Cardiology Flashcards
central, pleuritic chest pain and fever 4 weeks following a myocardial infarction suggests what?
Dresslers - Pericarditis following MI
traumatic accident with respiratory distress, hypotension, jugular venous distension, and absent lung sounds suggests what?
Tension pneumothorax
A third heart sound is considered normal
in patients under what age?
<30 years old
What are the common causative organisms of infective endocarditis?
Most common/IVDU - Staph aureus
Those with poor dental hygiene/post dental proceudure - Strep viridans
Following prosthetic valve surgery - Staph epidermidis
Widened mediastinum on CXR with severe chest pain suggests what?
Aortic dissection
In ALS, if IV drugs cannot be given, how should they be given?
Intraosseous
What is the most specific ECG finding in acute pericarditis?
PR depression
Type A (ascending) vs Type B (descending) aortic dissection?
A - chest pain
B - upper back pain
tall R waves in leads V1-3 are a classic finding for what?
Posterior MI
What score should be used to assess the risk of bleeding when starting someone on anticoagulation in AF?
Orbit
What are reversible causes of cardiac arrest?
Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins
When should warfarin be stopped prior to surgery?
5 days before
What is the key diagnostic finding of aortic dissection on CT?
False lumen
What are C/I to thrombolysis?
active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension
weak or absent carotid, brachial, or femoral pulse
variation in arm BP suggests what?
Aortic dissection
When can electrical cardioversion be considered for patients with AF?
If presenting within 48 hours
What medication should be stopped when patients are given a course of macrolides e.g. clarithromycin?
Statins
Thiazide-like diuretics should not be used in patients with what?
Gout
ST elevation and acute pulmonary oedema in a young patient with a recent flu-like illness suggests what?
Myocarditis
When should rhythm control be used for AF instead of rate control?
coexistent heart failure, first onset AF or an obvious reversible cause
Which medication can reduce hypoglycaemia awareness?
Beta blockers
Which medication can impair glucose tolerance?
Thiazides
Widespread ST elevation in V1-4 suggests what?
100% occlusion of the LAD
Erythromycin can cause which cardiac abnormality?
QT prolongation
What kind of bacteria is staph aureus?
Gram positive cocci
How should a patient with minor bleeding with INR > 8 be managed?
Stop warfarin and give IV Vitamin K with repeat dose of Vit K after 24 hours if INR still high
What drugs can cause hypokalaemia?
Loop diuretics e.g. furosemide
A new left bundle branch block should raise alarms for what?
ACS
What scoring system should be used to identify patients with a pulmonary embolism that can be managed as outpatients?
Pulmonary Embolism Severity Index (PESI)
How does fondaparinux work?
Activates antithrombin III
What is the management of AF if ChadsVasc is 0?
Echo to rule out valvular causes
What are ecg findings of hypokalaemia?
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
U waves
What is the second-line therapy in patients with HFrEF?
SGLT-2 inhibitors e.g Empagliflozin
inferior myocardial infarction and AR murmur suggests what?
Proximal aortic dissection
High dose statins should be commenced in stroke patients when?
48 hours after stroke
What criteria should be used for infective endocarditis?
Duke criteria
What criteria should be used for rheumatic fever?
Jones criteria
What drugs should be used for anticoagulation in those with mechanical heart valves?
Warfarin/LMWH
Complete heart block following an MI suggests the lesion is where?
Right coronary
Investigation of choice for aortic dissection?
CT Angio
Management of aortic dissection
Control BP with IV Labetalol and surgery
Most common ECG change of PE?
Sinus tachycardia
CP of pericarditis?
- pleuritic chest pain: worsen lying flat and relieved by sitting forward
- fever
- pericardial rub
- tachycardia and tachypnea
- non-productive cough
- dyspnoea
- flu-like symptoms
What may a pericardial rub indicate? (friction of heart against pericardium, sounds like sandpaper rubbed on wood)
pericarditis
Ix for pericarditis?
- all pts with suspected= TRANSTHORACIC ECHO
- ECG
- bloods: inflam markers, only 30% have elevated troponin
Pericarditis is associated with what?
pericardial effusion that can sometimes worsen to cardiac tamponade
ECG findings for pericarditis?
- PR depression
- ‘saddle-shaped’ ST elevation
PeRicardiTiS
Management of pericarditis?
NSAIDs plus colchicine
Until CP resolution and normal inflam markers (usually 1-2w) followed by tapering of dose recommended
PR Depression on ECG is indicative of what?
Pericarditis
Medical management of NSTEMI?
dual antiplatelet therapy, an ace inhibitor, a beta-blocker, and a statin
What is Beck’s triad?
- Raised JVP
- Muffled heart sounds
- Falling BP
What is Beck’s triad a sign of?
Cardiac tamponade
Management of major bleed with someone on warfarin?
stop warfarin, give intravenous vitamin K 5mg, prothrombin complex concentrate
How should episodic palpitations be investigated?
Holter monitoring
notching of the inferior border of the ribs suggests what?
Aortic coarctation
Management of PE with low PESI score?
Can be managed as an outpatient with DOAC
Nitrates for MI are contraindicated when?
Patients with hypotension
What is the treatment for torsades de pointes?
IV Mag Sulph
What is a normal cardiac variant in athletes?
First degree heart block
Investigation of choice for someone with PE and renal impairment?
V/Q scan
What is normal in an athlete and does not require any intervention?
First degree heart block
If angina is not controlled by a beta blocker, what should be added?
Amlodipine
What should be used if atropine if not helping with bradycardia?
- transcutaenous pacing
- transvenous pacing
Sydenham’s chorea is a complication of what?
Rheumatic fever
Management of persistent myocardial ischaemia following fibrinolysis
PCI even if time elapsed
What on echo is used to determine the severity of aortic stenosis?
Trans-valvular pressure gradient
What is Buerger’s disease?
aka thromboangiitis obliterans
- A small/medium vasculitis which is associated with smoking
- CP: intermittent claudication, Raynaud’s, ischaemic ulcers, superficial thrombophelbitis
What is the mode of action of statins?
Decrease intrinsic cholesterol synthesis by inhibiting HMG-CoA reductase enzyme
How to manage a strong suspicion of PE whilst waiting for scan?
Start treatment dose anticoagulant
Electrical alternans is a sign of what?
Cardiac tamponade
J waves are associated with what?
Hypothermia
Hypertrophic obstructive cardiomyopathy is associated with what?
Wolf-Parkinson-White
Management of acute heart failure not responding to furosemide?
Consider CPAP
What is a complication of MI?
Pulmonary oedema
SVT Management?
- Valsalva
- IV Adenosine upto 3 doses
- Electrical cardioversion
Criteria for rate control vs anticoag/cardioversion?
- Under 65
- No Hx of IHD
Thrombus in aVL, which artery?
Left circumflex
What is Framingham risk score?
estimate the 10-year risk of heart attack
severe hypertension and bilateral retinal hemorrhages and exudates
Malignant HTN
Endocarditis - which valves are affected?
Mitral - most common
Aortic
Tricuspid - IVDU
A patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination
VSD
Treatment for cardiac tamponade?
Urgent pericardiocentesis: Pericardial needle aspiration
What is Kussmaul sign?
- JVP rises on inspiration
- Sign of constrictive pericarditis
holosystolic murmur, high-pitched and ‘blowing’ in character
Mitral regurg
Tachycardia and tachypnoea with no signs
Think PE
Can warfarin be used when breast feeding?
Yes
What electrolyte abnormality do thiazide diuretics cause?
- Hypokalaemia
- Hyponatraemia
- Hypercalcaemia
- Gout
- Impaired glucose tolerance
Management of irregular broad complex tachycardia
Seek cardiology input
What is Takayasu’s arteritis?
- Systemic features of vasculitis
- Unequal BP in upper limbs
- Carotid tenderness
- Absent/weak peripheral pulses
- Associated with renal artery stenosis
- MRA/CTA to treat with steroids
Low pitched diastolic murmur?
Mitral stenosis
Acute mitral valve regurg + pulmonary oedema
Think MI
What is the dose of adrenaline used in cardiac arrest?
1mg of IV adrenaline
Breathing problems with clear chest
PE
What is Brugada syndrome?
- AD disorder which can cause sudden death
- autosomal dominant; more common in Asians
- can be caused by mutation in SCN5A gene (encodes for myocardial sodium ion channel protein)
- ECG shows ST elevation and T wave inversion (may become clearer after giving flecainide- Ix of choice)
- Mx is implantable cardioverter-defib
Most common place of inhaled foreign body?
Right inferior bronchus
Findings for aortic stenosis?
narrow pulse pressure
slow rising pulse
a thrill palpable over the cardiac apex
a fourth heart sound (S4) indicative of left ventricular hypertrophy
a soft/absent S2
Which medications can cause torsades de pointes?
Macrolides e.g. azithromycin
What condition are ACE inhibitors C/I with?
Renovascular disease
What causes the acute mitral regurg following MI?
Rupture of the papillary muscle/ischaemia
When can you commence spironolactone for HTN?
When already taking ACE, CCB and thiazide-like diuretic + K is below 4.5
When should adrenaline be given for shockable rhythms?
After 3 unsuccessful shocks
Pericarditis vs Myocarditis?
Myocarditis -> elevated troponin
Which markers can you test for STEMI?
Troponin, CK, AST, LDH
What ECG changes might be seen following STEMI?
T wave inversion, pathological Q waves
Driving rules post MI
- No need to inform DVLA
- Can drive after1 week if successful angioplasty
- Can drive after 4 weeks if no angio/unsuccessful angio
Complication of coronary angio
Bleeding, haemorrhage, infection, MI, stroke, damage to coronary vessels, death
What triggers are there for angina?
Exertion, cold weather, emotions such as anger, vivid dreams
How does aspirin work?
Inhibits COX which inhibit thromboxane which inhibits platelets aggregation
Abnormally large drop in BP during inspiration?
Pulsus paradoxus -> Cardiac tamponade
How should diabetes be managed following MI?
Use IV insulin infusion and stop the oral diabetes meds
patients with a GRACE score > 3% should have what?
Coronary angio within 72 hours
Management of persistent MI following fibrinolysis
PCI
What is the treatment of broad complex tachycardias?
- Amiodarone
Single episode of paroxysmal AF?
ChadsVasc and consider DOAC
Management of IE causing congestive cardiac failure
Emergency valve replacement
What is the alternative to 3 weeks of anticoagulation for someone having cardioversion with AF?
Transoeseophageal echo to exclude left atrial appendage thrombus
What are warfarin INR targets for mechanical valves?
Aortic - 3.0
Mitral - 3.5
What is the NYHA heart failure classification?
Class 1 - no symptoms and no limitations
Class 2 - mild symptoms with slight limitation (some fatigue, dyspnoea)
Class 3 - moderate symptoms with marked reduction in activity (symptoms anytime except rest)
Class 4 - severe symptoms and symptoms of HF present even at rest
When is AAA screening done?
Men aged 65
How is AAA screening managed?
< 3 cm - normal
3 - 4.44cm - rescan every 12 months
4.45 - 5.4cm - rescan every 3 months
>5.5 - refer to vascular surgery within 2 weeks
Other referral criteria
- Rapidly growing (>1cm per year)
What is the biggest indicator of a poor prognosis in someone with MI?
Cardiogenic shock
What would an ABG for pulmonary embolism show?
Respiratory alkalosis -> hyperventilation
When is staph epidermidis the most common organism causing endocarditis?
If <2 months post valve surgery
Why is verapamil C/I in heart failure + VT?
It can slow down contractility of the heart even further
What is the most common cause of death in patients post MI?
V Fib
Haemoptysis can be a symptom of what?
Mitral stenosis
mid-diastolic low-pitched rumbling murmur
mitral stenosis
Management of BP > 180/120 in GP
If unstable/signs of papilloedema/retinal haemorrhages -> refer to specialist
If stable then arrange urgent investigations for organ damage eg. bloods, urine ACR, ECG
What is the normal QRS value?
<0.12s / 3 small squares
What are signs of left ventricular failure?
Dyspnoea, reduced exercise tolerance, fatigue, paroxysmal nocturnal dyspnoea, orthopnoea, wheeze, cough (worse at night), pink, frothy sputum
What are signs of right ventricular failure?
Peripheral oedema, facial engorgement and abdominal distension
What are causes of AF?
Pneumonia, MI, PE, Alcohol excess, HF, Endocarditis
What are signs of aortic regurg?
- Collapsing pulse
- Early diastolic murmur
- Wide pulse pressure
- Displaced apex
- Carotid pulsation: Corrigans sign
- pulsation of nail bed: Quincke’s sign
Absent arm pulses in a young woman?
Think Takayasu’s arteritis
AF + mass in left atrium
Cardiac myxoma - bengin tumour of the heart
Patients with aortic valve IE are at risk of what?
Developing aortic valve abscess (prolongation of PR can be first sign)
What pulse can you get with heart failure?
Pulsus alternans - strong and weak beats due to varying systolic pressure
When is rhythm control used in AF treatment over rate control?
- Coexistent HF
- First onset AF
- Obvious reversible cause
- Use amiodarone/flecainide
What is the inheritance of HOCM?
AD
What is the pathophysiology of HOCM?
- Diastolic dysfunction as LVH causes decreases compliance and decreased CO
- Biopsy shows myofibrillar hypertrophy with disarrayed myocytes
ECG findings for hypercalcaemia?
Short QT
What are the components for JONES criteria?
Joint involvement
<3 - Myocarditis
Nodules
Erythema marginatum
Sydnehams chorea
Post MI patient develops pulmonary oedema and has pansystolic murmur?
Think acute mitral regurg
What can cause orthostatic hypotension?
- Excercise induced
- After meals
- After prolonged bed rest
- Drugs such as CBB, Levodopa
QT prolongation with no electrolyte abnormalities?
Think hereditary long QT syndrome -> caused by loss of function/blockage of K+ channels
When should LFTs be checked with statins?
Baseline, 3 months and 12 months
What murmur do you get with VSD?
Pansystolic murmur - entire systolic period
Which drug when used alongside clopidogrel can make it less effective?
Omeprazole/Esomeprazole
What dose of amiodarone is given in ALS?
Initially 300mg
After 5th shock, an additional 150mg can be given alongside 1mg of adrenaline
What will type A aortic dissection cause?
Acute aortic regurg
What is the treatment for rheumatic fever?
IM BenPen or Oral PenV with NSAIDs
Patients taking isosorbide mononitrate should use what dosing regime?
Asymmetric dosing interval to prevent nitrate tolerance
NSTEMI in an unstable patient?
Immediate coronary angio
Which antihypertensive cause hyperkalaemia?
ACE
What is tongue and facial swelling?
Angioedema -> ACE inhibitor
What are examination signs of pericarditis?
-Pericardial rub
- Quiet heart sounds
- Raised JVP
What are causes of pericarditis?
- Infective: coxsackie, TB
- Trauma
- Malignancy eg. lung/breast
- MI complication
- SLE
- RA
- hypothyroidism
3 main investigations for IE?
