.
72
Signs + Symptoms of Mitral stensosis
Malar flush Haemoptysis / Dyspnoea AF - L atrium struggles to push blood through stenotic valve leading to strain + electrical disruption Low volume pulse Loud S1 + Opening snap (thick valves require large systolic force to shut) Tapping apex beat (palpable closure of mitral valve) ECG changes = P mitrale (late stage sign due to atrial hypertrophy)
73
Causes of Mitral stenosis
Rheumatic heart disease (most common + main complication of rheumatic HD) Congenital Left atrial Myxoma Connective tissue disorder Mucopolysaccharidosis
74
Aortic regurgitation murmur
Early diastolic soft murmur with decrescendo pattern
75
How can you emphasise an aortic regurg murmur?
Get pt sat up, leant forward and hold expiration or handgrip manoeuvre
76
Austin flint murmur
This is the murmur that can be heard in severe AR. It is an early diastolic rumbling murmur heard over the apex. Caused by a backflow of blood through the aortic valve and some over mitral valve (causing it to vibrate)
77
5 Clinical signs of Aortic regurgitation
1. Corrigans sign = visible distension and collapse of carotid arteries in neck 2. De Musset's sign = head bobbing with each heart beat 3. Quincke's sign = pulsations in nail bed with each heartbeat when nail bed is lightly compressed 4. Traube's sign = pistol shot sound heard when stethoscope placed over femoral artery during systole and diastole 5. Mullers sign = Uvula pulsations are seen with each heartbeat
78
Pulse characteristics in Aortic regurgitation
Corrigan's pulse (Collapsing pulse) = rapidly appearing and disappearing pulse at carotid. Also wide pulse pressure
79
Causes of Aortic regurgitation
1. Valvular disease - congenital bicuspid aortic valve, Rheumatic heart disease, Infective endocarditis 2. Aortic root dilation = Aortic dissection, Connective tissue disease (marfans), Aortitis.
80
Main complication of aortic regurg
Heart failure
81
Mitral regurgitation murmur
Pan systolic, high-pitched, whistling murmur with radiation to the left axilla.
82
How to emphasise a mitral regurgitation murmur
Left lateral decubitus position, on expiration
83
Causes of mitral regurgitation
1. Infective endocarditis 2. Acute MI (papillary muscle rupture) 3. Rheumatic heart disease 4. Congenital defect of valve 5. Cardiomyopathy
84
What is the gold standard investigation for Aortic stenosis?
Transoesophageal echocardiogram
85
Gold standard Invx for Mitral stenosis / Regurg and Aortic regurg
Doppler transthroacic echocardiogram
86
Management of acute aortic regurgitation
Medical emergency! Ionotropes + Vasodilators + Aortic valve replacement
87
Management of chronic aortic regurg
If asyptomatic / EF >50% - Yearly review If symptomatic / EF <50% - Aortic valve replacement. if not surgical candidate then vasodiators + ACEi
88
Acute management of Mitral regurg
Emergency mitral valve replacement
89
Management of Aortic stenosis
If asymptomatic then 3-5 year monitoring If symptomatic (or LV dysfunction/+ve exericse tolerance test or valvular gradient >40mmHg) then Aortic valve replacement is needed. If high risk pt then can do a transcatheter replacement (TAVI)
90
Management of symptomatic mitral stenosis
Diuretic + Balloon valvotomy/replacement Treat rheumatic heart disease or AF.
