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Cardio-resp > Cardio > Flashcards

Cardio Flashcards

1
Q

What are the risk factors for IHD?

A

modifiable: smoking, diabetes, hypertension, hypercholesterolaemia
non-modifiable: age, family history

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2
Q

Describe the NYHA heart failure classification

A

I - No limitation of physical activity
II - Slight limitation of physical activity
III - marked limitation of physical activity
IV - symptoms at rest

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3
Q

When is the third heart sound normal?

A

children and young adults <30

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4
Q

What are causes of a third heart sound?

A

heart failure, myocardial infarction, cardiomyopathy, hypertension

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5
Q

what are causes of a 4th heart sound?

A

always abnormal

heart failure, MI, cardiomyopathy, hypertension

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6
Q

Describe the grading of murmurs

A

1 - very faint
2 - soft
3 - heard easily
4 - loud, with a palpable thrill
5 - very loud, with thrill, may be heard with stethoscope slightly off chest
6 - very loud, with thrill, may be heard with stethoscope off chest

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7
Q

what are causes of mitral stenosis?

A

50% have a history of rheumatic fever or chorea, old age and calcification

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8
Q

describe the mitral stenosis murmur?

A

rumbling mid-diastolic murmur, best heard with he bell of the stethoscope at the apex with the patient lying on their left

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9
Q

what signs might you see in a patient with mitral stenosis?

A

pulse - AF
face - malar flush
palpation - tapping apex beat
CXR - enlarged left atrium, pulmonary oedema

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10
Q

what are the signs of pulmonary oedema on a CXR?

A 
same as heart failure (idiot)
a alveolar oedema
b kerley b lines
c cardiomegaly
d dilated upper lobe vessels
e pleural effusion
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11
Q

what are the causes of mitral regurgitation?

A

prolapsing mitral valve, rheumatic mitral regurge, papillary muscle rupture, cardiomyopathy, CT disorders

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12
Q

Describe the murmur in mitral regurgitation

A

pansystolic murmur radiating to the axilla

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13
Q

what are signs of mitral regurge

A

pulse - sinus
face - malar flush
palpation - displaced apex beat and palpable thrill
CXR - caridomegaly
ECG - bifid p, left ventricular hypertrophy

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14
Q

aortic stenosis causes

A

bicuspid aortic valve
age related calcification (over 65)
rheumatic fever

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15
Q

symptoms of aortic stenosis

A

exercise induced syncope, angina and dyspnoea

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16
Q

signs of aortic stenosis

A

pulse - slow rising, low volume with narrow pulse pressure
palpation - forceful apex beat
CXR - relatively small heart with dilated ascending aorta
ECG - left ventricular hypertrophy and left ventricular strain pattern (depressed ST and T inversion)

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17
Q

describe the aortic stenosis murmur

A

ejection systolic murmur radiating to the carotids

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18
Q

what causes aortic regurgitation

A

rheumatic fever, bicuspid valve, infective endocarditis, marfans, tertiary syphylis

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19
Q

what are signs of aortic regurge

A 
pulse - collapsing, wide pulse pressure
quinkes - capillary pulsation
de Musset's - head nodding
pistol shot femorals
palpation - displaced apex beat
ecg - left ventricular hypertrophy
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20
Q

describe the aortic regurge murmur

A

high pitched early diastolic murmur, best heard at the left sternal edge in the 4th ICS leaning forward with breath held

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21
Q

how do you work out rhythm on an ECG?

A

300/ big squares in R-R interval or rhythm strip x 6

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22
Q

describe the ECG in AF

A

irregular rhythm and no P waves

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23
Q

describe the ECG in atrial flutter

A

saw tooth p waves,

factors of 300

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24
Q

describe the ecg in VT

A

fast 120-180 bpm, broad complexes, always serious, may need cardioversion

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25
Q

describe v fib

A

patient arrested, look for capture or fusion beats, concordance

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26
Q

what are causes of left axis deviation?

