Cardiology Flashcards
Ischaemic heart disease (IHD) / Coronary artery disease (CAD) / Coronary heart disease (CHD)
All interchangeable terms for the condition of inadequate perfusion of the myocardium due to atherosclerosis of the coronary arteries leading to ischaemia & hypo perfusion of myocardial tissue
leading cause of mortality in the UK
incidence ↑ with age
IHD / CAD / CHD risk factors
↑ age smoking hypertension hyperlipidaemia diabetes obesity elicit drug use male gender inacitivity / sedentary lifestyle Family history of IHD
Presentations of IHD / CAD / CHD
angina pectoris (cardinal symptom)
-retrosternal chest pain / pressure
-may radiate to L arm/neck/jaw
dyspnoea, dizziness, palpitations, nausea & vomiting, sweating
Stable vs unstable angina
Stable angina:
- brought on by exercise
- symptoms are reproducible
- symptoms subside with rest or use of GTN
Unstable angine:
- a type of ACS
- symptoms start randomly, including at rest
- not reproducible
Investigations for IHD / CAD / CHD (angina)
resting ECG (often normal) FBC Cholesterol HbA1c coronary angiogram (Gold standard) consider exercise testing
Management of angina pectoris
For all patients with IHD:
- sublingual glyceryl trinitrate (GTN)
- 75mg aspirin
- 80mg statin
1st line:
- beta blockers or calcium channel blockers (CCB)
- CCB monotherapy use rate limiting agents e.g. diltiazem or verapamil
- Beta blocker monotherapy use atenolol/bisoprolol/propanolol
- NB if poor response go to max dose of either drug
2nd line:
- Beta blocker + CCB
- use dihydropyridine CCB e.g. MR nifedipine/amlodipine
- DO NOT combine beta blocker with cerpamil/diltiazem due to risk of severe bradycardia
-less prefers options in combination with either a beta blocker or CCB include long acting nitrates (e.g. isosorbide mononitrate), ivabradine, ranolazine, nicorandil
3rd line:
- CCB + beta blocker + long acting nitrate/ivabradine/ranolazine
- only add 3rd drug if pt awaiting revascularisation e.g. with PCI/CABG
What calcium channel blockers should not be combined with beta blockers
DO NOT combine beta blocker with verapamil/diltiazem due to risk of severe bradycardia
NB ivabradine should also not be used with verapamil or diltiazem
beta blockers are safe to combine with dihydropyridine CCBs e.g amlodipine/nifedipine/felodipine
1st line angina treatment
Beta blockers or calcium channel blockers (CCB)
- CCB monotherapy use rate limiting agents e.g. diltiazem or verapamil
- Beta blocker monotherapy use atenolol/bisoprolol/propanolol
- NB if poor response go to max dose of either drug before adding a further medication
2nd line angina treatment
Add a 2nd drug
Preferred 2nd line treatment
- Beta blocker + CCB
- use dihydropyridine CCB e.g. MR nifedipine/amlodipine
- DO NOT combine beta blocker with verpamil/diltiazem due to risk of severe bradycardia
Other 2nd line options
-Beta blocker or CCB + long acting nitrates (e.g. isosorbide mononitrate)/ivabradine/ranolazine/nicorandil
NB ong acting nitrates (e.g. isosorbide mononitrate)/ivabradine/ranolazine/nicorandil can all be used as monotherapy fi both beta blockers & CCB contraindicated or not tolerated
3rd line angina treatment
Add a 3rd drug
CCB + beta blocker + long acting nitrate/ivabradine/ranolazine
-only add 3rd drug if pt awaiting revascularisation e.g. with PCI/CABG
Nitrate tolerance
pts taking nitrates long term experience reduced efficacy as tolerance develops
asymmetrical dosing should be used to counteract this
pts taking standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance
NB this is not seen with OD MR isosorbide mononitrate
Acute coronary syndrome (ACS)
a spectrum of acute myocardial ischaemia and/or infarction
medical emergency requiring immediate hospital admission
Types of Acute coronary syndrome (ACS)
Unstable angina:
- acute myocardial ischaemia not severe enough to caused detectable quantities of myocardial injury
- troponin not elevated
- no ST elevation
Non-ST elevation myocardial infarction (NSTEMI)
- ↑ troponin
- no ST elevation on ECG
- ECG may show non specific ST depression, T wave inversion
ST segment elevation MI (STEMI)
- troponin ↑
- ST elevation in 2 contiguous leads on ECG
General presentation of Acute coronary syndrome (ACS)
angina at rest/with minimal exertion angina not relieved by rest / GTN spray prolonged angina >20 min severe, persistent/worsening angina chest pain radiating to L arm, neck, jaw diaphoresis, syncope, palpitations, nausea, vomiting
Investigations for Acute coronary syndrome (ACS)
ECG
troponin
consider echocardiogram
coronary angiogram
Risk assessment on Acute coronary syndrome (ACS)
GRACE score
TIMI score
Management of unstable angina
aspirin 300mg IV morphine for pain (if required) IV/sublingual nitrates O2 if needed offer antithrombin therapy e.g. fondaparinux offer clopidogrel/ticagrelor
PCI/coronary angiography is reserved for pts who are clinically unstable (immediate) or if GRACE score >3% (within 72h)
Myocardial infarction (MI)
ischaemic necrosis of myocardial tissue usually secondary to IHD/CAD/CHD
most commonly affects anterior or inferior territories
Risk factors for Myocardial infarction (MI)
atherosclerosis ↑ age male gender FH of IHD premature menopause smoking diabetes obesity HTN hyperlipidaemia physical inactivity south asian / indian heritage
Presentation of Myocardial infarction (MI)
chest pain (often central)
- radiating to L arm, neck, jaw
- may present as epigastric pain
- substernal pressure, squeezing, crushing
diaphoresis nausea & committing dyspnoea fatigue palpitations pt is pale, clammy altered mental state
atypical presentations are seen in women, elderly and diabetics
Investigations for Myocardial infarction (MI)
ECG
Investigations for Myocardial infarction (MI)
ECG (ST elevation or ST depression, peaked T-waves, T-wave inversion, Q waves, new onset conduction defects e.g. LBBB)
FBC (leukocytosis common)
U&Es, lipid profiel. CRP
cardiac enzymes e.g. troponin (↑)
CXR
coronary angiogram/myocardial perfusion scan
ECG features of Myocardial infarction (MI)
hyperacute T waves ST elevation or ST depression T wave inversion Q waves new onset LBBB
ECG leads representing septal myocardium
Leads V1 & V2
ECG leads representing anterior myocardium
Leads V3 & V4
ECG leads for anteroseptal MI
V1, V2, V3, V4
ECG leads for lateral MI
I, aVl, V5, V6
ECG leads for inferior MI
II, III, aVF
ECG leads for posterior MI
ST depression in leads V1, V2, V3
ECG leads for posterior MI
ST depression in leads V1, V2, V3
also Tall, broad R waves, Upright T waves, Dominant R wave in V2
Vessel affected in anterospetal MI
Left anterior descending artery
Vessel affected in inferior MI
left circumflex artery
Vessel affected in lateral MI
right coronary artery or left circumflex depending on L or R dominance
NB 70% of people are right dominant
Vessel affected in posterior MI
Posterior descending artery
In approximately 70% of the population, the right coronary artery (RCA) supplies the posterior descending artery (PDA)
NSTEMI management
Initial management
- ECG (ST depression, T wave inversion)
- troponin (↑)
- 300mg aspirin
- IV/sublingual nitrates
- O2 & Morphine as needed
calculate GRACE score to asses risk of cardiovascular event
PCI:
- GRACE score >3% = PCI within 72h
- PCI immediately if unstable e.g. hypotension
- NB give
NSTEMI/unstable angina management
Initial management
- ECG (ST depression, T wave inversion)
- troponin (↑)
- 300mg aspirin (+fondaparinux if no immediate PCI planned)
- IV/sublingual nitrates
- O2 & Morphine as needed
calculate GRACE score to asses risk of cardiovascular event
PCI:
- GRACE score >3% = PCI within 72h
- PCI immediately if unstable e.g. hypotension
- NB give ticagrelor/prasugrel & UFH pre PCI
Conservative management:
- give fondaparinux with aspirin initially if no PCI planned
- give ticargelor
STEMI management
Initial management
- ECG (ST elevation, new onset LBBB)
- troponin (↑)
- 300mg aspirin (+fondaparinux if no immediate PCI planned)
- IV/sublingual nitrates
- prasugrel/clopidogrel/ticagrelor (ticagrelor is preferred)
- O2 & Morphine as needed
- UFH/LMWH (pre PCI)
Percutaneous coronary intervention (PCI)
- gold standard
- ideally within 12h of symptom onset
- if pt presents within 12h of symptom onset PCI should happen with 120min of presentation
- if PCI cannot be offered within 120min of presentation give thrombolysis e.g. alteplase/streptokinase
Longterm management
-CABG, not acute
Antiplatelet therapy post MI
dual anti-platelet therapy (aspirin + another drug)
if high risk of bleeding give clopidogrel/prasugrel
if low risk of bleeding give ticagrelor
Secondary prevention post Myocardial infarction (MI)
dual anti-platelet therapy:
- low dose aspiring plus clopidogrel/ticagrelor (ticagrelor is preferred)
- min 4 weeks duration but given longer
beta blockers:
-initially IV on admission then continued PO
ACE inhibitors/ARBS:
Statins
-80mg as secondary prevention e.g. atorvastatin
GRACE score
Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment post MI
composed of:
- age
- heart rate, blood pressure
- cardiac (Killip class) and renal function (serum creatinine)
- cardiac arrest on presentation
- ECG findings
- troponin levels
score >3% is an indication for PCI in NSTEMI & unstable angina
Anti-platelet therapy post Myocardial infarction (MI)
dual anti-platelet therapy (aspirin + another drug)
if high risk of bleeding give clopidogrel/prasugrel
if low risk of bleeding give ticagrelor
Driving post Myocardial infarction (MI)
Must inform the DVLA
Normal driving license:
