Cardiology Flashcards
(153 cards)
1
Q
CVS DDx for chest pain
A
- acute coronary syndrome
- angina
- aortic dissection
- arrhythmia
- valve disease
- acute pericarditis (pleuritic)
- cardiac tamponade
2
Q
DDx for pleuritic chest pain
A
- pneumonia
- PE
- pneumothorax
- pericarditis
- viral pleurisy
- lung cancer
- pleural effusion
3
Q
GI DDx for chest pain
A
- GORD
- Peptic ulcer disease
- gallstones
- pancreatitis
4
Q
Other DDx for chest pain (apart from CVS, pleuritic, GI)
A
- MSK: trauma, costochondritis
- anxiety: panic attack
- functional: chest wall syndrome
- shingles. Pain may come before rash
5
Q
DDx for bilateral leg swelling
A
- venous insufficiency
- right heart, liver or renal failure
- dependent oedema: effect of gravity when sitting for a prolonged period
- pregnancy
- calcium channel blockers
- hypothyroidism
6
Q
DDx for unilateral leg swelling
A
- venous insufficiency
- DVT
- Cellulitis
- lymphoedema
7
Q
Causes of atrial fibrillation
A
PIRATES
* Pulmonary: PE, pleural effusion, COPD, lung cancer, pneumonia
* Ischaemic heart disease: HTN, HF, cardiomyopathy, pericardial disease, myxoma
* Rheumatic valve disease and mitral stenosis
* Alcohol, smoking, caffeine
* Thyrotoxicosis
* Electrolyte abnormalities
* Sugar (diabetes), sepsis
8
Q
Epidemiology of atrial fibrillation
A
- most common arrhythmia, affecting 10% over 80 years old
- more common in men
9
Q
Symptoms of atrial fibrillation
A
- palpitations
- syncope
- SOB
- angina, reflecting age-related ischaemia
- 20% are asymptomatic
10
Q
Signs of atrial fibrillation
A
- tachycardia
- irregularly irregular pulse
- hypotension
11
Q
Investigations in atrial fibrillation
A
ECG
* absent P waves
* irregularly irregular RR interval
Blood
* FBC: anaemia may exacerbate HF
* U+E and TSH to look at cause
* Investigate other CV risk factors: lipids, glucose
* LFT and coag pre-warfarin
Imaging
* trans-thoracic echo
* CXR: may show HF
12
Q
Indications for thrombophylaxis in atrial fibrillation
A
- consider in all patients with chronic AF with a CHA2DS2-VASc >= 1 and weigh against bleeding risk with ORBIT score
- important in any patient undergoing cardioversion
13
Q
What drugs are used for thrombophylaxis in AF
A
- Direct oral anticoagulants
- Warfarin
14
Q
Mechanism of action of DOACs
A
- thrombin inhibitor: dabigatran
- factor Xa inhibitors: rivaroxiban, apixaban, edoxaban
15
Q
Indication for DOACs
A
- non-valvular AF
- DVT
- PE
16
Q
Mechanism of action of warfarin
A
- vitamin K antagonist which works by inhibiting vitamin K1 reductase = reduces hepatic synthesis of clotting factors 2, 7, 9 & 10
- onset takes a few days as clotting factors have half-life up to 80 hrs
17
Q
Management of patients on warfarin
A
- check FBC, LFT and coag at baseline
- check INR initially after 48 hrs, then daily until in range (aim for 2.5 - 3.5)
- monitor INR monthly
18
Q
Contraindications for warfarin
A
- bleeding disease
- haemorrhagic stroke
- active PUD
- pregnancy
- severe HTN
19
Q
Drug interactions with warfarin
A
**Agents which raise levels
* abx: macrolides, metronidazole, ciprofloxacin, isoniazid
* CV: statins, amiodarone
* Psych: SSRIs, valproate
* omeprazole
* liver disease
* diet: acute alcohol, grapefruit, cranberry juice
Enzyme inducers lower levels (PC-BRAS)
* Phenytoin
* Carbamezapine
* Barbiturates
* Rifampicin
* Chronic Alcohol
* St Johns wort and smoking
Aspirin and NSAIDs
* increased bleeding due to antiplatelet effect**
20
Q
Side effects of warfarin
A
- bleeding
- GI: nausea, vomiting, diarrhoea
- hepatic: jaundice, hepatic jaundice
- skin necrosis, especially with protein C or S deficiency
21
Q
Rate control management in AF
A
1st line options
* beta blocker: metoprolol, bisobrolol
* rate-limiting CCB: verapamil, diltiazem
* consider digoxin if they are stationary
2nd line. combine any 2 of
* beta blocker, diltiazem, and/or digoxin
22
Q
Rhythm control management in AF
A
Electrical cardioversion
* preferred choice if there is haemodynamic instability: SBP<90, syncope, acute HF, MI
* shock carried out under short-acting general anaesthetic, followed by second shock with higher joules if no success with first
Pharmocological cardioversion
* indications: if symptoms are milder and situation is less urgent. Bolus followed by infusion if AF continues. Again anticoagulate first.