A

left ventricular hypertrophy, left anterior hemiblock

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27
Q

describe the different types of heart block

A

1 - prolonged p-r interval
2a -progressive pr lengthening until one QRS dropped
2b - intermittent failure of AVN to conduc - 2:1, 3:1
3 - no relationship between p-p and R-R

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28
Q

Describe the ECG territories for MI

A 
V1-V2 - septal
V3-V4 - anterior
V5-V6 - lateral
I, aVL - high lateral
II, III, aVF - inferior
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29
Q

describe the ECG changes in PE

A

S1, Q3, T3, right axis deviation, tachycardia

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30
Q

describe the ECG changes in hyperkalaemia

A

flat p waves, broad QRS, tall tented t

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31
Q

what are the three main causes of heart failure?

A

IHD (70%), non-ischaemic dilated cardiomyopathy (25%), hypertension (5%)

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32
Q

what are more niche causes of heart failure?

A 
valvular disease
congenital heart disease
arrhythmias
hyperdynamic circulation
pericardial disease
right heart failure
alcohol and drugs
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33
Q

what are normal physiological changes in heart failure?

A

ventricular dilatation, myocyte hypertrophy, neurohumeral increased ANP, salt and water retention, sympathetic stimulation, peripheral vasoconstriction

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34
Q

what are early compensation mechanisms in heart failure?

A

normally if CO decreases, venous return increases leading to increased end diastolic volume restoring starlings law
if mild myocardial depression there is no decrease in cardiac output as it is maintained by an increase in venous pressure and sinus tachycardia, there is a decrease in ejection fraction

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35
Q

what are late compensatory mechanisms in heart failure?

A

cardiac output is maintained by large increases in venous pressure and sinus tachycardia at rest, they are unable to maintain a normal CO during excercise, increase VP leads to dyspnoea, hepatic enlargement, ascites and dependent oedema

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36
Q

what are the changes in severe heart failure?

A

decreased CO even at rest despite increased venous pressure and sinus tachycardia

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37
Q

what are causes of left heart failure?

A

IHD
non ischaemic dilated cardiomyopathy
hypertension
mitral/aortic valve disease

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38
Q

what are symptoms of left heart failure?

A

fatigue, exertional dyspnoea, orthopnea/PND

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39
Q

what are the physical signs of left heart failure

A

displaced apex beat (cardiomegaly)
gallop rhythm
features of mitral regurge
crackles at lung bases (pulmonary oedema)
dependent pitting oedema (activation of RAA)

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40
Q

what are causes of right heart failure?

A

chronic lung disease
PE or pulmonary hypertension
tricuspid/pulmonary valve disease

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41
Q

what are the symptoms of right heart failure?

A

fatigue, dyspnoea, anorexia

42
Q

what are the physical signs of right heart failure?

A

increased jugular venous distension, cardiomegaly, hepatic enlargement (tender and smooth), ascites, dependent pitting oedema

43
Q

describe the NYHA classification of heart failure?

A 
class I - no limitation of physical activity
class II - slight limitation of physical activity
class III - marked limitation of physical activity
class IV - symptoms at rest
44
Q

what is the general management for heart failure?

A 
low level exercise
low salt diet
stop smoking
education
vaccination
45
Q

what is the medical management of heart failure?

A

1) diuretics - furosemide, bumetanide, add thiazide
2) ace inhibitor, swap to arb if dry cough
3) beta blocker
4) spironolactone
5) inotropic agent - dopamine, dobutamine, digoxin
6) nitrates
7) anticoagulation

46
Q

describe the pathophysiology of atherosclerosis

A

endothelial injury
oxidation of lipoproteins which are taken up by macrophages to make foam cells
release of cytokines leads to an accumulation of fat and smooth muscle proliferation
plaque formation

47
Q

describe the physiology of acs

A

rupture of coronary artery plaque, platelet aggregation and adhesion, localised thrombus, vasoconstriction, myocardial ischaemia

48
Q

what are risk factors for ACS?

A

non modifiable - increased age, male hender, family history, ethnic origin
modifiable - smoking, diabetes, hypertension, hypercholesterolaemia

49
Q

initial management of ACS?