91
What is the normal diameter of the aortic valve
3-4cm
92
what is the diameter of the aortic valve in severe aortic stenosis
<1cm
93
Causative agent of rheumatic fever
Streptococcus pyogenes
94
Clinical features of rheumatic fever
1. Erythema marginatum (rash which quickly dissapears) 2. Sydenham's chorea / st Vitus dance 3. Polyarthritis 4. Carditis + Valvulitis (think mitral stenosis) 5. Subcutaneous nodes 6. Pyrexia
95
Investigations for Rheumatic fever
Bloods = raised inflammatory markers Raised Anti-streptococcal antibody titre
96
Treatment for Rheumatic fever
Oral Penecillin + NSAIDs
97
Diagnostic criteria for Rheumatic fever
Jones criteria; 1. Evidence of recent group A streptococcal infection (e.g +ve throat swab, raised ASO) 2. 2 major or 1 major + 1 minor criteria Major = 'JONES' - Joint involvement - myOcarditis - Nodules (subcutaneous) - Erythema marinatum - Sydenham Chorea Minor = 'Cafe Pal' - CRP raised - Arthralgia - Fever - ESR raised - Prolonged PR interval - Anaemensis of rheumatism - Leukocytosis
98
Causes of pericarditis
1. Mainly idiopathic 2. Viral - Cocksackie B or echo virus, HIV. Very painful 3. Post-MI (Dressler's syndrome) 4. Uremic (secondary to CKD) 5. Bacterial - e.g staphyloccocus aureus (rare) 6. Tuberculosis - usually constrictive pericarditis. pts will have TB symptoms 7. Malignant - secondary to lung/breast/hodgkins lymphoma 8. Other = radiation, fungus, hypothyroidism
99
Risk factors for pericarditis
Male, Age 20-50, autoimmune disease, past cardiac surgery, previous MI, Dialysis
100
Clinical presentation of pericarditis
Chest pain - may be pleuritic in nature + may radiate to neck or shoulders. Typically relieved by sitting forwards, exacerbated by lying flat Pericardial friction rub - best heard at left lower sternal edge with pt leaning forward and expiring Pyrexia + Leukocytosis (if infective) Dyspnoea Tachypnoea Tachycardia
101
ECG changes in pericarditis
Global + widespread changes. 1. ST elevation which is saddle-shaped (concave + upwards) in all leads 2. PR depression in all leads
102
Management of pericarditis
NSAIDs + Colchine (until symptoms resolution or normalisation of inflammatory markers) Treat underlying cause Avoid strenuous physical activity
103
What is brugada syndrome + What is the inheritence?
An inherited (Autosomal dominant) CVD which may present with sudden death. Due to a mutation in the SCN5A gene
104
Features of Brugada syndrome
Convex elevation / Down-sloping ST segment (mainly in V1-V3) Partial RBBB
105
What is the investigation of choice for Brugada syndrome
Injection of flecainide or ajmaline - this will make ECG changes more pronounced.
106
Management of brugada syndrome
implantable cardioverter-defibrillator
107
Features of Tetralogy of Fallot
1. Ventricular septal defect 2. Pulmonary valve stenosis 3. Misplaced aorta 4. Right ventricular hypertrophy
108
If a younger patient is presenting with chest pain on a history of recent viral illness what must you consider as a cause?
Myocarditis
109
Causes of Myocarditis
Viral : Coxsackie, HIV Bacteria : Diptheria, Clostridia Lyme disease Chaga disease Toxoplasmosis Autoimmune Doxarubicin antracycline chemotherapy agent.
110
Clinical Features of myocarditis
Typically younger pt with a history of a recent viral illness with new chest pain. May also have dyspnoea, signs of acute HF (Pulmonary oedema or orthopnoea) and arrythmias
111
Investigation findings in myocarditis
May have elevated tropnin, BNP and inflammatory markers. Tachycardia ECG may show focal ST elevation (e.g V1-V4) or global T wave inversion
112
What are the RF of infective endocarditis
Prior endocarditis Prior heart survery Prosthetic heart valves Valvular heart disease Dental procedures or poor dental hygeine IV catheter or implanted pacemaker IVDU Cardiomyopathy
113
Most common causes of Infective endocarditis
1. Staphylococcus aureus: esp in IVDU 2. Streptococcus viridians: associated with dental procedures or poor dental hygiene 3. Steptococcus epidermis: in first 2 months following prosthetic heart valve surgery 4. Streptococcus bovis: in colorectal cancer
114
Which valve is most commonly affected by Infective endocarditis + what type of murmur does it case?
