Cardio Flashcards
Define postural hypotension
recurrent drop in systolic blood pressure ≥ 20 mmHg (risk of syncope and falls).
what waves are found on ECGs in hypothermia
J waves = osbourne waves
(hypothermia - body temp <35 degrees)
In IE
- what side of the heart are IVDUs more at risk of gettign valve disease
Right side
IVDU: predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditi
what triad is found in cardiac tamponade
Becks triad
- hypotension
- muffled heart sounds
- raised JVP
difference between SOB & orthopnoea
orthopnoea = SOB on lying down
which valve condition gives the following findings on auscultation:
a diastolic decrescendo murmur
best heard at the left sternal border
and a wide pulse pressure.
aortic regurgitation
which valve condition gives the following findings on auscultation:
low-pitched, diastolic rumble at the apex with an opening snap.
Mitral stenosis
which valve condition gives the following findings on auscultation:
harsh systolic murmur
Aortic stenosis
which valve condition gives the following findings on auscultation:
holosystolic murmur at the apex, radiating to the axilla.
mitral regurgitation
which valve condition gives the following findings on auscultation:
holosystolic murmur at the left lower sternal border, which increases with inspiration.
tricuspid regurgitation
Define SVT (bpm & QRS width on ECG
SVT -any narrow complex tachycardia (100bpm & QRS width <q20ms)
give examples of SVTs
AF
AV re-entry tachcardia (AVRT)
AV Nodal Re-entry Tachycardia (AVNRT)
Management of SVt in pts with adverse features is….
synchronised DC cardiovesion
HISS - HF, Ischaemia, Shocj and syncope afre the 4 adverse features of SVT
1st and 2nd line of management in SVT with a regular rhythym
1 regular vagal manoeuvres (e.g/ carotoid sinus massage)
2 IV Adenosine 6mg
what conditions cause
- arterial ulcers
- venous ulcers
- mixed ulcers
arterial - peripheral artery disease
venous - venous insufficiency, causes pooling of blood & waste products
mixed - arterial and venous disease
which of arterial or venous ulcers occur at the on the toes/dorsum of foot
arterial ( these affect more peripheral places first)
venous - gaiter area ( top of foot to bottom of calf uscle)
which type of ulcer is small deep with well-defined borders
arterial - “punched out” look
venous - larger, irregular border, more superficial, more likely to bleed
a pt presents complaining of left leg pain. upon inspection, they have an ulcer, what is this ulcer most liekly to appear as
punched out appearance ( deep, small, regular border) - arterial ulcer
these are painful
worse when lying/elevating leg)
what investigation is appropriate in a patient with a leg ulcer
ABPI - ankle-brachial pressure index (ratio of systolic blood pressure (SBP) in the ankle (around the lower calf) compared with the systolic blood pressure in the arm.)
this tests for arterial disease but is used in both
Normal: 0.9 - 1.2. Values
Arterial disease: <0.9 (or >1.3 - e.g. in diabetics due to calcification of ulcers )
critical ischaemia : <0.3
1st line Mx in arterial ulcer
the management of peripheral artery disease - referral to vascular - consider revascularisation
( do not use compression/debridement)
Mx in venous ulcers
Most important: Compression therapy
Pentoxifylline ( orally - improves healing).
Abx in infection, analgesia (NOT NSAID) in pain)
what is intermittent claudication
crampy, achey paiun in muscle due to fatigue following ischaemia which occurs during exertion.