- if treated with PCI can drive after 1 week as long as LVEF >40% & not urgent revascularisation planned
- if not treated successfully treated with PCI then no driving for 4 weeks
heavy goods/passenger carrying
-must stop driving for minimum 6 weeks, then can have a medical assessment before continuing
Complications of Myocardial infarction (MI)
- Cardiac arrest (usually due to VF)
- chronic heart failure
- ventricular septal rupture / free wall rupture
- Dresslers syndrome (pericarditis 2-10 weeks post MI without infectious cause)
- Acute mitral regurg (due to ischaemic rupture of papillary muscles, has early-to-mid systolic murmur)
- LV aneurysm
- cardiogenic shock
Ventricular septal rupture / free wall rupture
presents 7-14 days post MI
septal rupture:
- new onset harsh pansystolic murmur, shock, pulmonary oedema, angina
- diagnosed on echo
- requires surgical closure
free wall rupture:
- usually 1-2 weeks post MI
- leads to cardiac tamponade & often death
- requires urgent percardiocentesis & thoracotomy
LV aneurysm
presents with persistent ST elevation and left ventricular failure
Thrombus may form within the aneurysm increasing the risk of stroke
Dresslers syndrome
2-10 weeks post MI, thought to be autoimmune reaction, so no infective cause found
characterised by a combination of fever, pleuritic pain, pericardial effusion, pericardial friction rub and a raised ESR (may also have fever)
treated with NSAIDs ± colchicine
Hypertension (HTN)
a common condition that is usually asymptomatic & detected on routine examination or after the occurrence of a complication
3rd biggest risk factor for premature death / disability
> 1/4 adults have HTN
Aetiology of Hypertension (HTN)
Primary (essential) HTN
- most common
- unknown cause
Secondary HTN
-e.g. due to renal disease (most common cause of secondary HTN), pregnancy, primary hyperaldosteronism and other endocrine causes e.g. phaeochromocytoma, medication e.g. steroids/COCP/NSAIDs/Leflunomide
Risk factors for Hypertension (HTN)
obesity excessive dietary salt intake stress lack of exercise alcohol intake ↑ age Family history male gender
Defining Hypertension (HTN)
Stage 1:
BP in surgery/clinic ≥140/90
ABPM/HBPM 135/85-149/94
Stage 2:
BP in surgery/clinic ≥160/100
ABPM/HBPM ≥150/95
Stage 3:
sBP ≥180 or dBP ≥120
Malignant hypertension:
sBP >200, dBP>130 both with signs of end organ damage
White coat HTN:
clinical BP >20/10 higher than ABPM/HBPM
NB offer HBPM/ABPM to any pt with BP ≥140/90
Investigations for Hypertension (HTN)
measure BP in every adult every 5 yrs minimum till age 80 then annually
FBC, U&Es, ruine dipstick, ECG, HbA1c, lipid profile
investigate possible secondary cause if suspected
Management of hypertension
Lifestyle interventions
- ↓salt intake
- ↓ caffeine intake
- smoking cessation
- ↓ weight
- ↑ exercise
Always treat stage 2 HTN pharmacologically
treat Stage 1 pharmacologically if <80 y/o + endoscopic organ damage / renal disease / established CVD / diabetes / Risk ≥10%
Step 1
- pt <55 y/o / background of T2DM = ACE-Is e.g. ramipril/ARBs e.g losartan (may use ARB if ACE-I causes dry cough)
- pt ≥55 y/o / black african / afro-caribbean heritage = CCB e.g. amlodipine
Step 2
- if taking ACE-I/ARB add CCB or thiazide like diuretic e.g. indapamide
- if taking CCB add ACE-I/ARB or thiazide like diuretic
Step3
- add third drug
- ACE-I/ARB + CCB + thiazide like diuretic
Step 4
- add 4th drug
- if K+ ≤4.5 add spironolactone
- if K+ >4.5 add alpha or beta blocker
Step 5
specialist referral
Conditions for pharmacologically treating Hypertension (HTN)
Always treat stage 2 HTN pharmacologically
-i.e. BP in surgery/clinic ≥160/100 or ABPM/HBPM ≥150/95
treat Stage 1 pharmacologically if <80 y/o + endoscopic organ damage / renal disease / established CVD / diabetes / Risk ≥10%
-i.e. BP in surgery/clinic ≥140/90 or ABPM/HBPM 135/85-149/94
Step 1 Hypertension (HTN) management
pt <55 y/o / background of T2DM
- ACE-Is e.g. ramipril or ARBs e.g losartan
- may use ARB if ACE-I causes dry cough
pt ≥55 y/o / black african / afro-caribbean heritage
-CCB e.g. amlodipine
NB ACE-Is have reduced efficacy in these ethnicities
Step 2 Hypertension (HTN) management
if taking ACE-I/ARB add CCB or thiazide like diuretic e.g. indapamide
if taking CCB add ACE-I/ARB or thiazide like diuretic
NB if afro-carribean add ARB rather than ACE-I as these have better effect
Step 3 Hypertension (HTN) management
add third drug
ACE-I/ARB + CCB + thiazide like diuretic
Step 4 Hypertension (HTN) management
add 4th drug after assessing for orthostatic hypotension & discussing adherence
if K+ ≤4.5 add spironolactone
if K+ >4.5 add alpha or beta blocker
BP targets
age >80yrs = 150/90 or HBPM of 145/85
age <80yrs = 140/90 or HBPM 135/85
in T2DM = < 140/90 mmHg
Hypertensive crisis
BP ≥180/120
presents with headaches, fits, N&V, visual disturbances and chest pain
management is specialist, BP lowering within 24-48h
usually with IV nitroprusside/labetalol/nifedipine
NB in pregnancy use hydralazine
NB if pheochromocytoma use phentolamine
if not treated quickly leads to end organ damage in retinas & kidneys
Acute Heart failure (HF)
life threatening emergency of sudden onset/worsening of HF symptoms
may be de novo i.e. no HF background but ~75% of cases are decompensation of known HF
usually seen in age >65yrs
Acute Heart failure (HF) presentation
dyspnoea
SOB
↓ exercise tolerance
peripheral/pulmonary oedema
Acute Heart failure (HF) investigations
ECG
echo
CXR
BNP/NT-proBNP
Acute Heart failure (HF) management
IV furosemide 20-50mg (or bumetanide)
O2 (sats 94-98%)
vasodilators e.g. nitrates (not routine)
CPAP (if respiratory failure)
if hypotensive/cardiogenic shock give inotropes e.g. dobutamine & pressors e.g.noradrenaline
-if refractory consider LVAD
Heart failure (HF)
heart is unable to generate sufficient cardiac output to meet the metabolic demands of the body without increasing diastolic pressure
NB congestive heart failure is a term reserved for pts with breathlessness & abnormal Na+, along with water retention leading to oedema
Types of Heart failure (HF)
HF with ↓ ejection fraction (HFrEF) = LVEF <40%
HF with preserved ejection fraction (HFpEF) = LVEF >40%
Epidemiology of Heart failure (HF)
average age of diagnosis is 77yrs
incidence ↑ with age
HFpEF tend to be older & female compared to HFrEF pts
Aetiology of Heart failure (HF)
CHD/IHD & HTN (most common causes) valvular heart disease post MI cardiomyopathies toxins e.g. alcohol, cocain
Presentation of Heart failure (HF)
Symptoms:
- dyspnoea on exertion, fatigue, orthopnoea (breathless lying flat), paroxysmal nocturnal dyspnoea
- peripheral oedema & pulmonary oedema
- weight gain (fluid retention)
- syncope, light headedness
- nocturnal cough ± pink frothy sputum
O/E
- displaced apex beat
- RV heave
- ↑ JVP
- narrow pulse pressure
- pulsus alternans
- bilateral basal end insinuatory crackles
- tachypnoea
- peripheral oedema (ankles & sacrum)
Investigations for Heart failure (HF)
Echocardiogram
-dilated LV/RV, ↓LVEF, abnormal diastolic filling pressure
B-type natriuretic peptide (BNP) / N-terminal pro BNP (NT-proBNP)
- both ↑
- if BNP >400 μL/ml or NT-proBNP >2000 μL/ml = assess with echo in 2 weeks
- if BNP 100-400 μL/ml or NT-proBNP 400-2000μL/ml = assess with echo in 6 weeks
CXR
-pleural effusion, Kerley B lines, Bat wing sign, cardiomegaly, upper lobe diversion
FBC, U&Es, LFTs, HbA1c, lipid profile, TFTs, ECG, urinalysis
cardiac MRI
-gold standard for wall motion & ventricular volumes
Staging system for Heart failure (HF)
New York Heart Association (NYHA) classification of HF
Class I:
no symptoms on ordinary physical exercise
Class II:
slight limitation of physical activity by mild symptoms
no symptoms at rest
Class III:
moderate limitation of less than ordinary physical activity by moderate symptoms
no symptoms at rest
Class IV:
symptoms present even at rest
↑symptoms with any physical activity
Chest Xray findings for Heart failure (HF)
A - Alveolar oedema (Bat wing sign) B - Kerley B lines C - Cardiomegaly D - dilated upper lobe vessels E - (pleural) effusion
Management of Heart failure (HF)
Lifestyle:
-smoking cessation, ↓dietary salt (~2-3g/day), alter fluid intake, exercise, ↓alcohol
1st Line:
- Beta blocker + ACE-I/ARB
- beta blockers e.g. bisoprolol/carvedilol/nebivolol
- ACE-Is e.g. ramipril/perindopril/lisinopril
- ARBs e.g. candersartan/losartan
2nd line:
- add aldosterone antagonist e.g. epleronone/spironolactone to ACE-I + Beta blocker
- monitor K+ as both ACE-Is and aldosterone antagonists cause ↑ K+
3rd line: (started by HF specialist)
-add ivabradine/sacubitril with valsartan/digoxin/hyrdalazine with a nitrate
Symptomatic:
furosemide / diuretics for fluid overload
Drugs to avoid in Heart failure (HF)
CCBs e.g. verapamil & diltiazem TCAs lithium NSAIDs corticosteroids QT prolonging drugs e.g. erythromycin
1st line management for Heart failure (HF)
Beta blocker + ACE-I/ARB
- beta blockers e.g. bisoprolol/carvedilol/nebivolol
- ACE-Is e.g. ramipril/perindopril/lisinopril
- ARBs e.g. candersartan/losartan
2nd line management for Heart failure (HF)
add aldosterone antagonist e.g. epleronone/spironolactone to ACE-I + Beta blocker
monitor K+ as both ACE-Is and aldosterone antagonists cause ↑ K+
3rd line management for Heart failure (HF)
started by HF specialist
-add ivabradine or sacubitril with valsartan or digoxin or hyrdalazine with a nitrate
Aortic stenosis (AS)
usually develops secondary to aortic sclerosis of the tricuspid aortic valve
most common valvular heart disease
most commonly due to calcification & fibrosis
↑ risk if bicuspid aortic valve