Mitral valve (regurg) Then aortic valve (regurg)
115
Signs + Symptoms of Infective endocarditis
mneumonic = 'For James' Fever Osler's nodes Roth spots Janeway lesions Anemia Murmur (mitral/aortic regurg) Emboli Splinter haemorrhages
116
Modified Duke's Criteria for IE
Diagnosis based on either +ve Pathological criteria / 2 major criteria / 1 Major + 3 minor / 5 minor Major = 2 x blood cultures +ve / +ve Echocardiogram / New valvular regurg Minor = Predisposing heart condition / Fever >38 / Signs + symptoms / immunological phenomenon e.g GN
117
Management of Infective endocarditis
1st line = Amoxicillin +/- Gentamycin (if pen allergic or severe sepsis/MRSA - Vancomycin + gentamicin) If prosthetic heart valve = Vancomycin + Rifampicin + Gentamicin
118
Poor prognostic factors in infective endocarditis
1. Staphylococcus aureus +ve 2. Prosthetic heart valve 3. Culture -ve 4. Low complement levels
119
Clinical features of cardiac tamponade
Beck's triad; 1. Hypotension 2. Raised JVP 3. Muffled heart sounds Additional: Dyspnoea, Tachycardia, Chest pain, Pulsus paradoxus
120
ECG findings and JVP characteristic in Cardiac tamponade
Absent Y descent on JVP ECG = electrical alternans (alternating amplitude/axis of QRS complex)
121
What diagnosis should be considered in a patient presenting with shock but no tension pneumothorax
Cardiac tamponade
122
Gold standard investigation for cardiac tamponade
Echocardiogram - will show a pericardial effusion / ventricular collapse
123
Management of Cardiac tamponade
Definitive treatment = Thoracotomy Unless pt is in peri-arrest = perform urgent needle pericardiocentesis to buy some time.
124
Gold standard invx for aortic injury
CT with contrast
125
CXR findings in aortic injury
Widened mediastinum (>8cm) Loss of aortic knuckle Tracheal deviation to the R
126
Troponin guidelines in suspected MI
Troponin on admission + repeat after 6-12hours. If <14 after 6+ hours then can exclude NSTEMI/STEMI If 14-30 then should repeat in 3 hours (If inc by 50% then STEMI/NSTEMI) if >30 = STEMI/NSTEMI
127
For how long does troponin stay elevated for
10-14 days
128
Other causes of raised troponin (other than MI)
CKD Sepsis PE Aortic dissection Myocarditis
129
Evolution of ECG changes in STEMI
Initially = tall, pointed upright T waves and ST elevation After a few hours = T wave inversion and R wave voltage decreases. Q waves begin to develop After a few days = ST elevation returns to normal After a few weeks = Pathological Q waves develop and T wave returns to normal
130
Initial management of suspected NSTEMI/STEMI
Aspirin 300mg 02 via nasal cannula 2-4l/min Morphine if severe pain (+/- antiemetic) Nitrates (Sublingual GTN x2) Gain IV access and take bloods. Do ECG.
131
What is a GRACE score
Global registry of acute coronary events Used to estimate 6 month mortality in NSTEMI/Unstable angina
132
Definitive management of NSTEMI/Unstable angina
High risk/haemodynamically unstable = urgent CA + PCI + Dual antiplatelets Intermediate risk = Early coronary angiography + PCI (<72hrs) Low risk = BATMAN 1. Beta-blockers 2. Aspirin 300mg stat 3. Ticagrelor 4. Morphine 5. Anticoagulant (e.g fondiparinaux) 6. Nitrates (E.g GTN - avoid in HTN)
133
Management of STEMI
1. Dual antiplatelet therapy = Aspirin + Presagurel / ticagrelor (or clopidogrel if already taking anticoagulant e.g apixaban) 2. PCI (should be done <2hrs) - give unfractionated heparin before 3. If PCI can't be done, thrombolyse with tPA then recheck ECG after 60 mins.
