Cardio Flashcards
Rare causes of MI
Other rare causes (consider in young pt/risk factors)
- Coronary artery embolus (from LA/LV, mitral/aortic valve) - Congenital: (e.g. Coronaries from pulmonary artery) - Vasculitis: kawasaki's in children - Dissecting aneurysm (and coronary artery occlusion)
Cause of MI
Atheromatous plaque rupture and thrombosis in coronary vessels
Where is the damage in LAD MI
Anterior LV and septum.
Where is the damage in right coronary artery MI
Inferior LV, RV and septum
Where is the damage in L circumflex artery MI
Lateral and posterior walls of LV
Which arteries are the most commonly involved in MI?
- LAD
- RCA
- Lcircumflex
Signs of MI on auscultation
- 4th heart sound (common)
- 3rd heart sound if heart failure
- mitral regurg (if papillary muscle dysfunction/ventricular dilatation)
- VSD due to septal rupture (rare)
Lung bases crackles (heart failure)
ECG changes in hyperkalaemia
Flat P wave, broad QRS, tall tented T waves
ECG changes in hypokalaemia
Long PR, depressed ST, flat T, prominent U waves
Management of suspected MI
- pain relief
- oxygen
- aspirin 300mg (chew)
- nitrates (relieves ischaemic pain and control BP and treat heart failure)
- transfer to specialists (reperfusion)
Reperfusion therapies
- Thrombolysis within 12h (best if within 6h)
- streptokinase
- alteplase/duteplase (rTPA) - Primary per cutaneous coronary intervention
- if rapidly available (door to balloon time target = 90min)
Contraindications for thrombolysis
- recent bleeding (bleeder)
- severe hypertension >200/120
- active peptic ulceration (belching?)
- recent stroke
Evidence for PCI v. Thrombolysis
PRAGUE-2: long transport for PCI is safe (especially if present >3h after onset)
CARESS-in-AMI: high-risk patients STEMI: half dose reteplase/abciximab AND immediate transfer.
Primary PTCA results better in long and short term than thrombolysis.
Definition of MI
(2007, EuSC/ACCF/AHA/WHF) diagnosis of acute MI if… There is a rise in biomarkers of cardiac injury (preferably troponin)
AND ONE of the following
- Symtpoms of MI
- ECG changes indicative of new ischaemia (new ST segment or T wave changes or LBBB)
- Development of pathological Q-waves
- Evidence of new loss of viable myocardium OR new regional wall motion abnormality on imaging
Pathognomonic Signs of Aortic regurgitation
Corrigan’s sign: visibly pulsating carotids
De Musset’s sign: the head nods with each heartbeat
Duroziez’s sign: systolic and diastolic murmur over femoral during gradual compression
Hill’s sign: higher BP in legs compared to arms
Mueller’s Sign: pulsation of uvula
Quincke’s Sign: capillary pulsation
Apex beat characteristics
Heaving (forceful sustained impulse): pressure loaded- concentric hypertrophy. E.g. AS, systemic HTN, HOCM, Coarctation of aorta.
Thrusting (Displaced, diffuse, non-sustained): volume loaded- LV dilatation and hypertrophy e.g. MR, AR, DCM
Tapping= palpable first heart sound. Mitral Stenosis.
To complete my Cardio examination…
Observations: BP, Temp, O2 sats.
Peripheral vascular examination/Peripheral pulses.
Fundoscopy: hypertensive changes (silver/copper wiring, blot retinal haemorrhages, AV nicks, cotton wool spots), Roth’s spots (IE retinal infarcts)
Urine dip: microscopic haematuria (IE), proteinuria (CCF).
Minimum presentation of cardiovascular examination (normal)
On examination of X’s cardiovascular system I found him to be comfortable at rest in bed with no peripheral stigmata of cardiovascular disease, with no evidence of oedema, cyanosis or anaemia. Pulse rate is 72 and regular, blood pressure is 110/70. JVP is not raised. Apex beat is of a normal character in the 5th intercostal space, mid-clavicle line. There were no heaves or thrills. Heart sounds 1 and 2 were normal with no added sounds. In conclusion X presents with a normal cardiovascular examination.
Ways to distinguish JVP from carotid
- Biphasic waveform: undulating and expansile
- Heptojugular reflux or valsalva manoevre (increase RAP) = transient rise in JVP, but in L/R sided heart failure, may remain elevated for duration of manoevre.