Most common valvular heart disease (VHD)
Aortic stenosis
Presentation of Aortic stenosis (AS)
chest pain / angina, dyspnoea
dizziness, exertional syncope
narrow pulse pressure & slow rising pulse
thrill present
soft/absent S2, possible S4, systolic click
ejection systolic crescendo-decrescendo murmur radiating to the carotids
-loudest in R 2nd intercostal space
Aortic stenosis (AS) murmur
ejection systolic murmur
- crescendo-decrescendo
- radiating to the carotids
- best heard in R 2nd intercostal space
Aortic stenosis (AS) pulse
slow rising pulse
narrow pulse pressure
Investigations for valvular heart disease (VHD)
Echocardiogram ECG CXR coronary angiogram (needed pre-op, if concomitant CAD can be treated in same operation) cardiac MRI
Investigations for Aortic stenosis (AS)
Echo (↑ aortic pressure gradient)
ECG (LV hypertrophy)
CXR
coronary angiogram (pre-op to determine risk)
Management of Aortic stenosis (AS)
asymptomatic pts:
- observed & monitored
- consider surgery if valvular gradient >40mmHg & LV dysfunction
symptomatic pt:
- transcatheter aortic valve implantation (TAVI)
- balloon vavluloplasty if critical stenosis
Aortic regurgitation (AR)
characterised by incomplete closure of the aortic valve leaflets leading to reflux of blood into the LV rapidly leading to LV function deteriorating
Aetiology of Aortic regurgitation (AR)
bicuspid aortic valve rheumatic fever infective endocarditis Marfans & Ehler Danlos degenerative aorta valve disease
Rheumatic heart disease is the most common cause world wide
In developed world degenerative disease is most common
Presentation of Aortic regurgitation (AR)
sudden severe dyspnoea, pulmonary oedema, HF, fatigue
soft S1
de Mussets sign = head bobbing
quinickes sign = nail bed pulsation
wide pulse pressure, collapsing (waterhammer) pulse
Austin flint murmur (in severe AR, mid-diastolic murmur loudest at apex)
early diastolic murmur
- best heard in R 2nd intercostal space
- accentuated by pt leaning forward in expiration
Murmur of Aortic regurgitation (AR)
early diastolic murmur
- best heard in R 2nd intercostal space
- accentuated by pt leaning forward in expiration
Pulse characteristic in Aortic regurgitation (AR)
wide pulse pressure collapsing pulse (water hammer pulse)
Management of Aortic regurgitation (AR)
Mild to moderate:
-review yearly & echo every 2 years
severe:
-urgent surgery via TAVI
otherwise TAVI should be offered on a non urgent elective basis
Mitral stenosis (MS)
caused by ↑ L atrial & ↑ pulmonary arterial pressures
most commonly due to rheumatic fever
other causes include degenerative calcification, SLE, RA
Presentation of Mitral stenosis (MS)
progressive dyspnoea, orthopnea, paroxysmal nocturnal dyspnoea
malar flush*
↑ JVP
signs of right HF (peripheral oedema, ascites, pulsatile hepatomegaly)
loud S1 with opening snap
irregularly irregular pulse (with AF)
RV heave
Low-pitched, rumbling mid diastolic murmur loudest in 5th intercostal space midaxillary line
Murmur of Mitral stenosis (MS)
diastolic murmur
- Low-pitched, rumbling
- mid-diastolic
- best heard in 5th intercostal space mid-clavicular line
- loudest with pt in left hand lateral position, with bell in 5th intercostal space mid-axillary line on expiration
Echo finding for Mitral stenosis (MS)
hockeys tick sign shaped mitral deformity
Complications of Mitral stenosis (MS)
Atrial fibrillation
- ↑ risk of thromboembolic event
- Right HF
- Pulmonary HTN
Management of Mitral stenosis (MS)
percutaneous mitral commissurotomy (PMC) = 1st line
-may require pre-surgical trans-oesophageal echo
surgical valve replacement can be used if pt not a candidate for percutaneous intervention
Mitral regurgitation (MR)
2nd most common valvular heart disease after aortic stenosis
causes include degenerative MR (most common), post MI or infective endocarditis
Presentation of Mitral regurgitation (MR)
generally tolerated well especially if chronic so is asymptomatic
dyspnoea left HF, pulmonary oedema, palpitations, pulmonary HTN
quiet S1, split S2
pansystolic murmur
- blowing
- loudest at apex & radiating into axilla, especially in inspiration
Management of Mitral regurgitation (MR)
valve repair is preferred over replacement (especially if degenerative)
papillary muscle rupture post MI requires urgent surgery after haemodynamic stabilisation with inotropes and intra-aortic balloon pump
Murmur of Mitral regurgitation (MR)
pansystolic murmur
- blowing
- loudest at apex
- radiating into axilla
- accentuated in left lateral position with bell over the mid-axillary line in inspiration
Tricuspid regurgitation
can be secondary to pulmonary HTN or infective endocarditis (especially in IVDU)
pansystolic murmur heard east in L 4th intercostal space
prominent/giant V waves on JVP with pulsatile hepatomegaly & left parasternal heave
Pulmonary stenosis
crescendo-decrescendo ejection systolic murmur heard in L 2nd intercostal space at sternal edge
may radiate to back
widely split S2 may be present
Anticoagulation post valve replacement
Biological (bioprosthetic) valves:
- e.g. porcine or bovine valves
- give 3 months of warfarin and then lifelong aspirin
Mechanical valves
- lifelong warfarin anticoagulation
- Target INR
- aortic: 3.0
- mitral: 3.5
Atrial fibrillation (AF)
the most common sustained cardiac arrhythmia, its a type of supra ventricular tachyarrythmia characterised by uncontrolled atrial activation
Types of Atrial fibrillation (AF)
acute: onset in previous 48h
paroxysmal: spontaneous termination of AF within 7 days
persistent: not self terminating, lasting >7 days
Persistent: cannot be cardioverted
Aetiology of Atrial fibrillation (AF)
CHD/IHD
HTN
valvular heart disease
hyperthyroidism
Presentation of Atrial fibrillation (AF)
often asymptomatic
palpitations, dyspnoea, chest pain, dizziness, tachycardia
irregularly irregular pulse*
may present with TIA or stroke (due to ↑ thrombotic risk)
Investigations for Atrial fibrillation (AF)
ECG
-variable R-R intervals, indiscernible/absent P waves, tachycardia
NB if paroxysmal AF suspected then use 24h ambulatory ECG monitoring
Investigations for Atrial fibrillation (AF)
ECG
-variable R-R intervals, indiscernible/absent P waves, tachycardia
TFTs, FBC, U&Es, LFTs, coagulation screen
echocardiogram
NB if paroxysmal AF suspected then use 24h ambulatory ECG monitoring
Management of Atrial fibrillation (AF)
1st line rate control unless:
- AF has a reversible cause e.g. sepsis
- AF believed to be primarily caused by HF
- new onset AF (i.e. within <48h)
- for pts where rhythm control is deemed more suitable based on clinical judgement
Rate Control: (generally 1st line)
1st line
-Beta blockers (except sotalol)
-consider rate limiting CCB e.g. verapamil/diltiazem (avoid in HF)
2nd line
-digoxin (especially if pt has sedentary lifestyle)
Rhythm control: (consider if pt symptomatic despite rate control)
- DC Cardioversion (if >48h of AF its the preferred method, after 3 weeks of anticoagulation ± TOE)
- Pharmacological
- Flecainide (avoid in structural heart disease & IHD)
- Amiodarone (especially in HF & LV impairment)
- Beta blockers
Dronedarone is used post successful cardio version to maintain sinus rhythm
Anticoagulation:
- 1st line is DOACs e.g. apixaban/edoxaban/riveroxaban for all pts with CHA2DS2-VASc score ≥2
- 2nd line is warfarin
Rate control of Atrial fibrillation (AF)
1st line
- Beta blockers (except sotalol)
- consider rate limiting CCB e.g. verapamil/diltiazem (avoid in HF)
2nd line
-digoxin (especially if pt has sedentary lifestyle or if co-existing HF)
Rhythm control of Atrial fibrillation (AF)
consider if pt symptomatic despite rate control or if new onset AF, or clear underlying cause
DC Cardioversion (if >48h of AF its the preferred method, after 3 weeks of anticoagulation ± TOE)
Pharmacological
- Flecainide (avoid in structural heart disease & IHD)
- Amiodarone (especially in HF & LV impairment)
- Beta blockers
Dronedarone is used post successful cardio version to maintain sinus rhythm
Indications for rhythm control 1st line in Atrial fibrillation (AF)
- AF has a reversible cause e.g. sepsis
- AF believed to be primarily caused by HF
- new onset AF (i.e. within <48h)
- for pts where rhythm control is deemed more suitable based on clinical judgement
Anticoagulation for Atrial fibrillation (AF)
Assess stroke risk with CHA2DS2-VASc tool & bleeding risk using the ORBIT score
If CHA2DS2-VASc score ≥2 then anticoagulate
Anticoagulation:
1st line is DOACs e.g. apixaban/edoxaban/riveroxaban
2nd line is warfarin
NB do not withhold anticoagulation simply due to age or risk of falls
Tool to determine stroke risk
CHA2DS2-VASc tool
C Congestive heart failure 1
H Hypertension (or treated hypertension) 1
A2 Age ≥ 75 years 2
Age 65-74 years 1
D Diabetes 1
S2 Prior Stroke, TIA or thromboembolism 2
Va Vascular disease (including ischaemic
heart disease and peripheral arterial
disease) 1
S Sex (female) 1
Tool to determine bleeding risk
ORBIT score
NB Previously the HAS-BLED scoring system was recommended
CHA2DS2-VASc tool scores
Score of 0
=No treatment
Score of 1
=Males: Consider anticoagulation
=Females: No treatment (this is because their score of 1 is only reached due to their gender)
Score ≥2
=Offer anticoagulation
Atrioventricular block (Heart block)
characterised by the interrupted or delayed conduction between the atria & ventricles
First degree atrioventricular block
PR interval fixed at >0.2 sec/200msc
usually asymptomatic
no treatment needed, low chance of progression
rate of SA node is HR
Second degree atrioventricular block
Mobitz Type I (Wenckenbach)
