Cardiology- complete Flashcards
What are STEMI criteria?
STEMI criteria
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or
≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)
What is the initial drug therapy for all patients with ACS?
aspirin 300mg
oxygen if sats < 94%
morphine for patients with severe pain
nitratesn (SL or IV)- should be used in caution if patient hypotensive
Management of STEMI
Aspirin 300mg
Is PCI possible within 120 minutes?
Yes
for PCI
Give Prasugrel, give unfractionated heparin + bailout gylcoprotein IIb/IIIa inhibitor, and use a drug-eluting stent
No
for fibrinolysis
Give an antithrombin at the same time
Give Ticagrelor after
for onging ischemia consider PCI
Assumptions for STEMI management
Pt presented within 12 hours of symptoms AND PCI can be delivered within 120 minutes - if not then fibrinolysis
if pt high risk of bleeding then swap prasugrel for ticagrelor/ and swap ticagrelor for clopidogrel
if pt on oral anticoagulation then swap prasugrel for ticagrelor
When to consider PCI after thrombolysis?
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
How do you manage NSTEMI/ unstable angina?
Aspirin 300mg
Fondaparinux if no immediate PCI planned
then-
** estimate 6 months mortality using GRACE
if low risk (3 or less)
- Ticagrelor
if high risk (more than 3)
- PCI (immediate if unstable vs 72 hrs if stable)
- Give prasugrel or ticagrelor
- give unfractionated heparin
- Drug-eluting stent
Assumptions not high bleeding risk and not on oral anticoagulations
Following an ACS, all patients should be offered?
dual antiplatelet therapy (aspirin plus a second antiplatelet agent such as an adenosine diphosphate receptor (ADP) receptor inhibitor)
ACE inhibitor
beta-blocker
statin
what are adenosine diphosphate receptor (ADP) receptor inhibitors?
clopidogrel, ticlopidine, prasugrel and ticagrelor
they impair platelet aggregation and fibrinogen-mediated platelet cross-linking
What are the ECG features of a LBBB?
QRS duration > 120ms
Dominant S wave in V1 (W shape rS in V1)
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Prolonged R wave peak time > 60ms in leads V5-6
(M shape R in V6)
Absence of Q waves in lateral leads
Associated features include:
Left axis deviation (LAD);
Poor R wave progression in precordial leads, and
Appropriate discordance (discussed below)
https://litfl.com/left-bundle-branch-block-lbbb-ecg-library/
Pulmonary embolism ECG findings?
Sinus tachycardia is most common
finding
Classical is the ‘S1Q3T3 pattern’ or the McGinn-White Sign: a large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain.
WiLLiaM vs MaRRoW
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
Causes of new LBBB
New LBBB is always pathological.
Causes of LBBB include:
MI
HTN
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
Sgarbossa Criteria
Used to help diagnose MI in patients with new LBBB
Concordant ST elevation ≥ 1 mm in ≥ 1 lead
Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave
Peri-arrest Arrhythmias?
Rhythm abnormalities that occur in the peri-arrest period may be considered in two main categories:
- Arrhythmias that may lead to cardiac arrest.
- Arrhythmias that occur after initial resuscitation from cardiac arrest - these often indicate that the patient’s condition is still unstable and that there is a risk of deterioration or further cardiac arrest.
Peri- arrest arrhythmias: Tachycardia or bradycardia with life threatening features (shock/ syncope/ MI/ HF)?
Tachycardia -> synchronised DC shocks up to 3 attempts
if unsuccessful (amiodarone 300mg IV over 10-20 min/ rpt DC shock)
bradycardia -> atropine 500 mcg IV
if unsuccessful
do this as interim measures whist seeking expert help
atropine up to 3 times
isoprenaline/ adrenaline infusion titrated to response
or transcutaneous pacing
seek expert help and arrange for transvenous pacing
Potential risk of asystole in those with peri-arrest arrhythmia?