- Non-palpable
- Occlude vein close to clavicle: vein will fill and waveform disappears.
- Moves on respiration: JVP decreases on inspiration (if increases = Kussmaul’s sign, constrictive pericarditis)
Causes of S3 on examination
Low frequency early diastolic sound
Physiological (
Causes of S4 on cardiovascular examination
Low frequency late diastolic sound, caused by rapid. Influx of blood into poorly compliant ventricle during atrial contraction (so NOT heard in AF), usually due to impaired left ventricular function.
- Left: AS, MR, systemic HTN, IHD, old age, ACS
- Right: pulmonary HTN, PS
Typical features of Aortic stenosis on examination
Harsh grade 3-4 ejection systolic murmur.
Loudest in expiration over 2nd RICS
Radiation to both carotids
Loudest with pt sitting forward at the end of expiration.
Clinical markers of severity:
- narrow pulse pressure
- low volume pulse
- slow rising plateau pulse
- heaving (pressure overload) apex beat
- systolic thrill in aortic area/upper sternum
- long systolic murmur with late systolic peaking
- soft S2 (A2)
- splitting of A2
- Pulmonary HTN
- Signs of heart failure.
Typical features of Aortic regurgitation on examination
High pitched decrescendo early diastolic murmur
Loudest in expiration over 4th LICS (Also at aortic area in expiration and apex.)
Thrusting (volume) displaced apex.
Collapsing or ‘water hammer’ pulse
Often exists with aortic stenosis.
May Ejection Systolic murmur (flow?)due to quantity of CO.
Markers of severity in aortic regurgitation
Wide pulse pressure Long duration of decrescendo diastolic murmur S3 (Passive ventricular filling) Austin Flint murmur Pulmonary hypertension Signs of LVF
What is an Austin Flint murmur?
Mid-diastolic low pitch rumbling heard at apex.
Austin Flint murmurs occur in aortic regurgitation due to the vibration of the anterior leaflet of the mitral valve as it is buffetted simultaneously by the blood jets from the left atrium and the aorta
Typical heart sounds of Mitral stenosis on examination
Low pitched rumbling mid-late diastolic murmur
Heard best with pt in left lateral position.
Louder after exercise.
Opening snap
Loud S1
Tapping apex (palpable S1)
No radiation
Clinical markers of severity of mitral stenosis
S1 opening snap
Increased length of murmur
Signs of pulmonary HTN ( e.g. Graham Steell murmur- PR and MS)
Low pulse pressure
Typical signs of mitral regurgitation
Pansystolic blowing murmur, softer than AS
Loudest in expiration at the apex of heart.
Radiates towards axilla
Displaced apex beat
Mid-systolic click may be heard in prolapse. (Around grade 4)
?systolic thrill at apex.
Clinical markers of severity of mitral regurgitation
Soft S1 S3 and S4 (only if in sinus rhythm) Displaced apex beat (LVF dysfunction) Systolic thrill over mitral area Signs of pulmonary HTN Mid-diastolic flow murmur Widely split S2
Typical features of Tricuspid regurgitation (on examination)
Rarely seen in isolation, often co-exists with MR (whole valve annulus stretched in CCF) Loudest in tricuspid area About grade 2 Does not radiate Associated with signs of RVF: - raised JVP - peripheral oedema - ascites - Pulsatile liver
Causes of SVT
Sinus tachycardia AV nodal re-entry tachycardia AVNRT AV reciprocating tachycardia complexes AVRT Atrial fibrillation Atrial flutter Atrial tachycardia Multifocal atrial tachycardia Accelerated Junctional tachycardia
Commonest causes of Aortic stenosis
Calcific degeneration
Bicuspid valve disease
Rheumatic valve disease
= 95% of AS
Commonest causes of Aortic regurgitation
Aortic root dilatation Post-endocarditis Rheumatic fever = 95% of AR REALM Rheumatic, endocarditis, Ank Spond/Ao Dissect, Luetic heart disease, Marfan's
Cardiomyopathies
- HCM: genetic (variable penetrance); sarcomeric proteins (B myosin heavy chain; tropomyosin; troponin)
1b. HOCM: hypertrophy, disarray, fibrosis - Arrhythmogenic cardiomyopathy ACM: fibrofatty infiltration of RV (+LV) Desmosomal protein complex genes e.g. Plakoglobin, desmoplakin, desmoglein.