- progressive lengthening of PR interval until a dropped beat occurs (i.e. normal P wave not followed by QRS complex)
- low risk of progression
Mobitz Type II
- PR interval is constant & prolonged with intermittent absent QRS complexes
- usually follow regular conduction pattern e.g. 3:2 (3 P waves : 2 QRS complexes)
- high risk of progression to complete heart block
Third degree degree atrioventricular block (complete heart block)
complete dissociation of P waves & QRS complexes (AV dissociatio)
risk of progression to cardiogenic shock/cardiac arrest is high via ventricular asystole
Presentation of Atrioventricular block (Heart block)
generally asymptomatic especially if 1st degree of Mobitz Type I
complete heart block may present with:
- syncope, HF, wide pulse pressure, fatigue, dizziness, dyspnoea
- Stoke-Adams attacks (sudden LOC lasting a few seconds due to intermittent ventricular asystole)
Management of Atrioventricular block (Heart block)
all symptomatic pts and pts with Third degree (complete heart block) or Mobitz Type II should be treated
- atropine can be used to counteract bradyarrythmias
- transcutaneous pacing
- Pacemaker implantation* (KEY)
Left bundle branch block (LBBB)
causes of LBBB include MI, HTN, aortic stenosis, cardiomyopathy, digoxin toxicity
ECG:
- Deep S waves forming W shape in V1
- wide notched R waves forming M shape in V5, V6 (also I & aVL)
- William (W in V1, M in V6)
NB new onset LBBB is always pathological (should usually be treated as ACS)
Right bundle branch block (RBBB)
can be normal variant especially with ↑ age
other causes include RV hypertrophy, PE, cor pulmonate, ASD, MI
ECG:
- secondary R waves in leads V1 & V2 forming M shape (or Rabbit ears)
- deep slurred S waves in V6 & I forming W shape
- MarroW (M in V1, W in V6)
Supraventricular tachycardia (SVT)
a group of narrow complex tachyarrythmias arising from abnormalities in pacemaker activity and/or conduction of the atria and/or AV node
generally paroxysmal arrhythmia, i.e. episodes of SVT that self terminate
Types of Supraventricular tachycardia (SVT)
Atrioventricular nodal re-entrant tachycardia (AVNRT)
-~2/3 cases
Atrioventricular re-entry tachycardia (AVRT)
-due to accessory pathways e.g. in Wolff-Parkinson white syndrome
Presentation of Supraventricular tachycardia (SVT)
symptoms may be minimal
palpations, syncope, light-headedness, chest pain, dizziness
during attacks tachycardia (140-250bpm)
ECG findings in Supraventricular tachycardia (SVT)
narrow QRS complexes (<120ms)
rate typically >150bpm
rhythm is regular
consider 24h Holter monitor to catch paroxysmal episodes
NB wide QRS complexes may be seen in aberrant conduction)
Management of Supraventricular tachycardia (SVT)
1st line:
-vagal manoeuvres e.g. Valsalva (blow into empty syringe) or carotid sinus massage
2nd line:
-IV adenosine if vagal manoeuvres fail (6mg → 12mg if no effect → 18mg if still no effect)
3rd line:
-DC cardioversion
Prevention:
beta blockers & radio frequency ablation
NB adenosine can cause chest pain & impending sense of doom
Wolff-Parkinson white syndrome (WPW)
AVRT (a type of SVT) due to congenital accessory pathway conducing between atria & ventricles
can degenerate into VF (leading to sudden death)
may present with headaches, palpitations, syncope, light headedness
ECG findings
- short PR interval
- wide QRS with slurred upstroke (delta wave)
- left axis deviation if right sided pathway or vice versa
mangement include radio frequency ablation / surgical ablation (curative)
and acute epsiodes are terminated with vagal manoeuvres & adenosine
ECG features in Wolff-Parkinson white syndrome (WPW)
short PR interval
wide QRS with slurred upstroke (delta wave)
left axis deviation if right sided pathway or vice versa
Atrial flutter
a form of SVT characterised by a succession of rapid atrial depolarisation eaves
ECG:
- saw tooth pattern
- atrial rate often ~300/min so heart rate is determined by degree of AV block
- e.g. if 2:1 block then ventricular rate is ~150/min
managed similar to AF but meds are less affected
may be amenable to cardioversion
Ventricular tachycardia (VT)
broad complex tachyarrhythmia originating from ventricular atopic focuses
potentially life threatening
Types of Ventricular tachycardia (VT)
monomorphic VT:
- commonly due to MI
- QRS complexes all look similar
polymorphic VT:
- e.g. due to long QT syndrome / QT prolongation, drug toxicity or electrolyte imbalances
- QRS complexes are dissimilar
- can lead into Torsades des pointes
Presentation of Ventricular tachycardia (VT)
regular tachycardia palpitations shock syncope hypotension dyspnoea dizziness
if sustained i.e. lasting >30sec causes haemodynamic instability
ECG features of Ventricular tachycardia (VT)
rate >100 bpm (usually 150-200)
regular
QRS complexes (>120ms or >3 small squares)
NB to be considered VT needs to affect >3 consecutive beats
Management of Ventricular tachycardia (VT)
Pulseless VT
-as per cardiac arrest guidelines, with defibrillation
unstable VT (↓ CO) -immediate cardioversion (usually low voltage)
stable VT
- amiodarone 300mg initially then 900mg IV over 24h
- lidocaine/procainamide
- if ineffective cardioversion
- high risk of deterioration into unstable rhythm
Torsades des pointes:
-IV magnesium sulphate
NB ICDs should be considered for all pts to prevent sudden cardiac arrest
Ventricular fibrillation (VF)
life threatening broad complex tachyarrhythmia characterised by disorganised high-frequency ventricular contractions leading to diminished CO & haemodynamic collapse
most commonly encountered arrhythmia in cardiac arrest
ECG features of Ventricular fibrillation (VF)
arrhythmic fibrillation baseline usually >300bpm
indiscernable QRS complexes
no atrial P waves
NB ventricular flutter usually has a ventricular rate of 250-300 but can deteriorate into VF
Management of Ventricular fibrillation (VF)
as per cardiac arrest guidleines
immediate cardioversion via a defibrillator
Brugada syndrome
a form of inherited cardiovascular disease that presents with sudden death, most commonly seen in asian populations
autosomal dominant mutation in SCN5A gene
ECG
- convex ST segment elevation >2mm in >1 of V1/V2/V3 followed by negative T wave
- partial RBBB
- change of appearance after giving flecainide/ajmaline
Mangement is an ICD
Long QT syndrome
inherited condition associated with delayed depolarisation of the ventricles, which can deteriorate into torsades des pointes / VT and cause sudden cardiac death
LQT1 & LQT2 are the most common types and are due to defects in slow delayed rectifier K+ channels
Normal QT interval
430ms in males
450ms in females
Causes of a prolonged QT
Long QT syndrome Jervell-Lange-Nielsen syndrome (includes deafness) Romano ward syndrome amiodarone sotalol TCAs SSRIs (especially citalopram) haloperidol erythromycin ondansetron chloroquine
Features of long QT syndrome
Long QT on ECG
exertional syncope (especially while swimming) in LQT1 emotional stress syncope in LQT2
sudden cardiac arrest
Management of long QT syndrome
ICD
beta blockers (not sotalol as it can prolong QT)
avoid QT prolonging drugs & other precipitants e.g. strenuous exercise
Reversible causes of cardiac arrest
4 H’s and 4 T’s
The H’s
- hypoxia
- hypovolaemia
- hyper/hypokalaemia
- hypothermia
The T’s
- thrombosis (coronary or pulmonary)
- tension pneumothorax
- tamponade (cardiac)
- toxins
Types of rhythm in cardiac arrests
Shockable rhythms:
- VF
- pulseless VT
Non shockable rhythms:
- PEA (pulseless electrical activity)
- asystole (flat line)
Chest compression in cardiac arrest
ratio of chest compressions to ventilation is 30:2 in adults
rate of compression is 100-120 bpm regardless of age
NB CPR should continue while the defibrillator is charging
Defibrillation rules in cardiac arrest
single shock for VF/pulseless VT followed by 2min of CPR, then repeat the shock
NB if witnessed arrest and VF/pulseless VT then 3 stacked shocks may be delivered before commencing CPR
Drug delivery in cardiac arrest
IV is 1st line
IO (Intraosseous) is 2nd line if IV access not possible
Adrenaline use in cardiac arrest
1mg of adrenaline (10ml 1:10,000) is generally used
Non shockable rhythm
-give as soon as possible
Shockable rhythm:
-give once CPR has restarted after 3rd shock
Repeat adrenaline every 3-5min while ALS continues
Amiodarone in cardiac arrest
only used in shockable rhythms
give 300mg after 3rd shock
then give 150mg after the 5th shock
NB lidocaine can be used as an alternative
Thrombolytic drugs in cardiac arrest
given if PE is suspected cause
must continue CPR for 60-90min post administration to allow agents to work
Peri-arrest algorithm for tachyarrhythmias
if adverse features e.g. shock/syncope/MI/HF
Step 1:
- synchronised DC shocks (up to 3)
- seek expert help
Step 2:
- 300mg amiodarone IV over 10-20min
- repeat shock
- 900mg amiodarone over 24h
Peri-arrest in rhythm with broad QRS (>120ms)
irregular:
-seek expert help (may be AF + bundle branch block)
regular:
- if VT/uncertain rhythm = 300mg amiodarone IV over 10-20min then 900mg over 24h
- if known SVT with bundle branch block = treat as regular narrow complex tachycardia
Peri-arrest in rhythm with narrow QRS (<120ms)
irregular:
- probably AF = control rate with diltiazem or beta blockers
- if in HF consider amiodarone/digoxin
- consider anticoagulation after assessing thrombotic risk
regular:
- vagal manœuvres
- if vagal manoeuvres fail = adenosine 6mg rapid IV bolus
- if no effect give another 12mg
- if still no effect give a further 12-18mg
Peri-arrest with bradyarrhythmias
