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Cardiology Flashcards

1
Q

asthlersoscleoriss

A

athlerosclerosis
fatty deposits in artery walls that harden and form plaques

affects medium and large arteries

chronic inflammation and acitvation of the immune ssytem casue athelroscleorriss
casuing depostiion of lipids in arterial walls and then devleop fibrous athermoatous plaques

the plaques can casue:
stiffening of walls=> ht, strain on heart as increased resistance
plaque rupture=> thrombosis=>block distal artery casuing ischmeia eg. ACS
stenosis=> decreased blood flow eg. angina

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2
Q

end resutls of athlerosclerosis

A

angina
MI
stroke
TIA
unstbale angina
peripheral vascualr disease
chronic mesenteric ischemia

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3
Q

risk factors of cardiovascualr disease

A

non modifiable:
increased age
male
fam hx

modifiable:
obesity
stress
alcohol
smoking
poor diet
low exercise
poor sleep

medical co morbiditits:
diabetes
ht
CKD
inflammation conditions- RA
atypical antipsycotic meds

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4
Q

preventions of cardiovascualr disease

A

optomise modifiable factors;
loose weight
stop smoking
stop alcholol
optomise medical co morbidiits

primary prevention- never had any cvd:
QRISK 3 score
if over 10% risk of having MI/stroke in 10 yrs then start them on a statin- atorvastatin 20mg at night

if had t1dm/ ckd for 10yrs or more then start on statin no matter their score

secondary prevention= patients developed MI, angina, TIA, stroke, peripheral vascualr disease :
4As
aspirin (and another antiplatlelt for 12 months - clopidogrel)
atenolol- or other beta blocker = titrate to max dose
atorvastatin 80mg
ACEi- titrated to max dose

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5
Q

checks for statins

A

check lipids after 3 months startijg
increase dose so aim to have 40% reduction in non HDL cholesterol- before increase dose though make sure they are adhering to their meds

do LFTs 3 months ater starting then 12 months- then no more
can casue rise in ALT and AST in first few weeks

stop if the rise is more than 3x the upper limit of normal

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6
Q

se for statins

A

muscle pain= myopathy- if pt muscle pain/weakness then check creatine kinase levels
T2DM
harmoerrhagic stroke- rare
constipation, diarrhoea
tendon damage
hepatits - feel flu like
pancreatitis - stomach pain

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7
Q

cardiovascualr disease

A

angina
MI
storke
coranry artery disease

due to athlerosclerosis

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8
Q

stable angina

A

insifficent blood supply not able to match the demand for it but relived on rest/ GTN spray

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9
Q

casues of stable angina

A

athleroscleorirs!!- late sign cus enoh so that its occluding some of the artery

vasosapsm
embolsim
ascending arotic dissection thats exaserbated by tachycardia, coranry arteritits eg. can get in SLE

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10
Q

presentation of stable angina

A

chest pain thats triggered on exertion/stress- anything that increases demand of heart
pain can be constricing, tight, dull, heavy
pain can radiate to arm/jaw
sob
dizzy
nausea
no pain can occur if neuopathy- b12 deficiency/diabetes

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11
Q

suspect pt stable anging qu to ask

A

rf for cvd- had before, diet, exercise, smoking, fam hist of heart/ atherlosclerosis
onset
trigger- doing at time
reliving factors- sitting
dizzy
nausea
sob
pain ofc
duration
how did you feel before- feel it coming on
how did feel after
loose consiousneess?

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12
Q

investigations for stable angina

A

diagnosist = ct coroanry angiogrpahy- involves contrast
physcial examination- heart sounds, bmi
fbc- anemia?
u and e- prior to startijg acei
lft- prior to starting statins
lipid profile
thyroid function
hba1c and fasting glucose- diabetes

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13
Q

managment of stable angina

A

ramp
refer to specialst
advise of managemnt and dx
medical managment- immediate + long term + 2 prevention
procsdures/surgical

medical:
immediate = GTN sprey when needed. if not gone after 5 mins use again. if after 2nd time pain not gone then ring 999

long term relief = betablocker- bisoprolol 5mg OD
or
CCB- amlodipine 5mg OD
if not controlled then can use both

other options for long term relieft that arnt first line:
long acting nitrates- isosoribide mononitrate
ivabradine
nicorandil
ranolazine