- DCM: impaired contraction of both ventricles, genetic/post-viral/alcoholic/cocaine/post-partum/ idiopathic
- Restrictive cardiomyopathy: endocardial fibrosis/EMF (endomyocardial fibrosis of Equatorial Africa) OR granulation tissue (Loffler eosinophilic endomyocardial disease e.g. Amyloidosis)
SADS: characteristics and causes
Sudden Arrhythmic death syndrome: family history (drowning); micro and macroscopically normal heart; 20-50% have channelopathy e.g.
- Long QT syndrome: Na and K channels (LQT1 swimming/exertion; LQT2 auditory/postpartum; LQT3 sleep/rest)
- Brugada syndrome: Na channel
ECG changes in an inferior MI? Likely artery?
ST elevation on leads II, III, aVF. With/without q waves
RCA: 80% = med-inf walls + inf septum.
LCx/RCx: lat-inf wall + left post-basal.
(Rarely LAD wraparound)
ECG changes in an inferior MI? Likely artery?
ST elevation on leads II, III, aVF. With/without q waves
RCA: 80% = med-inf walls + inf septum.
LCx/RCx: lat-inf wall + left post-basal.
(Rarely LAD wraparound)
Signs of infective endocarditis
Splinter haemorrhages, clubbing, change in murmur, splenomegaly, macroscopic haematuria (and then Roth spots, janeway lesions, osler’s nodes)
Signs of Right ventricular failure
Pt would look ill, AF, extra heart sounds, basal crackles, pleural effusions
ECG signs of LV aneurysm?
Persistent ST elevation
Causes of AF
Ischaemic heart disease, rheumatic heart disease, thyrotoxicosis.
Causes of a 4th heart sounds?
Atrial contraction into a non-compliant/hypertrophied ventricle. Low pitched, always pathological.
Heart failure, myocardial infarction, cardiomyopathy, hypertension (pressure overload)
Causes of 3rd heart sound?
Physiological: <30y, fit young people
Pathological: heart failure, myocardial infarction, cardiomyopathy, hypertension (pressure overload), mitral and aortic regurgitation (volume overload), constrictive pericarditis.
Elements of clubbing?
Increased fluctuant you of the nail bed
Loss of angle
Increased curvature of nail
Expansion of terminal phalanx
Causes of AF?
Ischaemic heart disease
Rheumatic heart disease
Thyrotoxicosis
How to differentiate causes of irregular heart beat
AF: irregular at rest or on exercise
Ventricular ectopics: become regular on exercise
Why can there be a difference betweeen the pulse taken at the wrist and heart rate auscultated in AF?
Pulse deficit. Due to irregular rhythm in AF (and sometimes the fast ventricular response)impulses may be too close to allow sufficient diastolic filling for a cardiac output (i.e. No palpable pulse for that beat)
Management of AF?
Rate control: B-blockers, Ca-antagonists, digoxin to slow ventricular rate by increasing a-v delay.
Anticoagulation: target INR 2.5 (2-3)
Sings of mitral stenosis on imaging?
ECHO: obviously
CXR: prominent left atrium with no LV enlargement ( in pure stenosis)
Causes of LVF pressure overload?
Hypertension Aortic stenosis, Coarctation of aorta, Hypertrophic cardiomyopathy (+LVOT)
How to differentiate aortic stenosis and aortic sclerosis?
Aortic sclerosis: thickened valve leaflet, no haemodynamic significance. Unlikely to radiate to neck, pulse normal, ECG noraml, apex beat normal
Aortic stenosis: radiates to neck, slow rising pulse, hypertrophic heave in pressure overload,
COmplications of MI?
PRAED street? Pump failure Rupture of papillary muscles/septum Aneurysm and arrthymias Embolism Dresler's syndrome ( and acute early pericarditis)
What is needed for a diagnosis of ACS?
2/3 of
- cardiac chest pain
- positive troponin (change with 2 6/8h readings)
- ECG changes
What ECG changes are needed for an ACS diagnosis?
T wave inversion, ST depression, ST elevation, Q waves, new LBBB
Independent risk factors for ACS?
Smoking Hyperlipidaemia, Hypertension Diabetes Family history CKD
Initial investigations to include in ?ACS
FBC:
U+Es: poor renal function may give false positive troponin, also need baseline before starting ACEi, chekc fo hypo/hyperkalaemia.