if adverse features e.g. shock/syncope/MI/HF
-atropine 500 micrograms IV
- if not successful consider
- repeat atropine 500 micrograms IV to max 3mg (i.e. 6 doses)
- transcutaneous pacing
- isoprenaline 5 micrograms/min IV
- adrenaline 2-10micrograms/min IV
- if still no success
- arrange expert help
- arrange transcutaneous pacing
If no adverse features but risk of asystole e.g. recent asystole/Mobitz type II/complete heart block with broad QRS/ventricular pace >3sec
- atropine 500mcg IV (repeat up to 3mg)
- transcutaneous pacing
Shock & circulatory failure
a life threatening circulatory disorder leading to tissue hypoxia, a disturbance in microcirculation and end organ damage
Types of shock
septic shock hemorrhagic shock (a type of hypovolaemic shock) neurogenic shock cardiogenic shock anaphylactic shock obstructive shock
Presentation of the shocked pt
tachycardia tachypnoea hypotension altered level of consciousness agitation / confusion lethargy ↓ GCS oliguria cold, mottled extremities slow cap refill diaphoretic / clammy
NB if signs of HF e.g. ↑JVP, crackles at lung bases = suggestive of cardiogenic shock
General management of shock
ABDCE assessment Resuscitation vascular access identify type of shock (ABG, CXR, ECG, USS, etc) call for help
Management of Hypovolaemic shock
stop bleeding
blood products if haemorrhage
IV fluids if fluid loss
Management of Cardiogenic shock
elevate head
resp support if signs of fluid overload
careful use of IV fluids
Management of obstructive shock
fluids
vasopressors/inotropes
treat underlying cause e.g. PE or cardiac tamponade
Management of distributive shock
i.e. septic/anaphylactic/neurogenic shock
fluid resuscitation
vasopressors
treat underlying cause
Carotid artery stenosis
a narrowing of the lumen of the carotid artery most commonly due to atherosclerotic plague formation in the cervical carotid artery
one of the main risk factors for the cerebrovascular events
area of bifurcation of the common carotid arteries is the most common location
Presentation of Carotid artery stenosis
most pts are asymptomatic
pts may presents with TIAs or strokes i.e. contralateral weakness/sensory disturbances, ipsilateral vision loss, dysphasia, aphasia, speech ataxia
carotid bruit may be audible on auscultation
Investigations for Carotid artery stenosis
Carotid artery dopple USS
- helps quantify luminal stenosis
- moderate = 50-69%
- severe ≥70%
CT angiogram head/neck/chest
ECG (MI is biggest cause of mortality post carotid endarterectomy)
Management of Carotid artery stenosis
BP control
Statins
antiplatelets
Surgical (carotid endarterectomy)
- especially helpful for severe stenosis
- consider if stenosis ≥50%
- urgently if pt is symptomatic (within 48h)
Renal artery stenosis
narrowing of the renal artery lumen considered angiographically significant if >50% reduction in vessel diameter present, mostly secondary to atherosclerosis
accounts for ~90% of renal vascular disease
Presentation of Renal artery stenosis
hypertension (severe or early onset)
flash pulmonary oedema
abdominal bruit
CKD (due to ischaemic nephropathy)
Investigations for Renal artery stenosis
U&Es (↑ creatinine, ↓K+) aldosterone:renin ratio (<20) duplex USS (shows stenosis) CT angiography (but beware of use of contrast if ↓ renal function)
Management of Renal artery stenosis
angioplasty with stenting (generally 1st line if surgical intervention required)
if stable then medication preferred
- treat HTN (ACE-Is/ARBs, CCB, beta blockers)
- statins
- consider antiplatelets
Fibromuscular dysplasia
proliferation of the connective tissue & muscle fibres within arteries leading to stenosis generally seen in middle aged females
accounts for ~10% of renal artery stenosis
presents with HTN, flats pulmonary oedema, abdominal bruit, CKD
management of choice is percutaneous tranluminal angioplasty
NB if young female with AKI after staring ACE-I think about fibromuscular dysplasia
Acute mesenteric ischaemia
essential a stroke of the bowel, most commonly due to an arterial embolism
commonly affects the superior mesenteric artery (SMA)
Most pts will have background of AF
Most pts are >60y/o
Presentation of Acute mesenteric ischaemia
moderate to severe colicky/constant abdo pain
- sudden onset
- poorly localised
- pain is disproportionate to clinical findings
later signs
- vomiting & nausea
- bloody diarrhoea
- peritonitis
- shock
Investigations for Acute mesenteric ischaemia
CT angiogram is gold standard
Management of Acute mesenteric ischaemia
emergency laparotomy is usually required
the prognosis is for if laparotomy is delayed
NB with treatment mortality is 50-90%
Chronic mesenteric ischaemia (intestinal angina)
chronic atherosclerotic disease of the vessels supplying the intestines (very uncommon)
presents with colicky/constant abdo pain, history of weight loss, postprandial pain (intestinal angina) and a feat of eating
diagnosed with CT angiogram
treated with open/endovascular revascularisation
Ischaemic colitis
compromised blood flow to the colon, this is the most common form of intestinal ischaemia
usually affects watershed areas e.g. splenic flexure between SMA & IMA territories
presents with acute abdomen, bloody stools, peritonitis, and septic shock
AXR shows thumb printing (oedematous thickened mucous indents bowel wall)
management is generally supportive especially if not severe, but laparotomy with bowel resection may be necessary
Peripheral arterial disease (PAD)
NB also known as peripheral vascular disease
includes a range of arterial syndromes that are caused by atherosclerotic obstruction of the lower extremities arteries most commonly
Risk factors include smoking, HTN, diabetes, hyperlipidaemia, obesity, physical inactivity
NB the most commonly affected vessel is the femoropopliteal artery leading to calf claudication
Presentation of intermittent claudication
pain/cramping/paraesthesia/burning on exertion
pt usually walks for a predicted distance before symptoms start
symptoms are relived by rest
Leriche syndrome (seen in cortoiliac disease)
- bilateral hip/buttock/thigh claudication
- erectile dysfunction
- absent/diminished femoral pulses
Presentation of critical limb ischaemia
rest pain lasting >2 weeks
pain worse at night
limb ulceration
gangrene
Presentation of acute limb threatening ischaemia
pale pulseless painful paralysed paraesthetic perishing with cold
General presentation of Peripheral arterial disease (PAD)
absent/diminshed pulses dry atrophic, shiny skin cool peripheries loss of hair on legs brittle nails livido reticularis
NB you must check all lower limb pulses
Investigations for Peripheral arterial disease (PAD)
Ankle brachial pressure index (ABPI)
- ≤0.90 is diagnostic
- ≥1 is normal
- 0.6-0.9 =claudication
- 0.3-0.6 = rest pain
- <0.3 = impeding/critical
USS Doppler (shows location of stenosis) MRI/CT angiogram (shows location of stenosis)
Management of Peripheral arterial disease (PAD)
smoking cessation*, weight loss, increased exercise
optimise HTN & diabetes management
All pts to start on 80mg statin (i.e. secondary prevention)
clopidogrel for all symptomatic pts
supervised exercise programmes for all pts
Surgery:
endovascular revascularisation (i.e. bypass, angioplasty or stenting)
amputation is last resort
Arterial Ulcers
ulceration due to impaired blood flow
risk factors include CHD, history of stroke/TIA, diabetes, PAD, obesity, immobility
presents as distal ulcers (often on dorms of foot/toes), with a punched out appearance and well defined borders, base is greyish granulation tissue & there is minimal bleeding on debridement, they are severely painful especially at night
the limb may show signs of chronic ischaemia e.g. hairlessness, pale skin, weak pulses or nail dystrophy
requires specialist referral
Differentiating venus & arterial ulcers
Ankle brachial pressure index is helpful
severe nocturnal pain points to arterial ulcer
signs of PAD (e.g. hairlessness, pale skin, weak pulses & nail dystrophy) also point to arterial cause
venous ulcers tend to be painless with stasis dermatitis around ulcer, hyperpigmentation and oedema
Venous Ulcer
chronic defects of the skin that do not spontaneously heal due to chronic venous insufficiency
risk factors include varicose veins, history of DVT/phlebitis, FH of venous disease
ulcers a typically above medial malleolus with a large shallow appearance and irregular borders, often ooze blood when handled but are painless/mildly painful
the limb may have stasis dermatitis around ulcer, hyperpigmentation and peripheral oedema
1st line management are graduated compression bandages, ± debridement and pentoxifylline
Neuropathic ulcers
often seen in diabetic neuropathy
usually ulcers ulcer calluses or over pressure points on plantar surface of the foot
have punched out appear cane with deep sinuses, tend to be painless, with ↓ sensation in surrounding area
managed by improving diabetic control or treating the underlying neuropathy
close attention should be paid to shoes & socks to reduce pressure points
Dry gangrene
gangrene secondary to ischaemia with causes including PAD, vasculitis e.g. Raynauds/scleroderma
presents as areas with grey-black discolouration (usually with clear demarcation between viable & gangrenous tissue), coldness & pallor, numbness
THERE IS NO DISCHARGE
management includes restoring blood supply or amputation if not salvageable (NB auto-amputation possible)
Wet gangrene
dry gangrene with a superinfection (e.g. strep or staph), or secondary to infection causing blockage of blood vessels
