Cardiology Flashcards
What are the features of MS?
Mitral facies (rosy cheeks not crossing nose, blue cyanosed face)
Mid-diastolic, pre-systolic murmur, with opening snap Loud S1 Loud P2 Low-pitched Evident after exercise
What are the features of AR?
Decrescendo early diastolic blowing murmur
Best heard over aortic areas sitting up in held expiration
AR causing premature closure or mitral valve –> Austin flint murmur (mid diastolic)
Widened pulse pressure
Waterhammer pulse, dancing carotids (corrigans pulse) (characterised by rapid systolic rise and rapid diastolic collapse)
Soft A2
Quincke’s sign (pulsation of capillary bed in nail)
De Musset’s sign (rythmic nodding of head in syncrhony with heartbeat)
Traube’s sign is pistol shot sounds heard over femoral artery
Duroziez’s sign (systolic and dialostic bruit heard over femoral artery)
What are the common causes of AR?
Marfan’s
Ankylosing spondylitis
Syphillis
Aortic dissection
What are the common causes of AS?
Age-related progressive calcifications (>50%) (65-70y/o)
Calcification of congenital bicuspid valve (30-40%) (40-50y/o)
Acute rheumatic fever (<10%)
What are the features of AS
Ejection systolic, crescendo-decrescendo
Radiates to carotids
Syncope, Angina, Dyspnoea (SAD)
What are the common causes of MR?
Marfan’s, RA, cardiomyopathy, rheumatic fever, MVP, IHD
What are the common causes of MS?
Rheumatic fever
Uncommonly: calcifications and congenital heart disease
Features of MR
Pan systolic murmur, loudest at apex, radiates to axillae
LVS3
Differential diagnoses for pansystolic murmur
MR, TR, VSD, HOCM (midsytolic murmur), aorto-pulmonary shunt
Differential diagnoses for midsystolic murmurs
AS (loudest in midsystolic), PS, HOCM
Differential diagnoses for late systolic murmurs
MVP, papillary muscle dysfunction, HOCM
What dynamic manouvres do you know and what murmurs do they accentuate?
Inspiration - right heart murmurs (increased venous return, and preload)
Expiration - left heart murmurs
Valsava - decreased preload during strained phase, everything softer (except HOCM and MVP)
Stand-to-squat - increased venous return and systemic arterial resistance, increased stroke volume and arterial pressure, most murmurs louder (LV size increased, reducing obstruction to outflow)
Isometric exercise - e.g. hand grip, increased afterload, AS may become softer (often unchanged) most murmurs become louder
How do you differentiate JVP from carotid pulse?
JVP, occlude it and it will fill from the top
JVP has double-flicker with each cardiac cycle
JVP bounded by two heads of sternocleidomastoid
JVP decreases on inspiration
JVP visible but not palpable
JVP more prominent inward movement
How do you measure the JVP?
Position at 45 degree angle
Turn head slightly to the left
Measure vertical height of column of blood in jugular vein from the sternal angle in line with base of the neck by:
Identifying the highest point of pulsation
Extending a long rectangular card/ruler horizontally from this point and a centimeter ruler vertically from the sternal angle (make an exact right angle)
Measure the vertical distance (in centimeters) above the sternal angle where the horizontal card crosses the ruler
Add to this distance 4 cm (the distance from the sternal angle to the centre of the right atrium)
Normal from sternal angle <3cm
Normal from RA <8cm
Signs of LHF
Fluid overload (SOB, orthopnoea, PND) (lung crackles, LVS3, functional MR), poor cardiac output (cyanosis, hypotension, tachycardia), signs of RHF
Signs of RHF
Fluid overload (sacral, ankle, abdominal edema), anorexia, nausea Raised JVP, RVS3, functional TR, pulstile liver, hepatojugular reflux (when pressure is applied to liver, JVP remains elevated for >10-20s suggesting RHF) Pulmonary HTN (palpable P2, parasternal impulse)
Causes of LHF
IHD, volume overload (AR, MR, PDA), pressure overload (AS, systolic HTN)
Causes of RHF
LHF, IHD, volume overload (TR, ASD), pressure overload (PS, pulmonary HTN)
SYSTOLIC HTN –> LHF –> PULMONARY HTN –> RHF
SYSTOLIC HTN –> LHF –> PULMONARY HTN –> RHF
What is cor pulmonale?