it is relieved by rest
what is critical limb ischaemia
end-stage peripheral arterial disease, with pain at rest, non-healing ulcers, gangrene
what are the 6 s&s of critical limb ischaemia
6 Ps
* Pain
* Pallor
* Pulseless
* Paralysis
* Paraesthesia (abnormal sensation or “pins and needles”)
* Perishing cold
Mx in peripheral arterial disease ( medical and surgical)
Medical treatments:
* Atorvastatin 80mg
* Clopidogrel 75mg once daily (aspirin if clopidogrel is unsuitable)
* Naftidrofuryl oxalate (5-HT2 receptor antagonist that acts as a peripheral vasodilator)
Surgical options:
* Endovascular angioplasty and stenting
* Endarterectomy – cutting the vessel open and removing the atheromatous plaque
* Bypass surgery – using a graft to bypass the blockage
what are the 4 rhythms that may occur in a pulseless patients, which ones are shockable and which are non-shockable
Shockable :
Ventricular tachycardia
Ventricular fibrillation
Non-shockable :
* Pulseless electrical activity (everything but VF/VT, incl. sinus rhythm without a pulse)
* Asystole
what is the size of a normal QRS complex ( small squares/ seconds
small squares - 3
seconds - 0.12
give 4 main differentials of narrow complex tachycardia
narrow complex tachycardia
sinus tachycardia
Supraventricular tachycardia
atrial fibrillation
atrial flutter
broad complex tachycardia is defined as
fast HR w/ broad QRS (>0.12s/ 3small squares)
give 4 types of broad complex tachycardia
Ventricular tachycardia - tx I
what causes atrial flutter
a re-entrant rhythm in either atrium: extra electrical pathway
atrial rate is approx 300 bpm - conduction typically ina 2:1 ratio - but can be more ( so atria 300bpm, ventricles, 150bpm)
how does Atrial flutter appear on an ECG (x3)
Sawtooth appearance
repeated Pwave approx. 300/min
Narrow complex tachycardia (QRS<3 small boxes/ 0.12s)
Tx for atrial flutter
Rate/rhythm control ( as with AF)
plus anticoagulation (based on CHA2DS2-VASc score)
Permaent solution - radiofrequency ablation of re-entrat rhythm
QT interval
- what section does it measure
- what is QTc
- what is a prolonged QT interval in men/women
QT - from start of Q wave to end of T wave
QTc = corrected QT interval if the HR were 60 bpm
prolonged
>440ms in men
>460 ms in women
give 3 electrolyte imbalances which cause prolonged QT
hypokalaemia, hypomagnesaemia hypocalcaemia
Ventricular ectopics are premature ventricular beats which occur in all ages/health status. How does it appear on an ECG?
as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.
Whats is Bigeminy
when every other beat is a ventricular ectopic
ECG: normal beat (P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, repeated
Management options in ventricular ectopics
- reassurance (no tx) in otherwise health people
2.Specialist advice: underlying heart disease/ concerning Sx ( chest pain/ syncope), FHx heart disease/ sudden death
B-Blockers ( Sx Mx)
how many types of heart block are there
4
1st degree - delayed conduction to AVN, so PR interval prolonged ( >200 ms)
otherwise, everthing present, regular rhythm
2nd degree type 1 ( Wenckebach)
Progressive prolongation of PR interval, until QRS drops, then repeats
2nd degree type 2 (Mobitz 2)
Pwave present, fixed PR interval, regular, but regular non-conducted Pwave, so dropped QRS wave . The intermittent failure of AVN conduction is at a set ratio ( e.g. 3:1)
3rd degree (complete heart block) - completely unrelated P waves and QRS complexes - Pwaves regular
give 3 potential causes of bradycardia
meds ( B-blockers)
heart block
sick sinus syndrome (any condition causing SAN dysfunction)
in which type of heart block is there a risk of asystole
3rd degree heart block
AND
2nd degree type 2
stepwise management of bradycardic patients who are unstable/ at risk of asytole
1st line - 500mcg IV atropine
2 Inotropes (e.g. adrenaline)
3. temporary cardiac pacing
(transcutaneous - e.g. pads/ transvenous e.g. catheter for direct stimulation of the heart)
4. permanent pacemenker
500mcg IV atropine is the 1st line in unstable bradycardic patients, what are its side effects? (x4)
Atropine - antimuscarinic
so inhibits parasympathetic nervous system
pupil dilation, dry mouth, urinary retention, contstipation
give 4 risks factors a for asystole in a bradycardic patient
- complete heart block with broad complex QRS
- recent asystole
- Mobitz type II AV block
- ventricular pause > 3 seconds
what ECG leads can be used to Dx bundle branch block
V1 and V6 (WiLLiaM MaRRoW)
the QRS complex is also wde in both (>120)
an ejection systolic murmur which radiates to the carotids is associated with which heart murmur
Aortic stenosis
closure of which valves cause S1?