* Flecainide or propafenone IV (class IC) if there is no structural heart disease.
* Amiodarone (class 3) if there is structural or IHD. given through central line
Maintaining long term rhythm control post cardioversion
* 1st line = beta blocker
* other options: amiodarone, sotalol, flecainide, propafenone
23
Q
Complications of AF
A
- stroke
- acute HF and pulmonary oedema
- cardiomyopathy and heart failure
24
Q
What is a supraventricular tachycardia
A
tachycardia due to faulty impulse formation or conduction which is sustained by tissue about the ventricle
25
signs and symptoms of SVT
* palpitaions
* dizziness
* SOB
* chest pain
26
Investigations for SVT
ECG
* HR>100 bpm
* QRS: narrow complex. wide in WPW
* P waves: sinus tachy = +ve in all leads except aVR; atrial tachy = inverted (ectopic), varying morphology (multifocal), sawtooth (atrial flutter), or absent (AF); junctional tachy = inverted, hidden within QRS and/or following QRS
Echo
* usually normal
* if there is LVF, then increased risk of sudden cardiac death and class 1 drugs are contraindicated
27
Acute management of SVT
* Vagal maneuvers: carotid sinus massage
* IV drugs: 1st line adenosine, 2nd line verapamil, 3rd line beta blocker, flecainide, or amiodarone
* if haemodynamically unstable or atrial flutter, 1st line synchronised electrical cardioversion
28
ECG findings in ventricular tachycardias
* HR is usually 150-250
* broad QRS (>0.12s)
* QRS complex can be monomorphic or polymorphic
* signs of AV dissociation
29
Management of ventricular tachycardia
In cardiac arrest
* VF and pulseless VT are shockable rhythms
If there is a pulse VT is treated with
* synchronised DC shocks if unstable, followed by amiodarone 300mg IV over 20 mins, further shock, then amiodarone 900mg over 24h
* straight to amiodarone IV if stable
30
What is sinus bradycardia?
sinus rhythm <60 bpm
31
Causes of sinus bradycardia
* myocardial: inferior MI, myocarditis
* CV drugs: beta blockers, alpha agonists, rate limiting CCBs, digoxin, amiodarone
* CNS drugs: opioids, benzodiazapine
* sick sinus syndrome
* metabolic: hyperkalaemia, hypothyroidism, hypothermia
* physiological staes: high levels of fitness, pain
* anorexia nervosa
* cushings reflex: response to increased ICP
32
What is sick sinus syndrome
* aka sinus node dysfunction
* usually due to idiopathic SA node fibrosis
33
Presentation of sinus bradycardia
often asymptomatic. otherwise:
* syncope
* fatigue
* palpitations
34
Causes of atrioventricular (AV) block
* idiopathic
* RCA infarct (as this supplies the AV node)
* myocarditis
* drugs: beta blockers, CCBs, adenosine, digoxin, cholinesterase inhibitors
35
how does type 1 heart block present on an ECG
Prolonged PR interval (>0.2 seconds = 5 small squares)
NOTE: no treatment required
36
How does 2nd degree heart block - Mobitz type 1 present on an ECG
Progressively prolonged PR interval until a P wave fails to transmit to the ventricles
NOTE: no treatment required
37
How does 2nd degree heart block - Mobitz type 2 present on an ECG
constant PR interval but intermittent failure to transmit to the ventricles
NOTE: high risk of progression to 3rd degree block so often requires pacemaker treatment
38
How does 3rd degree heart block present on an ECG
* No transmission of P waves into ventricles, with a ventricular escape rhythm taking over
* QRS is usually wide
* HR 20-40
NOTE: this requires a pacemaker
39
Causes of left bundle branch block
* anterior MI (LAD)
* HTN
* myocarditis
* cardiomyopathy
* aortic valve disease
40
How does left bundle branch block present on ECG
* broad QRS (>120ms)
* Dominant S wave in V1
* Broad monophasic R in lateral leads (I, aVL, V5-6)
* Absence of Q waves in lateral leads
* Prolonged R wave peak time >60ms in leads V5-6
41
Causes of right bundle branch block
* increased RV pressure: primary pulmonary HTN, cor pulmonale
* acquired heart disease: anterior MI (LAD), myocarditis, cardiomyopathy
* congenital
* iatrogenic e.g. cardiac catheterisation
* can also be a normal ECG variant in healthy individuals
42
How does right bundle branch block present on an ECG
* QRS duration >120ms
* RSR' pattern in V1-3 (M shaped QRS complex)
* Wide slurred S wave in lateral leads (I, aVL, V5-6)
43
Acute management of bradycardia
1. atropine 500 mcg IV if there is cardiac ischaemia, syncope, SBP <90, or HF
2. Further measures if there is inadequate response or risk of asystole: further atropine (up to 3mg), transcutaneous pacing, adrenaline infusion, or isoprenaline infusion