134
Secondary prevention after MI
Aspirin Anti-platelet (Ticagrelor or Clopidogrel for 12 months) Atorvastatin 80mg Acei Atenolol / beta-blocker Aldosterone antagonist (if HF) e.g spirinolactone
135
Driving rules following MI
Cannot drive for 4 weeks or 1 week if succesfully treated with angioplasty
136
Complications of MI
Think 'Drreaad' Death Regurg (mitral) Rupture (septum or Left ventricular wall) Edema Arrythmia (VT / VF / Bradyarrythmia) Aneurysm (in left ventricle) Dresslers syndrome
137
Dressler's syndrome
Localised immune response leading to pericarditis Occurs 2-6 weeks post MI Sx = pleuritic chest pain, worse on lying flat, low grade fever, pericardial rub.
138
Investigations for Dressler's syndrome
ECG shows saddle-shaped global ST elevation + PR depression Echocardiogram = pericardial effusion
139
Management of Dresslers syndrome
NSAIDs + Pericardiocentesis
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What investigation can you do to confirm if a patient with recent ACS has had a reinfarct
CK-MB
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Causes of Atrial Fibrillation
'MRS SMITH' Mitral Rerug/Stenosis Sepsis MI / IHD Thyrotoxicosis HTN
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Acute rate/rhythm control in AF
Two principles = Rate/rhythm control + Anticoagulation 1. Rate control 1st line (unless a reversible cause, new onset or associated HF) = Beta-blockers. If Beta-blockers don't work/contraindicated then give CCB (diltiazem) or Digoxin (only in sedentary people) 2. Rythm control - if reversible / new onset / associated HF / failure to respond = Cardioversion - This should be done within 48hrs if new onset + stable - Pharmacological = Flecainide / Amiodarone (if structural HD) - Electrical cardioversion - if haemodynamically unstable
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Long-term management in AF
Think Rate/rhythm control + Anticoagulation 1st line = beta-blockers 2nd line = Drondedarone / Amiodarone (if HF of LVF) Anticoagulate with DOACs (e.g apixaban or rivoraxoabn) or give Warfarin if can't have DOAC (i.e severe hepatic disease)
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What food/drink must patients on warfarin avoid?
Vit K rich foods (e.g leafy greens) CYP450 enzyme effectors (e.g Cranberry juice + Alcohol)
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Management of Peri-arrest tachycardia
If life-threatening (i.e haemodynamic instability): 1. Synchronised DC shock. Give up to 3 attempts. must be sedated or anaesthetised if conciouss. 2. If unsuccessful give 300mg Amiodarone IV infusion over 10-20 mins then shock again. Broad complex (>0.12ms); 1. Regular rhythm = Assume VT + Give 300mg Amiodarone IV followed by 24hr infusion 2. Irregular rhythm = seek help (could be AF + BBB or TdP) Narrow complex (<0.12ms); 1. Regular rhythm = Vagal manoevre + IV Adenosine. 6mg, then 12mg, then 18mg. If unsuccessful consider atrial flutter and try beta-blocker / verapamil 2. Irregular = probably AF so consider cardioversion.
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Management of SVT
If Unstable = DC Cardiovert If stable; 1. Valsava manoevre 2. Carotid sinus massage 3. Adenosine - 6mg, then 12mg, then 18mg. 4. Verapamil 5. DC cardioversion
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Contraindications to adenosine
asthma / COPD / Heart failure / Heart block / Severe HTN
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Main side effect of adenosine
Sense of impending doom
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Management of peri-arrest bradycardia
If stable = observe If unstable = 1. IV Atropine 500mcg - can be repeated up to 6 times 3mg total 2. If still no improvement try Ionotropes (e.g noradrenaline / Isoprenaline) or transcutaneous cardiac pacing + defib
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main side effects of atropine
Pupil dilation Dry eyes Urinary retention Constipation Because it is an antimuscarinic
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Management of Acute Left ventricular failure
'pour SOD' 1. 'pour away' or stop their IV fluids 2. Sit up 3. Oxygen 4. Diuretics - IV 40mg Furosemide If severe shock = Ionotropes (dobutamine) or Vasopressors (norepinhephrine) If severe Pulmonary oedema = CPAP *also monitor fluid balance
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Debakey classification of Aortic dissection
Type 1 = originates in ascending aorta, propagates to atleast the aortic arch and possibly beyond (most lethal) Type 2 = Originates in and is confined to ascending aorta Type 3 = Originates in descending aorta, extends distally
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Management of Type B Aortic dissection
Type B = descending aorta Observe, Bed rest + IV Labetalol to prevent progression
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Management of Type A aortic dissection
Type A = ascending aorta Management = HTN control with IV labetaolol + Surgical repair (usually thoracic endovascular aortic repair)
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Main side effects of Nicorandil
Headache Flushing GI ulcers, anal ulceration + eye ulceration
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Which medications commonly reduce hypoglycemic awareness
Beta-blockers
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Anti-dote for dabigatran
Inadrucizumab = monoclonal antibody which binds directly to dabigatran with greater affinity than thrombin.