atrioventricular (mitral, tricuspid)
give 3 causes of aortic stenosis
calcification ( most common in developed countries - >65yo)
congenital abnormality
rheumatic disease
others :
- bicuspid aortic valve (most common cause in younger patients < 65 years)
- William’s syndrome (supravalvular aortic stenosis)
- subvalvular: HOCM
give 3 examination findings which indicate aortic stenosis
Ejection systolic murmur ( loudest at aortic region)
radiates to the carotids
manouevre: loudest on expiration when pt siting forwards
narrow pulse pressure, slow rising pulse, LVH/ failure are indicative of the severe form of which murmur?
aortic stenosis
Mx in aortic stenosis
if asymptomatic
if symptomatic
if symptomatic, with chest pain & pulmonary oedma - whilst awaiting referral
1 - asymptomatic, watch and wait
2 Sx - valve replacement
3- furosemide
what cardiac medication should NOT be given in AS
nitrites are contraindicated - risk of profound hypotension
ACEi may impair renal function and cause hyperkalaemia. What is the cut off for switching the ACEi for another anti-hypertensive in hyperkalaemia?
6.0mmol/l
( normal 3.5 - 5.0mmol/l)
give 4 S/E ACEi
cough ( raised bradykining)
angiooedema
hyperkalaemia
first-dose hypotension ( more common in diuretics pts)
ACEi cautions and contraindications in …
- pregnancy and breastfeeding
- renovascular disease -
- aortic stenosis
- starting ACEi in potassium >= 5.0 mmol/L
- pregnancy and breastfeeding - avoid
- renovascular disease - may result in renal impairment
- aortic stenosis - may result in hypotension ( same reason why GTN should be avoided in AS)
- hereditary of idiopathic angioedema
- specialist advice should be sought before starting ACE inhibitors in patients with a K+ >= 5.0 mmol/L
what is a potential adverse effect of prescribing ACEi to a pt on high-dose diuuretic ( e.g. furosemide 80mg/day)
hypotension
90% of HTN cases are essential HTN, what are the causes of secondary htn?
ROPED
- R – Renal disease*** most common cause of secondary HTN
- O – Obesity
- P – Pregnancy-induced hypertension or pre-eclampsia
- E – Endocrine ( e.g. hyperaldosteronism)
- D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
what are the cut offs ( clinic reading and ambulatory readings) for
stage 1
stage 2
stage 3
HTN
stage 1
>140/90, 135/85
stage 2
160/100, 150/95
stage 3
180/120
what are the 5 groups of medication used in HTN Mx
ABCD, ARB
* A – ACE inhibitor (e.g., ramipril)
* B – Beta blocker (e.g., bisoprolol)
* C – Calcium channel blocker (e.g., amlodipine)
* D – Thiazide-like diuretic (e.g., indapamide)
* ARB – Angiotensin II receptor blocker (e.g., candesartan)
A –> A+C/A+D –> A+C+D –> IF K+ <4.5 - spironolactone, if >4.5 -a/b blocker (doxazosin/ atenolol) –> specialist
what potassium diuretic can be used in the 4th stage of HTN Mx
spironolactone
U&E monitoring is essential in HTN mx what 3 groups of drugs in HTN can cause electrolyte disturbances
Spironolacton - potassium sparing diuretic –> hyperkalaemia
ACEi –> hyperkalaemia
Thiazide-like diuretics –> hypokalaemia
what is Accelerated/ malignant hypertension,
BP >180/120, with retinal haemorrhages or papilloedema.
so regular fundoscopy is important
Mx in accelerated HTN
same day referral
what is the typical cause of an ACS
thrombus ( from atherosclerotic plaque, made up of mainly of patelets ) blocking coronary artery
what are the 3 types of ACS
STEMI, Unstable angina, NSTEMI
(ACS SUN )
name the 4 main coronary arteries
right coronary artery (R side & under heart)
left coronary artery (LCA - splits into circumflex & LAD)
circumflex artery ( splits off LCA, round the top ant and posterior left heart)
Left anterior descending (middle of heart)
what areas of the heart are supplied by the right coronary artery?
Right atrium
Right ventricle
inferior left ventricle
posterior septal area
what areas of the heart are supplied by the circumflex artery
left atrium
posteriori left ventricle
what areas of the heart are supplied by the left anterior descending artery
left ventricle
anterior septum
how long should sx continue, at rest, to be classed as ACS
at least 15 mins
how does a STEMI present on an ECG (x2)
ST-segment elevation
new LBBB
how does an NSTEMI present on an ECG
ST segment depression
T wave inversion
diagnosis of NSTEMI is made when troponin high and either normal ECG/ pathological ECG
in ACS, pathologiucal Q waves typically appear >6hrs post symptom onset. What does their present indicate?
deep infarction - transmural ( full muscle) involvement
what ECG leads correspond to the Left anterior descending artery
LAD = V1-4 (anterior region)
what ECG leads correspond to the circumflex artery
V5-6, I, aVL
what ECG leads correspond to the right coronary artery
II, III, aVF
troponin levels are required to diagnose what type of ACS?