2ndry prevention:
aspirin 75mg OD
atorvastatin 80mg OD
acei
already on the beta blocker for the long term symtoom relive

procedural:
PCI with coronary angioplsaty - use acces via femoral/brachial artery so look for scars
or
CABG - slower recovery and more risk than pci

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14
Q

pt on statins and got muscle pains/ weakness

A

check creatine kinase as se can casue myopathy

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15
Q

pt is ill after pci from an mi

A

can have pappilary muscle rupture in mi so can casue murmur
Rupture of the papillary muscle due to a myocardial infarction → acute mitral regurgitation → widespread systolic murmur, hypotension, pulmonary oedema

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16
Q

why can an mi casue a murmur

A

Rupture of the papillary muscle due to a myocardial infarction → acute mitral regurgitation → widespread systolic murmur, hypotension, pulmonary oedema

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17
Q

cardiac tamponade ecg

A

electrical alternans
QRS morphology and amplitude changes as it swings in the pericardial fluid

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18
Q

cardiac tamponade presentation

A

becks triad- hypotension, rasied jvp, soft heart sounds
also esp if hx of chest trauma

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19
Q

pericarditis managment

A

first line- naproxen

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20
Q

ACS what in this category

A

unstable angina
NSTEMI
STEMI
= usally a result of a thrimbus from an athlerosclerotic plaque blocking a coronary a => normally made up of platelets hence antiplatelet meds treat

unstbale angina= no tissue damage. blocks off some of it at random times

STEMI = no blood at all. tissue death immediate and get changes to ecg as electrical activity changed

NSTEMI = some damage but not enough to affect electrical activity of heart in such a huge way

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21
Q

RCA supply and leads

A

r atrium
r ventricle
inferior aspect l venticle
psoterior septum
INFERIOR
II, III, aVF

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22
Q

II, III, aVF
affected

A

RCA- inferior aspect heart

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23
Q

LAD supply and leads

A

anterior apect heart
V1-V4
anteior L ventricle
anterior septum

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24
Q

circumflex artery supply and leads

A

lateral
I, aVL, V5-V6
l atrium
posterior aspect L ventricle

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25
Q

LCAsupply and leads

A

branches into circumflex and lad
anteriolaterlal
I, aVL, v3-v6

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26
Q

presentation of ACS

A

central constricting chest pain assocaite with:
nasuea and vomiting
dizzzy
palpitations
feeling impending doom
clammy and sweating
SO
ppain radiate to jaw/arm
CONTINUE AT REST FOR 20 MINS
if improve on rest then consider stable angina
silent MI - diabeteics may not have same sy ptoms- may not have the cp

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27
Q

investigations acs

A

ECG!
troponin- serial 0,6,12 hrs- rise
echo after to see functional damage
CT coroanry angiogram
CXR- asses for pulmonary odema and other cuases cp
examination
FBC- anemia
LFT
U E
thyroid funciton
lipid profile
HbA1c and fasting glucose

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28
Q

diagnosis of ACS

A

inital - ECG
if ST elevation/ new LBBB = STEMI
if no st eelveation or new LBBB then do tropnins levels
in raised troponin+/ other ECG changes (st depression, t wave inversion, pathological Qwave) = NSTEMI
if no raised troponin and normal ecg then unstbale angina - or consider other causes eg. MSK

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29
Q

ECG changes for STEMI

A

ST elevation in specific region
or
new LBBB
can haave raised tropnin too

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30
Q

ECG changes for NSTEMI

A

ST wave depression in spefic area
deep t wave inversion
patholigcal Q eaves- deep infarct and late sign
+/ raised troponin

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31
Q

ECG changes unstabel angina

A

non
normal troponin
= no tissue damage of heart occurs

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32
Q

when can torponin levels be raised

A

STEMI/NSTEMI - may not be. also rises 0,6,12 hrs
PE
sepsis
chronic heart failure
myocarditits
aortic dissection
=troponins are proteins found in cardiac muscle. rasied troponin doesnt mean ACS= they are non- specific

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33
Q

managemnt of ACS

A

mona
morphine
oxygen if less than 94%
nitrates- gtn be careful if low bp as vasodilator
aspirin- stat dose 300mg