3. Definitive management with transvenous and/or permanent pacemaker (PPM)
44
Pathophysiology of stable angina
* cardiac chest pain due to ischaemia
* usually caused by atherosclerosis
45
Epidemiology of stable angina
* affects 1/10 over 65 years old
* more common in men
46
Signs and symptoms of stable angina
intermittent, stable chest pain with 3 classic features (ECG)
* **E**xertion as a precipitant
* **C**onstricting discomfort of anterior chest, which may radate to neck, shoulders, jaw, or arms
* **G**TN or rest provides relief within 5 minutes
3/3 = typical angina, 2/3 = atypical angina, 1/3 = not angina
47
Investigations in stable angina
**Basic tests:**
* bloods: FBC (rule out anaemia), U&E (co-morbid CKD, ACEi baseline), and CVD risk factor investigations including BP, lipids, and glucose
* ECG: often normal, but may show ischaemic changes (Q waves or ST-T changes)
**Diagnostic testing for IHD should be offered to all those with typical/atypical angina or an ischaemic ECG**
* CT coronary angiogram (CTCA) is 1st line
* functional imaging using stress agent if CTCA is non-diagnostic: stress echo, myocardial perfusion scintigraphy, MR perfusion
* invasive angiography if functional imaging if functional imaging non-diagnostic
**For those with known IHD with chest pain of unknown cause, consider:**
* functional imaging
* exercise ECG. NOTE this is NOT recommended by NICE for initial diagnosis of IHD
48
Management of stable angina
**Anti-anginals**
* 1st line: beta blockers and/or CCBs. Use both if one is insufficient
* 2nd line: isosorbide mononitrate, nicorandil, ivabradine, ranolazine. Can be used as a monotherapy or in combination with 1st line
* consider revascularisation if not controlled by 2 drugs. PCI for 1 or 2 vessels; CABG for left main or triple vessel disease.
**Short-acting nitrate**
* GTN spray or sublingual tablet
* use before planned activity and when symptomatic
* if pain continues for 5 minutes after 1st dose, call ambulance and take 2nd dose
* side effects: headache, flushing and light headedness
**CVD prevention**
* aspirin for all (clopidogrel 2nd line), and consider statins and ACEi
* lifestyle changes, through simple advice as part of cardiac rehab, including exercise (30 mins per day but below anginal threshold), healthy weight, stop smoking, and Mediterranean diet
49
Pathophysiology of acute coronary syndrome
rupture of atheromatous plaque in coronary artery --> thrombus formation --> vessel occlusion locally or elsewhere in the heart
50
Types of acute coronary syndrome
* unstable angina: prolonged severe angina, usually at rest, possibly with ECG changes.
* NSTEMI: raised troponins and ischaemic symptoms or ECG changes
* STEMI: raised troponins and ST elevation on ECG
51
Symptoms of acute coronary syndrome
Evaluate chest pain using SOCRATES
* Site: central
* Onset: usually sudden, but can be more gradual
* Character: tight, crushing, but not sharp
* Radiation: left arm, neck, jaw
* Associated symptoms: sweating, clamminess, SOB, dizziness, faint, angor animin (impending sense of doom)
* Timing: duration >15 mins
* Exacerbating factors: exertion, emotion, eating.
* Severity: high
Atypical presentation seen in elderly or diabetics
* little or no chest pain
* SOB
* sweating
* nausea and vomiting
* sometimes no symptoms at all
52
Signs of acute coronary syndrome
* HR and BP may be increased or decreased
* pallor
* S3 or S4 heart sounds (especially in STEMI)
53
Investigations in acute coronary syndrome
**ECG**
* Do immediately, and if negative repeat after 20mins if pain continues or suspicion high
**Troponin T or I**
* test on admission and at 3-6 hrs. troponin peaks at 12-24 hrs, then declines over 10 days
* values >99th centile are diagnostic of acute MI. STEMI diagnosis is initially from the ECG alone so as not to delay treatment
**Other investigations**
* FBC: *anaemia may exacerbate heart strain, and baseline Hb and PLT needed before anticoagulation*
* U+E: *baseline before anticoagulants and ACEi, and screens for co-morbid renal disease from HTN*
* Glucose: *tight control improves outcomes*
* Lipids: *check on admission, as cholesterol can dip 24hrs post-MI*
* CXR: *rule out other causes and check for HF*
* Exercise tolerance test: *consider in low risk patients*
54
ECG findings in STEMI
**Changes over time**
* Acute: peaked T waves (<5 mins) then ST elevation (<20 mins). Resolve in hours to days.