RVH caused by pulmonary pathology leading to scarring and sustained pulmonary hypertension. Eventually lead to RHF.
How would you take blood pressure?
Position patient, arm at heart level
Do not use arms with pathology e.g. post-mastectomy lymphoedema
Using appropriately sized, fully deflated cuff,
1) Wrap cuff over patients upper arm with the cuff marker overlying the brachial artery (palpate to locate)
2) Palpate radial pulse, inflate cuff until radial pulse can no longer be felt to estimate systolic BP
3) Open valve, and deflate BP cuff
4) Place diaphragm of stethoscope over brachial artery
5) Inflate cuff to 20-30mmHg above estimated SBP
6) Deflate cuff at slow rate of 2-3mmHg/s
7) Listen for pulsatile noise, pressure at which first korotkoff sound is heard is the SBP
8) Continue to deflate until pulsatile noise completely disappears, the 5th and last korotkoff sound is DBP
Sounds
1) Thud
2) Blowing/ swishing sound
3) Thud softer than 1
4) Soft blowing
5) Disappearing
Important history in infective endocarditis
- Preenting symptoms e.g. malaise, fever, symptoms of anaemia
- CHF e.g. PND, orthopnoea, SOB
- Embolic phenomena in large vessels: e.g. brain, viscera (focal neurological deficits) or small vessels e.g. kidney (AKI, haematuria, loin pain)
- Risk factors/ recent precipitating event: dental work, endoscopic procedures, IVDU (tricuspid and pulmonary valve regurgitation), history of rheumatic fever,
- Antibiotic use (prophylaxis for procedures/ treatment): how long, which antibiotics, allergies
- History of any valve surgery (when, surgeon performed, type of valve, any complications)
- PMHx especially those associated with immunosuppression e.g. renal transplantation/ steroid use
Duke’s criteria
Pathological Criteria (either is evidence)
- Microorganisms in a vegetation (demonstrated by culture or histologic examination)
- Pathologic lesion (vegetation of intra-cardiac abscess confirmed by histology)
Major Criteria (if both positive, diagnosis definite)
- Blood cultures positive for IE with typical microorganisms consistent from 2 separate blood cultures
- Evidence of endocardial involvement (echocardiogram positive for IE)
Minor Criteria (if all positive, diagnosis definite)
- Predisposing heart condition or injecting drug use
- Fever
- Vascular phenomenon )major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, Janeway’s lesions)
- Immunologic phenomena (Glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
- Microbiological evidence (positive blood culture not meeting major criteria)
Investigations for IE
Bedside: ECG (might see AF), U/A (haematuria, proteinuria)
My diagnostic investigations of choice would be 3-6 sets of blood cultures taken from 3 different peripheral sites (over 24 hours, 3 in 1st hour), and a trans-oesophageal echocardiogram (2D + doppler) looking for any vegetations (must be more than 2mm to be detected) (TOE more sensitive 86-92% vs 17-36% and better at picking up complications such as abscesses), evidence of heart failure
Other investigations include FBC (anaemia, neutrophilia), ESR/CRP, EUCs, LFT, Coagulation studies (INR), G+H, CXR (look for any LV/RV hypertrophy, increased pulmonary artery markings, Kerley B lines, valve calcification in lateral film to rule out any ddx, complications)
Signs of IE
New murmur/ prosthetic valve murmur
Peripheral stigmata of IE
o Hands: clubbing, splinter haemorrhages, Osler’s nodes (rare immunologic embolic phenomenon, painful and on finger pulp), Janeway lesions (rare non-tender erythematous maculopapular vascular lesions containing bacteria on palms or pulps)
o Eyes: Roth’s spots in fundus, conjunctival petechiae
o Abdomen: splenomegaly (late sign)
o Neurological signs of embolic disease: cranial nerve, UL + LL
Management of IE
Management will require MDT approach with early involvement of cardiac surgeon, ID, cardiology
Empiric antibiotics after blood cultures in haemodynamically unstable patients
Prosthetic valves: Flucloxacillin + vanc + gent
Native valve Fluclox + benpen + gent
Tailored therapy for 6-8 weeks (prosthetic), 4-6 (native) after sensitivity testing
Consider surgery if haemodymic instability, cardiac failure due to valvular dysfunctiom, persistently positive BC despite treatment, paravalvular abscesses/infection causing conduction disturbances
Valvular AF
“Valvular AF” according to the European Society of Cardiology Guidelines only refers to patients with moderate to severe mitral stenosis or prosthetic heart valves (and valve repair in North American guidelines), and should be treated with Vitamin K Antagonists. Valvular
What is the HASBLED score?