Glucose: ?diabetic aim for physiological levels
LFTs: baseline before statins, hepatic impairment = relative CI to ticagrelor
Lipids, Serial troponin, ECG.
Initial management of ?STEMI
Morphine + metaclopramide
Oxygen if desaturating
Nitrates sublingual
Aspirin 300mg stat
Definitive management of STEMI?
Primary percutaneous intervention w/i 2h
- ticagrelor 180mg stat
Angioplasty + stenting -> treat the culprit lesion.
If not possible in 2h ?fibrinolytic therapy (alteplase)
Post-PCI management of STEMI?
A: ACEi B: B-blocker C: cholesterol lowering (atorvastatin) D: dual antiplatelet therapy- 90mg ticagrelor bd E: Echo to assess LV.
How much elevation is needed on an ECG for STEMI diagnosis?
at least 1mm in limb leads
At least 2mm in 2 adjacent chest leads
What if LBBB on ECG and ?STEMI?
Is the LBBB new? If so treat as if a STEMI, you cannot assess ST segment if LBBB present.
Signs of a posterior MI?
ST depression, R waves in V1 + V2. = STEMI
What change is seen on a full thickness infarct?
Q-waves
Initial management of all ACS?
Morphine + metaclopramide
Oxygen if desaturating
Nitrate SL
Aspirin 300mg stat
Management of NSTEMI/unstable angina?
Risk stratify!
Signs of mitral stenosis on examination
Malar flush
Atrial fibrillation
JVP not raised until late in disease process
Apex beat not displaced
Tapping apex beat (loud palpable first heart sound)
LUB de derrr (rumbling diastolic murmur at apex)
Signs of LVF?
Pt looks unwell, pale and grey Cold clammy peripheries ?cyanosis Frothy blood stained sputum Orthopnoea (using accessory muscles) May wheeze (cardiac asthma) Sinus tachycardia or AF Systolic hypotension Cardiomegaly: displaced apex beat, signs of valve disease) S3 and S4 Right sided/bilateral pleural effusions Basal crackles
Signs of haemodynamic shock?
Pale anxious SHOCKS Sinus tachycardia Hypotension Oliguria Cold Klammy Slow cap refill
Define chronic limb ischaemia?
Intermittant claudication.
ABPI >0.4
1y mortality 4%
?lifestyle limiting claudication.
Define Critical limb ischaemia
Rest pain needing opiate analgesia for >2/52 OR
Evidence of tissue necrosis, ulceration or gangrene
(ABPI <0.4- maybe falsely raised in calcified vessels)
1y mortality 12%
Define Acute limb ischaemia (thrombosis or embolus)
Sudden decrease in limb perfusion that causes a threat to limb viability. ABPI <0.1 (maybe falsely raised in calcified vessels)
1y mortality 20%
Six Ps of acute limb ischaemia
Pale, Pulseless, painful, paraesthetic, paralysed, perishingly cold.
Management of PAD?
(1. Watchful waiting)
2. Brest medical treatment (antiplatelets, statins, BP and diabetic control)
3. Endovascular treatments (angioplasty ± stent)
4. Surgical reconstruction
5. Amputation
Targets for best medical treatment of PAD (BP, cholesterol, diabetes)
Syst BP≤ 140
Total Cholesterol≤ 4mmol
LDL ≤2mmol
HbA1c ≤59mmol (‘good’ diabetic control)
How to differentiate arterial/venous/neuropathic ulcers?
Arterial: small, painful, punched out margin, lateral malleolus + pressure points (back of heel, plantar aspect of big toe)
reduced ABPI cold foot, absent pulses.
Venous: medial calf or ankle + asn skin changes (venous eczema)
Neuropathic: painless, warm foot, dry skin, loss of ankle jerk/sensation
Well’s criteria for DVT. 5 pt and 5 leg
WELLS PENIS (leg signs, pt factors) Whole leg swollen Edema- pitting, worse on one side Leg tender over deep veins (calf/thigh) Leg big (>3cm difference in calf diameter) Superficial veins dilated Previous DVT Explanation (other explanation likely) Neoplasia Immobilised leg Surgery in past month.
Likely cause of an inferior MI?
75% RCA supplies Posterior desc
25% L circumflex