* Within days: Q waves then T wave inversion
* Long term: Q waves, ST changes
**Leads affected based on territory**
* inferior MI (RCA): II, III, aVF
* anterior MI (LAD): V1-4
* lateral MI (circumflex): I, aVL, V5-6
55
ECG findings in NSTEMI or unstable angina
* ST depression and/or T-wave inversion
* unlike STEMI, difficult to localise lesion based on ECG
56
Management of acute coronary syndrome
**Initial medical treatment**
* dual antiplatelet therapy: aspirin and P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel). Loading doses for both
* analgesia PRN: morphine IV and/or nitrates
* other therapies: oxygen if hypoxemic, beta blockers IV if tachycardic/hypertensive (but not if unstable)
**Anticoagulation**
* unfractionated heparin in those going gor immediate or early angiography
* fondiparineux or enoxaparin SC for those without angiograpyh planned
**Reperfusion for STEMI presenting within 12 hrs of onet**
* immediate (within 90-120 mins) primary PCI
* if PCI not available within 120 mins, consider thrombolysis (alteplase, reteplase) and transfer to PCI centre
* patients presenting beyond 12 hrs are essentially managed like NSTEMI
**Reperfusion in NSTEMI or unstable angina**
* angiography +/- revascularisation within 72 hrs if 6 month mortality risk >3% as per GRACE or TIMI score. Revascularisation is usually PCI, but sometimes CABG if left main or triple vessel disease
* immediate PCI if unstable, refractory chest pain, or acute severe heart failure
* conservative management otherwise
**Further management - start BAGS within 24 hrs**
* **B**eta blocker PO, metoprolol, atenolol
* **A**CEi
* maintain **G**lucose <11mmol/L
* **S**tatin
**Further management - Other issues**
* anticoagulation is usually stopped post-PCI, or continued until discharge in those managed without reperfusion. However, it is continued for 3 months in anterior MI
* Discharge on CVD secondary prevention medication and offer cardiac rehab
* avoid NSAIDs, especially diclofenac
57
Prognosis of acute coronary syndrome
1/3 MIs are fatal: 20% pre-hospital, and a further 10% within 30 days
58
Complications of acute coronary syndrome
Electrical
* heart block or sinus bradycardia post anterior MI
* Bundle branch block
* ventricular fibrillation
Structural
* acute mitral regurg
* papillary muscle rupture
* ventricular septal rupture
* ventricular aneurysm
Inflammatory
* peri-infarction pericarditis
* Dressier's syndrome: pericarditis weeks later
Heart failure
59
CVD risk calculation
* 10 year risk of MI or stroke can be quantified using QRISK2 or the Framingham risk equation
* Those with previous CVD automatically have a 10 year risk >30%
60
CVD prevention - lifestyle
* weight loss and dietary change. The Mediterranean diet (fruit, veg, olive oil, fish). Also recommend reducing sugar intake and replacing starch with wholegrains
* Physical activity: 150mins/week moderate activity
* smoking cessation
* reduce alcohol intake: =<14 units/week
61
CVD prevention - medical
Secondary prevention post-ACS
* Beta blocker
* ACEi, aiming for BP 140/90
* Aspirin for life
* Clopidogrel or ticagrelor for 1 year after an ACS
* Statin: high dose e.g. atorvastatin 80mg
62
What is heart failure
1/70
63
What is heart failure
it is when the heart fails to provide adequate blood flow to meet body's needs
64
Types of heart failure
* **LEFT VENTRICULAR FAILURE**
1. heart failure with reduced ejection fraction (HFrEF)
2. heart failure with preserved ejection fraction (HFpEF)
* **RIGHT VENTRICULAR FAILURE**
* **CONGESTIVE HEART FAILURE**
* **HIGH OUTPUT HEART FAILURE**
65
What is HFrEF
* left ventricular ejection fraction <40%
* also known as systolic heart failure
66
Causes of HFrEF
* IHD/MI
* HTN
* Diabetes
* Dilated cardiomyopathy
* valve disease
* arrhythmias
* drugs or alcohol
67
What is HFpEF
* LV relaxation failure --> inadequate filling --> decreased stroke volume despite normal ejection fraction (>= 50%)
* also known as diastolic heart failure
68
Causes of HFpEF
* HTN
* diabetes
* constrictive pericarditis
* cardiac tamponade
* restrictive cardiomyopathy
69
Causes of right ventricular failure
* cor pulmonale: primary lung disease (e.g. COPD) --> vasoconstriction in poorly ventilated lung tissue to correct lower V/Q --> pulmonary HTN --> RVF
* LVF --> pulmonary HTN --> RVF
* pulmonary valve stenosis
70
What is congestive heart failure
heart failure with fluid overload, especially pulmonary oedema
71
What is high output heart failure
Normal heart but increased needs. Due to:
* anaemia
* pregnancy
* hyperthyroidism
72
Respiratory symptoms of LVF
* SOB
* Orthopnea. Aksk how many pillows they sleep with
* paroxysmal nocturnal dyspnoea and nocturnal cough