The following are risk factors for asystole. Even if there is a satisfactory response to atropine specialist help is indicated to consider the need for transvenous pacing:
complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds
NYHA classifications?
Class I
no symptoms
no limitation
Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
Class IV
severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
MGT of massive PE with haemodynamic instability ?
thrombolysis
MGT of pt with recurrent PEs who are on recommended anticoagulation?
IVC filters
What does PESI score stand for?
the Pulmonary Embolism Severity Index (PESI) score
this can be use to determine the suitability of outpatient treatment
MGT of suspected/ confirmed PE?
- Use a DOAC (apixaban or rivaroxaban) once diagnosis is suspected
if not suitable then in order use - LMWH –> dabigatran or edoxaban
- LMWH –> warfarin
for PE in pts with severe renal impairment or antiphospholipid syndrome the use LMWH –> Warfarin
when is the Pulmonary embolism rule-out criteria (PERC) used?
When there is a low suspicion of PE
if all criteria are negative then this can be used to rule out PE
if there is a high suspicion that PE is the likely diagnosis then Wells score should be used
Wells score- what is included?
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
An alternative diagnosis is less likely than PE 3
Heart rate > 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less
MGT of CHF
1st line - ACE-inhibitors and a beta blocker (bisoprolol, carvedilol, and nebivolol)
2nd line- Minralocorticoid receptor antagonist (MRA)
3rd line- should ne initiated by a specialist (ivabradine/ sacubitril-valsartan/ digoxin/ hydralazine/ cardiac resynchronisation therapy)
4Hs and 4Ts
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
When to give adrenaline during CPR?
ASAP for non-shockable rhythms
for VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock
repeat adrenaline 1mg every 3-5 minutes whilst ALS continues
When to give amiodarone in ALS?
https://bnf.nice.org.uk/medicines-guidance/life-support-algorithm-image/
After the third shock
Does grapefruit interact with simvastatin?
Grapefruit juice is a potent inhibitor of the cytochrome P450 enzyme CYP3A4
When are statins used: primary and secondary preventions?
primary (atorvastatin 20mg)
- QRISK >10%
- T1DM
- CKD if eGFR <60
secondary (atorvastain 80mg)
- known IHD, CVD, PAD
- when uptitrated if no >40% reduction in non-HDL is achieved with 20mg
MGT of HTN if <55yrs or T2DM
Step 1: A
Step 2: A+C or A+D
Step 3: A+C+D
step 4
if K 4.5 or less low dose spironolactone
if K more than 4.5 add an alpha or beta blocker
if BP on 4 drugs then for specialist review
MGT of HTN if 55 or more and no T2DM or black African or African-carribean ethnicity
Step 1: C
Step 2: C+A or C+D
Step 3: A+C+D
if pt is black then ARB is preferred to ACE
step 4
if K 4.5 or less low dose spironolactone
if K more than 4.5 add an alpha or beta blocker
if BP on 4 drugs then for specialist review
ECG: coronary territories and their arteries
Anteroseptal
V1-V4
lt anterior descending artery
Inferior
II III aVF
Rt coronary
Anterolateral
V4-6, I, aVL
lt anterior descending or lt circmflex
Lateral
I, aVL +/- V5-6
Lt circumflex
Posterior
changes in V1-3
Reciprocal changes of STEMI are typically seen
horizontal ST depression +
tall, broad R waves+
upright T waves+
dominant R wave in V2
Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)
Lt circumflex also rt coronary
HTN medications that can worsen gout
bendroflumethiazide
what is J wave classically a feature of?
Hypothermia
A J-wave is a positive deflection at the start of the ST interval, following the QRS complex.
In patients with chronic AF - what score should be used to decide on treatment?
CHA2DS2VASc
NICE suggest using the CHA2DS2-VASc score to determine the most appropriate anticoagulation strategy.
