Cardiology Flashcards

1
Q

What is heart failure?

A

A syndrome where cardiac output is not sufficient to meet the body’s requirements

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2
Q

What is systolic failure? What causes it (top 3)

A

Inability of the ventricle to contract normally, reduced CO, ejection fraction typically <40%

Causes: IHD, MI, cardiomyopathy (hypertension)

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3
Q

What is diastolic failure? What causes it (5)

A

Inability of the ventricle to relax and fill normally, increased filling pressure. Typical ejection fraction >50%.
Causes include ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity

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4
Q

What are the symptoms of left ventricular failure?

A

Dyspnoea, poor exercise tolerance, fatigue, orthopnea, PND, nocturnal cough (+/- pink frothy sputum), wheeze, nocturia, cold peripheries, weigh loss.

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5
Q

What are the symptoms of right heart failure ?

A

Peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis

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6
Q

NY classification of heart failure

A

I: no undue breath,Essenes
II: Breathlessness during ADLs, not limiting
III: breathlessness during ADLs, limiting
IV: breathlessness at rest

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7
Q

Chest x-ray findings in heart failure (5)

A

Alveolar Oedema (bat wing appearance)
kerley B lines (interstitial oedema, also known as septal lines)
Cardiomegally (>50% cardiothoracic ratio)
Dilated prominent upper lobe vessels (diversion due to oedema)
Effusions (blunted costophrenic angle and cardiac border)

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8
Q

How should you investigate suspected heart failure?

A

BNP and ECG. If either abnormal echocardiogram. If abnormal ever to cardiology.

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9
Q

Management of heart failure (not specific drugs, 5 things)

A

1) treat cause e.g. valvular heart disease, arrhythmia.
2)treat exacerbating factors e.g. anaemia,infection
3 )lifestyle modification e.g smoking cessation, alcohol reduction, reduced salt diet, healthy eating, weight loss.
4)avoid exacerbating factors e.g. NSAIDS and negative inotropes e,g, verapamil
5) annual flu vaccine and one off pneumococcal vaccine

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10
Q

Pharmacological management of heart failure. (3 core things + 2 to add on)

A

Reduce workload of heart.

1) diuretics - furosemide or bumetanide
2) ACEi or ARB
3) beta blocker e.g. bisoprolol. Start low and go slow.
4) spironolactone if renal function allows and potassium >3.4 or arrhythmia or digoxin therapy. Use if other diuretics not achieving adequate symptom control or if LVSD in post MI patients
5) digoxin considered in all who have LVSD who are still symptomatic with above management.

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11
Q

Palliative care considerations for heart failure patients (5)

A

1) treat and prevent comorbid conditions e.g. flu vaccine
2) good nutrition, allow alcohol
3) involve GP - discuss prognosis
4) treat symptoms - consider opiates for pain and dyspnoea
5) be realistic about prognosis

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12
Q

Hypertension management (not drugs)

A

If >135/85 in clinic, monitor, lifestyle advice
If >140/90 in clinic, home recordings
If at home >135/85 then stage 1 hypertension.
No comorbid disease or over 80- monitor
Comorbid disease and under 80- drug treatment
If in clinic >150/95 drug treatment

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13
Q

Pharmacological management of hypertension

A

A=ACEi
C= CA2+ blocker
D= thiazide diuretic

if <55yrs or diabetic = A
if >=55yrs or Afro-Caribbean =C
Then A and C
Then A and C and D

Then consider adding spironolactone or increasing D, if not tolerated add an alpha or beta blocker
If doesn’t tolerate ACEi use ARB

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14
Q

What is the cardiac output of an average male at rest

A

5L/min

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15
Q

Leads I and aVL on an ECG refer to which territory and which artery is likely to supply this area?

A

Septal or lateral - circumflex artery

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16
Q

Leads II, III and aVF on an ECG refer to which territory and which artery is likely to supply this area?

A

Inferior - RCA or Circumflex

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17
Q

Leads V1 to V4 on an ECG refer to which territory and which artery is likely to supply this area?

A

Anteroseptal - LAD

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18
Q

Leads V1 to V6 (+/- aVL) on an ECG refer to which territory and which artery is likely to supply this area?

A

Anteriorlateral - LAD

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19
Q

What ECG change would make you suspicious of a posterior myocardial infarction? What should you do to confirm your suspicions?