* pink frothy sputum
* wheeze
73
non-respiratory symptoms of LVF
* Palpitations
* poor exercise tolerance
* fatigue
* reduced weight (cachexia) or increased weight (fluid retention)
74
signs of LVF
* crackles
* S3 heart sound, S4 more common in diastolic HF
* Murmurs
* cachexia
* cold peripheries
* displaced apex
75
Symptoms of RVF
* liver congestion leads to nausea, anorexia, early satiety, right upper quadrant pain
* epistaxis
* nocturia: on lying flat, fluid builds up from legs to kidneys
76
signs of RVF
* raised JVP
* peripheral oedema
* ascites
* hepatomegaly
* right ventricular heave due to pulmonary HTN
77
Investigations for diagnosis of heart failure
* Screen with BNP or NT-proBNP, and proceed to transthoracic echo if elevated. Consider going straight to echo if there is a prior history of MI
* If diagnosis not clear after echo, consider further tests: cardiac MRI, transoesophageal echocardiography
* HFrEF diagnosis: {signs and symptoms of HF} + {echo or MRI evidence of EF <40%}
* HFpEF diagnosis: {signs and symptoms of HF}+{EF>=50%}+{raised BNP/NT-proBNP} + {structural or functional heart disease such as left ventricular hypertrophy or left atrial enlargement}
78
Investigations in heart failure
Bloods
* FBC: anaemia may mimic or exacerbate symptoms
* U+E and LFTs: liver and kidney function can be affected in HF, and they are a differential for fluid retention
* TFT: thyrotoxicosis can cause high output failure, while hypothyroidism may cause symptoms of fatigue and oedema
* investigate cardiac RFs: cholesterol, blood glucose
CXR
* may show cardiomegaly and pulmonary oedema
ECG
* abnormal in 80%
* usually non-specific changes
* LVF: ST depression and T inversion in V5-6
* RVF: ST depression or T inversion in V1-3
79
Lifestyle and preventative measures in heart failure
* refer all stable patients to cardiac rehab
* stop smoking
* flu and pneumococcal vaccination
* monitor weight and fluid balance, advise moderate fluid restriction. Get help if rapid gain
* treat comorbidities such as IHD, AF, and dyslipidaemia
80
Pharmacological management for HFrEF
Most patients are on four agents, all of which except diuretics have a mortality benefit
* ACEi - any one should be offered to all, and titrated to evidence-based dose. ARB if intolerant
* beta blockers - bisoprolol, metoprolol - should also be offered to all and titrated to evidence-based dose
* diuretics - loop (furosemide) or thiazides - if there is fluid overload
* mineralcorticoid receptor antagonists - spironolactone should be added if patient remains symptomatic. Given to block effects of aldosterone on the heart as opposed to diuretic effect
81
Interventional and surgical management in HFrEF
* cardiac resynchronisation therapy
* implantable cardioverter defibrillator
* LV assist devices
* transplant if end-stage and no other options
82
Management of RVF and HFpEF
* Symptomatic relief with diuretics, management of co-morbidities, and lifestyle changes
* long term oxygen therapy is beneficial in cor pulmonale
83
Drug contraindications in HF
* NSAIDs, especially diclofenac. Low dose aspirin is OK
* Steroids
* Most CCBs, especially rate-limiting
* Pioglitazone
* TCAs
* beta agonists
84
Prognosis of heart failure
Death
* usually due to arrhythmia or pump failure
* 30% in 1 year, 50% in 5 years
85
Epidemiology of Aortic stenosis
* most common valve disease
* affects 4% of elderly
86
Causes of aortic stenosis
* calcification
* congenital: bicuspid valve
* rheumatic valve disease
87
Symptoms of aortic stenosis
SAD
* **S**yncope, which may occur on exertion
* **A**ngina
* **D**yspnoea on exertion
88
Signs of aortic stenosis
* ejection systolic murmur: best heard in aortic and left sternal area, radiating to carotids, loud on expiration
* slow rising pulse
* narrow pulse pressure
* non-displaced but sustained/heaving apex, lasting >50% of systole
* aortic thrill
89
Initial tests in aortic stenosis
* Echo with doppler: confirms diagnosis and assesses severity
* ECG: LVH, LBBB, poor R wave progression
* CXR is usually normal, otherwise: LVH, calcified valve, dilated ascending aorta
90
Further investigations in aortic stenosis
* Cardiac MRI, stress testing, angiography or catheterisation if indicated
* Multi-slice CT can help evaluate severity
* BNP may proved prognostic information
91
Medical management of aortic stenosis
* modify cardiovascular risk factors
* treat any secondary heart failure
* 6 monthly echo if severe
92
Surgical management of aortic stenosis
* Surgical aortic valve replacement
* transcatheter aortic valve implantation
* balloon valvuloplasty
93
Complications of aortic stenosis
* LVF or CHF