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34
Q

managment acute stemi

A

300mg aspirin stat dose
then
if within 12 hrs of onset:
primary pCI: if available within 2 hrs of onset
thrombolysis: if PCI is no availbale within 2 hrs onset
- strpotokinase, tenecleplase, alteplase

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35
Q

managment of nstemi

A

BATMAN
Betablocker
Aspirin 300mg stat dose
ticagrelor 180mg stat dose (clopidogrel 300mg alternative)
moprhine
anticoagulant - LMWH- enoxaparin 1mg/kg twice dailiy 2-8 days
nitrates- gtn- relive coroanry artery spasm

GRACE score
if med/high risk of recurrence death then consider PCI within 4 days of admission

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36
Q

for all ACS secondary prevtion

A

6 As for ACS
Aspirin 75mg OD
Atenolol
another antiopaltelt for max 12 motnhs- clopidofrel/ticagrelor
atorvastatin 80mg OD
ACEi
aldosterone antagonist if heart failure - epelerone

also lifestyle changes- stop smoking, no alchol, healthy diet, exercise sloly

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37
Q

complications of ACS

A

septum tupture/ papillary muscle rupture- murmur
death
arythmia/ aneurysm
Dresslers syndrome

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38
Q

whats dresslers syndrome

A

also called post mycocardial infarction syndrome
usally within 2-3 weeks after MI
caused by localised immune system causing pericarditits
presentation:
pleuritc chest pain, low grade fever, pericardial rub on auscultiation
can casue pericardial effusion and rarely pericardial tamponade

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39
Q

dx of dresslers synfrome

A

recent mi
ECG= global ST elevation and T wave inversion
echo can show pericardial effusion
raised inlfam markers- CRP and ESR

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40
Q

managment of dresslers syndrome (pericarditits after MI)

A

NSAIDS-aspririn/ ibruprofen/ naproxen
more severe cases= prednisolone

may need pericardocentesis to remove fluid around ehart

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41
Q

whats acute LVF and pulmonary oedema

A

left ventricle is unable to adeqyatley pum blood out the heart and so get a backlog of blood into the pulmonary veins and lungs
the veins have lots p so become leaky and fluid leadks out and cant reabsirb fluid==> pulmonary oedema and have decreased gas cexchange

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42
Q

casues of acute LVF and pulmonary oedema

A

iatrogenic- agresive fluids in frail elderly pt with already impaired LV function
MI- damage ehart tissue so cant pump blood out as well
Arythmias
sepsis

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43
Q

presention of acute LVF and pulmonary oedema

A

rapid onset breathlessnes
exaserbated by lying down
improved on sitting up
cough with frothy white/pink sputum
increase rr
tachycardia
dec oxygen sats
look and feel unwell
T1 resp failure- low oxygen normal co2
3rd heart sound
bilateral basal crackles
hypotension in severe cases- cardiogenic shock

may also see s and s of underlying cause
eg.
chesp pain in ACS
faver in spesis
palpiatatins with arrythmua
may also have Rheart failire- raised JVP, periheral oedema of ankles, calves and sacrum

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44
Q

pt rapid onset sob
cough with frothy white/pink sputum
chest pain
nasusa
dizzy
clammy
tachycardia
bibasal crackles on ausculttion of lungs

A

left ventricular heart failure with pulmonary oedema due to MI

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45
Q

investifations for acute LVF and oulmonary odedma

A

if clinical presentation shows then initate rx bedre dx is confirmed
confrim dx= echo/BNP
ECG - ishcemia/ arrythmia
ABG
CXR- mau show cardiomegaly, upper lobe venous diversion (the backpressure casues the upper lobe veins to also be encorged with lbood even when standing= see increased prominence of diameter of upper lobe vessels in cxr), bilateral pleural effusions, fluid in interlobular fissures, kerley lines
bloods- infection, kidney function, BNP, troponin if suspect mi
Echo- ejection fraction above 50% mormla

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46
Q

whats normal ejection fraction

A

over 50%

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47
Q

cxr findings o acute LVF and pulmonary oedema

A

bilateral pleureal effusions
upper lobe venous diversion
kerley lines
cardiomegaly
fluid in interlobular fissures