A

ST depression in V1 to V3, there may also be reciprocal change in aVR

Repeat ECG with leads V7, V8 and V9 which are placed on the back, below the left scapula. You would expect to see moderate ST elevation in these leads.

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20
Q

Where does the ductus arteriosus run, what is it’s purpose and what does it become after birth?

A

Between the pulmonary artery and the aorta. Allows most of the semi-oxygenated blood to bypass the foetuses lungs which are fluid filled and therefore at high pressure.

It becomes the ligamentum arteriosus

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21
Q

What is the foremen ovale, and what does it become?

A

The foremen ovale is a hole in the interatrial septum providing a shunt for oxygenated blood between the right and left atrium, allowing it to bypass the non-functioning lungs.

After birth the foramen closes forming the fossa ovalis

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22
Q

What is the ductus venousus purpose and what does it become?

A

The ductus venous provides a shunt from the umbilical vein to the IVC, preventing the liver from using most of the the oxygenated blood from the placenta.
Becomes the ligamentum venosum, which separates the caudate lobe of the liver

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23
Q

Give two examples of acyanotic congenital heart defects

A

Atrial septal defect

Ventricular septal defect

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24
Q

Give two examples of cyanotic congenital heart defects

A

Tetralogy of fallot

Transposition of the great arteries

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25
Q

What defects are present in tetralogy of fallot?

Which direction is the shunt?

A

Ventricular septal defect
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy

Produces right to left shunt, therefore some degree of cyanosis. Severity depends on level of pulmonary stenosis (and therefore amount of blood shunted)

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26
Q

What autonomic receptors are found in the heart?

A

Beta 1 adrenoreceptors - increase rate and contractility

M2 muscarinic ACh receptor - decrease rate

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27
Q

What is starling’s law?

A

The stroke volume of the heart increases if there is an increased volume of blood in the heart (i.e. a greater preload will result in greater contractility)

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28
Q

How do you calculate cardiac output?

A

CO= stroke volume * heart rate

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29
Q

What is preload?

A

The end diastolic pressure -the volume at which the ventricles are stretched the most.

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30
Q

What is afterload?

A

The tension within the left ventricle during systole -depends on arterial or pulmonary pressures

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31
Q

Describe Stable angina

A
  • transient ischaemia which is relived when O2 demand decreases
  • brief episodes of chest pain on breathlessness brought on by exertion or emotion and relieved by rest
  • resting ECG normal, ST depression on stress test, troponin normal
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32
Q

Describe unstable angina

A
  • ischaemia even at rest
  • ST depression at rest
  • no raised troponin as no necrosis
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33
Q

Describe an NSTEMI

A

ST depression or T wave changes pm ECG
Raised troponins
Some infarction but not full thickness

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34
Q

Describe STEMI

A

ST segment elevation on ECG with reciprocal changes
Troponins raised
Full thickeners infarction

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35
Q

When is troponin I most raised? How long will it remain raised? When would you look at creatinine kinase?

A

Troponin I reaches its peak level 24hours post infarction
It remains raised for approximately 1 week
CK may be used if there is a second episode of chest pain within 2 days of a confirmed MI

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36
Q

NYHA scale of dyspnoea in heart failure… go!

A

I - no symptoms or limitation
II - mild symptoms and slight limitation during ordinary activity
III - marked limitation on activity due to symptoms e.g. walking short distances. Only comfortable at rest.
IV - severe limitation, symptoms at rest, bed bound.

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37
Q

Causes of heart failure

A
Ischaemic heart disease 
Valvular disease
Hypertension 
Arrhythmia 
Hypertrophic cardiomyopathy
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38
Q

What general advice would you give to someone with heart failure?

A

Regular, low level exercise, such as brisk walking
Have a low salt diet
STOP SMOKING
Education about the disease and it’s progression
Vaccination

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39
Q

Define cardiogenic shock

A

The inability of the heart to eject enough blood e.g. following myocardial infarction

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40
Q

What is a third heart sound and what can cause it?

A

Due to a stiff or dilated ventricle suddenly reaching its elastic potential which decelerates the incoming blood. “Lub…dub de”
Normal in under 30s and children
Causes include HF, MI, cardiomyopathy, hypertension

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41
Q

What is a fourth hear sound and what does it mean?