NSTEMI
STEMIs can be dx using clinical findings and ECG findings
a high/ raisinng troponin ( on 3-hr repeat test) indicates what ACS?
NSTEMI
what are alternative causes of raised troponin
- Pulmonary embolism
- Chronic kidney disease
- Sepsis
- Myocarditis
- Aortic dissection
*
3 features used to diagnose unstable angina
ACS Sx but
troponin normal
ECG - normal / ST depression / T wave inversion
in chest pain where troponin & ECG are normal - think unstable angina or other cause, (e.g. MSK chest pain)
what are the 5 steps which form the initial management in ACS
CPAIN
Call ambulance
Perform ECG
Aspirin 300mg
IV morphine
Nitrate
refer to hospital, same-day assessmrent
STEMI mx
present
<12 hrs
refer for PCI (within 2 hrs of presenting)
Thrombolysis (if PCI not available within 2 hrs)
Mx NSTEMI
BATMAN
Base decision about angiography & PCI on GRACE score ( or in haemodynamically unstable pt)
Aspirin 300mg stat
Ticagrelor 180mg stat
Morphine
Antithrombin therapy w/ fondaparinux ( unlss bleeding risk )
Nitrate
O2 if sats <95%
(ACS – CPAIN, NSTEMI – BATMAN, STEMI - PIC/ thrombolysis, 6As for secondary prevention )
secondary prevention in ACS
6As
Aspirin 75mg OD
Another antiplatelet (ticagrelor/ clopidogrel) 12 months
Atorvastatin 80mg OD
ACEi (ramipril, high dose/0
Atenolol ( or other B-blocker e.g. bisoprolol)
Aldosterone antagonist ( in clinical heart failure e.g. eplerenone 50mg OD)
Give 5 complications of an MI
“DREAD”
* D – Death
* R – Rupture of the heart septum or papillary muscles
* E – “oEdema” (heart failure)
* A – Arrhythmia and Aneurysm
* D – Dressler’s Syndrome (2-3 weeks post MI, local immune response –> pericardium inflamation –> pericarditis): pleuritic chest pain, low-grade fever, pericardial rub ( footsteps on snow)
what are 3 options for m in dresslers syndrome
NSAIDS
Steroids 9 e.g. pred - if mrore severe)
Pericardocentesis ( if needed in significant pericardial effusion)
Sudden onset chest pain, maximal at onset with neurological symptoms indicates what condition?
aortic dissection
how does the pain in aortic dissection differ to that in ACS
Both can be central pain
but ACS - crushing/tight pain
aortic dissection - sharp pain
in what layers of the aorta does aortic dissection occur
intima ( inner layer, the media & adventitia are maintained but blood pools between the intima and media )
what are the 2 most common locations for aortic dissection
ascending aorta & aortic arch - most commons
what are the risk factors for aortic dissection
same as CVD ( age, male sex, smoking, etc)
big risk factor: HTN
a dramatic increase in BP ( heavy /cocaine use) can trigger it
Conditions/procedures e.g.
* Bicuspid aortic valve
* Coarctation of the aorta
* Aortic valve replacement
* Coronary artery bypass graft (CABG)
Connective tissue disease:
* Ehlers-Danlos Syndrome
* Marfan’s Syndrome
( typical exams: man approx 60 yo w/ PMHx HTN who presents with sudden onset tearing chest pain = aortic dissection.
remember Marfan’s and Ehlers-Danlos syndrome are for MCQ exam).