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48
Q

when can bNP be rasied

A

BNP is senstiv ebut no specific= good for excluding LVF (stretching of the ventricles more than its range as blood cant leave it as heart overloaded.) but can be psotive and be due to other things

overloaded heart
PE
COPD
sepsis
tachycardia
renal impairment

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49
Q

managment of acute LVF and pulmonay oedema

A

pourSOD
pour away- stop- IV fluids
Sit up
Oxygen if needd - if unfer 95% - be careful if got copd
diuretics- IV furosemide 40mg stat

monitor fluid balace- measure fluid intake, measure urine output, u and e and daily body weight

if severe acute pulmonary oedema/ cardiogenic shock may:
iv opiates ans morphine vasodilate but not always
NIV- cpap
intubaion and ventilation
inotropes
- noradrenalin
strenghten force of cotraction of the heart - needs monitoring

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50
Q

chronic heart failure

A

impaired LVF results in chronic back pressure of bloodd

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51
Q

casues of chroninc heart failure

A

systolic heart failure- impaired lv contraction => alcoholism, myocardium, IHD, dilated cardiomyopathy

diastolic heart failure- impaired lv relaxation
stiff LV -> amylodosis, sarcoidosis, hypertrophyic cardiomyopathy

ischemia heart disease
arrythmia- AF
valvular heart disease- aortic stenosis
hypertension- excessive overload

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52
Q

presentation of chronic heart failure

A

sob worsened on exertion
cough - frothy white/pink sputum
orthopnea- breathlessness lying flat, relived sit or stanidng - ask re pilllows at night
paroxysmal nocturnal dynsponea- wake up at night
peripheral oedema

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53
Q

investigations chronic ehart failure

A

NT-proBNP
then alsso ecg, ehco - look at ejection fractonover 50% normal

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54
Q

what levels of NT-proBNP suggest chronic heart fiaure

A

over 2000ng/l - refer speciaislt immediate 2ww
400-2000ng/l- specialst in 6 weeks
for these two then see specialst and do TOE to see heart

if under 400ng/l then prob not heart failure and look for other causes

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55
Q

managment of chronic heart fialure

A

specialsit- withi 6 weeks, or wothin 2 weeks if over 2000ng/l
surgical rx if severe aortic stenosis/ mitral regurg
see heart failure specialst nurse
yearly flu and pneumococcal vaccine
stop smoking
optomise co morbidities
exercise as tolerated

medical:
give loop diuretics for congestive symptoms and fluid retention - furosemide 40mg OD
then if preserved ejection fraction: manage co morbiditis
if reduced ejection fraction =
ACEi + Bblocker as tolerated titrate up to 10mg OD for both
(if acei not tolerated can give ARB)

if depsite ACEi + Bblocker symtpoms persist add aldosterine antagonist - spironolcation and eplereone

monitor u and e start and any dose change as diruetics, acei and aldosterone antagnoiss can casue electroylte disrubances.

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56
Q

mode of action ACE i intermes of how help chronic heart failure
se

A

reduce angiotnesin II
vaodialtion and decrease fluid retenion and decrease sns=> decrease preload and afterload
dry cough
postrual hypotension
increase potassium = hyperkalaemia
renal impairment

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57
Q

mode of action of beta blockers in terms of for chronic heart fialure
se

A

decrease workload of heart
triggers remodelling

se
postrual hypotnsion
dizzy
bradycardia
= possible syncope

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58
Q

heart rate on ecg how calculate

A

over 100= tachy
under 60 brady

regular can do 300/no big squares between r-r interval

if irregular- then number of complexes X 6

is the rate irregualry irregular- eg. AF
or is it regularly irregular- some form of pattern

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59
Q

once done rate of heart on ecg then look at axis of heart

what is left/right axis deviaition and whats normal

A

normal= lead II most positive defelction

left axis deviation- I and III leaving eachother
I moat positive delfection
II and III negative delfection
= conduction abnomality

right axis deviation- I and III towards eachother
I negative delfection
III most postiive deflection
- r ventricular hypertrophy

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60
Q

once looked at axis deviation then look at P waves what look for

A

present?
QRS after each?
duration, direction and shape
no p wave? is there saw tooth- flutter
chaotic baseline- fibrillation
flat- no atrial activity

