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Medicine > Cardio > Flashcards

Cardio Flashcards

1
Q

Rare causes of MI

A

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)
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2
Q

Cause of MI

A

Atheromatous plaque rupture and thrombosis in coronary vessels

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3
Q

Where is the damage in LAD MI

A

Anterior LV and septum.

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4
Q

Where is the damage in right coronary artery MI

A

Inferior LV, RV and septum

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5
Q

Where is the damage in L circumflex artery MI

A

Lateral and posterior walls of LV

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6
Q

Which arteries are the most commonly involved in MI?

A
  • LAD
  • RCA
  • Lcircumflex
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7
Q

Signs of MI on auscultation

A
  • 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)

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8
Q

ECG changes in hyperkalaemia

A

Flat P wave, broad QRS, tall tented T waves

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9
Q

ECG changes in hypokalaemia

A

Long PR, depressed ST, flat T, prominent U waves

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10
Q

Management of suspected MI

A
  • pain relief
  • oxygen
  • aspirin 300mg (chew)
  • nitrates (relieves ischaemic pain and control BP and treat heart failure)
  • transfer to specialists (reperfusion)
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11
Q

Reperfusion therapies

A
  1. Thrombolysis within 12h (best if within 6h)
    - streptokinase
    - alteplase/duteplase (rTPA)
  2. Primary per cutaneous coronary intervention
    - if rapidly available (door to balloon time target = 90min)
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12
Q

Contraindications for thrombolysis

A
  • recent bleeding (bleeder)
  • severe hypertension >200/120
  • active peptic ulceration (belching?)
  • recent stroke
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13
Q

Evidence for PCI v. Thrombolysis

A

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.

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14
Q

Definition of MI

A

(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

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15
Q

Pathognomonic Signs of Aortic regurgitation

A

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

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16
Q

Apex beat characteristics

A

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.

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17
Q

To complete my Cardio examination…

A

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).

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18
Q

Minimum presentation of cardiovascular examination (normal)

A

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.

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19
Q

Ways to distinguish JVP from carotid

A
  • 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)
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20
Q

Causes of S3 on examination

A

Low frequency early diastolic sound

Physiological (

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21
Q

Causes of S4 on cardiovascular examination

A

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
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22
Q

Typical features of Aortic stenosis on examination

A

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.

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23
Q

Typical features of Aortic regurgitation on examination

A

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.

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24
Q

Markers of severity in aortic regurgitation

A 
Wide pulse pressure
Long duration of decrescendo diastolic murmur
S3 (Passive ventricular filling)
Austin Flint murmur
Pulmonary hypertension
Signs of LVF
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25
Q

What is an Austin Flint murmur?

A

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

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26
Q

Typical heart sounds of Mitral stenosis on examination

A

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

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27
Q

Clinical markers of severity of mitral stenosis

A

S1 opening snap
Increased length of murmur
Signs of pulmonary HTN ( e.g. Graham Steell murmur- PR and MS)
Low pulse pressure

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28
Q

Typical signs of mitral regurgitation

A

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.

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29
Q

Clinical markers of severity of mitral regurgitation

A 
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
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30
Q

Typical features of Tricuspid regurgitation (on examination)

A 
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
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31
Q

Causes of SVT

A 
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
32
Q

Commonest causes of Aortic stenosis

A

Calcific degeneration
Bicuspid valve disease
Rheumatic valve disease
= 95% of AS

33
Q

Commonest causes of Aortic regurgitation

A 
Aortic root dilatation
Post-endocarditis
Rheumatic fever
= 95% of AR
REALM Rheumatic, endocarditis, Ank Spond/Ao Dissect, Luetic heart disease, Marfan's
34
Q

Cardiomyopathies

A
  1. HCM: genetic (variable penetrance); sarcomeric proteins (B myosin heavy chain; tropomyosin; troponin)
    1b. HOCM: hypertrophy, disarray, fibrosis
  2. Arrhythmogenic cardiomyopathy ACM: fibrofatty infiltration of RV (+LV) Desmosomal protein complex genes e.g. Plakoglobin, desmoplakin, desmoglein.
  3. DCM: impaired contraction of both ventricles, genetic/post-viral/alcoholic/cocaine/post-partum/ idiopathic
  4. Restrictive cardiomyopathy: endocardial fibrosis/EMF (endomyocardial fibrosis of Equatorial Africa) OR granulation tissue (Loffler eosinophilic endomyocardial disease e.g. Amyloidosis)
35
Q

SADS: characteristics and causes

A

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
36
Q

ECG changes in an inferior MI? Likely artery?

A

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)

37
Q

ECG changes in an inferior MI? Likely artery?

A

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)

38
Q

Signs of infective endocarditis

A

Splinter haemorrhages, clubbing, change in murmur, splenomegaly, macroscopic haematuria (and then Roth spots, janeway lesions, osler’s nodes)

39
Q

Signs of Right ventricular failure

A

Pt would look ill, AF, extra heart sounds, basal crackles, pleural effusions

40
Q

ECG signs of LV aneurysm?

A

Persistent ST elevation

41
Q

Causes of AF

A

Ischaemic heart disease, rheumatic heart disease, thyrotoxicosis.

42
Q

Causes of a 4th heart sounds?