1 CHF
1 HTN
2 Age 75 or more
1 Age 65-74
1 DM
2 Stroke/TIA/VTE
1 IHD/ PAD
1 Female
if the score is
0 no tx
1 or more if male anticoagulate
2 or more if female anticoagulant
ORBIT scoring system
2 if Hb <130 g/L for M and < 120 g/L for F, or Hct < 40% for M and < 36% for F
1 Age > 74 years
2 Bleeding history (GI, intracranial or haemorrhagic stroke)
1 Renal impairment (GFR < 60)
1 tx c antiplatelet agents
ORBIT score
0-2 Low
3 Medium
4-7 High
Tx of AF if anticoagulation is indicated?
1st line DOAC
2nd line Warfarin
Inv of choice to dx aortic dissection?
CT angiography is the investigation of choice for suspected aortic dissection (depending on stability of patient)
Transoesophageal echocardiography (TOE)
more suitable for unstable patients who are too risky to take to CT scanner
Mgt of aortic dissection
Type A (ascending aorta, 2/3 of cases)
surgical management, SBP aim of 100-120 mmHg whilst awaiting intervention
Type B (descending aorta, distal to left subclavian origin, 1/3 of cases)
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression
complications of Aortic dissection
Complications of backward tear
aortic incompetence/regurgitation
MI: inferior pattern is often seen due to right coronary involvement
Complications of a forward tear
unequal arm pulses and BP
stroke
renal failure
MGT of VT
If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated.
otherwise antiarrhythmics
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
Verapamil should NOT be used in VT
If these fail, then electrical cardioversion may be needed with synchronised DC shocks
If drug therapy fails
electrophysiological study (EPS)
implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
Mgt of polymorphic broad complex tachycardia/ Torsades de Pointes (TdP)?
TdP is often short-lived and self-terminating; however, it can be associated with haemodynamic instability and collapse. IV magnesium sulphate is the first-line pharmacological treatment option for sustained TdP and is shown to stabilise the cardiac membrane.
What are the types of VT?
monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval.
Causes of prolonged QT interval?
Congenital
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness)
Drugs
amiodarone
sotalol
class 1a antiarrhythmic drugs
TCA
fluoxetine
chloroquine
terfenadine
erythromycin
Others
hypocalcaemia, hypokalaemia, hypomagnesaemia
acute MI
myocarditis
hypothermia
SAH
Medications causing ototoxicity?
Loop diuretics
Aminoglycosides (gentamicin, streptomycin, …)
Cisplantin and Carboplatin - antineoplastic drugs
Salicylates in high doses (temporary hearing loss and tinnitus)
NSTEMI with low GRACE score (3 or less)
how to manage
Aspirin + either
Ticagrelor (if not high bleeding risk)
clopidogrel (if high bleeding risk)
Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately.
You would perform an immediate coronary angiography in an NSTEMI patient if they were clinically unstable. You would also offer one in 72 hours in patients with a GRACE score>3%.
Features of hypokalaemia/ hyperkalaemia on ECG
Hyperkalaemia
- Peaked T waves
- P wave widening/flattening
- PR prolongation
- Bradyarrhythmias: sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow AF
Conduction blocks (bundle branch block, fascicular blocks)
-QRS widening with bizarre QRS morphology
Hypokalaemia
- Increased P wave amplitude
- Prolongation of PR interval
- Widespread ST depression and T wave flattening/inversion
- Prominent U waves (best seen in the precordial leads V2-V3)
- Apparent long QT interval due to fusion of - T and U waves (= long QU interval)
Normal ECG variants
sinus bradycardia
junctional rhythm (originates from AV node or AV junction- https://www.youtube.com/watch?v=I6Hk-Zd8PdM)
first degree heart block
Mobitz type 1 (Wenckebach phenomenon)
Interations of Clopidogrel
Class of drugs (thienopyridine)
MoA antagonistt of the P2Y12 adenosine diphosphate (ADP) receptor
Interacts with
PPIs (omeprazole and esomeprazole of concern but lansoprazole okay)
When to give statin for 1ry prevention for T1DM?