Sx in aortic dissection
sudden onset, severe, “ripping” or “tearing” chest pain.
pain: anterior chest (ascending aorta) or back ( descending aorta) - may migrate over time
Other features:
* Hypertension
* Diff. in BP between the arms (>20mmHg)
* Radial pulse deficit (in one arm decreased or absent and does not match the apex beat)
* Diastolic murmur
* Focal neurological deficit (e.g., limb weakness or paraesthesia)
* Chest and abdominal pain
* Collapse (syncope)
* Hypotension as the dissection progresses
diagnostic investigations in aortic diseaction
CTA - initial confirmatory, can be done quickly
MRI angiogram - better detail
Mx in aortic dissection
surgical emergence
type A - midline sternotomy , remove and relace damaged area of aorta
type B - TEVAR ( thoracic endovascular aortic repair)
Stanford classification
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
give 6 potential complcations of aortic diseaction
MI, Stroke, paraplegia, cardiac tamponade, aortic valve regurgitation
death
Stable pt with an NSTEMI can be given aspirin and fondaparinux . what alternative medication should be administered if they are getting immediate angiography
aspirin and unfractionated heparin .
give 3 types of syncope
reflex syncope*
orthostatic syncope **
cardiac syncope**
- most common in all age groups
** progressively more common with age
what are the vasovagal, situational and vascular triggers of reflex syncope
Reflex syncope
= neurally mediated
* vasovagal: emotion, pain, stress
* situational: cough, micturition, gastrointestinal
* vascular: carotid sinus syncope
what are the triggers of orthostatic syncope
- primary autonomic failure: Parkinson’s disease, Lewy body dementia
- secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
- drug-induced: diuretics, alcohol, vasodilators
- volume depletion: haemorrhage, diarrhoea
causes of cardiac syncope
*arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (SVT, VT)
* structural: valvular, MI, hypertrophic obstructive cardiomyopathy
* others: pulmonary embolism
what Ix/ Examinations should be conducted in syncope?
*CV exam
* postural BP : fall in SBP> 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg
* ECG
- other tests depend on clinical features
In pts with typical features, no postural drop and a normal ECG –> no further Ix required
an eldery patient presents with light headedness and lying/standing BP shows postural hypotension. Which causes of this would also give a compensatory tachycardia on standing up
‘4Ds’ of postural hypotension with compensatory tachycardia.
Deconditioning.
Dysfunctional heart: aortic stenosis.
Dehydration: disease (acute illness, adrenal insufficiency), dialysis, drugs (diuretics, narcotics).
Drugs: anti-anginals, anti-parkinsonian medications (levodopa), antidepressants, antipsychotics, anti–benign prostatic hyperplasia drugs (tamsulosin).
what score is used to calculate the 6-monthly risk of death followign an NSTEMI
GRACE score
<3% - low risk
>3% - med/ high risk ( give early angiography / PCI in 72hours)
what score is used to decise giving an angiography/ PCI in NSTEMI
Grace score
global registry of acute coronary events
Hx - age, cardiac arrest at Presentation
Ex : HR & BP, signs of HF
Bedside tests: ECG changes
Lab tests: troponin & creatinine conc
Secondary prevention after coronary event
6As
Aspirin 75mg OD - permanent
Another Antiplatelet - 12 months
Atorvastatin 80mg OD
ACEi
Atenolol ( or other b-blocker)
Aldosterone antagonis( if clinical HF e.g/ eplerenon)
give 5 complications of an MI
DREAD
Death
Rupture of heart septum/ papillary muscles
E- oedema
Arrhythmia/ aneurosym
Dresslers syndorme ( post-MI syndrome)
how long after an MI might dressler’s syndrome occur
3 weeks
MI –> immunie response –> pericarditis ( pleuritic chest pain, low-grade fever, pericardial rub )
In dressler’s syndrome, what would the following investigations show
ECG
Echo
inflammatory markers
dresslers syndrome = post-MI pericarditis
ECG - global ST elevation, T wave inversion
Echo - pericardial effusion
inflammatory markers - raised
Mx in dresslers syndrome
NSAIDS ( aspirin/ ibuprofen)
If more severe - steroids
If significant effusion - pericardiocentesis
what are the types of MI
There are 4 types
Type 1 - traditional MI ( acute coronary event)
2 - Ischaemic MI ( increased demand and reduced supply of O2 - e.g. anaemia, hypotension, tachycardia)
3 - sudden cardiac death/ arrest ( ischaemic event)
4 - Iatrogenic ( PCI, stenting, CABG)
- Type 1: A – ACS-type MI
- Type 2: C – Can’t cope MI
- Type 3: D – Dead by MI
- Type 4: C – Caused by us MI