presents with oedema, blistering, discharge (may be pus), wet appearance, foul smelling odour, debridement
generally painful and area becomes black
management includes analgesia, broad spectrum Abx (e.g. metronidazole), surgical debridement
amputation if not controlled
Gas gangrene
also known as clostridia myonecrosis a life threatening bacterial infection with gangrene and the following 3 features -muscle necrosis -sepsis -gas production
due to rapid spread of clostridium perfringens from contaminated wound (surgical or traumatic)
presents with excruciating muscle pain (usually no skin changes only pain), massive oedema, cellulitic skin progressing to dark purple, overlying bullae/vesicles, would smelling discharge, surgical emphysema
also septic shock(tachycardia, hypotension, multi-organ failure)
investigated with CT/X-ray/MRI (gas in soft tissue, feathering pattern), blood cultures, ABG, FBC, U&Es, CRO, LFTs
management includes supportive therapy
surgical debridement (radical) ± amputation
IV Abx
Necrotising fasciitis
Uncommon but life threatening flesh latin disease usually with a polymicrobial cause
NB frequently seen in diabetic pts especially if taking SGLT-2 inhibitors
presents with systemically ill pts with disproportionately severe pain & only minor early skin changes
pain, swelling, erythema
skin necrosis, crepitus, vesicles/bulllae, grey discolouration, septic shock
clinical diagnosis (if strong clinical suspicion requires explorative surgery)
managed with early & aggressive surgical debridement of affected tissue (repeat daily until infection controlled)
IV broad spectrum Abx e.g. vancomycin + clindamycin + meropenem
Fournieres gangrene
necrotising fasciitis of the perineum/external genitalia that can rapidly spread to the anterior abdominal wall & gluteal muscles
Familial hyperlipidaemia
autosomal dominant condition resulting in high LDL cholesterol levels
suspect if total cholesterol >7.5 and/or personal/family history of premature CHD (<60y/o)
Diagnosis of familial hyperlipidaemia
Simon Broome criteria:
-total cholesterol >7.5 mmol/L in adults / 6.7mmol/L in a child & LDL cholesterol >4.9 mmol/L in adults / >4.0 mmol/L in children
+ tendon xanthomata or evidence of these signs in 1st/2nd degree relatives
OR
DNA evidence of LDL receptor mutation
NB must check to fasting LDL levels to confirm diagnosis
Management of familial hyperlipidaemia
refer to specialist lipid clinic
offer screening for 1st degree relatives
high dose statins e.g. 80mg atorvastatin
Secondary causes of hyperlipidaemia
hypertriglyceridaemia:
- T1DM
- T2DM
- obestiy
- alcohol
- CKD
- liver disease
hypercholesterolaemia:
- nephrotic syndrome
- cholestasis
- hypothyroidism
Presentation of hyperlipidaemia
xanthomas ( nodule lipid deposits in skin/tendons) xanthelasma (bilateral yellow flat plaques on upper eyelids) arcus senile (white/grey opaque ring in corneal margin)
Management of hyperlipidaemia
Primary prevention:
- 20mg of a statin (atorvastatin generally 1st line)
- give if QRisk >10% & age >40, or T1DM or CKD with eGFR < 60
Secondary prevention:
-80 mg statin
NB should take a further lipid profile 3 months after starting statins
Lifestyle modifications are vital
Pericarditis
an inflammation of the pericardium (outer layer of the heart)
acute: <6 weeks
Chronic: ≥ 4months
Aetiology of pericarditis
idiopathic viral infection e.g. cocksackie virus TB uraemia (causes fibrous pericarditis) trauma post MI (Dresslers syndrome) hypothyroidism malignancy radiation RA/SLE/Scleroderma
Presentation of acute pericarditis
pleuritic chest pain -worse on coughing/swallowing/deep inspiration -better sitting/leaning forward pericardial fiction rub (high pitched scratching on auscultation) non productive cough dyspnoea fever flu-like symptoms
Presentation of chronic pericarditis
constrictive (common post TB):
- dyspnoea, Right HF (↑JVP, ascites, peripheral oedema hepatomegaly)
- Kussmaul sign (↑JVP on inspiration)
- pericardial knock
- pulsus paradoxusus
effusive-constrictive:
-as above + signs of pericardial effusion (↓HS, ↑JVP)
Investigations for pericarditis
ECG
-saddle shaped ST elevation in all leads, PR depression
echo
-may show pericardial effusion or thickened pericardium
CXR
-pericardial calcification if constrictive
CRP (↑), FBC (↑WCC), troponin (may be ↑)
consider cardiac MRI
Management of pericarditis
treat underlying cause
if acute:
-1st line = Colchicine + NSAIDs
chronic constrictive:
-pericardioectomy (gold standard)
Pericardial effusion vs cardiac tamponade
Pericardial effusion:
-collection of fluid in the pericardial space
Cardiac tamponade:
-fluid in the pericardial space leading to ↓CO & circulatory collapse/shock due to compression of the heart
NB every tamponade is an effusion but not vice versa
Aetiology of pericardial effusion
haemopericaridum:
-trauma, aortic dissection, cardiac wall rupture, cardiac surgery
serous/serosanginous:
-idiopathic, acute pericarditis, malignancy, uraemia, autoimmune disorders, post-radiotherapy, drug induced (e.g. isoniazid/phenytoin)
Presentation of pericardial effusion
orthopnoea
retrosternal chest pain
hoarseness/nausea/dysphagia/hiccups (compressive symptoms)
Ewart sign (dullness on percussion of L lung base)
Presentation of cardiac tamponade
Becks triad:
- hypotension
- muffled heart sounds
- distended neck veins
dyspnoea, tachycardia, absent Y waves on JVP, pulsus paradoxus (drop in BP on inspiration)
obstructive shock
cardiac arrest with PEA
Investigations for pericardial effusion/cardiac tampoande
ECG
-low voltage, electrical alternans (seen mainly in tamponade) i.e. consecutive QRS complexes alter in height)
echocardiogram (gold standard)
-visualises effusion
consider CXR
NB in a cardiac arrest/unstable pt do not delay pericardiocentesis if a tamponade is suspected
Management of pericardial effusion
treat underlying condition
pericardiocentesis
-can be USS of CT guided
especially traumatic/purulent effusion may require surgical pericardotomy as pericardiocentesis is insufficent
Management of cardiac tamponade
may need immediate blind pericardiocentesis
if post traumatic (especially penetrating trauma) & in cardiac arrest then emergency thoracotomy is indicated
Infective endocarditis (IE)
an infection of the endocardial surface of the heart including valvular structures, the chordae tendinae and mural endocardium
most commonly affects mitral valve in normal people
in IVDU pts often causes tricuspid lesions
Pathogens causing Infective endocarditis (IE)
staph aureus
- most common overall
- especially acute IE in IVDU, and those with prosthetic valves/ICDs/Pacemakers
strep viridans
- previously the most common cause
- seen after dental procedures/with poor dental hygiene or developing countries
staph epidermis
-colonises indwelling lines so usually seen in pts post prosthetic valve surgery
NB can be culture negative e.g. HACEK or coxiella brunetti
Risk factors for Infective endocarditis (IE)
valvular heart disease valve replacement congenital heart disease previous IE IVDU poor dental hygiene
Most common sites for Infective endocarditis (IE)
most commonly affects mitral valve in normal people
in IVDU pts often causes tricuspid lesions
Presentation of Infective endocarditis (IE)
Generally:
fevers, chills, tachycardia, malaise, weakness, night sweats, arthralgia, myalgia, pleuritic chest pain
heart murmur (often new) generally regurg i.e. holsystolic palpitations, HF splinter haemorrhages Roth spots (round retinal haemorrhages with pale centre) Oslders nodes (painful nodules on pads of fingers) Janeway lesions (non tender macules on palms/soles)
emboli to brain / kidney / spleen
Criteria for Infective endocarditis (IE)
Modified Duke criteria: Infective endocarditis diagnosed if -pathological criteria positive, or -2 major criteria, or -1 major and 3 minor criteria, or -5 minor criteria
Pathological criteria:
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria:
Positive blood cultures
-two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart
-three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis
-positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
-positive molecular assays for specific gene targets
Evidence of endocardial involvement
- positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
- new valvular regurgitation
Minor criteria:
- predisposing heart condition or intravenous drug use
- microbiological evidence does not meet major criteria
- fever > 38ºC
- vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
- immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
Investigations for Infective endocarditis (IE)
Blood cultures:
- do not delay Abx if pt unwell
- take 3 sets of cultures from different sites prior to Abx therapy
- take monitoring cultures to monitor treatment
echo
-valvular or mobile vegetations
CRP/ESR (↑), FBC (↑WCC)
Management of Infective endocarditis (IE)
Initially empirical Abx:
- native valve = amoxicillin ± low dose gentamicin
- penicillin allergy/MRSA/severe sepsis = vancomycin + low dose gentamicin
- prosthetic valve = rifampicin + vancomycin + low dose gentamicin
Staph endocarditis:
- native valve = flucloxacillin
- prosthetic valve = flucloxacillin + rifampicin + gentamicin
Strep endocarditis:
-Benzylpenicillin ± gentamicin
Surgery:
- for all IE pts affecting prosthetic valves
- also pts with HF, resistant infections or aortic abscesses
Prophylaxis for Infective endocarditis (IE)
Abx prophylaxis was previously recommended but this has now stopped
might still be considered in at risk pts e.g. IVDU but very rare
Modified duke criteria