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61
Q

once looked at p wave then look at what

A

PR interval

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62
Q

PR interval whats normal

A

normal 3-5 small squares
if more than5 small squares- more than 0.2 seconds then AV block

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63
Q

types of AV block

A

fisst degree heart block = prolonged fixed PR interval

second degree heart block type 1= mobitz type 1= progressvily longer PR interval until eventually QRS dropped
then this repeats = longer longer longer and then non

secind degree heart block type 2= mobitz 2=
fixed prolonged PR interval (like first degree) but then also QRS compleze is intermittently dropped and repeat cycle - if dropped afer every 3rd then 3:1 if dropped aftr every 4th p the 4:1
(first degree heart block and secind degree t2 are similar in that they both have a fixed prologned PR interval but in secind degree goes that bit further and qrs drops)

third degree heart block= compete heartblock
no electrical communication between atria and ventricles and so have p waves and QRS complex but no asscoaition between them

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64
Q

fixed prolonged PR interval

A

frist degree heart block

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65
Q

progressviely longer PR interval then QRS drops

A

secind degree heart block type 1

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66
Q

fixed prolonation PR interval and then QRS intermittently drops

A

second degree heart block t2= mobitz2

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67
Q

p waves there
qrs there
no assocaition with timings of the teo

A

thrid degree-complete heart block

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68
Q

cor pulmonale

A

r sided heart fialure due to resp disease
increase pressure and resitance in pulmonary arteries= pulmonary ht
the right ventricle is unable to effectively pump blood out the right side of the heart
back pressure of blood in the right atrium, vena cavca, systemic venous system

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69
Q

casues of cor pulmoanle

A

COPD!!!- most coomon
PE
CF
interstial lung disease
primary pulmoanry ht
left sided heart failure can cause it due to casuing pulmonary oedema and ht and then have increase afterload for right heart and then r ventricular failure

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70
Q

presentation cor pulmoanle

A

early- asymtpomatic
SOB- hard to tell as they also have resp disease- but if its worsening sob DEFO THINK OF COR PULMOANLE
SOBOE
hypoxia
cyanosis
syncope
hepatomegaly- back pressure in hepatic veins - pulsatile in tricuspid regurg
3rd heart sound
murmurs- tricuspid regurg pansystolic murmur
peripheral oedema
rasied JVP
chest pain
congestion of peripheral tissues:
oedema and ascited
gi congestion- weight loss and anorexia as poor absorbtion due to oedematous gut
liver congestion- impaired liver function- jaundice etc in late stagea

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71
Q

managment of cor pulmoanle

A

ecg- may show r ventricular hypertrophy
fbc- may have it due to polycythemia
abg
bnp
thoracic mri

main thing is treat symtoms and underlyin casue
give oxygen therapy and prognosis is poor

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72
Q

pt has copd
no fever
increasing sob

differnetilas

A

exaserbaion of copd
cor pulmonale

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73
Q

pt has copd
have increasing sob
peripheral oedema
hepatomegaly

A

cor pulmonale

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74
Q

casues of hypertension

A

essenetial ht- primary- no casue
secondary ht:
Renal disease- renal artery stenosis - esp consider if not repsonding to rx
obesity
pregnacy-pre eclampsia
endocrine- esp conns (hyperaldosteronsism) - check renin: aldosterone ratio- high aldosterone low renin

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75
Q

hypertension values satge 1 and 2

A

normal bp is under 120/80

if under 140/90 at clinic then check bp cevery 5 years
if 140/90-179/119 at clinic offfer Abulatory bp / home bo reading for few weeks throughout diff times of day and asses for cv risk and organ damage

stage 1=
clinic 140/90
home/ambulatory 135/85

stage 2=
clinic 160/100
home/abulatory 150/95

if under 40 and stage 2 consider specialst evaulation of secondary causes

180/120 or more then urgent specilsit if got compliactions or suspect phaeochromocytoma

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76
Q

complicatios ht

A

ishcemia heart diseasa
vascular dementia
aneurysm
CKD- hypertensive nephropathy
hypertensive retinopathy
cerebrovascualr accident - haemorrhage/stroke
peripheral arterial disease
aortic dissection