A

Low pitched sound of atrial contraction into a non-compliant or hypertrophied ventricle. “Le lub…dub”
Always abnormal
Heart failure, MI, cardiomyopathy, hypertension

42
Q

What is the grading system for murmurs?

A

1- very faint
2- soft
3- heard easily
4- loud, with palpable thrill
5- very loud, with thrill. Heard with stethoscope partly off the chest
6- very loud, with thrill. Heard with stethoscope completely off the chest

43
Q

What ECG changes in left ventricular hypertrophy?

A

S waves in V1 + r waves in V5/V6 = greater than 3.5 big squares

44
Q

ECG changes 1st degree heart block

A

Constant but prolonged PR interval

45
Q

Second degree heart block mowbitz 1 ECG changes

A

Progressively lengthening PR interval until a QRS is dropped

46
Q

What are the ECG changes in mowbitz II 2nd Degree heart block

A

Occasional Failure of the AV node to conduct atrial depolarisations to the ventricle. May occur in a fixed pattern I.e. 2:1 or 3:1

47
Q

What ECG changes in third degree heart block?

A

No relationship between the p waves and the qrs

48
Q

What ecg changes are suggestive of right ventricular hypertrophy?

A

Right axis deviation
Narrow QRS
Dominant R waves in V1 ( 7mm or taller)
Dominant S waves in V6 (7mm or deeper)

49
Q

ECG changes in LBBB

A

Wide QRS
W in V1, M in V6
(WiLLiaM)

50
Q

What ECG changes in RBBB?

A

Wide QRS
M in lead V1, W in lead V6

(MaRRoW)

51
Q

Heart failure changes on CXR (abcde)

A
Air space shadowing
Kerley B lines
Cardiomegaly
Diversion of blood to upper lobes
Effusions - pleural
52
Q

Class I antiarrythmics

Action

A

Sodium Channel Blockers (N -1 line)
Ia - quinidine - ventricular dysrhythmias, atrial fibrillation
Ib - lidocaine - VT & VF
Ic - flecainide - paroxysmal AF, recurrent tachycardias incl. WPW

53
Q

Class II antiarhytmics

Action, example

A
Beta Blockers (two lines for B)
Bisoprolol, atenolol, propanol
54
Q

Class III antiarhythmics

Action, example, use

A

K+ channel Blockers (3 lines to draw a K)

Amiodarone - end SVT in acute incl. WPW

55
Q

Class IV antiarrythmics

Action, example

A

Calcium channel blocker, verapamil or diltiazem

These are both examples of non-dihydropyridines which act centrally on the heart

56
Q

Adenosine

What is it?
What is it used for.

A

Antiarrythmic - unclassified

Rapid reversion to sinus rhythm of SVT including WPW
Don’t use in broad complex irregular tachycardias as could be preexcited AF because could cause VT

57
Q

Beta blockers
Examples
Action
Indications

A

Bisoprolol, atenolol, propranolol.
Negatively inotrophic (contractility) and chronotophic (rate)
Indicated for ischaemic heart disease, dysrhythmias such as AF and is a third line option for hypertension.

58
Q

Beta Blockers
Side effects
Contraindications

A

Vagal- GI disturbance, bradycardia, fatigue, cold peripheries, sexual dysfunction, exacerbation of Raynaud’s or intermittent claudication, bronchospasm.
Contraindications - brittle asthma, marked bradycardia, heart block, peripheral vascular disease

59
Q

Calcium channel Blockers

Two types - examples and uses

A

Non-dyhydropyridines - verapamil and diltiazem - act on myocardium - used in SVTs but should be cautioned in Heart failure
(especially in combination with beta blockers) can be used for hypertension
Dihydropyridines - act on arteries more than myocardium. E.g. amlodipine, felodipine,nifedipine 1st line for hypertension in over 55s and afrocarribeans of any age. Prevent angina.

60
Q

Side effects of calcium channel blocker

A

Non-dihydropyridines - CONSTIPATION, nausea, flushing, headache, dizziness, fatigue
Dihydropyridines - abdo pain, nausea, palpitations, flushing, oedema, headache, dizziness, fatigue

61
Q

Contraindications for calcium channel blockers

A

Non-dihydropyridines - Heart failure, 2nd or 3rd Degree heart block, cardiogenic shock

Dihydropyridines - unstable angina, significant atherosclerosis

62
Q

Nitrates
Examples
Indications

A

Isosorbide mononitrate - oral
GTN spray
Stable angina (prevention and treatment) unstable angina, acute heart failure, chronic heart failure.