The HASBLED score is used to assess risk of bleeding in patients on anticoagulation to assess risk benefit in AF care. Could be used as tool to potentially guide starting anticoagulation. Use in conjunction with CHADSVASC to determine in benefit of anticoagulation outweighs risk.
Hypertension (uncontrolled) Abnormal liver function Abnormal renal function Stroke Bleeding risk (personal medical history, previous bleeds) Labile INRs Elderly (age>65) Drugs (anticoagulants, NSAIDs, stuff that increase bleeding risk, excessive alcohol)
> 3 high risk of bleeding, use with caution with regular review
What is the CHADSVASC score and how is it used?
CHA2DS2VASC is used to estimate risk of stroke in patients with non-valvular AF
CCF Hypertension >140/90 or treated w meds Age >75 (2 points) Diabetes mellitus Stroke or TIA (2 points) Vascular disease (PAD, MI, aortic plaques) Age >65 (1 point) Sc (Sex Category) (Female +1)
0 in males or 1 in females no anticoagulant
≥2 consider anticoagulation
Duration of AF
First diagnosed
Paroxysmal (self terminating, <48 hours, usually but up to 7 days if cardioverted)
Persistent >7 days and cardioverted
Long standing persistent >1 year and decided to use rhythm control
Permanent AF when rhythm is NOT used bc patient accepts being in Afib . If rythmn control later used, reclassified to persistent.
Management of AF
The treatment of atrial fibrillation consists of:
- reduction of thromboembolism and stroke risk (anticoagulant therapy)
- symptom relief (rate and/or rhythm control)
- treatment of associated comorbidities, such as heart failure
- treat underlying aetiologies
If haemodynamicaly unstable –> accept risk of stroke if timing unknown, immediate direct current cardioversion (up to 3x), and then anticoagulate for 4 weeks
Stable (rate control preferred, control cardioverting after rate control achieved)
<48 hours: low risk of acute thromboembolism, initial rate or rhythm strategy might be considered and then if rhythm –> anticoagulate at time of cardioversion, continue anticoagulation for 4 weeks
> 48 hours: do not cardiovert unless ruled out left atrial thrombus via TOE or patient has had therapeutic anticoagulation for past 3 weeks, continue anticoagulation for 4 weeks. When thrombus ruled out, start IV UFH and then cardiovert within 24 hours.