> 40 years
Had T1DM >10 years
Have established nephropathy
Have other CVD risk factors (such as obesity and hypertension)
MGT of
Stable angina
- lifestyle changes
- Medications (below)
- PCT
- surgery
Medicaitons
- All given Aspirin and statin
- GTN to abort episode
- 1st line BB or CCB
- if using CCB only then use verapamil or dilimiazem
- if using CCB and BB then use a longer acting dihydropyridine CCB (nifedipine or amlodipine)
BB should not be prescribed with verapamil (risk of complete heart block)
Verapamil should be avoided in HF pt
If a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs:
a long-acting nitrate
ivabradine
nicorandil
ranolazine
if a patient is taking both a BB and a CCB then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
Thiazides
vs
Thiazide-like diuretics
vs
MRA
Thiazides are benzothiadiazine derivatives, like
- chlorothiazide
- hydrochlorothiazide, and they all end in -thiazide;
whereas thiazide-like diuretics, like
- metolazone,
- indapamide, and
- chlorthalidone, are sulfonamide derivatives
SE - hypokalaemia
MRA (potassium sparing)
spironolactone and eplerenone
Medicaitons causing long QT
amiodarone
sotalol
class 1a antiarrhythmic drugs
TCA
SSRIs (especially citalopram)
methadone
chloroquine
terfenadine
erythromycin
haloperidol
ondanestron
Angiotensin II receptor blockers
Azilsartan
Candesartan
Eprosartan
Irbesartan
Losartan
Olmesartan
Telmisartan
Valsartan
Wolff-Parkinson White syndrome
(delta wave)
caused by a congenital accessory conducting pathway between the atria and ventricles leading to an AVRT
can lead to rapid VT
ECG features:
short PR interval
wide QRS complexes with slurred upstroke (delta wave)
LAD or RAD depending on the side of the pathway
MGT
definitive radiofrequency ablation of the accessory pathway
medical therapy
Sotalol/ amiodarone/ flecainide
Associations of WPW
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
what is bicalutamide (Casodex)
anti androgen
used in the treatment of prostate CA
Torsades de pointes (‘twisting of the points’)
is a form of polymorphic VT associated with long QT –> might progress to V fib
MGT is IV MgSO4
causes of long QT
congenital
- Jervell-Lange-Nielsen syndrome
- Romano-Ward syndrome
antiarrhythmics: amiodarone,
sotalol,
class 1a antiarrhythmic drugs
TCA
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage
Combination antiplatelets and anticoagulation therapy- when is it appropriate?
2ndry prevention in stable CVD with an Indication for an anticoagulant - stop anti platelet and commence anticoagulant mono therapy
Post acute ACS or PCI
triple therapy (2 antiplatelets + 1 anticoagulant) for 4 weeks-6 months after the event and dual therapy (1 antiplatelet + 1 anticoagulant) to complete 12 months
VTE
use ORBIT
if low risk of bleeding then use both
if high risk stop antiplatelets
Risk factors for statin induced myopathy
macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course
Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
when should you initiate MRA post MI rx in pt with HFREF?
within 3-14 days of the MI, preferably after ACE inhibitor
Murmurs (aortic and mitral)
AR - diastolic murmur loudest over the aortic valve with a wide pulse pressure
AS- systolic murmur with narrow pulse pressure
MR- systolic murmur
MS- diastolic murmur with wide pulse pressure
AR Diastolic
AS Systolic
MR Systolic
MS Diastolic
Verapamil should NOT be used in VT
Ventricular tachycardia: management
Whilst a broad complex tachycardia may result from a SVT rhythm with aberrant conduction, the ERC advises that in a peri-arrest situation it is assumed to be VT
If the pt has adverse signs (systolic BP < 90, chest pain, HF, syncope) then immediate cardioversion is indicated.
In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks.