A

Atrial contraction into a non-compliant/hypertrophied ventricle. Low pitched, always pathological.
Heart failure, myocardial infarction, cardiomyopathy, hypertension (pressure overload)

43
Q

Causes of 3rd heart sound?

A

Physiological: <30y, fit young people
Pathological: heart failure, myocardial infarction, cardiomyopathy, hypertension (pressure overload), mitral and aortic regurgitation (volume overload), constrictive pericarditis.

44
Q

Elements of clubbing?

A

Increased fluctuant you of the nail bed
Loss of angle
Increased curvature of nail
Expansion of terminal phalanx

45
Q

Causes of AF?

A

Ischaemic heart disease
Rheumatic heart disease
Thyrotoxicosis

46
Q

How to differentiate causes of irregular heart beat

A

AF: irregular at rest or on exercise

Ventricular ectopics: become regular on exercise

47
Q

Why can there be a difference betweeen the pulse taken at the wrist and heart rate auscultated in AF?

A

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)

48
Q

Management of AF?

A

Rate control: B-blockers, Ca-antagonists, digoxin to slow ventricular rate by increasing a-v delay.
Anticoagulation: target INR 2.5 (2-3)

49
Q

Sings of mitral stenosis on imaging?

A

ECHO: obviously
CXR: prominent left atrium with no LV enlargement ( in pure stenosis)

50
Q

Causes of LVF pressure overload?

A

Hypertension Aortic stenosis, Coarctation of aorta, Hypertrophic cardiomyopathy (+LVOT)

51
Q

How to differentiate aortic stenosis and aortic sclerosis?

A

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,

52
Q

COmplications of MI?

A 
PRAED street? 
Pump failure
Rupture of papillary muscles/septum
Aneurysm and arrthymias
Embolism
Dresler's syndrome ( and acute early pericarditis)
53
Q

What is needed for a diagnosis of ACS?

A

2/3 of

  • cardiac chest pain
  • positive troponin (change with 2 6/8h readings)
  • ECG changes
54
Q

What ECG changes are needed for an ACS diagnosis?

A

T wave inversion, ST depression, ST elevation, Q waves, new LBBB

55
Q

Independent risk factors for ACS?

A 
Smoking
Hyperlipidaemia,
Hypertension
Diabetes
Family history
CKD
56
Q

Initial investigations to include in ?ACS

A

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.

57
Q

Initial management of ?STEMI

A

Morphine + metaclopramide
Oxygen if desaturating
Nitrates sublingual
Aspirin 300mg stat

58
Q

Definitive management of STEMI?

A

Primary percutaneous intervention w/i 2h
- ticagrelor 180mg stat
Angioplasty + stenting -> treat the culprit lesion.
If not possible in 2h ?fibrinolytic therapy (alteplase)

59
Q

Post-PCI management of STEMI?

A 
A: ACEi
B: B-blocker
C: cholesterol lowering (atorvastatin)
D: dual antiplatelet therapy- 90mg ticagrelor bd
E: Echo to assess LV.
60
Q

How much elevation is needed on an ECG for STEMI diagnosis?

A

at least 1mm in limb leads

At least 2mm in 2 adjacent chest leads

61
Q

What if LBBB on ECG and ?STEMI?

A

Is the LBBB new? If so treat as if a STEMI, you cannot assess ST segment if LBBB present.

62
Q

Signs of a posterior MI?

A

ST depression, R waves in V1 + V2. = STEMI

63
Q

What change is seen on a full thickness infarct?

A

Q-waves

64
Q

Initial management of all ACS?

A

Morphine + metaclopramide
Oxygen if desaturating
Nitrate SL
Aspirin 300mg stat

65
Q

Management of NSTEMI/unstable angina?

A

Risk stratify!

66
Q

Signs of mitral stenosis on examination

A

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)

67
Q

Signs of LVF?

A 
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
68
Q

Signs of haemodynamic shock?

A 
Pale anxious SHOCKS
Sinus tachycardia
Hypotension
Oliguria
Cold
Klammy
Slow cap refill
69
Q

Define chronic limb ischaemia?

A

Intermittant claudication.
ABPI >0.4
1y mortality 4%
?lifestyle limiting claudication.

70
Q

Define Critical limb ischaemia

A

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%

71
Q

Define Acute limb ischaemia (thrombosis or embolus)

A

Sudden decrease in limb perfusion that causes a threat to limb viability. ABPI <0.1 (maybe falsely raised in calcified vessels)
1y mortality 20%

72
Q

Six Ps of acute limb ischaemia

A

Pale, Pulseless, painful, paraesthetic, paralysed, perishingly cold.

73
Q

Management of PAD?

A

(1. Watchful waiting)
2. Brest medical treatment (antiplatelets, statins, BP and diabetic control)
3. Endovascular treatments (angioplasty ± stent)
4. Surgical reconstruction
5. Amputation

74
Q

Targets for best medical treatment of PAD (BP, cholesterol, diabetes)

A

Syst BP≤ 140
Total Cholesterol≤ 4mmol
LDL ≤2mmol
HbA1c ≤59mmol (‘good’ diabetic control)

75
Q

How to differentiate arterial/venous/neuropathic ulcers?

A

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

76
Q

Well’s criteria for DVT. 5 pt and 5 leg

A 
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.
77
Q

Likely cause of an inferior MI?

A

75% RCA supplies Posterior desc

25% L circumflex

Medicine (16 decks)

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