- Blood cultures
- Echo
- ECG
What are some triggers for worsening pulmonary oedema?
- Arrhythmia
- MI
- Sepsis
What is the most common cardiomyopathy?
Dilated
management of mitral stenosis?
Asymptomatic - Monitor with regular echo
Symptomatic - Percutaneous mitral commissurotomy
When fibrinolysis is done for ACS, when should ECG be repeated?
60-90 minutes
What are the ChadsVasc categories?
Congestive HF
HTN
Age >75 (2), >65 (1)
Diabetes
Stroke/TIA/VTE
Vascular disease
Sex (Female)
Where is access preferred for PCI?
Radial artery
Which medications can worsen glucose tolerance?
Thiazides
widespread pansystolic murmur, hypotension, pulmonary oedema post MI?
Acute mitral regurg
Management of suspected HF in GP?
Measure BNP and refer for TTE if elevated
What does a loud opening snap indicate?
The mitral valve leaflets are still mobile in mitral stenosis
What can indicate the severity of the mitral stenosis?
Length of murmur increases
What are components of orbit score?
- Haemoglobin
- Age
- Bleeding history
- Renal impairment
- Treatment with anti platelets
Nailed pulsation?
Quincke’s sign -> aortic regurgitation
Rate control for AF?
Beta blocker
CCB
Digoxin
Management of continued pain post PCI for MI?
Urgent CABG
Reverse nike sign?
Digoxin
Persistent ST elevation post MI?
Left ventricular aneurysm
What are signs of aortic coarctation?
- radio-femoral delay
- mid systolic murmur
- weak peripheral pulses in legs
- Left ventricular heave
Investigations to confirm aortic coarctation?
- Echo
- CT aorta
- Cardiac catheterisation
Management options for aortic coarctation?
- Open surgery
- Balloon angioplasty and stent insertion
- Mild cases can be controlled with antihypertensives
What carries the worst prognosis in symptomatic aortic stenosis?
Exertional syncope
What medication should be avoided in someone with aortic stenosis?
Nitrates
When should adenosine be avoided?
Asthmatics
What is the definitive management of bradycardia?
Permanent pacemaker
Which organisms often cause rheumatic fever?
Strep pyogenes
Stroke + AF?
2 weeks of aspirin then warfarin/DOAC
ADPKD is associated with what?
Mitral valve prolapse
S3 vs S4 sounds
CCF - 3 letters - S3
HOCM - 4 letters - S4
What does aortic dissection cause?
Weak/absent carotid, brachial or femoral pulses
HF with rEF vs HF with pEF?
rEF - systolic dysfunction e.g. IHD, arrythmias
pER - diastolc dysfunction e.g. HOCM, cardiac tamponade
What can be done for patients not responding to medications for HF?
Cardiac resynchronisation therapy if wide QRS
Raised JVP, ankle oedema, hepatomegaly
Right sided HF
What are causes of torsades de pointes?
- Congenital
- Macrolides
- Subarachnoid haemorrhage
- Hypothermia
- Electrolyte disturbances
What is torsades de pointes?
Polymorphic VT
Heart failure management
- ACE + BB
- Spironolactone/Eplerenone
3rd lines
- Ivabradine if HR > 75 and reduced EF
- Hydralazine with nitrate for Afro-Caribbean patients
- Sacubitrtil-valsartan for patients with reduced EF after ACE/ARB wash out period
- Digoxin if sinus rhythm
What vaccines should be given to HF patients?
Annual flu
One off PCV
Sudden heart failure, raised JVP, pulsus parodoxus post MI?
Left ventricular free wall rupture
What ABG picture will hyperaldosteronism cause?
Metabolic alkalosis with hypokalaemia
What can cause high output heart failure?
Anaemia
When is DC cardioversion done for arrhythmias?
Systolic < 90
How to manage HTN when patient is on ACE/CCB/Thiazide and K+ > 4.5?
Add alpha/beta blocker
AF with sudden onset abdo pain?
Think acute mesenteric ischaemia -> treat with immediate laparotomy
Management of ruptured AAA?
Crossmatch 6 units of blood
When is amiodarone preferred for pharmacological cardioversion?
Evidence of structural heart disease
Chest pain + neurology?
Think aortic dissection
new BP >= 180/120 mmHg + new-onset confusion, chest pain, signs of heart failure, or acute kidney injury
Refer for assessment
CCB side effects
headache, flushing, ankle oedema
Amlodipine can cause what?
Gingival hyperplasia
What is the cut off for aortic valve surgery if no symptoms?
Valvular gradient > 40 with features of left systolic dysfunction
pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles
Wolf-Parkinson-White
Gallop rhythm is a sign of what?
Left sided heart failure
Prosthetic vs mechanical valve?
Mechanical last longer so are given to younger patients
What can be considered in CPR if a PE is supected?
Thrombolytic drugs such as alteplase
How should 80+ year olds with raised BP be managed?
Lifestyle advice
Nifedipine can cause what?
Peripheral vasodilation which can cause reflex tachycardia
What is an alternative to amiodarone in arrest?
Lidocaine
What drugs are an alternative to atropine?
Isoprenaline/adrenaline infusion
How long should CPR be continued when thrombolytic drugs are being given?
60-90 minutes
Tension pneumothorax can cause what?
Pulseless electrical activity
Clinically unstable aortic dissection?
Transoesophageal echo
What is the most common cause of aortic stenosis in young patients?
Congenitally bicuspid valve
Hyperlipidaemia can cause what?
Pseudohyponatremia -> serum osmolality will be normal
Premature supraventircular beats vs premature ventricular betas on ECG?
Supraventricular - narrowed QRS complexes
Ventricular - widened QRS complexes
What is cardiac tamponade?
Accumulation of pericardial fluid causing increased pericardial pressure which compromises ventricular filling, resulting in a
reduced cardiac output.
cardiomyopathy + diabetes + joint pain + hepatomegaly
Think haemochromatosis
What antibiotic is recommended in COPD patients who continue to have exacerbations?
Azithromycin
Chronic infection with Pseudomonas and Bulkholderia in CF
Increased risk of morbidity or mortality
Pericarditis vs STEMI ECG?
STEMI will have ST elevation greater in lead III than lead II
Aortic dissection can cause what?
Neuro deficits
Persistent ST elevation with fatigue
Left ventricular aneurysm
When do CK levels normalise after an MI?
48-72 hours -> good to check if suspecting a reinfarction
When should sacubitril-valsartan be initiated?
Following an ACE/ARB wash out period
What part of the QRS is electrical cardioversion synchronised to?
R wave
Mitral regurg is associated with which conditions?
- Marfans
- Ehlers-Danlos
DC cardioversion vs unsynchronised cardioversion?
DC- Tachyarrhythmias
Unsynchronised - Cardiac arrest (VT, VF)
What is the management of atrial flutter?
- Beta blocker/CCB
- Consider cardioversion
- Catheter ablation curative
Sudden increase in BP associated with ACS?
Treat with IV GTN
Elderly patient with ECG with periods of sinus bradycardia + atrial tachycardia?
Sick sinus syndrome
What is a normal PR interval?
0.12-0.20s
3-5 small squares
Absent P waves + regular rhythm of QRS
SVT
What stroke is most likely during cardiac catheterisation?
Embolic -> debris can be scraped from aortic wall
Most common cause of left ventricular hypertrophy in a healthy person?
Hypertrophic cardiomyopathy
Heart failure + wide QRS?
Consider resynchronisation pacemaker device
2nd line investigation for endocarditis if echo is negative but high suspicion?
PET CT
What is the PR interval?
Start of P wave to start of QRS complex
Indications for DC cardioversion in tachyarrhythmias except shock?
- Syncope
- MI
- Heart failure
What are the 2 options for aortic valve replacement?
Surgical - low risk patients
Transcatheter - high risk patients
When to do 1 shock vs 3 shocks in shockable rhythms?
3 shocks - if witness cardiac arrest
1 shock - if not witnessed
What is a common cause of tricuspid regurg?
Pulmonary HTN e.g. COPD
Investigation of choice for cardiac tamponade?
Echo
When in CABG indicated?
More significant coronary artery disease e.g. triple vessel
Abx for MRSA resistant endocarditis?
Prosthetic valve - Vancomycin, Rifampicin and Gentamicin
Normal valve - Vancomycin and Rifampicin
Thiazides can precipitate what?
Digoxin toxicity
De Musset sign is a sign of what?
Aortic regurgitation
What is acute coronary syndrome? (ACS)
umbrella term covering number of acute presentations of ischaemic heart disease
Presentations of acute coronary syndrome?
1) STEMI
2) NSTEMI
3) unstable angina
As a rise in troponins may take hrs, it may be hard to distinguish between unstable angina and NSTEMI initally so what do you do?
Treat like NSTEMI until troponin result is known
When is unstable angina considered to be present in patients? (an acute coronary syndrome)
pts with ischaemic symptoms suggestive of ACS and NO elevation in troponins, with or without ECG changes indicative of ischaemia
ACS generally develops in what patients?
Those with known or unknown ischaemic heart disease
What are other terms for ischaemic heart disease (all have the SAME meaning)?
coronary heart disease, coronary artery disease, IHD all mean same thing
What causes IHD?
gradual build up of fatty plaques within walls of coronary arteries
What does IHD lead to?
1) gradual narrowing of coronary arteries therefore less oxygen reaching myocardium at times of increased demand -> angina
2) risk of sudden plaque rupture -> sudden occlusion of coronary artery -> no oxygen reaching area of myocardium
Unmodifiable RFs for IHD
increasing age, male, FHx
Modifiable RFs for IHD
smoking, DM, HTN, obesity, hypercholesterolaemia
IDH pathophysiology: inital endothelial dysfunction is triggered by what?
factors eg. smoking, HTN, hyperglycaemia
Inital endothelial dysfucntion results in what changes to the endothelium in IHD?
pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
IHD pathophysiology: endothelial dysfunction is triggered and there are a number of changes to the endothelium; fatty infiltration of the subendothelial space by what then occurs?
Low-density lipoprotein (LDL) particles
IHD pathophysiology: role of monocytes in the progagation of the inflammatory process?
monocytes migrate from the blood and differentiate into macrophages; these then phagocytose oxidised LDL, slowly turning into large ‘foam cells’. As these macrophages die, the result can further propagate the inflamm process
IHD pathophysiology: what forms the fibrous capsule covering the fatty plaque?
smooth muscle proliferation and migration from tunica media into intima results in formation of fibrous capsule covering fatty plaque
What pathophysiological changes can be seen in IHD over number of years?
- intial endothelial dysfunction
- results in a number of changes to endothelium
- fatty infitration of subendothelial space by LDL
- formation of ‘foam cells’ and inflammatory process
- smooth muscle proliferation and migration to form fibrous capsule covering fatty plaque
Cx of atherosclerosis?
angina
MI
How does atherosclerosis cause angina?
plaque forms physical blockage in lumen of coronary artery; may cause reduced blood flow (and so oxygen) to myocardium, partically at times of increased demand
How can atherosclerosis cause myocardial infarction?
plaque may rupture, potentially causing a complete occlusion of coronary artery
Function of endothelium of arteries?
protects vessel wall and prevents clotting
Pathophysiology of atherosclerosis?
- damage to endothelium wall allows LDL to enter
- monocytes enter and break LDL down by oxidation, causes macrophage to die
- then deposits under damaged endothelium: called foam cells
- when macrophages die, also release cytokines that causes more monocytes to enter endothelium and break down more LDL
- foam cells build up to form a lesion called a fatty streak
- fatty streak is thrombogenic meaning blood can clot on it
- platelets gather at damaged endothelium and release platelet dervived growth factor which encourages growth of smooth muscle cells
- smooth muscle meant to stay in middle layer (tunica media) but starts to growth in tunica intima where they multiply
- smooth muscle cells secrete collagen, proteoglycans, elastin fibrous cells that form a wall around fatty streak preventing blood clotting= extracellular matrix wall of fibrous cap
- fibrous cap + fatty streak = plaque
Why in atherosclerosis do the walls of the arteries become stiff?
- smooth muscle also starts depositing calcium into the plaque creating crystals
- Ca crystals normally deposited by LDL and removed by HDL, but plaque stops HDL removing Ca
- causes build up of Ca in vessel wall and crystallises= stiffens walls of arteries
Why might a high CRP indicate atherosclerosis?
atherosclerosis is an inflamm disease as immune sysytem invl (macrophages). Therefore high CRP
CPS of acute coronary syndrome?
- left-sided/central chest pain
- may radiate to jaw or L arm
- ‘crushing’ ‘heavy’
- dyspnoea
- sweating
- nausea
What pts with ACS may not experience any chest pain?
Diabetics; elderly
Physical signs of ACS
- BP, HR, T, O2 often normal or mild eg. tachy
- unless HF
- pale, clammy
Most important Ix when assessing pt with chest pain
- ECG
- cardiac markers eg. troponin
Deep and widespread ST depression is associated with what?
very high mortality because it signifies severe ischaemia usually of LAD or left main stem
Aims of treatment of ACS?
1) prevent worsening (further occlusion)
2) revascularise (unblock) vessel if occluded (STEMI)
3) Mx pain
Acute Mx of ACS
M.orphine (IV)
O.xygen (if <94%)
N.itrates (IV or subling)
A.spirin (300mg)
When should oxygen be given in Mx of ACS?
if sats <94%
Secondary prevention for pts who have had an ACS?
Aspirin
Antiplatelet eg. clopidogrel
BB
ACE inhibitor
Statin
STEMI?
ST-elevation MI= ST-segment elevation + elevated biomarkers of myocardial damage
NSTEMI?
non ST-elevation MI= ECG change but no ST-segment elevation + elevated biomarkers of myocardial damage
Groups of Mx for acute coronary syndromes?
- STEMI
- NSTEMI/unstable angina
- Secondary prevention
Dose of aspirin to give in acute Mx?
300mg
Acute Mx of ACS: nitrates should be used in caution if the pt is…
Hypotensive
Overview of Mx in pt with suspected ACS?
1) acute Mx
2) ECG findings- ?STEMI
3) STEMI confirmed= eligability for coronary reperfusion therapy
STEMI criteria?
CP consistent with ACS ≥ 20mins with persistent >20mins ECG features in ≥ 2 contiguous leads
STEMI ECG criteria in men?
ECG features in ≥ 2 contiguous leads of….
Men <40yrs=
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3
Men >40yrs= ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3
PLUS 1 mm ST elevation in other leads & new LBBB (LBBB should be considered new unless there is evidence otherwise)
STEMI ECG criteria in women?
ECG features in ≥ 2 contiguous leads of…
1.5 mm ST elevation in V2-3
STEMI Mx?
1) 300mg aspirin (+other acute Mx)
2) PCI OR Fibrinolysis
3) dual antiplatelet therapy: Clopidogrel + aspirin (if high bleeding risk) or tricagrelor + aspirin (low risk)
4) stenting indicated? Cardiac rehab and secondary prevention
2 types of coronary reperfusion therapy in STEMI?