A 
ABC
IV access
12-lead ECG
morphine
oxygen
nitrates
aspirin
bloods - FBC, U&amp;E, LFTs, glucose, lipids, CK, troponin
50
Q

ECG findings in a STEMI

A 
ST elevation Anteroseptal = V1-4 (LAD)
Lateral = V5-6 (Cx)
High Lateral = I, aVL (Cx)
Inferior = II, III, aVF (RCA)
new LBBB
T wave inversion
pathological Q waves
51
Q

What are indications for thrombolysis?

A

<12 hours onset of pain
+ any 1 of the following
- ST elevation >1mm in 2+ consecutive limb leads
- ST elevation >2mm in 2+ consecutive chest leads
- posterior infarct
- new onset LBBB

52
Q

what are thrombolysis contraindications?

A 
absoloute:
haemorrhagic or ischemic stroke < 6 months
CNS neoplasia
recent trauma or surgery
GI bleed <1 month
bleeding disorder
aortic dissection
relative:
warfarin
pregnancy
advanced liver disease
infective endocarditis
53
Q

what are possible complications of thrombolysis?

A 
bleeding
hypotension
intracranial haemorrhage
reperfusion arrythmias
systemic embolaisation of thrombus
allergic reaction
54
Q

what are indications for PCI?

A

same as thrombolysis
if does not fill thrombolysis criteria or thrombolysis contraindicated
if symptomatic post thrombo-lysis or develops

55
Q

what are complications of a STEMI?

A 
s- sudden death
p - pump failure
r - rupture papillary muscles or septum
e - embolism
a - aneurysm
d - dressler's syndrome
56
Q

what are the discharge medications and advice post STEMI?

A 
Dual antiplatelet - aspirin and clopidogrel
ACE inhibitor
B-blocker
Statin
Address modifiable risk factors
1 month off work
inform DVLA - no driving for 4 weeks
57
Q

how to you distinguish between NSTEMI and unstable angina?

A

check troponin I 12 hours after onset of pain to distinguish, NSTEMI will have positive troponin I and unstable angina will have a negative troponin

58
Q

Describe the management of NSTEMI/ UA

A

morphine
nitrates, ACE inhibitor, beta blocker, calcium channel blocker, statins
antiplatelet - aspirin and clopidogrel
LMWH

59
Q

when would you consider PCI as the management for NSTEMI/UA?

A 
raised troponin I
recurrent angina/ ischaemic ECG changes
features of heart failure
poor LV function
haemodynamic instability
PCI <6 months/previous CABG
60
Q

describe the presentation of acute pulmonary oedema

A

acute breathlessness
cough and frothy pink sputum
orthopnoea, PND
collapse, arrest, cardiogenic shock

61
Q

describe signs you’d find in acute pulmonary oedema

A

distressed, pale, sweaty
tachycardic
fine crepitations bilaterally
gallop rhythm, 3rd heart sound

62
Q

what are the commonest causes of LVF?

A

myocardial ischemia
hypertension
aortic stenosis or aortic incompetence

63
Q

what are the radiological signs of heart failure?

A 
airspace shadowing
kerley B lines
cardiomegaly
diversion of blood to upper lobes
effusions
64
Q

what are the mechanisms causing tachyarrythmias?

A

accelerated automaticity - an area of myocardial cells depolarises faster than the SAN
triggered activity - myocardial damage
re-entry - propagating action potential keeps meeting excitable myocardium, must be 2 pathways around area of conduction block

65
Q

what are precipitating factors for VT?

A 
metabolic
IHD
cocaine
cardiomyopathy
MI
66
Q

what are precipitating factors for SVT?

A 
IHD
thyrotoxicosis
caffeine
alcohol
smoking
67
Q

what are precipitating factors for AF?

A 
same as SVT +
mitral vlave disease
hypertension
lung disease
post op
pericardial disease
cardiomyopathy
68
Q

describe the management of SVT

A 
ABC, O2, IV access
vagal manoeuvres
adenosine
SEEK HELP
antiarrythmic
DC cardioversion if haemodynamically unstable
69
Q

what are the differences between SVT and VT?

A

SVT is slowed/terminated by vagal manoeuvres or adenosine, there is atrial and ventricular coupling
VT has QRS >160ms, indipendent atrial activity, presence of fusion/capture beats

70
Q

what is the management for broad complex tachycardia?