Drug therapy
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
If drug therapy fails
- electrophysiological study (EPS)
- implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
SE of ACE
Side-effects:
cough
occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
Cautions and contraindications
pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
Interactions
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension
MGT of HF
- for all pt IV loop diuretics (furosemide/ bumetanide)
- if sats >94% oxygen
- if MI/ severe HTN/ valve disease - consider using vasodilator/ nitrates (SE hypotension)
- CPAP if resp failure
- for pt in caridogenic shock SBP <85
- inotropic agents e.g. dobutamine if shock reversible
- vasopressor agents norepinephrine if insufficient response to inotropes and end organ hypo perfusion
*mechanical circulatory assistance (intra-aortic balloon counter pulsation or ventricular assist devices)
When should you discontinue BB when treating acute HF
General points
regular medication for heart failure such as beta-blockers ACE-inhibitors should be continued
beta-blockers should only be stopped if the patient has heart rate less than 50 beats per minute, second or third degree atrioventricular block, or shock
AV blocks
First-degree heart block
PR interval > 0.2
asymptomatic commonly and does not need treatment
Second-degree heart block
type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
Third-degree (complete) heart block
there is no association between the P waves and QRS complexes
Infective endocarditis in intravenous drug users most commonly affects the tricuspid valve
Causes
staph aureus
strep viridian’s
coagulase-negative staphylococci e.g. staph epidermis
Strep bovis
non-infective (SLE and malignancy/ mar antic endocarditis)
Culture negative causes
prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
ECG findings in acute pericarditis
ECG changes
are often global/widespread
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
all patients with suspected acute pericarditis should have TTE
Management
treat the underlying cause (viral/ TB/ uraemia/ trauma/ Dressler’s (post MI)/ CTD/ hypothyroidism/ malignancy)
a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis
Which MI presents with a 1st degree heart block
Inferior MI
the MI must affect the inferior leads (right coronary arteries also provide blood supply to the AV node).
NICE NSTEMI/unstable angina guidelines are based on 6 month mortality risk:
if > 1.5% clopidogrel for 12 months
if > 3% angiography within 96 hours
nil
cardiac tamponade vs constrictive pericarditis
Cardiac tamponade
JVP Absent Y descent
Pulsus paradoxus Present
Kussmaul’s sign Rare
Constrictive pericarditis
JVP X + Y present
Pulsus paradoxus Absent
Kussmaul’s sign Present
Characteristic features Pericardial calcification on CXR
Beck’s triad for cardiac tamponade
Classical features - Beck’s triad:
hypotension
raised JVP
muffled heart sounds
Other features:
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans
MGT of cardiac tamponade
Management
urgent pericardiocentesis
Statins are contraindicated in
Pregnancy
with macrolide treatment
Causes for raised NTproBNP
LVH
MI
AF
pulmonary HTN
hypoxia
PE
right ventricular strain
COPD
liver failure
spesis
DM
renal impairment
in women
pt >70 years old
Causes for low NTproBNP
Heart failure is unlikely if BNP levels are low (<100). However, aldosterone antagonists, ACE inhibitors, angiotensin-II receptor antagonists, beta-blockers and diuretics can all falsely lower BNP levels, as can obesity.
Causes for low NTproBNP
Heart failure is unlikely if BNP levels are low (<100). However, aldosterone antagonists, ACE inhibitors, angiotensin-II receptor antagonists, beta-blockers and diuretics can all falsely lower BNP levels, as can obesity.
Dx of CHF and further management
First line NTproBNP
if high –> specialist assessment (including TTE) within 2 weeks
if raised –> specialist assessment (including TTE) within 6 weeks
When would you treat type 1 HTN 135/85 or more
treat all pt who are less than 80 and have
traget organ damage
established CVD risk
renal disease
diabetes
QRISK of 10% or more
When is cardiac resynchronisation therapy indicated?
in pt with symptomatic HF despited optimal medical management - pt would have LVF, ejection fracture <37%, and QRS duration >120ms
An Implantable cardiac defibrillator (ICD) is indicated in patients with previous sustained ventricular tachycardia, ejection fraction <35% and symptoms no worse than NYHA class III of the New York Heart Association functional classification.