1) PCI: dual antiplatelet therapy before; then during give either unfractionated heparin with bailout GPI if radial access or bivalirudin with bailout GPI if femoral access
2) Fibrinolysis + antithrombin drug
In STEMI Mx when should pt get PCI?
<12hrs of symptoms and can be delivered in 120mins. Consider >12hrs if CG shock or continue ischaemia.
PCI for Mx of STEMI?
1) dual antiplatelet therapy before PCI:
aspirin + prasugrel or clopidogrel
2) PCI with radial access: + unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)
OR
2) PCI with femoral access: bivalirudin with bailout GPI
Dual antiplatelet therapy to give pt with STEMI prior to PCI?
Aspirin +
clopidogrel if taking oral anticoag
or
prasugrel if not taking oral anticoag
In STEMI Mx when should pt get fibrinolysis?
if <12hrs and PCI not possible in 120mins
Patients undergoing fibrinolysis should also be given what?
Antithrombin drug eg. fondaparinux or LMWH
When should ECG be done after fibrinolysis?
60-90mins after
STEMI Mx: is radial or femoral access preferred?
Radial
What if pt with STEMI gets ECG 90mins after fibrinolysis and it fails to show resolution of ST elevation?
PCI
Mx of NSTEMI/unstable angina overview?
1) 300mg aspirin + fondaparinux or unfractionated heparin
2) GRACE score
3) low risk= dual antiplatelt therapy (aspirin + ticagrelor or clopidogrel)
3) intermediate/high risk= PCI immediately/within 72hrs; give aspirin + prasugrel or ticagrelor (if pt on oral anticoag give clopidogrel); give unfractioned heparin; use drug-eluting stents
4) assess LV function and consider angiography (eg. if develop ischaemia)
5) cardiac rehab and secondary prevention
What is dual antiplatelet therapy (DAPT)?
aspirin + P2Y12 inhibitor eg. clopidogrel, prasugrel or ticagrelor
How to know what drugs to use for DAPT?
Apirin +
prasugrel (during PCI) if not taking anticoag
clopidgorel (during PCI) if taking anticoag
ticagrelor if low bleeding risk
clopidogrel if high bleeding risk
How do you decide if you use fonaparinux or unfractionated heparin initally in the Mx of NSTEMI/unstable angina?
- fondaparinux= low risk of bleeding and no immediate angiography
- unfractionated heparin= immediate angiography planned or creatinine is > 265 µmol/L
What does GRACE score stand for?
The Global Registry of Acute Coronary Events
What is the GRACE score?
Predicts 6m mortality and risk of cardiovascular events
In Mx for NSTEMI/unstable angina, as well as the GRACE risk score what else needs to be included in the risk assessment?
history, examination; ECG; bloods (troponin I or T, creatinine, glucose, Hb); balance possible benefits of Mx against bleeding risk
What factors does the GRACE score account for?
age
HR, BP
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels
GRACE score: what is low risk?
predicted 6m mortality ≤ 3%
GRACE score: what is intermediate or higher risk?
predicted 6-month mortality > 3%
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) immediateley?
clinically unstable eg. hypotensive
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) within 72hrs?
pts with GRACE score >3%
When should coronary angiography be considered for pts with NSTEMI/unstable angina?
if ischaemia is experienced after admission
What is cardiac rehabilitation used as the final Mx for ACS?
before discharge; assessment 10days after discharge
physical activity, lifestyle advice, stress management and health education
Drug therapy for secondary prevention for ACS (STEMI, NSTEMI, unstable angina)?
- ACE inhibitor
- DAPT
- Beta-blocker
- Statin
DAPT for secondary prevention of ACS?
Aspirin + second antiplatelet for up to 12m
Drug titration of beta-blockers for secondary prevention of ACS?
titrate to max tolerated or target dose
Drug titration for ACE inhibitors for secondary prevention of ACS?
titrate up (with monitoring) every 12-24hrs; complete titration in 4-6w of hospital discharge.
What should you monitor in pts before starting and 1-2w after starting an ACE inhibitor?
renal function, electrolytes and BP
Secondary prevention for ACS: if pt already on anticoag, offer clopidogrel for how long?
Up to 12m if had PCI
Poor prognostic factors of ACS?
age; Hx or development of HF; PVD; reduced systolic blood pressure; Killip class; inital serum creatinine conc; elevated initial cardiac markers; cardiac arrest on admission; ST segment deviation
What is the name of the system used to stratify risk post MI?
Killip class
Killip class features and 30 day mortality?
I= no signs HF (6%)
II= lung crackes, S3 (17%)
III= frank pulmonary oedema (38%)
IV= cardiogenic shock (81%)
Cx of myocardial infarction?
Cardiac arrest
Cardiogenic shock
Chronic heart failure
Tachyarrhythmias
Bradyarrhythmias
Pericarditis
Left ventricular aneurysm
LV free wall rupture
Ventricular septal defect
Acute mitral regurgitation
Most common cause of death following MI
Cardiac arrest
Why can cardiac arrest occur after MI?
pt develops ventricular fibrillation
Cardiac arrest Mx
ALS with defibrillation
Why may pt develop cardiogenic shock after MI?
if large part of V myocardium damaged by infarction the EF may decrease to the point the pt develops CG shock
Causes of cardiogenic shock?
post MI; mechanical Cx (LV free wall rupture)
Pt with cardiogenic shock may require what?
Inotropic support and/or intra-aortic balloon pump
Cardiogenic shock?
Heart suddenly can’t pump enough blood to meet body’s needs as it has been damaged so much. Life-threatening- can lead to organ failure.
Why may MI lead to chronic HF?
ventricular myocardium may be damaged and dysfunctional
Arrhythmias that may develop post MI?
Ventricular fibrillation (most common cause of death following MI); ventricular tachy; bradyarrhythmias
Atrioventricular block is more common following what type of MI?
Inferior
What is common (10%) in first 48hrs following a transmural MI?
Pericarditis
Pain worse lying flat and better leaning forward; pericardial rub may be heard; may see pericardial effusion on echo
Pericarditis
Dressler’s syndrome?
Pericarditis that can occur 2-6w following an MI.
Fever, pleuritic pain, pericardial effusion and raised ESR?
Dressler’s
Pathophysiology of Dressler’s?
autoimmune reaction against antigenic proteins formed as myocardium recovers
Mx of dressler’s?
NSAIDs
Ischaemic damage following MI may weaken the myocardium and result in LV aneurysm forming. What is this associated with?
Persistent ST elevation and LV failure.
Why may LV aneurysm increase risk of stroke?
thrombus may form within the aneurysm
Pts with LV aneurysm are what?
Anticoagulated
When could a LV free wall rupture occur after MI?
1-2w after (3% of MIs)
Acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)?
LV free wall rupture
Mx for LV free wall rupture?
urgent pericardiocentesis and thoracotomy
Pulsus paradoxus?
When BP decreases with inhalation eg. in cardiac tamponade
When would rupture of interventricular septum occur post MI (1-2% pts)?
in 1st week
Features of ventricular septal defect post MI?
Acute HF associated with pan-systolic murmur
Diagnosis of ventricular septal defect post MI?
ECHO diagnostic and will exclude acute mitral regurg (presents similar)
Mx of ventricular septal defect post MI?
Urgent surgical correction
What may cause acute mitral regurgitation post MI?
infero-posterior infarction and may be due to ischaemia or rupture of papillary muscle
CP of mitral regurg post MI?
acute hypotension, pulmonary oedema; early-mid systolic murmur
Mx for pt with mitral regurg post MI?
vasodilator therapy but often require emergency surgical repair.
Secondary prevention of ACS: dietary advice?
Mediterranean style diet; switch butter and cheese for plant oil based products; do NOT recommend eating oily fish
Secondary prevention of ACS: exercise advice?
20-30mins a day until pt slightly breathless
When can sexual activity resume after an uncomplicated MI?
4w after. Sex does not increase likelihood of further MI
When can PDE5 inhibitors eg. sildenafil be used in pts post MI?
6m after MI but avoid in pts prescribed nitrates or nicorandil
DAPT post ACS?
aspirin + ticagrelor (stop T after 12m)
DAPT post PCI?
aspirin + prasugrel or ticagrelor (stop P or T after 12m)
When might the 12m period for DAPT be altered in patients?
If at high risk of bleeding or high risk of further ischaemic events
What should be initiated after ACE inhibitor theraoy in pts who had an acute MI and have symptoms/signs of HF and LV systolic dysfunction for secondary prevention?
Aldosterone antagonists eg. eplerenone 3-14days post-MI
Abdominal aortic aneurysm (AAA)?
Permanent pathological dilation of abdominal aorta with diameter >1.5 times the expected anteroposterior diameter of the segment given the person’s sex and body size
Threshold for diagnosis of AAA?
abdo aortic diameter of 3cm or more
RFs for AAA?
male, age, smoking, HTN, FHx, DM, COPD, hyperlipidaemia
When is screening for AAA offered?
All men the yr they become 65yrs
AAA screening test?
abdo USS to detect any bulging or swelling of aorta
AAA screening: no aneurysm found?
<3cm- no further scans requried
AAA screening: small AAA?
3-4.4cm. Placed under surveillance and repeat scan in 12m (repeat every 12m)
AAA screening: medium AAA?
4.5-5.4cm. Under surveillance and repeat scan in 3m (repeat every 3m)
AAA screening: large AAA?
5.5cm+. Referred to vascular surgeon within 2w for probable intervention.
How long does AAA screening take?
15mins; told results at appointment
Why is there screening for AAA?
majority asymptomatic and if rupture then high mortality.
What AAA have a low rupture risk?
asymptomatic, diameter <5.5cm (small and medium)
High rupture risk AAA?
Symptomatic, diameter >=5.5cm or rapidly enlarging (>1cm/yr)
How are large high risk AAA surgically managed?
Elective endovascular repair (EVAR) or open repair. EVAR stent placed into abdo aorta via femoral artery to prevent blood from collecting in aneurysm
Cx of EVAR for AAA?
endo-leak: stent fails to exclude blood from aneurysm; asymptomatic on routine follow up
Why do AAA occur?
As result of the failure of elastic proteins in the matrix.
Loss of intima with loss of elastic fibres from the media, associated with increased proteolytic activity and lymphocytic infiltration.
Normal diameter abdo aorta in men and women >50yrs?
F: 1.5cm
M: 1.7cm
Aneurysms typically represent dilation of…
all layers of the arterial wall; most caused by degenerative disease
Rare causes of AAA?
Syphilis; connective tissue disorders eg. Ehlers Danlos type 1 and Marfan’s
Peripheral arterial disease (PAD)?
narrowing or occlusion of peripheral arteries affecting blood supply to lower limbs
Types (symptoms) of peripheral arterial disease?
Acute limb ischaemia
Intermittent claudication
Chronic limb-threatening ischaemia
Asymptomatic
PAD: acute limb ischaemia?
sudden decrease in limb perfusion that threatens limb viability- CP <2w
PAD: intermittent claudication?
diminished circulation leads to pain in lower limb on walking or exercise, relieved on rest
Most common symptom of PAD?
Intermittent claudication
PAD: chronic limb-threatening ischaemia?
chronic, inadequate tissue perfusion at rest and is defined by ischaemic rest pain, with or without tissue loss
Asymptomatic PAD?
early stage in the condition and may progress with symptoms of intermittent claudication or chronic limb-threatening ischaemia
PAD of the lower limbs is most commonly caused by?
Atherosclerosis
Cause of acute limb ischaemia (PAD)?
thrombosis within diseased artery when plaque ruptures
RFs for PAD?
smoking, DM, HTN, hypercholesterolaemia
CP of acute limb ischaemia (PAD)?
pain, pallor, pulseless, perishing with cold, paraesthesia and power loss
CP of chronic limb ischaemia (PAD)?
progressive development of cramp-like pain in calf, thigh or buttock on walking; not relieved by rest; unexplained foot or leg pain; non-healing wounds on lower limb. ?absent foot pulses.
Pt with pain in leg worse at night, sleep with leg hanging out of bed or sleep in a chair?
Chronic limb-threatening ischaemia
Why do pts with chronic limb-threatening ischaemia report pain worse at night?
decrease of BP when asleep and no gravity when lying down
CP of intermittent claudication (PAD)?
pain in lower limb on walking or exercise, relieved by rest (within 10mins), aching, burning, distal extremity before proximal. Uni or bilateral
Ix for PAD?
ankle brachial pressure index (ABPI)
What reading of an ABPI suggests the presence of PAD?
0.9 or less
Mx of acute limb ischaemia?
ABC, IV opioids, IV unfractionated heparin then:
Urgent assessment by vascular specialist: endovascular therapies (eg. percutaneous catheter-directed thrombolytic therapy) or surgical interventions (eg. surgical thromboembolectomy)
Mx of chronic limb-threatening ischaemia?
- urgent referral to vascular
- pain Mx: paracetamol, weak/strong opioids
- advice
Mx of intermittent claudication?
- supervised exercise programme (2hrs per w for 3m)
- lifestyle advice
- referral for consideration of angioplasty or bypass surgery
- if don’t want surgery= naftidrofurl oxalate
What if supervised exercise programme is not available in pts with intermittent claudication?
30mins exercise 3-5 times per week; walking until onset of symptoms then rest
All people with PAD should be given what?
Advice and treatment for secondary prevention of CVD
Physical signs in someone with PAD?
dry shiny skin; elevation pallor; hair loss over dorsum of foot; muscle atrophy; thickened toenails; ulceration on heel
Ruptured AAA?
catastrophic (sudden collapse) or sub-acute (persistent severe central abdo pain with developing shock). 80% mortality
CP of ruptured AAA?
severe central abdo pain radiating to back; pulsatile expansile mass in abdo; may be shocked (hypoten, tachy) or collapsed
Severe central abdo pain radiating to back?
ruptured AAA
Ruptured AAA Mx?
immediate vascular review for emergency surgical repair.
if stable may get CT angiogram to confirm
Tear in the tunica intima of the wall of the aorta
aortic dissection
Associations with aortic dissection?
HTN
trama; bicuspif aortic valve; marfans; turner’s and noonan’s; pregnancy; syphillis
Severe and sharp tearing cheat and upper back pain
aortic dissection
Aortic dissection CP
tearing sharp chest and upper back pain; weak or absent pulse; variation (>20) in SBP between arms; aortic regurg; HTN
Aortic dissection if involves cornonary/spinal arteries/distal aorta?
1) anginga
2) paraplegia
3) limb ischaemia
Are there ECG changes in aortic dissection?
non-specific or no ECG changes. Some: ST-elevation in inferior leads
Stanford classification of aortic dissection?
- Type A (2/3)= ascending aorta
- Type B (1/3)= descending aorta, distal to L subclavian origin
Ix for aortic dissection?
- CT angiography of chest, abdo and pelvis GOLD (if stable)
- Tranoesophageal echo (if unstable)
- CXR: widened mediastinum
Finding on CT angiography of chest, abdo and pelvis for aortic dissection?