Pharmacological Cardioversion: flecainide 1.5mg/kg up to 150mg (10 min)or amiodarone 300mg by IV (1-2 hours) followed by 900mg over 24 hours
Rate vs Rhythm control in AF
Meta-analysis showed no significant difference between rate and rhythm control for all-cause mortality, cardiovascular mortality or ischaemic stroke in patients with atrial fibrillation
Rate control –> asymptomatic, normal left ventricular function
Rhythm control –> highly symptomatic, or have left ventricular dysfunction that might be secondary to atrial fibrillation
electrical over pharmacological cardioversion
Causes of AF
Heart failure Elevated blood pressure (see blood pressure reduction) Valvular heart disease Diabetes mellitus Excess body weight Obstructive sleep apnoea Hazardous alcohol use Hyperthyroidism
Drug choice for rate control in AF
usually beta blocker –> metoprolol
if not, CCB (non dihydropyridine)
if LV dysfx: consider digoxin/ amiodarone
Management of ACS
- Stabilise. + MONA (morphine, O2, nitrates, aspirin chewable)
- STEMI (reperfusion by PCI within 90 minutes or fibrinolysis within 30 minutes if PCI not possible)/N-STEMI (plaque stabilisation and prevention of occlusion and then consider revascularisation based on risk stratification, no fibrinolysis)
If PCI –> give anticoagulaiton and antiplatelet before, and if fibronylisis load antiplatelets and then anticoagulate after - Long term management with: SAAB-C (statin, aspirin, anticoagulant, beta-blocker, clopidogrel)
Criteria for STEMI
Refer to PACSA or LHD guidelines:
Ongoing chest pain
AND
ST elevation of 1mm or more in 2 or more adjacent leads (except v2 and v3 which require ≥2.5mm in men < 40 or ≥2mm in men >40 and ≥1.5 or more in any woman)
OR
LBBB + haemadynamically unstable
OR
LBBB , HD stable with positive modified sgarbossa criteria.
OR
Posterior infarct (ST depression in V1-V3)
OR dewinter T waves
Management of ACS
- Stabilise. + MONA (morphine, O2, nitrates, aspirin chewable), dobutamine in cardiogenic shock. do NOT administer nitrates in right ventricular infarct (present with inferior ecg changes, hypotension, elevated JVP, hepatomegaly, clear lungs) as will cause cardiovascular collapse
- STEMI (reperfusion by PCI within 90 minutes or fibrinolysis within 30 minutes if PCI not possible)/N-STEMI (plaque stabilisation and prevention of occlusion and then consider revascularisation based on risk stratification, no fibrinolysis)
If PCI –> give anticoagulaiton and antiplatelet before, and if fibronylisis load antiplatelets and then anticoagulate after - Long term management with: SAAB-C (statin, aspirin, ACE-I, beta-blocker, clopidogrel)
ECG changes in STEMI
Perform:
0 and 2 hours
When repeating trops
Every 30 minutes if ongoing symptoms
Minutes - Hyperacute/ peaked T waves, large T waves, loss of ST segment
Minutes to hours: ST segment changes (ST elevation or depression), inverted T waves (onset of myocardial necrosis)
Days: pathological Q waves (represents total loss of electrical activity due to scar tissue in an area that had transmural infarction)
Investigations for ACS
Serial ECGs,
Serial troponins
Preferably use high sensitivity (I and T) troponins, looking for rise and/or fall
Other: FBC (infection, anaemia), EUC, LFT, Coags, Group + Hold, VBG, BSL
CKMB for recurrent infarction down the track (quicker return to baseline than troponins)
CXR for APO, and to rule out respiratory causes of chest pain
What is the third heart sound?
Occurs 120-160ms after 2nd heart sound, low-pitched, best heard with bell of stethostcope
Not dependent on atrial contraction, not influenced by presence of AF
Associated with RAPID ventricular filling
Normal before 30 years, not normal above 40 years (always implies ventricular disease)
Commonly heard in LVF, as after MI, severe MR, constrictive pericarditis (where 3rd heart sound represents cessation of ventricular filling)
What is syncope?
Symptom that presents with an abrupt, transient, or complete loss of consciousness, associated with inability to maintain postural tone, with rapid and spontaneous recovery.
Presumed mechanism of cerebral hypoperfusion.
Should not have other clinical features e.g. seizure, antecedant head trauma, or apparent loss of consciousness
What is pre-syncope?
Symptoms before syncope such as extreme light-headedness; visual sensations (tunnel vision/ graying out); variable degrees of altered consciousness without complete loss of consciousness. Could or could not progress to syncope.
What are the common types/ causes of syncope?
- Orthostatic - syndrome consisting of constellation of symptoms that include frequent, recurrent, or persistent light-headedness, palpitations, tremulousness, generalised weakness, blurred vision, exercise intolerance, and fatigue upon standing. Can occur without orthostatic tachycardia, orthostatic hypotension, or syncope.