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Anti-dote for factor Xa inhibitors (Apixaban or Rivoroxaban)
Andexanet alfa
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Anti-dote for Warfarin
Phytomedandione (vitamin K)
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Anti-dote for heparin
Protamine = Peptide which binds and sequesters heparin modules
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Pulseless electrical activity management
1mg Adrenaline ASAP!!! CPR 30:2 Secure airway + ventilate Recheck rhythm after 2 minutes, if no response then repeat 1mg Adrenaline every 3-5 minutes + continue CPR
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Anticoagulation in pts with AF post-stroke
2 weeks post stroke = Warfarin of DOAC (e.g 5mg Apixaban BD)
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what causes a slurred upstroke on QRS complex
Wolf-Parkinson White syndrome
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How can you differentiate between an aortic stenosis and pulmonary stenosis murmur
Pulmonary stenosis is louder on inspiration and does not radiated (unlike AS which radiates to carotids and is loudest on expiration)
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Lateral MI ECG territories and arteries
I, aVL and V5,V6 Left circumflex artery
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Inferior MI ECG territories
II, III, aVF Right coronary artery
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Anterolateral/Septal MI ECG territories + arteries
V1 - V4 sometimes V1-V6 + aVL Left Anterior Descending (LAD)
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Posterior MI ECG territories and Arteries
V1-V3 ST DEPRESSION!!! Also often causes horizontal ST depression, Tall broad R waves, upright T waves + Q waves in posterior leads (V7-V9) Usually left circumflex or right coronary
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HOCM murmur
Ejection systolic murmur, louder on valsalva maneouvre + Quieter on squatting
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cause of worsening renal function in a young pt shortly after starting ACEi for hypertension
Bilateral renal artery stenosis - if ACEi are started before diagnosis of this it can cause significant renal impairment
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How can you distinguish between tricuspid regurgitation and mitral regurg?
Both cause pansystolic murmur however TR is loudest on inspiration and is best heard at left lower sternal border and radiates to right lower sternal border Whereas MR is best heard at apex and in left lateral decubitus position.
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ECG changes in PE
Most often sinus tachycardia is seen S1Q3T3 is seen in 20% of patients. this is when there is a large S wave in lead 1, Q wave in lead 3 and a inverted T wave in Q3.
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ECG findings in hypercalcemia
Short QT interval
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What causes persistent ST elevation months after an MI
Left ventricular thromboembolism/aneurysm
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Loop diuretics side effects
e.g Furosemide, Bumetanide SE's; - Ototoxicity - Hypotension - Hyponatremia - Hypokalemia - Hypomagnesemia - Hypochloremic acidosis - Hypocalcemia - Renal impairment - Hyperglycemia (not as much as thiazide diuretics) - Gout
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Which medications can cause torsades de pointes?
1. Macrolide antibiotics (e.g azithromycin / Clarithromycin) 2. Antiarrythmics e.g amiodarone, sotalol 3. TCAs 4. Antipsychotics 5. erythromycin 6. Chloroquine
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Causes of a raised JVP
Pulmonary HTN / PE / PS / Pericardial effusion (CT) Quantity of fluid (i.e fluid overload) RVF SVC obstruction Tamponade / TR
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Why must ACEi be stopped prior to starting subcutril-valsartan?
Subcutrl-valsartan contains valsartan (ARB). Using both together increases the risk og angiodema as it would result in higher levels of bradykinin (as they both inhibit bradykinin degredation) 36 hour wash out period must be done.