False lumen
Mx for Type A aortic dissection?
- surgery but BP must be controlled of S target of 100-120 whilst awaiting
Mx for Type B aortic dissection?
conservative, bed res, reduce BP IV labetalol to prevent progression
Complications of a backward tear in aortic dissection?
aortic incompetence/regurg
MI: inferior due to right cornonary invol.
Complications of a forward tear in aortic dissection?
unequal arm pulses and BP; stroke; renal failure
Aortic regrurg is the leaking of the aortic valve of heart that causes….
blood to flow in reverse direction during ventricular diastole
What can cause aortic regurg?
disease of aortic valve or dilation of aortic root and ascending aorta
Causes of aortic regurg due to valve disease?
Chronic= RF, calcific valve disease, connective tissue diseases (RA, SLE), bicuspid aortic valve
Acute= infective endocarditis
Causes of aortic regurg due to aortic root disease?
Chronic= bicuspid aortic valve, spondylarthropathies, HTN, syphilis, Marfan’s
Acute= aortic dissection
What type of murmur is aortic regurgitation?
Early diastolic murmur
Where is aortic regurg best heard?
loudest at the left sternal edge
Features of aortic regurg?
- collapsing pulse
- wide pulse pressure
- early diastolic murmur
Signs in aortic regurg?
Quincke’s sign (nailbed pulsation) and De Musset’s sign (head bobbing)
What can you get in severe aortic regurg?
mid-diastolic Austin-Flint murmur: due to partial closure of anterior mitral valve cusps caused by regurg streams
Ix for aortic regurg?
echo
Mx for aortic regurg?
- medical Mx for any HF
- surgery if indicated
Indications for surgery in aortic regurg?
symptomatic patients with severe AR
or
asymptomatic patients with severe AR who have LV systolic dysfunction
What type of murmur is aortic stenosis?
Ejection systolic murmur; has crescendo-decrescendo quality.
Where is aortic stenosis heard loudest?
over aortic valve (2nd R ICP) and commonly radiates to carotid arteries. Loudest on espiration and when pt is sitting forward
CP of aortic stenosis
- slow rising pulse with narrow pulse pressure
- non-displaced heaving apex beat (LV hypertrophy)
- reduced or absent S2
- reverse splitting of S2
Causes of aortic stenosis?
- degenerative calcification (>65yrs)
- bicuspid valve disease (<65yrs)
- RF
- William’s syndrome (supravalvular aortic stenosis)
Crescendo vs decrescendo vs crescendo-decrescendo murmur?
C= murmur increases in intensity
D= decrease in intensity
C-D= increase in intensity followed by decrease in intensity
Is aortic stenosis C, D or C-D?
Crescendo-decresendo
Is aortic regurg C, D or C-D?
Decrescendo
Is mitral regurg C, D or C-D?
Crescendo-decrescendo
Is mitral regurg C, D or C-D?
Decrescendo
Mx for aortic stenosis
- asymptomatic= observe
- symptomatic= valave replacement
- asymptomatic but valvular gradient >40mmHg and features eg. LV systolic dysfunction= valve replacement
Mitral regurg occurs when blood leaks…
back through mitral valve on systole
Where is mitral valve located?
between LA and V so regurg leads to less efficient heart as less blood pumped through body with each contraction
What can happen as the degree of mitral regurg becomes more severe?
oxygen demand > heart can supply; leads to thicker myocardium; then fatigued when comes less efficient -> irreversible HF
RFs for mitral regurg?
female, lower BMI, age, renal dysfunction, prior MI, prior mitral stenosis, collagen disorders
Causes of mitral regurg?
post MI, mitral valve prolapse, infective endocarditis, RF, congenital
What type of murmur is mitral regurg?
Pansystolic murmur heard loudest over apex and radiating to axilla. Severe may cause widely split S2.
Where to listen for mitral regurg?
L 5th ICP mid-clav line; then left axilla.
CP of mitral regurg?
most asymptomatic; symptoms due to failure of LV, arrythmias or pulmonary HTN so SOB, fatigue, oedema
Ix for mitral regurg?
ECHO
- ECG: broad p
- CXR: cardiomegaly (enlarged LV and LA)
What does mitral regurg sound like?
Like a high-pitched blowing, constant whoosh
What can sometimes be felt with aortic stenosis?
palpable thrill
What does aortic stenosis sound like?
Whoosh (starts soft, then loud, then soft again)
Mx for mitral regurg?
Acute: nitrates, diuretics, +ve iontropes and intra-aortic balloon pump to increase cardiac output
Acute severe: surgical repair/replacement
Mitral stenosis is when there is an obstruction of blood flow across…
the mitral valve from LA to LV; leads to high P in LA, pulmonary vessles and R heart
Causes of mitral stenosis?
RHEUMATIC FEVER
What type of murmur is mitral stenosis?
mid-late diastolic murmur best heard in expiration and loud in S1
CP of mitral stenosis?
dyspnoea; haemoptysis (pink frothy or sudden haemorrhage); opening snap; low volume pulse; malar flush; AF
What does an opening snap indicate in mitral stenosis?
mitral valve leaflets are still mobile
Ix for mitral stenosis?
- echo: cross section of mitral valve <1sqcm (normal 4-6)
- cxr: may see LA enlargement
Mx for mitral stenosis?
- asymptomatic= monitor regular with echo
- symptomatic= percutaneous mitral balloon valvotomy or mitral valve surgery
- if AF: warfarin
Bicuspid aortic valve?
1-2% of population; asymptomatic in childhood
The majority of pts with bicuspid aortic valve eventually develop what?
aortic stenosis or regurg; higher risk of aortic dissection and aneurysm formation (on ascending aorta)
What is bicuspid aortic valve associated with?
a left dominant coronary circulation (posterior descending artery arises from circumflex not right coronary) and Turner’s
Around 5% of patients with what also have coarctation of the aorta?
bicuspid aortic valve
What are biological heart valves usually made from?
Bovine or porcine
Disadvantage of biological heart valves?
structural deterioration and calcification over time; so >65/70yrs receive
Is long-term anticoag needed for biological heart valves?
No; may give warfarin for first 3m; low-dose aspirin long term
Most common type of mechanical heart valve?
Bileaflet valve
Pro and con of mechanical heart valve?
low failure rate but increased risk of thrombosis so long term anticoag needed
Is long term anticoag needed for mechanical heart valve?
Yes, warfarin
Target INR for mechanical heart valve anticoag?
Aortic: 3.0
Mitral: 3.5
Why do you manage pts with AF?
reduce the increased risk of stroke
What is atrial fibrillation (a supraventricular tachyarrhythmia)?
uncoordinated atrial electrical activation and so ineffective atrial contraction, causing an irregular and abnormally rapid vetricular rhythm
How would you describe the rhythm of AF?
Irregularly irregular
Example of regularly irregular rhythm?
Ventricular ectopics
Classification of AF?
- paraoxysmal (episodes terminate <7days of onset)
- persistent (>7d)
- longstanding persistent (>12m)
- permanent (no more attempts to restore sinus rhythm)
RFs for AF and its maintenance?
HTN, IHD, HF, valvular disease, intercurrent illness, electrolyte disturbances, thyrotoxicosis, alcohol XS
CP of AF
usually asymptomatic, undetected and undiagnosed
Cx of AF?
stroke, HF, mortality, tachycardia-induced cardiomyopathy
When should you suspect a diagnosis of AF?
irregular pulse with or without symptoms eg. SOB, palpitation, chest pain, dizziness, syncope
Ix for AF?
- exam: pulse, auscultate heart and lungs
- ECG
- consider bloods, cxr, echo, ambulatory ecg monitoring (if paroxysmal AF)
Routine review of someone with AF?
managing Cx; lifestyle modification; stroke and bleeding risk; monitor meds. Review symptoms, HR & rhythm, BP, adherence and adverse effects
When should you arrange a prompt cardio referral in someone with AF?
recurrent or persistent symptoms despite rate and/or rhythm control treatment
When to urgently admit someone to hospital with AF?
severe CP, haemodynamically unstable, decompensated HF
When should you seek urgent cardio advice in someone with AF?
new onset within 48hrs, associated with structural disease or uncertainty about Mx
Mx for pt with AF?
- assess stroke and bleeding risk
- lifestyle advice
- consider DOAC for stroke prevention eg. apixaban (or wafarin 2nd line)
- consider meds for rate control (BB or CCB)
Signs of haemodynamic instability?
tachycardia (>150bpm); hypotension (S<90); severe dizziness, syncope, loss of consciousness; ischaemic chest pain or acute pulmonary oedema
ECG for AF
absence of p waves, iregguarly-irregular R-R intervals,narrow QRS, ventricular rate 90-170bpm
When should you arrange a transthoracic echo in someone with AF?
- high risk/suspicion of underlying functional or structural heart disease and this will influence Mx
- cardioversion (electrical or drug) is being considered
Risk score for stroke?
CHA2DS2-VASc
Assess pts bleeding risk?
ORBIT bleeding risk score
When to offer a DOAC for pt with AF?
- chadvasc score 2 or more
- or if man and score of 1
DOAC stands for and example?
direct-acting oral anticoag
apixaban, rivaroxaban
What is warfarin?
vit KK antagonist; anticoag
When to not offer rate control drug for pt with AF?
reversible cause; HF caused by AF; newonset AF <48hrs
How to monitor pt on vit K antagonists eg. warfarin?
International normalised ratio (INR) until in therapeutic range
What indicates that a pt on warfarin has sub-optimal anticoag control?
- TTR <65%
- 2 INR higher than 5, or one higher than 8 within 6m
- 2 IRN <1.5 within 6m
What factors may cause sub-optimal anticoag control for pt on warfarin?
impaired cognitive function, poor adherence, acute illness, lifestyle eg. XS alcohol; medications
What meds may interact with warfarn?
antiplatelets, SSRIs, NSAIDs
When should you review someone who has just started rate control drugs eg. BB?
within 1 week of starting or each dose titration
Ventricular rate targets for someone on rate control drugs eg. BB?
<80bom at rest and <110bpm during moderate exercise.
<100bpm at rest may be appropriate
When is the highest risk for embolism leading to stroke in AF?
During cardioversion- thrombus in fibrillating atrium suddenly pushed out when sinus rhythm restored. SO make sure pt anticoag before (at least 3w prior)
What is electrical cardioversion synchronised to?
R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when V fib can be induced
Types of cardioversioN?
Electrical (DC cardioversion) or pharmacological eg. amiodarone, flecainide
Following a TIA, when should anticoag for AF be started?
immediately once excluded haemorrhage
In acute stroke pts, in absence of haemorrhage, when should anticoag for AF be started?
after 2w. In the intervening period give antiplatelet
When should pt be electrically cardioverted if have AF?
if haemodynamically unstable
Form of supraventricular tachy characterised by succession of rapid atrial depolarisation waves?
Atrial flutter
Flutter waves in atrial flutter may be more visible following what?
carotid sinus massage or adenosine
What features suggest VT rather than SVT?
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
What does the Mx of bradycardia depend on?
1) presence of signs indicating haemodynamic compromise
2) potenial risk of asystole
what factors indicate haemodynamic compromise and so the need for Mx in bradycardia?
- shock
- syncope
- MI
- HF
Signs of shock?
hypotension (SBP <90), pallor, sweating, cold, clammy extremities, confusion, impaired consciousness
Mx of bradycardia and tachycardia
- asssess with A-E
- give O2 if appropriate and gain IV access
- monitor ECG, BP, Sp02
- Treat any reversible causes eg. electrolyte abnorm
- any life threatening signs? (follow the different pathways)
Life-threatening signs in someone with brady/tachy?
haemodynamically unstable; shock; syncope; MI; HF
What may be signs that indicate risk of asystole (flat-line)?
- recent asystole
- Mobitz II AV block
- complete heart block with broad QRD
- V pause >3secs
Mx for bradycardia with life threatening features?
Atropine 500mcg IV
Mx if haemodynamically unstable with bradycardia and no response to atropine 500mcg IV or if there is a risk of asystole?
- repeat atropine up to 3mg
- isoprenaline 5mcg min-1 IV
- adrenaline 2-10mcg min-1 IV
- OR transcutaneuous pacing
Mx for tachycardia if there are life threatening features?
Synchronised DC shock up to 3 attempts
- if unsuccessful: amiodarone 300mg IV over 10-30mins and repeat shock
Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is irregular?
could be:
1) AF with BBB: same Mx as irregular narrow QRS tachy
2) polymorphic VT (eg. torsades)= gve Mg 2g over 10mins
Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is regular?
1) VT (or uncertain)= amiodarone 300mg IV for 10-60min
2) previous diagnosis of SVT with BBB= Mx same as regular narrow QRS tachy
Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is irregular?
1) ?AF= BB, anticaog if >48hrs and amiodarone if evidence of HF
Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is regular?
1) vagal manoeuvre/fluids (normally decrease HR if sinus tachy)
if uneffective (usually SVT)
2) amiodarone 6mg rapid IV bolus, if unsuccessful give 12mg then if successful give 18mg AND monitor ECG
if uneffective
3) verapamil or BB
What does supraventricular tachycardia (SVT) refer to?
any tachycardia that is not ventricular in origin
SVT?
high HR, regular rhythm, narrow QRS.
Acute Mx of SVT?
- vagal manoeuvres eg. valsalva manoeuvre (eg. flow into empty syringe) or carotid sinus massage.
- fluids (both fluids and vagal normally work for sinus tachy)
- IV adenosine (usually needed)
- electrical cardioversion
Dose of adenosine in SVT?
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
Who is adenosine for SVT contraindicated in?
asthmatics- use veramil
Prevention of SVT?
BB
radio-frequency ablation
Torsades de pointes (rhythm strip can look like ribon- ‘twisting of the points’) is what?
Form of polymorphic ventricular tachy associated with long QT interval
Why can torsades de pointes lead to sudden death?
can deteriorate into V Fib
Causes of long QT interval?
- congenital
- drugs
- electrolyte: hypocal; hypokal; hypomag
- myocarditis
- hypothermia
- subarachnoid haemorrhage
Drugs that can cause long QT interval?
- antiarryhtmics eg. amiodarone
- tricyclic antidep
- antipyschotics
- chloroquine
- terfenadine
- erythromycin (macrolides)
Mx of torsades de pointes?
IV magnesium sulphate
Ventricular tachycardia?
broad complex tachy originating from ventricular ectopic focus
V tach can deteriorate to what?
V fib so need urgent Mx
2 types of V tach?
- monomorphic: commonly caused by MI. QRS complexes look same.
- polymorphic: eg. torsades de pointes. QRS complexes look different
Mx of V tach?
1) pulse? if no then ALS + defib +/- epi & amio
2) if pulse= adenosine
3) if doesn’t work then try other antiarrythmics: procainomide, amiodarone, lidocaine
4) prepare for synchronised electrical cardioversion
What drug should not be used in V tach?