* Aortic root dilation due to haemodynamic changes around valve
* infective endocarditis
* sudden cardiac death
94
Prognosis of aortic stenosis
* asymptomatic: 1 year mortallity 1%
* symptomatic: 1 year mortality 25% or 50% if high risk
* poor prognostic factors: age, IHD, raised BNP
95
Chronic causes of aortic regurgitation
* congenital: bicuspid valve
* aortic root dilation: Marfan's, Ehlers-Danlos
* Inflammatory: SLE, RA or seronegative arthritis, rheumatic heart disease, syphilis
* appetite suppressants
* HTN
96
Acute causes of aortic regurgitation
* infective endocarditis
* aortic dissection
97
Symptoms of aortic regurgitation
* LVF symptoms: SOB, orthopnea, PND
* Sense of pounding heart beat, worse on lying down on left side
98
Signs of aortic regurgitation
* murmur: high-pitched early diastolic murmuer, aortic and left sternal area
* collapsing pulse
* wide pulse pressure
* hyperdynamic apex beat
* eponymous signs: visible carotid pulsation (Corrigan's sign), head nodding with beat (de Musset's sign), capillary pulsation in nail bed (Quincke's sign)
99
Investigations in aortic regurgitation
* echo is diagnostic
* ECG: LVH
* CXR: LVH, dilated ascending aorta
* multi-slice CT may help visualise aortic root dilation in Marfan's
100
Management of aortic regurgitation
* Manage LVF if present: ACEi (especially in HTN), beta blockers (especially in Marfan's)
* Monitor: regular echo, 6 monthly if severe or every 2 years if mild-moderate
* Surgery indications: severe AR with symptoms or LVF. Threshold is lover if there is underlying disease such as Marfan's or bicuspid valve
101
Primary causes of mitral regurgitation
* mitral valve prolapse (causes 50%)
* calcification
* rheumatic heart disease
* infective endocarditis
* congenital
* papillary muscle rupture due to MI
* appetite suppressants
* trauma
102
secondary causes of mitral regurgitation
* LV dilation due to IHD
* Dilated cardiomyopathy
* HCM
* Aortic regurgitation
103
symptoms of mitral regurgitation
* SOB
* fatigue
* chest pain
* LVF symptoms
* symptoms of AF
104
Signs of mitral regurgitation
* pansystolic murmur heard at apex, radiates to axilla
* hyperdynamic apex beat
* systolic thrill over apex
* soft S1
* LVF signs: S3, crackles
105
Investigations for mitral regurgitation
* **Echo** is diagnostic
**ECG**
* AF
* P-mitrale if in sinus rhythm
* LVH
**CXR**
* enlarged left ventricle and atrium: double right heart border
* valve calcification
**Further tests**
* cardiac MRI, angiography, and cathetisation, if indicated
* BNP may be provide prognostic information
106
Medical management of mitral regurgitation
* manage AF and HF if present
* manage acute MR as acute heart failure with the addition of sodium nitroprusside to reduce afterload, and intra-aortic balloon pump if hypotensive
* 6-monthly follow up and annual echo if severe
107
Surgical management of mitral regurgitation
* indications: symptomatic MR, acute severe MR, or MR complications
* Procedure: open repair is 1st choice. Valve replacement or percutaneous repair are other options
* anticoagulation: 3 months after valve repair or bioprosthetic replacement, lifelong after metallic replacement
108
Complications of mitral regurgitation
* structural changes: left ventricular and atrial enlargement, CHF
* pulmonary HTN
* AF
* infective endocarditis
109
Prognosis of mitral regurgitation
5 year mortality in severe asymptomatic MR: 20%
110
causes of mitral stenosis
* rheumatic valve disease
* calcification
* autoimmune: RA, SLE
* carcinoid syndrome
* congenital
111
Symptoms of mitral stenosis
* SOB, orthopnoea, PND
* Haemoptysis
* pink frothy sputum
* fatigue
* features of AF
* RVF symptoms
* hoarseness from recurrent laryngeal nerve compression
112
signs of mitral stenosis
* mid-diastolic murmur heard at apex with bell. Follows opening snap in early diastole
* loud S1
* Tapping apex beat
* Malar flush
* RVF signs
113
Investigations in mitral stenosis
* Echo is diagnostic
ECG
* AF
* P-mitrale if in sinus rhythm
* RVH
CXR
* enlarged left atrium: double right heart border
* valve calcification
114
Medical management of mitral stenosis
* anticoagulation if there is AF, thrombus in left atrium or prior thrombus
* diuretics or long-acting nitrates for SOB, and beta blockers or rate-limiting CCBs to improve exercise tolerance
* annual echo
115
Surgical management of mitral stenosis
* indications: severe symptoms or complications
* percutaneous balloon mitral commissurotomy is 1st line
* other options: valve replacement
116
Complications of mitral stenosis
* left atrial enlargement --> oesophageal and recurrent laryngeal nerve compression, AF
* pulmonary HTN, RVF, tricuspid or pulmonary regurgitation
* infective endocarditis