Antihypertensives causing hypokalaemia
Indapamide
bendroflumethiazide are both thiazides diuretics; these cause hypokalaemia.
Bumetanide is a loop diuretic; this also causes hypokalaemia.
Antihypertensives causing hyperkalaemia?
Renin–angiotensin–aldosterone system (RAAS) inhibitors, such as angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and aldosterone antagonists, can increase the risk of hyperkalemia.
How to manage rises in U&Es following initiation of ACE inhibitors?
U&Es should be checked before treatment is initiated and after increasing the dose
A rise in the creatinine and potassium may be expected after starting ACE inhibitors
Acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
Significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
The DVLA guidance on driving after an acute coronary syndrome is as follows
If successfully treated by coronary angioplasty, driving may recommence after 1 week provided:
No other urgent revascularisation is planned. (Urgent refers to within 4 weeks from acute event)
Left ventricular ejection fraction is at least 40% prior to hospital discharge.
There is no other disqualifying condition.
If not successfully treated by coronary angioplasty, driving may recommence after 4 weeks provided:
There is no other disqualifying condition.
If the patient in this scenario was a bus, taxi or lorry driver the DVLA would need to be informed and driving would need to cease for at least 6 weeks.
Mgt of HOCM
Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500.
Management
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
Drugs to avoid
nitrates
ACE-inhibitors
inotropes
Complications of MI: immediate
1) Cardiac arrest
Mi -> V fib
Rx as per the ALS protocol with defibrillation.
2) Cardiogenic shock
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.
MI complications: early & late
- CHF
Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure. - Tachyarrhythmias
Ventricular fibrillation is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia. - Bradyarrhythmias
Atrioventricular block is more common following inferior myocardial infarctions. - Pericarditis
Common in the first 48 hours following a transmural MI (c. 10% of patients). A pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram. - Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
- Left ventricular aneurysm
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated. - Left ventricular free wall rupture
This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required. - Ventricular septal defect
Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed. - Acute mitral regurgitation
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.
When is prophylaxis against infective endocarditis recommended in the UK?
NICE recommends the following procedures DO NOT require prophylaxis:
dental procedures
upper and lower gastrointestinal tract procedures
genitourinary tract; this includes urological, gynaecological and obstetric procedures and childbirth
upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy
The guidelines do however suggest:
any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
It is important to note that these recommendations are not in keeping with the American Heart Association/European Society of Cardiology guidelines which still advocate antibiotic prophylaxis for high-risk patients who are undergoing dental procedures.
Inv in stable angina
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography
Examples of non-invasive functional imaging:
myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
stress echocardiography or
first-pass contrast-enhanced magnetic resonance (MR) perfusion or
MR imaging for stress-induced wall motion abnormalities
When should you add Alteplase during ALS
Thrombolytic drugs should be considered during CPR if a PE is suspected
What are the side effects of nicarandil
Adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Contraindications
left ventricular failure
Mgt of high INR?
Major bleeding
- Stop warfarin
- vitamin K 5mg IV
- Prothrombin complex concentrate - if not available then FFP*
INR > 8.0
Minor bleeding
- Stop warfarin
- vit K 1-3mg IV
- rpt vit K if INR still too high after 24 hours
- Restart warfarin when INR < 5.0
INR > 8.0
No bleeding
- Stop warfarin
- Give vit K 1-5mg orally, using the IV preparation orally
- Repeat dose of vitamin K if INR still too high after 24 hours
- Restart when INR < 5.0
INR 5.0-8.0
Minor bleeding
- Stop warfarin
- vit K 1-3mg IV
- Restart when INR < 5.0
INR 5.0-8.0
No bleeding
- Withhold 1 or 2 doses of warfarin
- Reduce subsequent maintenance dose
SE of thiazide diuretics
Common adverse effects
dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence
Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
Who is at risk for infective endocarditis?