Verapamil
Shockable rhythms?
Ventricular fibrillation and pulseless ventricular
tachycardia
Non-shockable rhythms?
pulseless electrical activity and asystole
Most dangerous rhythms?
V tach and V fib
Adult advanced life support?
1) CPR 30:2 (100-120/min), attach defib
2) assess rhythm
3) shockable: 1 shock, immediately resume CPR for 2mins
3) non-shockable: continue CPR
4) whilst doing this obtain IV or intraosseous access
5) give adrenaline 1mg every 3-5mins and amiodarone 300mg after 3 shocks and then 150mg after 5 shocks
Reversible causes of cardiac arrest?
H.ypoxia
H.ypovolaemia
H.yperkal, hypokal, hypogly, hypocal
H.+ (acidaemia)
H.ypothermia
T.hrombosis (coronary or pulmomary
T.ension pneumothorax
T.amponade (cardiac)
T.oxins
How old is an infant vs a child?
Infant= <1yr
Child= 1yr-puberty
Child advanced life support?
1) 5 rescue breaths
2) check femoral pulse
3) 15:2 (chest compressions 100-120/min)
Depth for chest compressions?
Lower half of sternum by at least 1/3 of anterior-posterior dimension of chest (4cm for infant, 5cm for child/adult)
Position for chest compressions in adults & children and infants?
- adults & children= lower half of sternum
- infants: 2 thumb encircling technique (on lower 1/3 of sternum)
Features of pulmonary oedema/HF on CXR?
A.lveolar and interstitial oedema (bat’s wing appearance)
B. Kerley B-lines
C.ardiomegaly
D.ilated upper lobe vessels (increased blood flow to superior part of lung)
E.ffusion (pulmonary)
What do Kerley B lines represent?
Expansion of interstitial space by fluid
Symptoms of heart failure?
S.hortness of breath
O.rthopnea
F.atigue
A.nkle swelling
P.ulmonary oedema
C.old peripheries
cough worse at night, pink/frothy sputum; cardiac wheeze; cardiac cachexia
Signs of heart failure?
elevated jugular venous pressure, bibasal crepitations and peripheral oedema.
What causes heart failure?
structural and/or functional abnormality that produces raised intracardiac pressures and/or inadequate cardiac ouput at rest and/or at exercise
CP of right sided HF
raised JVP, peripheral oedema (ankle/sacral), hepatomegaly, weight gain due to fluid retention, anorexia (cardiac cachexia)
CP of left sided HF
pulmonary oedema: dyspnoea, cough, orthopnoea, paraoxysmal nocturnal dyspnoea, bibasal fine crackles
Heart failure is classified into what 3 main categories?
1) reduced ejection fraction
2) midly reduced EF
3) preserved EF
What is the New York Heart Association functional classification?
symptoms of heart failure are classified according to severity
HF is usually caused by what?
myocardial dyfunction, systolic or diastolic or move
most common underlying pathophysiology= coronary artery disease
Cx of HF?
arrhythmias, depression, cachexia, CKD, sexual dysfunction, sudden cardiac death
Steps to follow if HF is suspected clinically? (Ix)
- N-terminal pro b-type natriuretic peptide (NT-proBNP)
- if normal then HF unlikely, if raised then refer for specialist assessment and echo
What levels should NT-pro-BNP be to be referred for specialist assessment and transthoracic echo if suspected HF?
> 2000ng/L then urgent within 2w
400-2000 then refer within 6w
Ix for all people with suspected HF
- NT-pro-BNP (?may need transthoracic echo)
- 12 lead ECG
- Loop diuretic for symptom relief whilst waiting for assessment
-? CXR, bloods, urine dip (protein and blood), peak flow
Mx for HF with reduced ejection fraction?
- diuretic if fluid overload
- ACE inhibitor AND BB
- mineralcorticoid receptor antagonist (MRA eg. spironolactone) if still symptomatic
- specialist advice if still symptomatic
Mx for HF with mildly reduced EF?
- loop diuretic if fluid overload
- consider ACE, BB and maybe MRA eg. spirinolactone
Mx for HF with preserved ejection fraction?
low-medium dose loop diuretic if needed and refer if no response. Manage cormorbities eg. HTN, AF, IHD, DM
What to give all pts with confirmed HF?
- consider antiplatelet and statin
- offer personalised exercise based cardiac rehab programme
- lifestyle advice
- assess nutritional status
- screen for depression and anxiety
- offer appropriate vaccinations (influenza and pneumococcol)
RFs for HF?
Coronary artery disease, previous MI, HTN, AF, DM, drugs & alcohol, FHx sudden cardiac death <40yrs or HF
What should you examine for in pt with suspected HF?
1) tachy (>100bpm) and pulse rhythm
2) laterally displaced apex beat, murmurs, added heart sounds (gallop rhythm)
3) HTN
4) increased JVP
5) enlarged liver
6) resp signs: tachypnoea, basal crep, pleural effusions
7) leg or sacrum oedema, ascites
8) obesity
What is a common this for pts with HF to do?
sleep with lots of pillows (orthopnea)
Dose of loop diuretic for symptomatic relief for pts with HF?
furosemide 20-40mg daily
Natriuretic peptide levels may be reduced by what?
BMI >35
African-Caribbean origin
Drugs eg. diuretics, ACE, BB, ARB, mineralcortioid receptor antagonists eg. spironolactone
Natriuretic peptide levels may be elevated by what?
> 70yrs; LV hypertrophy, MI, tachy; RV overload; hypoxia; pulmonary HTN; pulmonary embolism; CKD; sepsis; COPD; DM; liver cirrhosis
Advice to give pt who has HF and is acutely unwell?
Maintain fluid intake and stop ACE, BB, MRA until eating and drinking normally
Specialist Mx of HF of reduced EF and ACE+BB+MRA not worked?
Either of….
1) <35% EF replace ACI (or ARB) with sacubitril
2) + ivabradine for sinus rhythm with HR >75 and EF <35%
3) + hydralazine and nitrate (esp if African-C descent)
4) digoxin for HF with sinus rhythm to improve symptoms
5) may need cardiac resynchronisation therapy or insertion of ICD (implantable cardioverter defib)
Ramipril initial and target dose for HF?
2.5mg once a day
then target of 5mg twice a day or 10mg once
Initial and target dose of bisoprolol for HF?
1.25mg once a day
then target 10mg once a day
(1.25-2.5 to 3.75-5 week 1; 5mg od 4w then 7.5 od for 4w then 10mg)
Dose of furosemide for HF?
20-40mg
When is b-type natriuretic peptide (BNP) or NTproBNP produced by the heart?
in response to strain
Why is exercise training good for HF?
improves symptoms but not hospital/mortality
When is cardiac resynchronisation therapy used for pts with HF?
- HF and wide QRS
- biventricular pacing
- improved CP and reduces hospitalisation in NYHA class III pts
How many classes in NYHA classication?
4
NYHA Class I
no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III
moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA 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
What is acute heart failure (AHF)?
sudden onset or worsening of the symptoms of HF
may be present with or without Hx of pre-existing HF
What is de-novo AHF?
acute HF without a past history of HF
What is decompensated AHF?
background history of HF
AHF is usually caused by a reduced…
cardiac output that results from functional or structural abnormality
Causes of de-novo AHF?
- increased cardiac filling pressures and myocardial dysfunction as a result of ischaemia -> reduced cardiac output and so hypoperfusion -> pulmonary oedema
- less common: viral myopathy, toxins, valve dysfunction
Causes of decompensated HF?
- acute coronary syndrome
- HTN crisis
- acute arrhythmia
- valvular disease
Patients with HF are broadly characterised into what groups based on what they present with?
- with or without hypoperfusion
- with or without fluid congestion
Symptoms of AHF?
breathlessness, reduced exercise tolerance, oedema, fatigue
Signs of AHF?
cyanosis, tachy, elevated JVP, displaced apex beat, bibasal crackles (maybe a wheeze), S3 heart sound
over 90% pts with AHF have a normal or increased…
BP
Ix for AHF
- BNP/NT-pro-BNO
- CXR
- bloods (?infection, electrolyte, anaemia)
- echo
Acute Mx for HF
1) IV loop diuretic eg. furosemide
2) O2
3) Do not routinely offer nitrates, opiates, inotropes or vasopressors
4) CPAP if resp failure
When to offer nitrates in acute Mx of HF?
pt with concomitant MI, severe HTN or regurgitant aortic/mitral valve
When to offer inotropes or vasopressors in the acute Mx of HF?
pts who have potentially reversible cardiogenic shock
eg. dobutamine (inotrope) and norepinephrine (vasopressor)
When should BB only be stopped in the acute Mx of HF?
if HR <50, second or third degree AV block or shock
HF with reduced ejection fraction level?
<35-40% (measured with echo)
HF with rEF typically has what type of dysfunction?
systolic (impaired myocardial contraction during systole)
HF with pEF typically has what type of dysfunction?
diastolic (impaired V filling during diastole)
Causes of systolic dysfunction (as so HF-rEF)?
IHD
Dilated cardiomyopathy
Myocarditis
Arrhythmias
Causes of diastolic dysfunction (as so HF-pEF)?
Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis
Most urgent symptom of acute HF?
LV failure causing pulmonary oedema
HR-rEF and HR-pEF typically develop what sided HF?
Left
Why may HR-rEF and HR-pEF develop left-sided HF?
increased LV afterload eg. arterial HTN or aortic stenosis; or increased LV preload eg. aortic regurg resulting in backflow to LV
What causes right sided HF?
increased RV afterload (eg. pulmonary HTN) or increased RV preload (eg. tricuspid regurg)
Left and right sided HF can be used to describe the consequences of HF ie. the backward failure of output of…
either RV or LV
What is high-output HF?
‘normal’ heart is unable to pump enough blood to meet metabolic needs of body
Causes of high-output HF?
anaemia, AV malformation, Paget’s, pregnancy, thyrotoxicosis, thiamine def
Angina?
chest pain/constricting discomfort caused by insufficient blood supply to myocardium
causes of angina?
CAD, valvular disease, hypertrophic obstructive cardiomyopathy or HTN heart disease
Stable angina?
occurs predictably with physical exertion or emotional stress and is relieved within mins of rest or with a dose of sublingual glyceryl trinitrate
Unstable angina?
New (usually <24hrs) onset angina or abrupt deterioration in previously stable angina, often occurring at rest. Requires immediate admission/referral to hospital.
Mx of stable angina?
- lifestyle advice
- Sublingual glyceryl trinitrate (GTN) for rapid relief
+ a BB or CCB (first line) - 2nd: long-acting nitrate eg. isosorbide mononitrate
- poor control then add another drug from different class, if still poor then referral to cardio
Drugs for secondary prevention of CV events for pts with angina?
low dose aspirin 75mg daily
ACE inhibitor
- Mx for lipid modification and HTN if appropriate
Hospital admission is recommended for people with possible unstable angina presenting with what symptoms?
- pain at rest (may be at night)
- pain on minimal exertion
- angina rapidly progressing despite medical Mx
Typical stable angina CP?
constricting discomfort in chest, neck, shoulders, jaw or arms + precipitated by exercise + relieved by rest or GTN within 5 mins
Atypical angina?
2/3 stable angina symptoms + GI discomfort +/or SOB +/or nausea
Factors that make diagnosis of stable angina more likely?
age, male, CVD RFs, Hx of coronary artery disease eg. previous MI, coronary revascularisation
Factors that make diagnosis of stable angina less likely?
continuous or prolonged pain, unrelated to activity; brought on my breathing; associated with dizziness, palpitations, tingling or diff swallowing
Ix for angina?
Clinical
Resting ECG
Hypertension?
Persistently raised arterial BP
Hypertension increases the risk of what conditions?
HF, CAD, stroke, CKD, peripheral arterial disease, vascular dementia
2 types of HTN?
primary and secondary
Primary HTN (essential HTN)?
90% of pts.
NO identifiable cause.
Secondary HTN?
has known underlying cause eg. renal, endocrine, or vascular disorder or use of certain drugs
When should HTN be suspected?
Clinic SBP >=140mmHg or DBP >=90
Ix for HTN?
- Clinic BP: if 140/90 to 179/119 offer ambulatory BP monitoring (ABPM) to confirm diagnosis. If unable offer home blood pressure monitoring (HBPM).
- If clinic 180/120 or higher= same day referral if indicated or Ix for target organ damage. Start antihypertensive Mx immediately.
What should be done whilst waiting for confirmation of diagnosis of HTN?
Ix for target organ damage and 2 causes of HTN.
Assess CV risk.
Classification of HTN (according to severity)?
- Stage 1= clinic BP 140/90 to 159/99 AND ABPM or HBPM average 135/85 to 149/94
- Stage 2= clinic 160/100 to 179/119 AND ABPM/HBPM 150/95 or higher
- Stage 3= clinic SBP 180+ OR clinic DBP 120+
Accelerated/malignant HTN?
severe increase in BP to 180/120 or higher (ofter >220/120) with signs of retinal haemorrhage and/or papilloedema (swelling of optic nerve)
White-coat HTN?
BP unusually raised when measured during clinic but normal in other ‘non-threatening’ situations eg. home. Suspect if discrepancy of more than 20/10mmHg between clinic and avergae ABPM/HBPM readings.
HTN referral for same day specialist assessment should be arranged when?
- clinic BP 180/120+ with signs of retinal haemorrhage/papilloedema OR life-threatening symptoms
- suspected phaeochromocytoma
Life-threatening symptoms for pt with HTN?
new onset confusion, chest pain, signs of HF, AKI
CP for suspected phaeochromocytoma?
labile or postural hypotension, headache, palpitations, pallor, abdo pain or diaphoresis
Overall things the Mx of HTN includes?
- lifestyle advice
- antihypertensive drug Mx
- ?statin
- monitor
When should pts with HTN be reviewed?
Annually= BP, review meds, discuss lifestyle, symptoms
Target BP for <80yrs?
clinic= <140/90
ABPM/HBPM= <135/85
Target BP for 80yrs+?
clinic= <150/90
ABPM/HBPM= <145/85
BP target for someone with postural hypertension?
Base on standing BP
How to measure BP in suspected HTN?
Relaxed setting, person quiet and seated with arm outstretched and supported.
Both arms.
If diff in reading between arms >15 then repeat. If still different use higher reading/
When might automated BP devices not be accurate?
If pulse irregularity eg. AF so measure BP manually using direct auscultation over brachial artery if pulse irregular
Measure BP for pt with suspected hypotension?
Measure seated/supine then again when standing for >1min before measurement. If SBP falls by 20+ when standing, measure subsequent BP with person standing
What if BP measured in clinic 140/90 or higher?
Take second measurement and record the lower of the 2
How to use HBPM?
For each BP reading: take 2, 1 min apart whilst seated. Record twice daily (morning and evening) for >4days (ideally 7). Discard first day measurements and use average of all values to confirm HTN.
When to confirm diagnosis of HTN?
Clinic BP 140/90 or higher AND ABPM/HBPM average of 135/85 or higher
When to suspect masked HTN?