A

ABC - if pulseless = arrest protocol
no adverse signs
amiodarone/lidocaine, K/Mg as needed, sedation and DC cardioversion
adverse signs
sedation, DC cardion, amidoarone/lidocaine

71
Q

what is the causative organism in infective endocarditis?

A

usually strep viridans

can be staph aureus - skin infections, abscesses, central lines, IV drug users

72
Q

describe the pathophysiology of infective endocarditis

A

1 - endothelial damage/damaged valve
2 - platelets and fibrin are deposited - sterile fibrin-platelet vegetation
3 - bacteraemia - delivers bacteria to surface of the valve
4 - adherence and colonaisation of bacteria
5 - fibrin aggregates protect the bacteria and vegetation from host defence mechanisms
leads to disruption of the valve cusps (regurgitation), vegetations embolise, deposition of immune complexes

73
Q

describe the clinical presentation of infective endocarditis

A

HEART MURMUR AND FEVER
systemic infection - malaise, pyrexia, myalgia, weight loss, fatigue
valvular/cardiac damage - changing murmur, heart failure, conduction abnormals
embolaisation - cerebral, pulmonary, coronary, renal
immune vasculitis - roth spots, oslers nodes, janeway lesions, clubbing, splinter haemorrhages, glomerulonephritis

74
Q

what is the criteria for diagnosing infective endocarditis?

A

Duke criteria
Major - Positive blood culture and evidene of endocardial involvement
Minor - predisposition, fever, vascular/immunological signs, positive blood criteria (doesn’t fit major criteria), postivie echo (doesn’t fit major)

need 2 major or 1 major, 3 minor or 5 minor

75
Q

what is the management for infective endocarditis?

A

ABC
involve micro and cardiology
empirical treatment is benpen and gent

76
Q

who’s at risk of infective endocarditis?

A

structural congenital heart disease
acquired valve disease
prosthetic valves
previous endocarditis

77
Q

what should you explain to a patient with infective endocarditis?

A

why antibiotic prophylaxis is no longer recomended
importance of maintaining good oral health
symptoms and when to seek help
risks of undergoing invasive procedures inc body piercing and tattoo

78
Q

describe the drainage of pericardial fluid

A

via thoracic duct and right lymphatic duct into right pleural space

79
Q

describe the pathophysiology of pericarditis

A

the pericardium is acutely inflamed
there is infiltration of polymorphonuclear leukocytes and pericardial vascularaisation which can lead to constrictive pericarditis or pericardial effusion

80
Q

what are causes of pericarditis?

A 
viral - most common (coxsackie)
idiopathic
tuberculosis
bacterial (causes purulent pericarditis)
neoplams
cardiovascular disease - MI, dressler's
renal failure
inflammatory - RA, sarcoidosis, SLE
81
Q

describe the features of pericardial pain

A 
sharp
worse on inspiration
central chest pain
radiating to left shoulder
eased sitting forwards
\+/- dyspnoea/ fever
82
Q

what signs would you see when examining a patient with pericarditis?

A

tachycardia + tachypnoea + fever
pericardial friction rub
if constrictive - right heart failure, hypotension, pulsus paradoxus, loud high pitched S3

83
Q

describe the ECG changes in pericarditis

A

1 - saddle shaped SST elevation
2 - ST returns to baseline, followed by T wave flattening
3 - T wave inversion
4 - ECG returns to pre-pericarditis baseline weeks to months after onset

84
Q

what is the treatment for pericarditis?

A 
treat cause
bed rest and oral NSAIDs unless its post MI when no NSAID (as assoc with myocardial rupture)
corticosteroids
pericardial window
pericardiectomy
85
Q

what is a pericardial effusion?

A

it is an abnormal accumulation of fluid in the pericardial cavity

86
Q

what is cardiac tamponade?