117
Location of pain and affected arteries in peripheral vascular disease
* upper 2/3 of calf = superficial femoral artery
* buttock and hip = aortic and iliac artery
* Thigh = iliac or common femoral artery
* Lower 1/3 of calf = popliteal artery
* foot = tibial or peroneal artery
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Signs and symptoms of chronic PVD
Claudication
* predictable, unrelieved pain on exertion caused by ischaemia of the muscles, which is relieved by rest
Critical limb ischaemia
* rest pain, unrelieved by medication for >= 2 weeks and/or evidence of tissue loss (ulcer or gangrene)
* pain is in the feet and toes rather than calves. Worse at night due to reduced gravitational pull
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Fontaine classification for chronic PVD
1. asymptomatic
2. intermittent claudication. 2a if stop >200m, 2b if <200m
3. rest or nocturnal pain
4. necrosis/gangrene
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Signs and symptoms of acute limb ischaemia
Presents with 6 Ps
* Pain at rest
* Pulseless
* Pale
* Paraesthesia
* Perishingly cold
* Paralysis is a late feature suggesting irreversible damage
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Investigations for PVD
**Diagnose with ankle-brachial pressure index (ABPI)**
* the ratio of systolic blood pressure at the ankle and arm, measured using doppler US
* procedure: take after 10 mins at rest, and use the sides with the highest measurements
* Results: roughly<0.9 is claudications, <0.6 is rest pain, <0.3 is impending gangrene
**Cardiovascular examinations**
* ECG
* Lipids
* glucose
* BP
**Duplex US**
* combines usual grayscale US image with colour-doppler US to visualise flow
* helps determine site of disease
**Angiography if surgery considered**
* MR angio is good choice when available
* CT angio is better for showing wall abnormalities
* Intra-arterial digital subtraction angiogram (invasive) = gold standard
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Conservative and medical management of PVD
* Advise patient to keep active. Can refer to exercise rehabilitation programme
* CVD prevention. Clopidogrel is 1st line antiplatelet therapy in PVD
* Foot care
* vasodilator naftidrofuryl can slightly increase walking distance
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Surgical managetment of PVD
Revascularisation
* surgical bypass, radiological angioplasty and stenting
* acute limb ischaemia: heparin IV and then embelectomy
Amputation
* last resort, considered in patients with ulceration and gangrene
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Complications of PVD
* arterial ulcers
* gangrene
* amputation
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Pathophysiology of cardiac tamponade
fluid in pericardial sac accumulates until increased pressure causes reduced ventricular filling and reduced cardiac output
126
Causes of cardiac tamponade
TAMP
* Trauma
* Aortic dissection
* Medical (iatrogenic)
* Pericardial effusion
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Signs and symptoms of cardiac tamponade
* Beck's triad: hypotension, reduced heart sounds, raised JVP
* tachycardia
* pulsus paradoxus: hypotension with inspiration
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Investigations in cardiac tamponade
* ECG: tachycardia, low voltage
* CXR: large cardiac sillhouette
* Echo
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Management of cardiac tamponade
urgent pericardiocentesis
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Causes of HTN
Primary
* essential HTN
* Non-pathologically raised during pain or anxiety
Kidney disease
* chronic kidney disease
* renal artery stenosis
Endocrine
* Conn's
* Cushing's
* Phaemochromocytoma
* Acromegaly
* Hyperparathyroidism
Other
* obstructive sleep apnoea
* pregnancy or pre-eclampsia
* aoarctation of the aorta
Medication (CE-LESS)
* Cyclosporin
* Estrogen (OCP)
* Liquorice
* EPO
* Steroids
* Sympathomimetics
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Signs and symptoms of HTN
* Symptoms of HTN itself are rare, and only occur in severe disease: headache, blurred vision
Symptoms suggesting secondary cause
* postural hypotension
* palpitations
* sweating
Only notable signs is hypertensive retinopathy
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How is hypertensive retinopathy graded
1. Silver wiring and tortuosity
2. AV nipping
3. Cotton wool spots and flame haemorrhages
4. Papilloedema
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Investigations for HTN
* Measure BP
Check for organ effects:
* eyes
* heart: LVF on ECG. CXR and echo are optional