If clinic BP normal (<140/90) but BP are higher using ABPM or HBPM
When to suspect secondary HTN?
Pts <40yrs or those with accelerated HTN or if suspicious of underlying cause eg. meds
What if HTN is not diagnosed?
- ?evidence of target organ damage
- if not then measure clinic BP every 5yrs after or more frequently if clinic BP close to 140/90
How to Ix for target organ damage in pt with HTN?
- haematuria
- urine albumin:creatinine ratio (?protein in urine)
- HbA1c
- electrolytes, creatine and eGFR (?CKD)
- examine fundi (HTN retinopathy)
- ECG
specialist Ix if target organ damage or 2 cause of HTN
Assess CV risk in pt with HTN?
- serum total cholesterol and HDL cholesterol
- QRISK
HTN Mx if <55yrs, with or without DMT2?
1) ACEi or ARB
2) ACEi or ARB + CCB or diuretic
3) ACEI or ARB + CCB + thiazide-like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice
HTN Mx if 55yrs or over, Black-African or African-Caribbean origin, without DMT2?
1) CCB
2) CCB + ACEi (or ARB) OR diuretic
3) ACEi/ARB + CCB + thiazide like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice
When should you use an ARB over an ACEi in HTN MX?
If ACEi side effects eg. cough not tolerated
When to use thiazide like diuretic over CCB in HTN Mx?
If not tolerated eg. because of oedema
When to use CCB first line in HTN Mx over ACEi/ARB?
if 55 yrs or over and DO NOT have DMT2
or
black African or African-Caribbean origin and don’t have DMT2
What to do in HTN Mx if have diabetes and are black African?
use ARB in perference to ACE
What to do in HTN Mx before offering another drug in addition to others?
review and ensure taking optimal tolerated doses; discuss adherence
ACEi example and dose for HTN Mx?
Ramipril
staring dose= 1.25-2.5mg OD
maintenance= 2.5-10mg OD
max= 10mg OD
ARB example and dose of HTN Mx?
Candesartan
starting= 8mg OD
maintenance= 8mg OD
max= 32mg OD
Thiazide-like diuretic example and dose for HTN Mx?
Indapamide
2.5mg in morning (immediate release) or 1.5mg (modified)
CCB example and dose for HTN Mx?
Amlodipine
start= 5mg OD
maintenance= 5-10mg OD
max= 10mg OD
Spironolactone dose for HTN Mx?
25mg OD with food
BB example and dose for HTN Mx (last line)?
Bisoprolol
start= 5mg OD in morning
maintenance= 10mg OD
max= 20mg OD
If pt BP is very high eg. >200/120mmHg what symptoms might they get? (HTN typically asymptomatic)
headaches, visual disturbance, seizures
Why do you go ECG, fundoscopy and urine dip on pt with newly diagnosed HTN?
ensure don’t have end-organ damage.
eg. F= HTN retinopathy
UD= renal disease (cause or consequence of HTN)
ECG= LV hypertrophy or IHD
How to measure BP in children?
- correct cuff size is 2/3 length of upper arm
- 4th Korotkoff sound used to measure DBP until adolescence, then 5th Korotkoff sound can be used
- compare results with graph of normal values for age
What is the most common cause of HTN in younger children?
secondary HTN eg. renal parenchymal disease
Causes of HTN in children?
- renal parenchymal disease
- renal vascular disease
- coarctation of aorta
- phaeochromocytoma
- congenital adrenal hyperplasia
- as child is older: essential/primary HTN
What drugs can cause HTN?
steroids, NSAIDs, COCP, monoamine oxidase inhibitors
Most common cause of secondary HTN?
Primary hyperaldosteronism (incl. Conn’s)
Renal causes of HTN?
glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis
Endocrine causes of HTN?
- primary hyperaldosteronism
- phaeochromocytoma
- Cushing’s syndrome
- Liddle’s syndrome
- congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
- acromegaly
Other causes of HTN?
pregnancy
coarctaation of aorta
Strongest RF for developing infective endocarditis?
previous episode of endocarditis
What valve is most commonly affected in endocarditis?
mitral
What types of pts are typically affected by endocarditis?
- prev normal valves
- rheumatic valve disease
- prosthetic valves
- IVDUs
- congenital heart defects
- recent piercings
Fever and new murmur
infective endocarditis likely
Causes of infective endocarditis?
staph aureus (most common)
strep viridans
staph epidermidis
poor oral hygiene/recent dental surgery- cause of IE?
strep viridans
Murmur in IE caused by strep viridans?
mitral/aortic regurg
Infective endocarditis in IVDU or acute presentation
staph aureus
Murmur in IE caused by staph aureus
Tricuspid (splitting of 2nd heart sound)
Infective endocarditis following prosthetic valve surgery
staph epidermidis
Streptococcus bovis (s. gallolyticus) that can cause infective endocarditis is associated with what?
colorectal cancer
Non-infective causes of endocarditis?
SLE
malignancy (marantic endo)
Culture negative causes of infective endocarditis?
prior Abx therapy
Coxiella burnetii
Bartonella
HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
Infective endocarditis?
inflam of endocardium (inner lining of heart) and valves primarily caused by bacteria
Criteria to diagnose infective endocarditis?
Modified Duke Criteria
When is infective endocarditis diagnosed using the Modified Duke criteria? (4)
1) pathological criteria positive, or
2) 2 major criteria, or
3) 1 major and 3 minor, or
4) 5 minor
Infective endocarditis: what is a positive pathological criteria on Modified Duke?
1) microorganisms in a vegetation on histology (autopsy or surgery)
OR
2) Pathologic legions on histology of vegetation or intracardiac abscess
Duke Modified Criteria for infective endocarditis: what is included in the major criteria?
1) Typical microorganisms consistent of IE from 2 separate blood cultures taken >12hrs apart
2) Evidence of endocardial involv. on ECHO
Duke Modified Criteria for infective endocarditis: what is included in the minor criteria?
1) Predisposing heart condition or IVDU
2) Fever >38
3) Vascular phenomena: conjunctival haemorrhages, Janeway’s lesions, intracranial haemorrhage, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, splinter H
4) Immunologic phenomena: Osler’s nodes, Roth’s spots, Glomerulonephritis, rheumatoid factor
5) Microbio evidence: +ve blood culture that doesn’t meet major criteria or serological evidence of active infection consistent with IE
Ix for infective endocarditis?
- Blood cultures (1st)
- Trans-oesphageal ECHO (vegetation)
- ECG: prolonged PR
Infective endocarditis CP?
F.ever >38
R.oth spots
O.cler’s nodes= fingertips, painful
M.urmur
J.aneway lesions: palm, painless
A.naemia
N.ail bed splinter haemorrhages
E.mboli
Predisposing heart condition, IVDU, recent dental surgery
Poor prognostic factors of infective endocarditis?
- staph aureus
- prosthetic valve
- culture -ve endocarditis
- low complement levels
Mortality of infective endocarditis according to organism?
staphylococci - 30%
bowel organisms - 15%
streptococci - 5%
Summary of Mx of infective endocarditis?
- inital blind Abx therapy
- then specific Abx therapy
- ?surgery
Mx of infective endocarditis: inital blind Abx therapy (empirical)? What is allergic/MRSA/sepsis? What if prosthetic valve?
- Amoxicillin, consider + low dose gentamicin
- MRSA, severe sepsis or penicillin allergic: vancomycin + low dose gentamicin
- If prosthetic valve: vancomycin + rifampicin + low dose gentamicin
Specific Abx therapy for infective endocarditis if native valve (normal) caused by staphlococci? Allergic/MRSA?
Flucloxacillin
Allergic/MRSA= vancomycin + rifampicin
Specific Abx therapy for infective endocarditis if prosthetic valve caused by staphlococci? Allergic/MRSA?
Flucloxacillin + rifampicin + low-dose gentamicin
Allergic/MRSA=
vancomycin + rifampicin + low-dose gentamicin
Specific Abx therapy for infective endocarditis if caused by fully-sensitive strep (eg. viridans)? Allergic?
Benzylpenicillin
Allergic= vancomycin + low-dose gentamicin
Specific Abx therapy for infective endocarditis if caused by less sensitive strep? Allergic?
Benzylpenicillin + low-dose gentamicin
Allergic= vancomycin + low-dose gentamicin
Typical Abx if allergic to penicillin or MRSA (eg. if use flucloxacillin)?
vancomycin
Indications for surgery in infective endocarditis?
- severe valvular incompetence
- aortic abscess
- infections resistant to Abx
- funal infections
- recurrent emboli after Abx
Pts with what cardiac conditions are at incresed risk of developing infective endocarditis?
- acquired valvular heart disease with stenosis or regurg
- hypertrophic cardiomyopathy
- previous IE
- structural congential heart disease
- valve replacement
Advice to give pts who are at increased risk of IE?
- benefits and risks of Abx prophylaxis and why it’s no longer recommeneded
- importance of good oral health
- CP of IE
- risks of invasive procedures incl. non medical eg. piercing or tattoos
Is Abx prophylaxis for IE routinely recommended?
No
What should pts who take standard release isosorbide mononitrate for stable angina Mx do to prevent development of nitrate tolerance and reduced efficacy?
use asymmetric dosing interval to maintain a daily nitrate-free time of 10-14hrs.
(not seen in pts who take modified release)
Another name for stable angina?
Angina pectoris
Causes of mitral valve prolapse?
usually idiopathic but can be associated with other conditions and CVD
Mitral valve prolapse? (Barlow syndrome)
the cusps of the mitral valve become enlarged or strecth and these bulge (prolapse) into LA as heart contracts
Usually doesn’t require Mx unless causes severe regurg
Mitral valve prolapse associations?
congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease
Features of mitral valve prolapse?
- atypical chest pain/palpitations
- mid-systolic click (later if pt squatting)
- late systolic murmur (longer if pt standing)
Cx of mitral valve prolapse?
mitral regurg, arrhythmias (long QT), emboli, sudden death
Myocarditis?
Inflamm of myocardium
Consider what is a young pt with acute chest pain?
myocarditis
Causes of myocarditis?
- viral: coxsackie B, HIV
- bacteria: diptheria, clostridia
- spirochaetes: Lyme disease
- protozoa: Chagas’ disease, toxoplasmosis
- autoimmune
- drugs: doxorubicin
CP of myocarditis?
- usually young pt with acute Hx
- chest pain
- dyspnoea
- arrhythmias
Ix for myocarditis?
- Bloods= Increased: CRP & ESR, cardiac enzymes and BNP, elevated troponin
- ECG
ECG findings in myocarditis?
- tachycardia
- arrhythmias
- ST/T wave changes incl ST elevation and T wave inversion
Mx for myocarditis?
- TUC eg. Abx if bacterial causes
- supportive treatment eg. of HF or arrhythmias
Cx of myocarditis?
- HF
- arrhythmia, possibly leading to sudden death
- dilated cardiomyopathy: usually a late complication
Classic features of cardiac tamponade?
Beck’s triad: hypotension, muffled heart sounds, raised JVP
CP of cardiac tamponade?
- Beck’s triad
- dyspnoea
- tachycardia
- absent Y descent on JVP (due to limited RV filling)
- pulsus paradoxus
- Kussmaul’s sign rare
ECG feature of cardiac tamponade?
electrical alternans (alternating QRS amplitude seen in any or all leads with no other changes to conduction pathways)
Pulsus paradoxus?
abnormally large drop in BP during inspiration
Kussmaul’s sign?
Paradoxical increase in JVP that occurs during inspiration. Seen in cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy
What does an absent Y descent mean?
when filling of RV is impaired following opening of tricuspid valve
eg. in cardiac tamponade:
TAMponade=TAMpaX (no Y)
Ix for cardiac tamponade?
transthoracic echo and ECG
What does X and Y mean in JVP?
X descent= RA relaxation
Y descent= RV filling (tricuspid opens)
Difference in features between cardiac tamponade and constrictive pericarditis?
CT= JVP absent Y descent; pulsus paradoxus present; Kussmaul’s sign rare
CP= X + Y present; absent pulsus paradoxus; present Kussmaul’s sign; pericardial calfication on CXR
Causes of constrictive pericarditis?
any cause of pericarditis, particularly TB
Constrictive pericarditis?
Granulation tissue formation in pericardium results in loss of pericardial elasticity leading to restriction in V filling
CP of constrictive pericarditis?
- dyspnoea
- RHF: elevated JVP, ascites, oedema, hepatomegaly
- JVP shows X and Y descent
- pericardial knock (loud S3)
- Positive Kussmaul’s sign
Ix for constrictive pericarditis?
CXR: pericardial calcification
Mx for constrictive pericarditis?
NSAIDs, diuretics
Only definitive Mx= pericardiectomy but use in caution if mild disease as high mortality
Causes of pericardial effusion?
infectious pericarditis: viral, tuberculosis, pyogenic spread from septicaemia and pneumonia
uraemia
idiopathic
post myocardial infarction (including Dressler’s syndrome)
malignancy
heart failure
nephrotic syndrome
hypothyroidism
trauma
Pericardial effusion can be made of what?
Transudates (low protein content)
Exudates (associated with inflammation)
Blood
Pus
Gas (associated with bacterial infections)
Pericardial effusion?
XS fluid collects within pericardial sac; can be cute or chronic; can fill entire pericardial cavity or only a localised section
Pericardial effusion: transudative effusion?
Results from increased venous pressure that can reduce drainage from pericardial cavity. May occur in congestive HF and pulmonary HTN.
Pericardial effusion: exudative effusion?
after any inflam process affecting pericardium (pericarditis) eg. infection, autoimmune, trauma, malignancy, methotrexate
Rupture of heart or aorta can cause bleeding into the pericardial cavity, resulting in rapid onset cardiac tamponade- rupture may be due to what?
MI, trauma or aortic dissection type A
CP of pericardial effusion?
chronic ones may be asymptomatic until pressure rises.
- chest pain, SOB, fullness in chest, orthopnoea
- quiet HS, pulsus paradoxus, hypotension, raised JVP, fever & pericardial rub (with pericarditis)
Pericardial effusion may compress surrounding structures causing other symptoms like….
- Phrenic nerve compression= hiccups
- Oseophageal= dysphagia
- Recurrent laryngeal nerve= hoarse voice
Ix for pericardial effusion?
- ECHO (gold & 1st)
- fluid analysis: underlying cause eg. protein content, bacterial culture, viral PCR, cytology & tumour markers
Mx for pericardial effusion?
- TUC eg. inflamm: NSAIDs and colchicine
- Draining: needle pericardiocentesis
Pericardial window?
surgical procedure where portion of pericardium removed creating a ‘window’/fistula to allow fluid to drain from pericardial cavity to pleural carvity/peritoneal cavity
Membrane that surrounds the heart?
Pericardium/pericardial sac
What is the pericardium made from?
2 layers with small amount of fluid in between (<50ml) providing lubrication to allow heart to beat without friction. These layers separate heart from rest of contents of mediastinum.