The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. The following types of patients are affected:
previously normal valves (50%, typically acute presentation)
the mitral valve is most commonly affected
rheumatic valve disease (30%)
prosthetic valves
congenital heart defects
intravenous drug users (IVDUs)
e.g. typically causing tricuspid lesion)
others: recent piercings
Murmurs AR MR AS MS PDA
This is a presentation of aortic regurgitation, including Corrigan’s pulse and De Musset’s sign.
A pansystolic murmur is associated with mitral regurgitation.
An ejection systolic murmur is associated with aortic stenosis.
A continuous ‘machinery’ murmur is associated with a patent ductus arteriosus.
A late diastolic murmur is associated with mitral stenosis.
GRACE assessment
NSTEMI management is determined by a risk assessment score such as GRACE
Important for meLess important
The doctor is calculating the 6-month mortality using a GRACE score - this includes age, ECG, troponin, renal function. Other factors that are considered include blood pressure, heart rate, and if the patient had a cardiac arrest on presentation. Renal function is important for consideration as the kidney is a common target organ that is injured in an acute myocardial infarction (AMI).
How to manage monitored cardiac arrest?
Although patients in VF/pulseless VT should receive one shock followed by two minutes of CPR, if they are witnessed having the cardiac arrest and are monitored (e.g. coronary care unit, critical care unit, catheter laboratory) then they should receive a maximum of three successive shocks instead. Chest compressions would then follow and CPR would be continued for 2 minutes.
Adrenaline 1mg IV and amiodarone 300mg IV are given once compressions restart following three shocks for shockable rhythms (VT/pulseless VF). This is then followed by adrenaline 1mg IV after alternate shocks (every 3-5 minutes).
Adrenaline 1mg IV is also given as soon as venous access is achieved for non-shockable rhythms (pulseless electrical activity/asystole) which would be done alongside CPR. Pulseless electrical activity is a cardiac arrest in which there is electrical activity (other than ventricular tachycardia) which would normally have an associated pulse.
Features of buerger’s dx?
Buerger’s disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
Features
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon
Nitrate tolerance
many patients who take nitrates develop tolerance and experience reduced efficacy
NICE advises that patients who take 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
this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate
S&S of mild vs severe airway obstructions
Mgt of airway obstruction
Mild airway obstruction
Response to question ‘Are you choking?’
victim speaks and answers yes
victim is able to speak, cough, and breathe
Severe airway obstruction
Response to question ‘Are you choking?’
victim unable to speak
victim may respond by nodding
victim unable to breathe
breathing sounds wheezy
attempts at coughing are silent
victim may be unconscious
Mgt
If mild airway obstruction
encourage the patient to cough
If severe airway obstruction and is conscious:
give up to 5 back-blows
if unsuccessful give up to 5 abdominal thrusts
if unsuccessful continue the above cycle
If unconscious
call for an ambulance
start CPR
Medications to reduce mortality in pts with LVF
The following drugs have all been shown to reduce mortality in patients with left ventricular failure:
ACE-inhibitors
Beta-blockers
Angiotensin receptor blockers
Aldosterone antagonists
Hydralazine and nitrates
LFT monitoring with statin
liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
Secondary causes of HTN?
It is thought that between 5-10% of patients diagnosed with hypertension have primary hyperaldosteronism, including Conn’s syndrome. This makes it the single most common cause of secondary hypertension.
Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include:
glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis
Endocrine disorders (other than primary hyperaldosteronism) may also result in increased blood pressure:
phaeochromocytoma
Cushing’s syndrome
Liddle’s syndrome
congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
acromegaly
Drug causes:
steroids
monoamine oxidase inhibitors
the combined oral contraceptive pill
NSAIDs
leflunomide
Other causes include:
pregnancy
coarctation of the aorta