63
Q

ECG Changes in posterior MI and which artery is most likely effected

A

Tall R waves in V1 and V2

usually left circumflex, can be right coronary

64
Q

CHADSVASc

A
Risk of thromboembolic disease in AF patients - used to inform anticoagulation decisions
Congestive HF
Hypertension
Age >75 =2, 65-74=1
Diabetes
Previous stroke or TIA =2
Vascular disease = IHD or PVD
Sex= female
65
Q

What is a third heart sound?

What causes it? (5)

A

‘lub dub DE’
blood rushing into ventricle during early diastole or a stiff or dilated ventricle suddenly reaches its limit and the incoming blood decelerates.

Causes:
Normal in under 30s
Heart failure
myocardial infarction
cardiomyopathy
hypertension
66
Q

What is a fourth heart sound?

What causes it? (4)

A

“LE lub dub”
atrial contraction into a non-compliant or hypertrophied ventricle.
low pitched

Causes:
ALWAYS ABNORMAL
Heart failure
MI
cardiomyopathy ( + hypertrophic)
hypertension
67
Q
Mitral Stenosis
How best heard?
What does it sound like?
Causes (2)
Effects
A

LUB De Derrr
Loud S1, Opening snap ‘De’ followed by rumbling mid-diastolic murmur.
Best heard with bell over apex with patient lying on left side.
Causes - calcification in old age or rheumatic fever.
Effects - raised LA pressure, pulmonary hypertension, eventually RHF.

68
Q

ECG and CXR Changes in Mitral Stenosis

A

AF, Pifid P waves, RHF - right axis deviation and tall R waves in leads V1 and V2.

69
Q
Mitral Regurgitation
How best heard?
What does it sound like?
Causes (5)
Effects
A

pan systolic murmur at the apex which radiates to the axilla
‘burrrrr’
Prolapsed mitral valve, rheumatic mitral regurgitation, papillary muscle rupture, cardiomyopathy, connective tissue disorder.
left atrial and left ventricular enlargement - LHF

70
Q

ECG and CXR Changes in Mitral regurgitation

A

bifid P wave, Left axis deviation due to LVH

CXR - cardiomegally

71
Q
Aortic Stenosis
How best heard?
What does it sound like?
Causes (3)
Effects
A

Ejection systolic, radiates to the carotid
Lub-whoshhh Dub
Bicuspid aortic valve (under 65), age related calcification, rheumatic fever.
Left heart failure

72
Q

ECG and CXR Changes in aortic stenosis

A

Left ventricular strain - ST segment depression and T wave inversion in left ventricular leads - chest leads
prominent, dilated aorta on CXR

73
Q
Aortic Regurgitation
How best heard?
What does it sound like?
Causes (5)
Effects
A

High pitched, early diastolic murmur - best heard at left sternal edge, 4th intercostal space, with the patient leaning forwards.
Lub Taaarrr
rheumatic fever, bicuspid valve, infective endocarditis, Marfan’s, tertiary syphilis
LV dilation

74
Q

Aortic regurge - changes on ECG

A

ECG - left ventricular hypertrophy

75
Q

Left axis deviation on ECG

A

If lead I is positive and lead II is negative - i.e. they are Leaving each other (aVF also negative)

76
Q

Right axis deviation on ECG

A

Lead I is negative and lead AVf is positive (I and II are Reaching for each other)

77
Q

ECG changes in bundle branch block

A

QRS is broad
up in V1, becoming progressively more negative = RBBB
down in V1, becoming progressively more positive - LBBB

78
Q

ECG changes in PE

A
TACHYCARDIA
S1, Q3, T3
Large S waves in I
Q wave inversion in III
T wave inversion in III
RAD
79
Q

Pathophysiology of atherosclerosis formation

A

Superficial endothelial injury causes:
-increased permeability causes lipoprotein accumulation
- cytokine release causing macrophage recruitment
macrophages phagocytose lipoproteins producing foam cells creating fatty plaque
inflammation causes smooth muscle cell migration and proliferation and collagen production, creating a fibrous cap

80
Q

pathophysiology of plaque thrombosis

A

the fibrous cap is ruptured or eroded
platelets adhere and aggregate
platelets release serotonin and thromboxane A2 causing localised thrombosis (which may embolise distally) and vasoconstriction
reduced coronary blood flow causes myocardial ischaemia and later necrosis, causing an increase in serum troponins.