Infective endocarditis diagnosed if
- pathological criteria positive, or
- 2 major criteria, or
- 1 major and 3 minor criteria, or
- 5 minor criteria
Pathological criteria:
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria:
Positive blood cultures
-two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart
-three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis
-positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci
-positive molecular assays for specific gene targets
Evidence of endocardial involvement
- positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
- new valvular regurgitation
Minor criteria:
- predisposing heart condition or intravenous drug use
- microbiological evidence does not meet major criteria
- fever > 38ºC
- vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
- immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
Rheumatic fever
an autoimmune disease that occurs due to an immunological reaction to recent (2-6 weeks ago) strep progenies (Group a Strep) infection e.g. strep throat
most commonly seen in school aged children
Presentation of rheumatic fever
constitutional symptoms e.g. fever, malaise, fatigue
migratory polyarthritis
CNS: sydenham chorea (often last, 1-8 month post infection)
skin: subcutaneous nodules, erythema marginatum (centrifugal expanding pink/red rash with well defined borders)
Cardiac: (Rheumatic heart disease)
- percarditis
- valvular lesions (~65% effect mitral valve, ~25% is aortic valve)
Jones diagnostic criteria
Used for rheumatic fever
-evidence of recent strep infection + 2 major criteria / 1 major & 2 minor
Evidence of recent strep infection
- ↑ streptococi antibodies
- +ve throat swab
- +ve rapid group A strep antigen test
Major criteria
- erythema marginatum
- sydenhams chorea
- polyarthritis (migratory)
- carditis & valvulitis
- subcutaneous nodules
Minor criteria
- ↑ESR/CRP
- pyrexia
- arthralgia
- ↑ PR interval
Most frequently affected valve in Rheumatic heart disease
Mitral valve ~65%
- early on leads to regurg
- later leads to stenosis
NB ~25% affects aortic valve
Diagnostic criteria for Rheumatic fever
Jones diagnostic criteria
-evidence of recent strep infection + 2 major criteria / 1 major & 2 minor
Evidence of recent strep infection
- ↑ streptococi antibodies
- +ve throat swab
- +ve rapid group A strep antigen test
Major criteria
- erythema marginatum
- sydenhams chorea
- polyarthritis (migratory)
- carditis & valvulitis
- subcutaneous nodules
Minor criteria
- ↑ESR/CRP
- pyrexia
- arthralgia
- ↑ PR interval
Investigations for rheumatic fever
throat swab anti streptococcal antibodies group a strep rapid antigen test ESR/CRP (↑) CXR Echo
Management of rheumatic fever
Abx
-PO penicillin V or benzylpenicillin
NSAIDs
treat complications e.g. HF
Myocarditis
an inflammation of the myocardium in the absence of predominant acute/chronic ischaemia characteristic of IHD
usually seen in young pts ~40 y/o
though to be the cause of ~10% of sudden deaths in young adults
Aetiology of myocarditis
viral (cocksackie B, HIV) bacteria (diphtheria, clostridium) lyme disease chagas disease autoimmune drugs e.g. doxorubicin
Presentation of myocarditis
may be asymptomatic with only ECG abnormalities
fatigue, chest pain, fever, dyspnoea, palpitations, tachycardia
viral prodrome
arrhythmia (sinus tachycardia, heart block, bradyarrhythmias, ventricular extrasystoles)
acute decompensated congestive HF + dilated cardiomyopathy
S3/S4 gallop on auscultation
Investigations for myocarditis
ECG
- non specific ST segment & T wave changes
- ST elevation/depression
CXR
-congestive HF signs (ABCDE)
creatine kinase/CK-MB (↑)
troponin (↑)
BNP (↑)
ESR/CRP (↑)
Management of myocarditis
supportive management e.g. give inotropes for hypotension
treat underlying cause e.g. Abx if bacterial
NB can cause dilated cardiomyopathy later on
Aortic dissection
describes a condition where a separation has occured in the aortic wall intimate causing blood flow into a new flash lumen channel composed of inner & outer layers of the tunica intima
MOST common emergency of the aorta
usually seen age 50-70
Risk factors for aortic dissection
HTN, smoking, ↑ cholesterol Trauma (especially deceleration injuries) connective tissues disease (ehler danlos, marinas) Turners & Noonas syndromes syphilis pregnancy cocaine/amphetamine use bicuspid aortic valve
Classification of aortic dissection
Standford classification:
- A: involves ascending aorta
- B: does not involve ascending aorta
DeBakey classification:
- I: aorta/ aortic arch & descending aorta
- II: ascending aorta only
- III: descending aorta distal to left subclavian
Types I & II are stanford A, while type III is stanford B
Presentation of aortic dissection
sudden severe tearing/ripping chest pain
- may radiate to back (intrascapular)
- pain migrates as dissection progresses
pulse deficit
- weak/absent carotid/brachial/femoral pulses
- wide pulse pressure
Hypertension*/hypotension
-variation >20mmHg of sBP between arms
syncope, diaphoresis
Investigations for aortic dissection
ECG
- may show MI
- non specific ST changes
- normla ECG
CXR
-widened mediastinum
CT/MRI angiogram
USS & dopple
Management of aortic dissection
resuscitation & ABCDE approach
- Stanford type A need immediate surgery
- Stanford type B can be conservatively managed
aggressively manage HTN
- aim for BP 100-120mmHg
- IV labetolol used
NB can lead to aortic rupture which presents as hemorrhagic shock
Acyanotic congenital heart defects
Ventricular septal defect (VSD)
Atrial septal defect (ASD)
Patent ductus arteriosus (PDA)
Coarctation of the aorta
Cyanotic congenital heart defects
Tetralogy of Fallot (TOF)
transposition of the great arteries
Ebstein anomaly
Epidemiology of congenital heart defects
VSDs are the most common
-make up ~30% of defects
ASDs are the most common heart defect diagnosed in adults but overall are less common than VSDs
Ventricular septal defect (VSD)
most common congenital heart defect, often detected on week 20 anomaly scan
causes include Down’s syndrome, Edward’s syndrome, pate syndrome, or intrauterine infections e.g. TORCH/s
presents with failure to thrive, HF (pallor, hepatomegaly, tachycardia, tachypnoea) and a pan systolic murmur ± a systolic thrill
small defects generally close spontaneously so only need monitoring but larger defects usually cause some degree of HF so need to be surgically closed
Ventricular septal defect (VSD) murmur
pan systolic murmur ± a systolic thrill
Atrial septal defect (ASD)
most common congenital heart disease diagnosed in adults, more common in females
associated with Down’s and metal alcohol syndrome
presents with ejection systolic murmur & fixed splitting of S2, and embolisms e.g. stroke
often close spontaneously in childhood but if children are symptomatic then surgery is required
Atrial septal defect (ASD) murmur
ejection systolic murmur & fixed splitting of S2
Patent ductus arteriosus (PDA)
failure of ductus arteriosus to close, usually associated with prematurity or maternal rubella infection
presents with left subclavicular thrill, heaving apex beat, a continuous machinery murmur and a large volume bounding & collapsing pulse with a wide pulse pressure
management include indomethacin* or ibuprofen (NSAIDs) for neonates which inhibits prostaglandin synthesis and promotes duct closure
Patent ductus arteriosus (PDA) murmur
continuous machinery murmur
Maintaining a Patent ductus arteriosus (PDA)
this may be desirable in pts with other congenital heart defects e.g. cyanotic defects such as transposition of the great vessels
duct is kept open until surgical management of other defect
potency can be maintained using prostaglandin E1
Patent foramen ovale (PFO)
seen in up to 25% of general population
generally asymptotic unless embolus passes into L atrium leading stroke
Coarctation of the aorta
congenital narrowing of the descending aorta associates with Turner’s syndrome and bicuspid aortic valves
presents with radio femoral delay, differential cyanosis (cyanosis of lower limbs), a mid systolic murmur, notching of the inferior ribs (only seen in adults), difference of BP in upper & lower limbs
management include prostaglandin E1 to maintain patency of ductus arteriosus with surgical correction or balloon angioplasty
Coarctation of the aorta murmur
mid systolic murmur
- loudest over back
- apical click from aortic valve
Tetralogy of Fallot (TOF)
most common cyanotic heart defect typically presenting age 1-2 months
Features are VSD, right ventricular hypertrophy, right ventricular outflow tract obstruction/pulmonary stenosis and an overriding aorta
presents with cyanosis, ejection systolic murmur, Tet spells (intermittent hypercyanotic, hypoxic episodes associated with physical/psychological stress)
classically a boot shaped heart is seen on CXR
management is usually a 2 part surgical repair
Features of Tetralogy of Fallot (TOF)
VSD
right ventricular hypertrophy
right ventricular outflow tract obstruction/pulmonary stenosis
overriding aorta
Tetralogy of Fallot (TOF) murmur
ejection systolic (due to pulmonary valve stenosis)
easy to remember this if you just know the components
Transposition of the great arteries (TGA)
also known as transposition of the great vessels
due to failure of aorticopulmonary septum to spiral during sepatation, risk is ↑ in children of diabetic mothers
presents with cyanosis, tachypnoea, loud single S2, prominent right ventricular impulse
on CXR see egg-on-string sign
management includes maintaining a patent ductus arteriosus with prostaglandin E1 and surgical correction within the first 2 weeks of life