What is between the 2 layers of the pericardium?
‘potenital space’ called pericardial cavity, layers usually touch eachother which is my it is only a potential space. Small amount of fluid.
Potential space of pericardial cavity fills with fluid?
Pericardial effusion. Creates inward pressure on heart making it more difficult to expand during diastole (filling of heart).
What is it called when the pericardial effusion is large enough to raise intra-pericardial pressure?
Cardiac tamponade. Leads to reduced filling of heart during diastole resulting in decreased cardiac output during systole.
Transudate?
Fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. Eg. due to increased hydrostatic pressure or decreased oncotic pressure
Exudate?
Fluid buildup caused by tissue leakage due to inflammation or local cellular damage.
Transudate vs exudate?
Transudate:
- Protein <30g/L
- Clear
- Low cell & protein content
- Causes: HF, liver cirrhosis, nephrotic syndrome
Exudate:
- Protein >30g/L
- Cloudy, yellow or bloody
- High cellular & protein content
- Causes: inflam eg. infections (eg. pneumonia), RA, malginancy
Are transudate and exudate both extracellular?
Yes they both accumulate in extracellular space eg. tissues or body cavities outside of cells.
Exudate diagnostic criteria?
High protein content (>3 g/dL).
High specific gravity (>1.020).
High LDH (lactate dehydrogenase) levels.
Transudate diagnostic criteria?
Low protein content (<3 g/dL).
Low specific gravity (<1.012).
Low LDH levels.
Reflex syncope?
Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
Most common cause of syncope?
Reflex syncope
Subtypes of reflex syncope subtypes?
- vasovagal (faiting)
- situational: cough, micturition, GI
- carotid sinus syncope
Vasovagal (reflex) syncope?
- ‘fainting’
- Typically in sitting or standing position & can be triggered by emotion pain or stress.
- CP: warm/hot or light headed prior
- <1-2mins
- prolonged fatigue/amnesia is usual after regaining consciousness
What can occur during uncomplicated vasovagal syncope?
brief myoclonic jerks
Carotid sinus syncope?
Type of fainting caused by exaggerated response to stimulation of carotid sinus located in neck. Leads to sudden drop in HR & BP -> reduced blood flow to brain and fainting.
Triggers= tight collars, neck pressure, head movements.
- Diagnosis= carotid sinus massage or tilt table test
- Mx: avoid triggers; severe- pacemaker to regulate HR
Signs of tricuspid regurg?
- pan-systolic murmur
- prominent/giant V waves in JVP
- pulsatile hepatomegaly
- left parasternal heave
Where is loin pain located?
Between lower ribs and buttocks on either side of the spine
Where can loin pain originate?
Kidneys, adrenal glands, parts of colon, MSK components, referred from abdo or pelvic organs
Renal capsule, ureter and muscles are supplied with what that transmit pain signals to the CNS?
nociceptors
Differential diagnosis for loin pain
- ruptured AAA
- renal colic
- pyleonephritis
- MSK pain
- radiculopathy (compression or inflam of spinal nerve roots may cause referred pain)
Ix for loin pain?
identifty life-threatening conditions eg. ruptured AAA; history; physical abdo renal and neuro exam; bloods (FBC, renal function); urinalysis; USS/CT; pain Mx
What may make atypical presentation of ACS more likely?
female, elderly, diabetic
Differential diagnosis for chest pain?
MI
pneumothorax
PE
pericarditis
dissecting aortic aneurysm
GORD
MSK chest pain
perforated peptic ulcer
shingles
Boerhaaves syndrome
Referral criteria for chest pain?
- current or <12hrs AND abnormal ECG= emergency admission
- chest pain 12-72hrs ago= refer for same day hospital assessment
- chest pain >72hrs ago= ECG and toponin then decide
Mx for pts in whom stable angina can’t be excluded by clinical assessment alone (eg. symptoms consistent with typical/atypical angina OR ECG changes)?
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (?reversible mycardial ischaemia)
3rd: 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
You can characterise congenital heart disease into what?
Cyanotic and acyanotic
Most common causes of acyanotic congential heart disease?
- Ventricular septal defects (VSD) (most common, 30%)
- atrial septal defect (ASD)
- patent ductus arteriosus (PDA)
- coarctation of aorta
- aortic valve stenosis
What are more common- VSDs or ASDs?
VSDs but in adults ASDs more common new diagnosis as generally present later
Most common causes of cyanotic congenital heart disease?
- tetralogy of Fallot
- transposition of great arteries (TGA)
- tricuspid atresia
What is more common- tetralogy of Fallot or TGA?
Fallot but at birth TGA is more common lesion as pts with Fallot’s generally present at around 1-2m
The presence of cyanosis in pulmonary valve stenosis depends on what?
the severity and any other coexistent defects
When is peripheral cyanosis eg. in hands and feet very common?
1st 24hrs of life and may occur when child is crying or unwell
Central cyanosis clinical diagnosis?
conc of reduced Hb in blood >5g/dl
What can be used to differentiate cardiac from non-cardiac causes of cyanosis in neonatal period?
Nitrogen washout test (hyperoxia test): infant given 100% O2 for 10mins then ABG taken. A pO2 of <15kPa= cyanotic congenital heart disease
Initial Mx of suspected cyanotic congenital heart disease?
supportive care + prostaglandin E1 eg. alprostadil
Why is prostaglandin E1 eg. alprostadil used in the inital Mx of suspected cyanotic congenital heart disease?
Used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect.
Acts as a holding measure until a definite diagnosis is made and surgical correction performed.
Acrocyanosis?
seen in healthy newborns and refers to cyanosis around the mouth and extremities (eg. hands & feet)
How is acrocyanosis differentiated from other causes of peripheral cyanosis with signif pathology?
occurs immediately after birth in health infants; common finding as may persist for 24-48hrs
Tetralogy of Fallot (TOF)?
most common cause of cyanotic congenital heart disease
When does TOF typically present?
1-2m old, may not be picked up until 6m
TOF is a result of what?
anterior malalignment of the aorticopulmonary septum
4 characteristic features of TOF?
- ventricular septal defect (VSD)
- RV hypertrophy
- overriding aorta
- pulmonary stenosis
what can cause RV outflow tract obstruction?
pulmonary stenosis
What is the heart defect- overriding aorta?
where aorta is positioned over both the LV & RV (not just the LV); causes it to override the VSD so that it receives blood from both the LV and RV (oxygen rich AND oxygen poor blood); so reduces amount of O2 body receives
What determines the degree of cyanosis and clinical severity in TOF?
severity of pulmonary stenosis (and so RV outflow tract obstruction)
CP of TOF?
- cyanosis
- ‘tet’ spells
- tachypnoea
- loss of consciousness
what are tet spells in TOF?
infants may develop episodic hypercyanotic tet spells due to near occulasion of RV outflow tract.
may become pale/blue (esp fingers and lips); diff breathing; irritable; loss of consciousness
Other features of TOF (shunt? murmur?)?
- causes R-to-L shunt
- ejection systolic murmur due to pulmonary stenosis (VSD doesn’t usually cause murmur)
- right-sided aortic arch in 25% pts
In TOF what does CXR and ECG show?
- cxr= boot-shaped heart
- ECG= RV hypertrophy
Mx of TOF?
- surgical repair often in 2 parts
- beta-blockers for cyanotic episodes to reduce infundibular spasm
Transposition of the great arteries (TGA)?
form of cyanotic congenital heart disease caused by the failure of the aorticopulmonary septum to spiral during septation (aorta and pulmonary artery swap places)
Who are at increased risk of TGA?
children of diabetic mothers
Basic anatomical changes in TGA?
- aorta leaves RV
- pulmonary trunk leaves LV
Clinical features of TGA?
- cyanosis
- tachypnoea
- loud single S2
- prominent RV impulse
- ‘egg-on-side’ appearance on CXR
Mx for TGA?
- maintenance of ductus arteriosis with prostaglandins
- definitive Mx= surgical correction
Coarctation of the aorta?
congenital narrowing of the descending aorta
Association of coarctation of aorta?
Turner’s syndrome.
But is more common in males.
Coarctation of aorta associations?
Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
Features of coarctation of the aorta?
- infancy: HF
- adult: HTN
Signs of coarctation of aorta on examination?
- radio-femoral delay
- mid systolic murmur, maximal over the back
- apical click from the aortic valve
- notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
What causes the first heart sound (S1)?
Closure of mitral and tricuspid valves
What causes the second heart sound (S2)?
aortic and pulmonary valve closure
S1?
closure of mitral and tricuspid valves
What causes soft S1?
if long PR or mitral regurg
What causes loud S1?
mitral stenosis
S2?
closure of aortic and pulmonary valves
What causes a soft S2?
aortic stenosis
Is splitting of S2 during inspiration normal?
Yes
What is a third heart sound (S3) caused by?
diastolic filling of the ventricle
When is a S3 normal?
If <30yrs old (may persistent in women up to 50yrs)
What is a gallop rhythm?
when S1 and S2 followed by pathological S3 and/or S4. commonly associated with LV failure
When may S3 be heard?
LV failure (eg. dilated cardiomyopathy), constrictive pericarditis and in mitral regurg
What is S3 called in constrictive pericarditis?
pericardial knock
When may a S4 (fourth heart sound) be heard?
in aortic stenosis, HOCM, HTN
What causes S4?
Atrial contraction against stiff ventricle; therefore coincides with P wave on ECG
In HOCM a double apical impulse may be felt as a result of a…
palpable S4
Site of auscultation for pulmonary valve?
Left 2nd ICP at upper sternal border
Site of auscultation for mitral valve?
Left 5th ICP just medical to mid clavicular line
Site of auscultation for aortic valve?
Right 2nd ICP at upper sternal border
Site of auscultation for tricuspid valve?
Left 4th ICS and lower left sternal border
Causes of loud S2?
- HTN: systemic (loud A2) or pulmonary (loud P2)
- hyper dynamic states
- ASD without pulmonary HTN
Causes of a soft S2?
Aortic stenosis
Causes of a fixed (in the middle) split of S2?
atrial septal defect
Causes of a widely split S2?
- deep inspiration
- RBBB
- pulmonary stenosis
- severe mitral regurg
Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)?
- LBBB
- severe aortic stenosis
- RV pacing
- WPW type B (causes early P2)
- patent ductus arteriosus
What does S2 sound like?
Higher pitched and shorter duration than S1. ‘dub’ section of ‘lub-dub’
What is S2 split into?
Closure of aortic (A2) and pulmonary (P2) valves at end of V systole
When do you hear the components of S2?
- A2 normally slightly before P2, P2 softer except in certain conditions it is more pronounced.
- Normal S2: ‘dub’
- Split S2: NORMAL during INSPIRATION where you can hear A2 and P2 distinctively (lub-d-dub’)
What does a split S2 mean?
In normal physiology, occurs during inspiration. The 2 components of S2 can be heard separately due to the delay in P2 (resulting in a split sound ‘d-dub’ A2-P2)
When is S2 split normal?
During inspiration- corresponds to A2 and P2. (d-dub)
NOT during expiration- sound be heard as a single sound (dub) and not a split
Types of split S2?
- physiological (normal in children and young adults, widens with inspiration and narrows with expiration)
- fixed split S2
- wide split S2
- paradoxical split S2
Fixed split of S2?
The split (between A2 and P2) remains constant during both inspiration and expiration.
What is associated with a fixed split of S2?
ASD
Wide split S2?
the split (sounds of A2 and P2) is wider than normal and persists during inspiration and expiration.
What is associated with wide split S2?
RBBB or pulmonary HTN
What is a paradoxical split s2?
Split (sounds of A2 and P2) occur during expiration and narrows or disappears during inspiration.
What is a paradoxical split S2 associated with?
conditions that delay the closure of aortic valve eg. LBBB, patent ductus arteriosus, severe aortic stenosis
Way to remember the type of S2 split that occurs in different conditions?
- normal during inspiration
- Reversed/paradoxical split (left): LBBB
- Widely split (right): RBBB
- Fixed split: ASD
- Loud S2: HTN
- Soft S2: aortic stenosis
Innocent murmurs heard in children?
- Ejection murmurs
- Venous hums
- Still/s murmur
Innocent murmurs in children: ejection murmurs due to?
Turbulent blood flow at outflow tract of the heart
Innocent murmurs in children: venous hums?
due to turbulent blood flow in great veins returning to the heart, heard as a continuous blowing noise just below the clavicles
Innocent murmurs in children: Still’s murmur?
low-pitched sound heard at the lower left sternal edge
Characteristics of an innocent ejection murmur ?
- soft-blowing murmur in the pulmonary area or short buzzing murmur in the aortic area
- may vary with posture
- localised with no radiation
- no diastolic component
- no thrill
- no added sounds (e.g. clicks)
- asymptomatic child
- no other abnormality
Types of murmurs? (6)
- ejection sytolic
- pansystolic (holosystolic)
- late systolic
- early diastolic
- mid-late diastolic
- continuous machine-like murmur
Causes ff ejection systolic murmur heard louder on expiration?
aortic stenosis and hypertropic obstructive cardiomyopathy
Causes of ejection systolic murmur heard louder on inspiration?
pulmonary stenosis and atrial septal defect
Causes of ejection systolic murmurs? (5)
- TOF
- aortic stenosis
- hypertrophic obstructive cardiomyopathy
- pulmonary stenosis
- ASD
Causes of holosystolic (pansystolic) murmurs? (3)
- mitral regurg (high pitched and blowing)
- tricuspid regurg (high and blowing)
- VSD (harsh)
Why does tricuspid regurg become louder during inspiration, unlike mitral regurg?
during inspiration, venous blood blow to RA and V are increased -> increases stroke volume of RV during systole
Causes of late systolic murmur? (2)
mitral valve prolapse and coarctation of aorta
Causes of early diastolic murmur?
- aortic regurg
- pulmonary regurg (Graham-Steel murmur)
Causes of mid-late diastolic murmur?
- mitral stenosis
- severe aortic regurg (Austin-Flint murmur)
Causes of continuous machine-like murmur?
Patent ductus arteriosus
What does mitral, tricuspid, aortic and pulmonary regurgitation sound like?
high pitched and blowing
What does a pansystolic murmur from VSD sound like?
harsh in character
What does mitral stenosis and severe aortic regurg sound like?
rumbling in character
What does RILE mean in regards to heart murmurs?
R.ight sided murmur -> heard best on I.nspiration
L.eft sided murmur -> heard best on E.xpiration
What does aortic stenosis sound like?
Harsh in character
Aortic vs mitral stenosis murmur sound?
Aortic: harsh systolic
Mitral: rumbling diastolic with opening snap
What is a leg ulcer?
break in the skin below the knee which has not healed within 2w
Venous leg ulcer?
Leg ulcer that occurs in the presence of venous disease (most common type of leg ulcer-60-80%)
Where do venous leg ulcers occur typically?
in the gaiter area of the leg (from ankle to mid calf)
Causes of leg ulceration?
venous disease; arterial disease; DM; RA; vasculitis; sickle cell; malignancy; drugs
What drugs can cause leg ulcers?