81
Q

STEMI Management

A

MONA and PCI or thrombolysis

82
Q

NSTEMI/Unstable angina management

A
Morphine
nitrates, ACEi, Beta blocker, calcium channel blocker, statin
aspirin, clopidogrel
LMWH
Consider PCI
83
Q

Causes of acute LHF (5)

A
MI
hypertension
aortic stenosis or aortic incompetence
mitral incompetence 
increased demand on heart i.e. shock - sepsis, hypovolaemia
84
Q

Acute HF Mx (9)

A
ABCDE
Sit upright
100% O2 via non-rebreathe
IV access and ECG monitoring
Morphine and antiemetic
If systolic BP >100 GTN infusion
Furosemide - caution if hypotensive
CPAP - think ceiling of care
address cause
85
Q

Mx of Tachyarrhythmia with adverse features and what are adverse features

A

Shock, snycope, MI, HF

A to E, periarrest call, prepare to DC cardiovery

86
Q

Mx narrow tachyarrhythmia

A

Regular - SVT so vagal manouvere, adenosine 6mg IV

Irregular - Probable AF - beta blocker if in HF consider digoxin or amiodarone

87
Q

Mx broad tachyarrhythmia

A

Regular - VT so amiodarone 300mg over 20-60 mins
if known SVT with BBB then beta blocker
Irregular - ? AF with BBB beta blocker
?Preexcided AF - ?amiodarone

88
Q

infective organism endocarditis

A

strep viridans most common

staph aureus in IVDU, central lines

89
Q

presentation of infective endocarditis

A

systemic infection - malaise, pyrexia, myalgia, weight loss, fatigue
Cardiac- heart murmur, heart failure, conduction abnormalities
Embolic disease
immune vasculitis - Roth spots, Osler’s nodes, Janeway lesions, clubbing, splinter haemorrhages, glomerulonephritis.

90
Q

Mx of infective endocarditis

A

involve micro and cardiology

empirical ABx gentamycin and penicillin IV

91
Q

presentation of pericarditis

A

chest pain - sharp, worse on inspiration, central, radiating to left shoulder, eased by sitting forward
+/- dyspnoea and fever

92
Q

ECG changes in pericarditis

A

1) saddle shaped ST elevation in most leads
2) days later - ST normalises, T wave flattening
3) T wave then inverts
4) Weeks to months later - ECG normalised.

93
Q

Ix Pericarditis

A

Bloods - FBC, U&E, LFT, CRP, CK, Trop I
Virology screen, blood culture
Rheumatology panal
Tuberculin and sputum for acid fast bacilli
Imaging - ECHO for effusion, CT/MRI

94
Q

Causes of pericarditis (7)

A
Viral - cocksakie
idiopathic
tuberculosis
bacterial 
secondary to MI, neoplasm
renal failure
rheumatological - RA, sarcoid, SLE
95
Q

Mx of pericarditis

A

treat cause
supportive care
high dose NSAIDs unless MI

96
Q

What is rheumatic fever

A

immunological reaction to a strep infection - usually URTI

97
Q

Diagnostic criteria for rheumatic fever

A
Confirmed Strep infection - swab or increasing antibodies
2 major or 1 major + 2 minor
Major:
   erythema marginatum
   sydenham's chorea
   polyarthritis
   carditis and valvulitis
   subcutaneous nodules
Minor:
   raised CRP/ESR
   pyrexia
   arthralgia if no arthritis 
   prolonged PR interval
98
Q

Ix rheumatic fever

A
blood culture
antistreptolysin titre
throat swab
ECG
Echocardiogram
CXR
99
Q

Mx Rheumatic fever

A

admit and bed rest
oral aspirin
IM penicillin 1.2mg followed by 10 day course
long term Abx may be required to prevent cardiac damage

100
Q

BP targets in diabetes

A

No end-organ damage - 140/80

End organ damage - 130/80