* kidney: urine dip, U+E, protein:creatinine ratio
Calculate 10 year CVD risk by checking
* glucose
* lipids
* using clinic BP measurement
If age<40, investigate underlying causes
* renal artery stenosis: kidney duplex USS
* CKD: urinalysis, U+E
* Endocrine: metadrenalines, cortisol, renin/aldosterone
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Stage 1 HTN criteria
Clinic BP >=140/90 and A/HBPM >=135/85
135
Stage 2 HTN criteria
Clinic BP >=160/100 A/HBPM >=150/95
136
Severe HTN criteria
Clinic BP >=180 systolic or >= 120 diastolic
137
Stepwise medical treatment in hypertension
Step 1: ACEi or ARB or CCB
* ACEi/ARB if <55 yrs old and non-black, or diabetic. Switch to ARB if ACEi causes cough
* CCB if >55yrs and non-diabetic or black
* common drug choices: lisinopril (ACEi), losartan (ARB), amlodipine (CCB)
Step 2: ACEi/ARB +CCB
* ARB not ACEi if black
* Thiazide-like diuretic is an alternative 2nd agent
Step 3: ACEi/ARB + CCB + thiazide-like diuretic
* thiazide-like (indapimide) is preferred to thiazide
Step 4: Diagnose resistant HTN, consider spironolactone
* confirm BP using A/HBPM, check for postural hypotension, check adherance
* spironolactone if K+ =<4.5, alpha or beta blocker if K+ >4.5
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Other considerations for HTN management
* monitor BP annually in clinic
* HTN during pregnancy: labetalol, methyldopa, nifedipine
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BP targets in HTN
* <80 yrs: 140/90
* >= 80 yrs: 150/90
140
Complications of HTN
* All major CVD: MI, stroke, PVD, HF, AF
* hypertensive crisis
* aortic aneurysm +/- dissection
* hypertensive nephropathy
141
Signs of hypertensive crisis
* papilloedema
* retinal haemorrhage
142
Management of hypertensive crisis
* labetalol IV or nitroprusside IV
143
Causes of primary dyslipidaemia
* familial hyperchylomicronaemia (T1)
* familial hypercholesterolaemia (T2a)
* familial combined hyperlipidaemia (T2b)
* familial remnant hyperlipidaemia (T3)
* familial hypertriglyceridaemia (T4)
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Causes of secondary dyslipidaemia
* obesity
* sedentary lifestyle
* diabetes
* endocrine: hypothyroidism, hypopituitarism
* hepatic: alcohol excess, cholestasis
* renal: nephrotic syndrome, CKD
* others: pregnancy, anorexia, gout, antipsychotics
145
Signs of dyslipidaemia
* eyelids: xanthelasma
* eyes: corneal arcus and retinal deposits
* tendon xanthoma
* palmar xanthoma
146
Investigations in dyslipidaemia
Lipid profile
* non-fasting sample is acceptable
* measured variables = total cholesterol, HDL, TG
* apolipoprotein levels may also help assess risk and guide treatment
Other = exclude secondary cause
* kidney disease: U+E, urinalysis
* Others: LFT, TFT, glucose, uric acid
147
Management of dyslipidaemia
* First consider and treat secondary cause: excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease, nephrotic syndrome
* Consider a familial syndrome
* Carry out a full CV risk assessment e.g. with QRISK
* For primary prevention discuss benefits of lifestyle changes, and amange other CV risk factors before offering a stain
* After these steps are taken, most patients still require a statin e.g. atorvastatin 20mg in primary prevention
148
Mechanism of action of statins
HMG-CoA reductase inhibitor --> reduced cholesterol synthesis and increased cholesterol uptake into liver via LDL receptor
149
Examples of statins
* simvastatin
* atorvastatin (1st line)
* rosuvastatin
150
Indications for statins
Isolated high cholesterol is not sufficient, they need factors for increased CVD risk or a familial syndrome
* existing CVD: IHD, stroke, TIA, PVD
* >=10% 10 year risk (QRISK2)
* T1DM and any one of: >40 yrs, >10 yrs duration, nephropathy or other CVD risk factors
* T2DM and >10% 10 year risk (QRISK2)
* CKD
151
Management when using statins
* start once daily in the evening, since that is when most cholesterol is synthesised
LFTs
* check at baseline and 3 and 12 months
* only stop if LFT rise 3x upper limit
Lipid levels
* check at 3 months, aiming for 40% reduction in non-HDL
* Consider increasing dose if not achieved
Myalgia:
* before starting stain: check CK if patient is complaining of muscle pain 7 if 5x upper limit, dont start on statin
* check CK if complaining of muscle pain after starting statin, rule out other causes and stop statin if 5x upper limit
152
Side effects of statins
* myalgia (increased CK)
* hepatitis
* rash
* GI symptoms
* altered sleep
* diabetes
153
Contraindications and interactions of statins
* macrolides
* azoles. stop statins if course is required
* for simvastatin, max 20mg daily if on amlodipine or rate-limiting CCBs
* Grapefruit juice