Classic orthostatic hypotension is a sustained reduction in blood pressure of systolic BP of more than 20mmHg or diastolic BP of more than 10mmHg.
Neurogenic OH - due to dysfunction of the autonomic system not solely due to environment e.g. dehydration or drugs. Neurogenic OH is due to lesions involving the central or peripheral nerves.
- Cardiogenic: syncope caused by bradycardia, tachycardia, or hypotension due to low cardiac index, blood flow obstruction, vasodilatation, or acute vascular dissection.
Cardiac factors: HR, contractility
Coupling factors: Preload, afterload
Things that affect CO.
- Reflex (neurally mediated)_ syncope: syncope due to a reflex that causes vasodilation, bradycardia, or both.
- -> Vasovagal - may occur with any posture with exposure t emotional stress, pain, or medical settings, typically characterised by diaphoresis, wartmh, nausea, and pallor, is associated with vasodepressor hypotension, often followed by fatigue.
- -> Carotid sinus syncope (more common in older patients)
- -> Situational syncope – syncope associated with specific actions such as coughing, laughing… closesly associated with specific physical features.
What other differentials for syncope (actual LOC)?
Seizures Sleep disturbances (narcolepsy, cataplexy) Falls leading to TBI Intoxication and metabolic disturbances Psychiatric (pseudoseizures)
Differentials for dizziness
Vertigo, pre-syncope, disequilibrium (imbalance when walking e.g. diabetic neuropathy, MSK, cerebellar), nonspecific (psychiatirc e.g. major depression, anxiety, hyperventilation)
What is vertigo?
Arises from acute asymmetry of vestibular system - there are both peripheral and central causes
Peripheral - BPPV, meniere’s, labyrynitis, ototoxicity
Central - migraine headache, MS, cerebellar haemorrhage/infarct, vertebrobasilar insufficiency
Distinguishing it from other types of dizziness:
Time course: Will not be longer than a few weeks, because CNS can adapt to defect. Constant dizziness lasting months –> psychogenic not vestibular. Vestibular - acute prolonged severe vertigo (vestibular neuronitis and stroke) vs recurrent spontaneous attacks (meniere’s and vestibular migraine) vs recurrent positional (BPPV) and chronic persistent (psychogenic, cerebellar ataxia)
Provoking factors: Spontaneous vs precipitated by manouvres that change head position. Positional vertigo vs pre-syncope: both assoc w dizziness on standing, differentiate: w/o lowering bp/cerebral blood flow e.g. lying down, rolling over in bed, bending neck to look back up –> suggest positional vertigo.
Aggravating: ALL VERTIGO MADE WORSE BY MOVING HEAD
Associated: generally accompanied by nystagmus and postural instability.
Ear involvement (e.g. hearing loss, tinnitus) suggestive of peripheral cause although absence does not exclude diagnosis.
Illusion of motion - ‘spinning sensation’ (not reliable)
Medications that predispose to syncope
- Hypovolaemia and electrolyte distyrbance: diuretics
- Hypotension: anti-hypertensives
- Long QT: anti-arrhythmics, anti-infectives (azole antifungals, fluoroquinolones, macrolides), antipsychotic, antidepressant
Management of orthostatic hypotension
If autonomic features present e.g. parkinsonionism, CNS features, peripheral neuropathies, underlying diseases –> refer for further evaluation (neurologist)
If orthostatic hypotension:
- Address reversible factors e.g. volume depletion or medications
- Non-pharm
- Review/remove suspected meds as above
- Modify behaviour: raise head of bed by 10-20deg, arise slowly from supine, isometric handgrip, dorsiflexing feet, liberalise salt and water intake (supplement sodium 1g PO with each meal), fitted compression stockings and abdominal binderds (not well tolerated) - Pharm
- Fludrocortisone (increases reabsoption of sodium, and plasma volume)
- Midodrine (alpha1agonist, improves symptoms of OH in patients with neurogenic OH)
- Droxidopa (metabolised to noradrenaline –> improves symptoms of neurogenic OH due to Parkinsons, pure autonomic failure, and multiple system atrophy), might reduce galls
All pharm meds are limited by supine hypertension