Ebsteins anomaly
low insertion of the tricuspid valve resulting in a large atrium and a small ventricle I.e. atrialisation of the right ventricle
commonly associated with in-utero exposure to lithium e.g. in mothers taking lithium
presents with cyanosis, cardiomegaly, HF, respiratory distress, tricuspid regurg (pansystolic murmur), RBBB, widely split S1 & S2
management include prostaglandin E1 to maintain ductus arteriosus and surgical repair
Eisenmengers syndrome
described reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension, secondary to uncorrected defects causing remodelling of the pulmonary vasculature
associated with VSD, ASD, PDA (long standing)
presents with disappearance of original murmur, cyanosis, clubbing, RV failure, haemoptysis and embolisms
management its a heart-lung transplant
Hypertrophic obstructive cardiomyopathy (HOCM)
an autosomal dominant disorder characterised by LV hypertrophy, impaired diastolic filling and abnormalities of the mitral valve
most common genetic heart disease & most common cause of sudden cardiac death in the young
Inherited cardiomyopathies
Hypertrophic obstructive cardiomyopathy (HOCM)
-autosomal dominant
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
-autosomal dominant
Presentation of Hypertrophic obstructive cardiomyopathy (HOCM)
most pts are asymptomatic
exertional dyspnoea, angina, syncope following exercise
sudden death (usually due to ventricular arrhythmias)
HF
jerky pulses
large ‘a’ waves
double apex beat
ejection systolic murmur
Investigations for Hypertrophic obstructive cardiomyopathy (HOCM)
ECG
-prminent Q waves, LV hypertrophy, ST/T wave abnormalities
Echo
-mitral regurg, systolic anterior motion, asymmetric hypertrophy
CXR
-cardiomegaly
exercise testing
cardiac MRI
genetic studies & family screening
MOST common area of hypertrophy is anterior ventricular septum
Mangement of Hypertrophic obstructive cardiomyopathy (HOCM)
amiodarone beta blockers/verapamil ICD (to prevent sudden death) dual catheter pacemaker endocarditis prophylaxis anticoagulation if pts in AF
NB avoid nitrates, ACE-Is, inotropes
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
autosomal dominant genetic CVD caused by fibro-fatty replacement of right ventricular myocytes
usually presents in adolescence or early adulthood
most common in males
2nd most common cause of sudden cardiac death in <35y/o only second to HCOM
Presentation of Arrhythmogenic right ventricular cardiomyopathy (ARVC)
palpitations, dyspnoea, angina
presyncope/syncope
RV failure (peripheral oedema, hepatomegaly)
sudden cardiac death (may be first presentation)
-often during exercise
Investigations for Arrhythmogenic right ventricular cardiomyopathy (ARVC)
ECG
- abnormalities in V1/V2/V3 (usually T wave inversion)
- epsilon waves i.e. terminal notch in QRS complex
Echo
- often subtle changes initially
- RV enlargement
- RV wall motion abnormalities
- ↓ RV ejection fraction
Cardiac MRI
-fibrofatty tissue in RV wall
Management of Arrhythmogenic right ventricular cardiomyopathy (ARVC)
sotalol (most widely used antiarrhythmic)
amiodarone ± a beat blocker
catheter ablation to prevent VT
ICD (to prevent sudden cardiac death)
Dilated cardiomyopathy
characterised by ventricular chamber enlargement & contractile dysfunction with normal LV wall thickness
most common for of cardiomyopathy accounting for ~90% of cases, more common in males
Aetiology of dilated cardiomyopathy
idiopathic (most common) myocarditis IHD HTN alcohol use disorder cocain abuse
Presentation of dilated cardiomyopathy
Heart failure -dyspnoea, weakness, fatigue, oedema, ↑JVP, pulmonary congestion, cardiomegaly loud S3/S4 exercise intolerance mitral/tricuspid regurg AF
Investigations for dilated cardiomyopathy
CXR
- ballooning heart
- cardiomegaly
- pulmonary oedema
Echo
- atrial/ventricular
- ↓ Lv ejection fraction
- wall motion abnormalities
ECG
-non specific ST/T changes
BNP (↑)
Management of dilated cardiomyopathy
Beta blockers (for all pts)
loop diuretics & thiazide diuretics for fluid overload
ACE-Is/ARBs if ↓ LVEF
spironolactone
nitrates (if diastolic dysfunction)
Heart transplant if medical management fails
Restrictive cardiomyopathy
a rare type of cardiomyopathy characterised by marked diastolic dysfunction, normal/near normal systolic function & normal ventricular volumes
least common cardiomyopathy, usually seen in elderly people
Aetiology of Restrictive cardiomyopathy
usually no underlying cause found
post radiation/surgery Löfflers endocarditis amyloidosis sarcoidosis haemochromatosis
Presentation of Restrictive cardiomyopathy
HF with normal systolic function
- dyspnoea, fatigue, loud S3, pulmonary oedema
- features of RV failure dominant e.g. peripheral oedema or hepatomegaly
AF
-seen in ~75% of pts
Investigations for Restrictive cardiomyopathy
ECG
- low voltage QRS complexes
- AF (absent P waves)
- conductive disorders e.g. RBBB/LBBB
Cardiac MRI
-to differentiate restrictive cardiomyopathy and constrictive pericarditis
endomyocardial biopsy
-with congo red stain
CXR, echo
Management of Restrictive cardiomyopathy
in children
-usually idiopathic so transplant is treatment of choice
in adults:
- management of HF
- amiodarone (if risk of arrhythmias)
- anti-coagulation if AF
- ICD
- heart transplant if medical management fails
Takotsubo cardiomyopathy (Broken-heart syndrome)
also known as stress induced cardiomyopathy, is a type of non-ischaemic cardiomyopathy associated with transient, reversible LV dysfunction & apical ballooning of the myocardium
can mimic ACS
NB 90% of pts are post menopausal women
Takotsubo cardiomyopathy presentation
retrosternal pain with typical features of angina dyspnoea syncope arrhythmias signs of HF/cardiogenic shock
Takotsubo cardiomyopathy investigations & management
ECG
-ST elevation in precordial leads (V1-V3)
Echo
- apical LV ballooning
- LV outflow tract obstruction
- ↓ LVEF
- global LV dyskinesia involving apex
coronary angiogram (normal)
Cardiac MRI
troponin (↑), BNP (↑), CK-MB (↑)
Mangement is supportive
Varicose veins
permanently dilated subcutaneous veins of ≥3mm diameter when measured in the standing position
NB the dilation is secondary to incompetent venous valves allowing retrograde blood flow
most commonly affects legs, due to reflux in the saphenous veins
more common in wome
Presentation of varicose veins
often the cometic presentation of varicose veins will prompt pts to come in
may have machine, throbbing, itching or leg cramps
skin changes:
-varicose eczema, venous stasis, haemosiderrin deposition, lipodermatosclerossi, atrophic blanche
bleeding, superficial thrombophlebitis, venous ulceration, DVT
Investigations for varicose veins
Trendelenburg test
Perthes manoeuvre
duplex USS
Management of varicose veins
conservative:
- for majority of pts
- leg elevation
- weight loss
- regular exercise
- compression stockings
secondary care
- endothermal ablation, foam sclerotherapy
- surgical ligation or stripping
Direct oral anticoagulants (DOACs)
e.g. Riveroxaban/Apixaban/Edoxaban (direct factor Xa inhibitors) & dabigatran (direct thrombin inhibitor)
indications:
- prevention of stroke in non-valvular AF
- treatment of DVT & PE
- prevention of VTE post hip/knee surgery
side effects include nausea & GI upset
Warfarin
affects Vit K dependent clotting factors i.e. clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
indications:
- mechanical heart valves
- 2nd line for VTE & AF
- secondary thromboprophylaxis in antiphospholipid syndrome
Monitored via INR (ratio of pts Prothrombin time (PT) and normal PT)
Managing ↑ INR
Major haemorrhage:
- stop warfarin
- give 5mg Vit K IV
- prothrombin complex concentrate (PCC)
INR >8.0:
- No haemorrhage
- stop warfarin
- PO Vit K
- minor haemorrhage
- stop warfarin
- IV Vit K
INR 5.0-8.0
- No haemorrhage
- withhold 1-2 doses & reduce subsequent warfarin dose
- minor haemorrhage
- stop warfarin
- IV Vit K
NB restart warfarin if INR <5.0
NB Vit K can be repeated if INR is still raised after 24h
Aspirin
block cyclooxyrgenase 1&2 (Cox 1/2) and blocking thromboxane A2 formation
Indications:
- secindary prevention of CVD (75mg)
- Acute MI & ischeamic stroke treatment (300mg)
- post TIA
- primary thromboprophylaxis in antiphospholipid syndrome
NB not used in children <16y/o due to risk of Reyes syndrome, the only exception being Kawasaki disease
P2Y12 receptor antagonists
examples include clopidogrel, ticagrelor and prasugrel
work by inhibiting platelet activation via the P2Y12 receptor
Indications:
- 1st line in secondary prevention post ischaemic stroke/MI/PAD (NB often combined with aspirin for dual antiplatelet therapy)
- acute MI (with aspirin, give ticagrelor or prasugrel)
NB generally used with aspiring together or as alternative to aspirin if there is an intolerance
Heparins
e.g. LMWH or UFH
work by activating antithrombin III
Indications:
- second line for treatment of PE/DVT
- management of DVT/PE in pregnancy
- antiphospholipid syndrome un pregnancy
- VTE prophylaxis
- ACS pre PCI
side effects include bleeding, thrombocytopenia, osteoporosis, ↑ K+
Heparin induced thrombocytopenia may be seen especially with UFH
NB given S/C
Benefits of unfractionated heparin (UFH)
useful in pts with renal failure or ↓ renal function
or in situations where high bleeding risk so rapid anticoagulation reversibility is desirable
increased risk of HIT over LMWH
Fondaparinux
activates antithrombin III
Indications:
- superficial thrombophlebitis
- ACS treatment if not a high bleeding risk & no immediate angiography
NB given S/C