NSAIDs, corticosteroids, nicorandil
What is venous leg ulceration caused by?
sustained venous HTN resulting from chronic venous insufficiency due to venous valve incompetence or impaired calf muscle pump
RFs for venous leg ulcer?
obesity, immobility, increasing age, varicose veins, Hx of DVT
Healing and recurrence rates of venous leg ulcers?
Repeat cycles of ulceration, healing and recurrence common.
12m recurrence: 26-69%.
6m healing rates= ommunity 45% and specialist 70%
How to examine venous leg ulcer?
- wound= site, edge, size, depth, wound bed, infection
- leg= oedema, varicose veins, venous skin changes, reduced ankle mobility
Ix for venous leg ulcers?
- examination
- Doppler assessment of both legs to determine ankle-brachial pressure index in both legs to exclude arterial insufficiency
- consider bloods
Primary care Mx of venous leg ulcer?
- cleaning and dressing wound
- compression therapy if appropritate (4 layer compression banding after excluding arterial disease)
- consider pentoxifylline improve healing
- advice
- follow up to assess
- Mx of Cx and associated conditions
- recurrent: refer to vascular specialist ?superficial venous surgery
Why may pentoxifylline be prescribed for venous leg ulcers?
to improve microcirculatory blood flow and improve ulcer healing (a peripheral vasodilator)
Lifestyle advice to promote leg ulcer healing and reduce recurrence?
compression therapy; keep mobile with walking regular (exercise calf muscle pump function); elevate legs when immobile; emollient frequently
When to arrange specialist referral for venous leg ulcer?
Delayed or no healing >2w of adequate Mx or uncertain diagnosis/cause.
For superficial venous surgery.
How to reduce risk of recurrence after leg ulcer has healed?
- long-term below-knee graduated compression hosiery
- lifestyle measures
- review and follow up
When should bacteriological swabs be taken for leg ulcer?
only if evidence of infection
In venous leg ulcers, after ABPI is done, may consider bloods- why?
-FBC: anaemia may delay healing; raised WBC & platelts- infection
- ESR & CRP
- urea and creatinine= high urea- ?dehyrdation which impair healing
- albumin= low may be associated wioth protein loss and malnutrition, may delay healing
- HbA1c: ?DM
What is the ankle brachial pressure index (ABPI)?
provides index of vessel competency by measuring ratio of SBP at ankle to that of the arm, valve of 1=normal.
always interpret in context of CP
ABPI ratio <0.5
severe arterial disease- compression treatment contraindicated and urgent referral for specialist vascular assessment
ABPI ratio >0.5 and <0.8?
arterial disease or mixed arterial/venous disease; refer and generally avoid compression
ABPI ratio 0.8-1.3?
no evidence of signif arterial disease and compression safe
ABPI >1.3?
may suggest presence of arterial calcification eg. in DM, RA, atherosclerosis, CKD.
may be misleadingly high so refer
Features of venous insufficency?
brown pigmentation, oedema, lipodermatosclerosis, eczema
Mx for infected leg ulcer?
500mg flucloxacillin 4 times a day for 7 days
or 500mg clarithromycin twice a day
Marjolin’s ulcer?
Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb
Arterial ulcers?
- Occur on the toes and heel
- Typically have a ‘deep, punched-out’ appearance
- Painful
- There may be areas of gangrene
- Cold with no palpable pulses
- Low ABPI measurements
Neuropathic ulcers?
- Commonly over plantar surface of metatarsal head and plantar surface of hallux
- The plantar neuropathic ulcer is the condition that most commonly leads to amputation in diabetic patients
- Due to pressure
- Management includes cushioned shoes to reduce callous formation
Pyoderma gangrenosum?
- Associated with inflammatory bowel disease/RA
- Can occur at stoma sites
- Erythematous nodules or pustules which ulcerate
Why can’t you use compression for arterial ulcers?
will reduce blood supply further, surgery may be needed to clear out blocked artery (angioplasty)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)?
form of inherited CVD that may present with syncope or sudden death; 2nd most common cause of sudden cardiac death in young after hypertrophic cardiomyopathy
Pathophysiology of ARVC?
- autosomal dominant
- RV myocardium is replaced by fatty and fibrofatty tissue
CP of ARVC?
palpitations, syncope, sudden cardiac death
Ix for ARVC?
- ECG= T wave inversion; 50% have epsilon wave (terminal notch in QRS complex)
- echo= subtle; enlarged hypokinetic RV with thin free wall
- MRI can show fibrofatty tissue
Mx of ARVC?
- sotalol (antiarrhythmic)
- catheter ablation to prevent V tach
- implantable cardio-verter defib
Naxos disease?
autosomal recessive variant of ARVC
triad= ARVC, palmoplantar keratosis and woolly hair
Atrial myxoma?
Most common primary cardiac tumour.
Females
75% in LA; commonly attached to fossa ovalis
Features of atrial myoxoma?
- systemic= dysponea, fatigue, weight loss, pyrexia of unknown origin, clubbing
- emboli
- AF
- mid-diastolic murmur, ‘tumour plop’
- echo= pedunculated heterogenous mass typically attached to fossa ovalis region of interatrial septum
Effects of BNP?
vasodilator
diuretic and natriuretic
suppressess both sympathetic tone and renin-angiotensin-aldosterone system
What may cause raised BNP?
produced by LV myocardium in response to strain
HF, MI, LV dysfunction, valvular disease
CKD
How to reduce BNP?
ACEinhh
ARB
and diuretics
<100pg/ml BNP makes what unlikely?
HF
Oxygenation of the blood in the heart?
- deoxygenated blood -> R side of heart via SVC and IVC, oxygen sat 70%; RA, RV, PA have oxyegn sat of around 70%.
- lungs oxygenate blood to around 98-100%; LA, LV and aorta should therefore have oxygen sat 98-100%
Oxygen sats you would expect if normal?
RA= 70%
RV= 70%
PA= 70%
LA= 100%
LV=100%
Aorta= 100%
Oxygen sats you would expect if ASD?
RA= 85%
RV= 85%
PA= 85%
LA= 100%
LV=100%
Aorta= 100%
Oxygen sats you would expect if VSD?
RA= 70%
RV= 85%
PA= 85%
LA= 100%
LV=100%
Aorta= 100%
Oxygen levels you would expect in PDA?
RA= 70%
RV= 70%
PA= 85%
LA= 100%
LV=100%
Aorta= 100%
Oxygen levels you would expect in VSD with Eisenmenger’s?
RA= 70%
RV= 70%
PA= 70%
LA= 100%
LV=85%
Aorta= 85%
Oxygen levels you would expect in PDA with Eisenmenger’s?
RA= 70%
RV= 70%
PA= 70%
LA= 100%
LV=100%
Aorta= 85%
Oxygen levels you would expect in ASD with Eisenmenger’s?
RA= 70%
RV= 70%
PA= 70%
LA= 85%
LV=85%
Aorta= 85%
What cardiac enzyme/protein marker is used to look for reinfarction?
CK-MB
Troponin T and Troponin I?
proteins found in cardiomyocytes; released into blood when heart muscle in damaged eg. MI.
Troponin T= binds the troponin complex to tropomyosin (another protein invl in muscle contraction)
Troponin I= inhibits the interaction between actin and myosin (proteins that cause muscle contraction) when the heart is at rest
How is Troponin T and Troponin I used to detect heart muscle damage eg. following MI?
troponins rise in the blood within 3-6hrs after heart muscle damage occurs; peak after 12-24hrs and can remain elevated for up to 1-2w
Troponin vs NT-proBNP?
T= diagnose MI; indicates heart muscle damage; highly specific to heart muscle injury
NT-proBNP= diagnose and manage HF (released by heart in response to increased pressure and vol overload eg. in HF); indicates heart strain or overload; reflects HF but can be elevated in other conditions eg. kidney disease, PE, old age
BNP vs NT-proBNP?
Both released by ventricles in response to increased pressure and vol overload eg. HF.
BNP is the active hormone and NT-proBNP is the inactive fragment.
NT-proBNP is more stable in the blood and has a longer half-life- 1-2hrs (BNP 20mins) so preferred marker for diagnosing & monitoring of HF.
Eisenmenger’s syndrome?
the reversal of a left to right shunt in a congenital heart defect due to pulmonary HTN; occurs when an uncorrected L-to-R shunt leads to copulmonale (pulmonary HTN and obstruction of pulmonary blood due to remodeling of pulmonary microvasculature).
What is Eisenmenger’s associated with?
VSD
ASD
PDA
Features of Eisenmenger’s?
- original murmur may disappear
- cyanosis
- clubbing
- RV failure
- haemoptysis, embolism
Mx of Eisenmenger’s?
heart-lung transplant required
Hypothermia?
unintentional reduction of core body temp:
mild= 32-35C
moderate/severe= <32C
What happens in the initial stages of hypothermia?
thermoreceptors in skin and subcut tissues sense low temp and cause regional vasocontriction; causes hypothalamus to stimulate release of TSH and ACTH; also stimulates heat production by promoting shivering
Causes/RFs of hypothermia?
- elderly and newborn babies
- exposure to cold environment
- inadequate insulation in operating room/general anaesthesia
- hypothyroidism
- impaired mental status
- homelessness
- cardiopulmonary bypass
Signs of hypothermia?
- shivering
- cold pale skin
- frostbite
- slurred speech
- Mild= tachypnoea, tachy, HTN
- moderate= resp dep, bradycardia, hypotension
- confusion/impaired mental state
Frostbite in hypothermia?
when skin and subcut tissue freeze, causing damage to cells
Hypothermia in babies?
can look healthy
may be limp; unusually quiet and refuse to feed.
Extremely common in newborns= hat and blanket soon after birth.
Ix for hypothermia?
- temp= tracked over time; low-reading rectal thermometers or thermistor probs
- ECG= acute ST-elevation and J waves or Osborn waes
- FBC + U&Es= Hb elevated, platelets & WBCs low (sequestration in spleen)
- Blood glucose= stress hormones increased so more resistance to insulin
- ABG
- Coag factors
- CXR
What should be monitored in hypothermia?
temp
potassium as can be hypokalaemic due to shift of potassium into intracellular space
Mx for hypothermia?
- remove from cold & any wet clothing
- warm with blankets
- secure airway and monitor breathing
- not responding to warming then maintain circulation using warm IV fluids or apply forced warm air directly onto body
- RAPID REWARMING can lead to PERIPHERAL VASODILATION AND SHOCK= so if severe prepare for CPR; avoid IV drugs if possible as likely to have drastic response to the drug
Advice for pubic on what NOT to do if pt has hypothermia (due to risk of cardiac arrest)?
- don’t put in hot bath
- don’t massage limbs
- don’t use heating lamps
- don’t give alcohol to drink
Mx for choking?
1) “are you talking”= if respond yes or able to speak, cough or breath then mild airway obstruction. If unable to speak/they nod, unable to breathe, wheezy, silent cough, unconscious then severe.
2) Mild= encourage pt to cough
2) Severe and conscious=
- 5 back-blows
- unsuccessful then 5 abdo thrusts
- if unsuccessful then repeat
2) if unconscious= call ambulance and start CPR
Isolated systolic HTN (ISH)?
Common in elderly; 50% of >70yrs.
Mx in same way as standard HTN.
Where is a non-pulsatile JVP seen?
superior vena caval obstruction
Kussmaul’s sign: paradoxical rise in JVP during respiration?
seen in constrictive pericarditis
JVP: jugular vein waveform= ‘a’ wave?
atrial contaction
- large if atrial pressure eg. tricuspid stenosis, pulmonary stenosis, pulmonary HTN
- absent in AF
JVP: jugular vein waveform= cannon ‘a’ waves?
- caused by atrial contractions against a closed tricuspid valve
- seen in complete heart block, V tachy/ectopics, nodal rhythm, single chamber ventricular pacing
JVP: jugular vein waveform= ‘c’ wave?
closure of tricuspid valve
- not normally visible
JVP: jugular vein waveform= ‘v’ wave?
- due to passive filling of blood into atrium against closed tricuspid
- giant v waves in tricuspid regurg
JVP: jugular vein waveform= ‘x’ descent?
fall in atrial pressure during V systole
JVP: jugular vein waveform= ‘y’ descent?
opening of tricuspid valve
Long saphenous vein?
may be harvested for bypass surgery or removed as Mx for varicose veins with saphenofemoral junction incompetence
Path of the long saphenous vein?
- Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the foot
- Passes anterior to the medial malleolus and runs up the medial side of the leg
- At the knee, it runs over the posterior border of the medial epicondyle of the femur bone
- Then passes laterally to lie on the anterior surface of the thigh before entering an opening in the fascia lata called the saphenous opening
- It joins with the femoral vein in the region of the femoral triangle at the saphenofemoral junction
Long saphenous vein tributaries?
- Medial marginal
- Superficial epigastric
- Superficial iliac circumflex
- Superficial external pudendal veins
Short saphenous vein path?
- Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the foot, which attaches to the great saphenous vein.
- It passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along the posterior aspect of the leg (with the sural nerve)
- Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein, approximately at or above the level of the knee joint.
Path of the subclavian artery?
- The left subclavian comes directly off the arch of aorta
- The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into the subclavian and the right common carotid artery.
- From its origin, the subclavian artery travels laterally, passing between anterior and middle scalene muscles, deep to scalenus anterior and anterior to scalenus medius. As the subclavian artery crosses the lateral border of the first rib, it becomes the axillary artery. At this point it is superficial and within the subclavian triangle.
Branches of the subclavian artery?
- Vertebral artery
- Internal thoracic artery
- Thyrocervical trunk
- Costocervical trunk
- Dorsal scapular artery
Takotsubo cardiomyopathy?
type of non-ischaemic cardiomyopahty associated with a transient, apical ballooning of the myocardium.
may be triggered by stress
Pathophysiology of Takotsubo cardiomyopathy?
Takotsubo= Japanese word that for octopus trap
- apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap)
Features of Takotsubo cardiomyopathy?
- chest pain
- features of HF
- ECG= ST elevation
- normal coronary angiogram
Mx and prognosis of Takotsubo cardiomyopathy?
Mx is supportive.
Prognosis= most improve with supportive treatment.
Wolf-Parkinson White?
caused by congenital accessory conducting pathway between A & Vs leading to atrioventricular re-entry tachy (AVRT). As the accessory pathway doesn’t slow conduction, AF can degenerate rapidly to VF.
Possible ECG features of Wolf-Parkinson White?
- short PR interval
- wide QRS with slurred upstroke- delta wave
- left axis deviation if right-sided accessory pathway; right axis D if left sided A P (majority have left axis deviation)
Differentiate between type A and B of WPW syndrome?
type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1
Associations of WPW syndrome?
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
Mx of WPW syndrome?
definitive treatment= radiofrequency ablation of the accessory pathway
medical therapy= sotalol***, amiodarone, flecainide
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