A

it is a pericardial effusion causing haemodynamically significant cardiac compression, the increased pressure impedes venous return to the heart resulting in reduced cardiac output, hypotension and shock

87
Q

describe the presentation of cardiac tamponade

A

depends on how fast the fluid accumulates
commonly - cardiac arrest, hypotension, confusion, shock
slow developing - SOB, cough, hiccoughs, dysphagia

88
Q

what are the signs of cardiac tamponade

A

Beck’s triad - increasedJVP, low BP, muffled heart sounds
tachycardia
kussmauls sign (JVP increase with inspiration)
pulsus paradoxus (decrease in palpable pulse and decrease in systolic BP on inspiration)

89
Q

describe the management of effusion/tamponade

A

MEDICAL EMERGENCY

pericardiocentesis - needle tip inserted at level of xiphisternum, aim for tip of left scapula, aspirating continously

90
Q

Describe the class I antidysrhytmics

A

Na channel blockers
Ia - qunidine - delays
Ib - lidocaine - opes channels, aborts premature beats
Ic - flecanide - not specefic to damage cells, suppresses re-entrant rhythms

91
Q

Class II antidysrhythmics

A

beta blocker e.g. bisoprolol, atenolol, propanolol
negatively chronotropic and ionotropic
indications - hypertension, angina, post MI, AF
SE - GI disturbances, , bradycardia, fatigue, cold peripheries, heart failure, hypotension, dizziness, sexual dysfunction, peripheral vasoconstriction, bronchospasm
CI - asthma, marked bradycardia, heartblock, uncontrolled heart failure, PVD, prinzmetals angina, hypotension, cardiogenic shock

92
Q

what should beta blockers not be used in conjunction with?

A

verapamil and diltiazem (non-dihydropyridines) in heart failure due to their additive effects (decrease HR, contractility, CO)

93
Q

What are class III antidysarythmics?

A

K+ channel blockers e.g. amiodarone

94
Q

What are class IV antidysarrythmics?

A

calcium channel blockers e.g. verapamil, diltiazem (non dihydropyridines)
amlodipine, felodipine, nifedipine
(dihydropyridines)
SE - v

95
Q

describe the nitrates

A

e.g. isosorbide mononitrate, GTN infusion, GTN spray
indications - stable angina,unstable angina, acute heart failure, chronic heart failure
CI - hypersensitivity, hypotension, hypertrophic cardiomyopathy, AS, MS, cardiac tamponade, constrictive pericarditis, marked anaemia

96
Q

describe ACE inhibitors

A

e.g. ramipril, lisinopril
inhibit conversion of agiotensin 1 into angiotensin 2 inhibiting its effects:
-increasing sympathetic activity
- fluid retention by kidney (via increase aldosterone and direct)
- arteriolar vasodilation
- stimulate ADH secretion
indications - hypertension, HF, post MI, IHD risk, diabetic nephropathy, progressive renal insufficiency
side effects - renal impairment, dry cough, , angioedema, rash, hypotension, pancreatitis, hyperkalaemia, GI effects
CI - hypersensitivity, renal artery stenosis, pregnancy, AS,

97
Q

describe statins

A

e.g. atorvastatin, simvastatin
MOA - block HMG-CoA-reductase so inhibit liver cholesterol synthesis and upregulation of LDL receptors
SE - myositis, rhabdomyolysis, headache, altered LFTs, parasthesia, GI effects
CI - active liver disease, pregnancy, breast feeding

98
Q

Aspirin

A

Supresses production of prostaglandins and thromboxane by irreversibly inactivating the COX enzyme, irreversibly blocks formation of thromboxane A2 in platelets, inhibiting platelet aggregation

99
Q

describe clopidogrel

A

inhibits ADP induced aggregation through n active metabolite

100
Q

describe dipyridamole

A

phosphodiesterase inhibitor

101
Q

compare UFH and LMWH

A

LMWH - inhibits factor Xa but not thrombin, LMWH not fully reversible with Protamine

UFH - binds to ATIII which is an endogenous inhibitor of coagulation, increases ATIII ability to inhibit factors IXa,Xa, XIa, XIIa and thrombin, fully reversible with protamine

102
Q

MOA of warfarin

A

inhibits vitamin k dependent clotting factors - II,VII, IX, X, protein C& S

Cardio-resp (1 decks)

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