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77
Q

BP targets for pt on treatment

A

80 or over:
clinic less than 150/90
home/ambulatory= less than 145/85

under 80:
- under stage 1 so
clinic= under 140/90
home/ ambulatory= under 135/85

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78
Q

treatment for hypertension

A

life style advice for all- dec salt less 6g per day, regular exercise, stop smoking

anyone woth T2DM or under 55 = ACEi (or ARB)
if over 55 or black/african carribean = CCB

add in the opposite or thiazide like diuretic:
anyone woth T2DM or under 55= ACEi (ARB) + CCB or thiazide like diurtic
if over 55 or black african carribean = CCB + ACEi (ARB) or thiazide like diuretic

all three:
ACEi (ARB) +CCB + thiazide like diuretic

confrim resitant ht with home/ ambulatory bp, check postural hypotension and adherenace if is still ghihg then:
expert adivce
or
add low dose spirinolcatone if K 4.5mm/l or less
or
add alpha blocker/beta blocker if K more than 4.5mm/l

expert if BP unctorlled on 4 drugs

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79
Q

pt on ACEi + CCB + thiazide like diruetic and still ht
what do

A

look at potassoum levels
if 4.5 or less then give spironolactone
if more than 4.5mm/l postassium in blood then give alpha blcoker/beta blocker

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80
Q

what can ht drugs do to potassoim

A

thiazide like diuretics= hypokalaemia
ACEi + aldosterone antagonsists (spirinolactone) = hyperkalaemia

= monitor u and e if on ACEi or all diuretics

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81
Q

indapamide drug

A

thiazide like diruetic

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82
Q

ccb drus

A

amlodopine
verapamil

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83
Q

ACEi frug

A

ramipril

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84
Q

ARB drug

A

candesartan

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85
Q

S1

A

sound of atrioventricular valves closing as ventricles start contraction- systole

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86
Q

S2

A

sound of pulmonary and aortic valve shutting as heart start diastole- end of systole

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87
Q

S3

A

can be normal in youg
sound of fast filling ventricles as then chordae tendiane pulled
can be sign of heart failure as ventrcels and chordae are stiff and so limit is faster met
just after S2

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88
Q

what fills theventricles

A

diastole of ventrciles- very important - as get older this decreases
systole of atria

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89
Q

S4

A

sound before S1 always abnormal

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90
Q

what casues left atrial hypertrophy

A

mitral stenosis- atria having to push harder to get blood thorugh

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91
Q

what casues left ventricular hypertrophy

A

aortic stneosis - ventricle have to push harder to get blood through aortic valve

92
Q

what casues left atrial dilatation

A

mitral regurgitation

93
Q

what casues left ventricualr dilitation

A

aortic regurgitation

94
Q

hypetrophy of heart is bad too becasue

A

becasue theres thickening outward sbut also inwards of the chamber so actually end up sometimes iwth less space in the ventricle

95
Q

mid diastolic low pitch murmur

A

mitral stneosis

96
Q

mitral stenosis heart murmur and assocaitions with mitral stensosis and casues

A

casue:
rheumatic fever
infective endocarditits

mid diastolic low pitched murmur
loud S1 as thick valves so need high force to shut them
can palpate tapping apex beat

assocaitaitons:
malar flush- blood no able g through into ventricle so back log in l atrium and so icnrease pressure in rthe pulmonary system and so increase co2 and vasodialtion occurs

AF- atria having to push hard to get blood through and so casues strain,electrical disruotion and result in fibrillation

97
Q

malar flush assocaited with which murmur

A

mitral stensosi

98
Q

AF asscoaited with which murmur

A

mitral stenosis

99
Q

pan systolic high pitch mumur

A

mitral regurigitation

100
Q

mitral refugitation murmur and other sigs and casueses

A

mitral regurg= as heart contracts the blood flows through leaky mitral valve back into the left atrium
so happening all the time throughout systole and systole casues high flow so high pitch
- pan systoluc, high pitch murmur thatcan radiate to axilla
may hear S3

results in congestive heart failure as reduced ejection fraction and back log of blood in left heart

casues:
idiopathic age weakening of valve
rheumatic heart disease
ischeia heart disease- MI!! can ruptur ppillary msucles
infective nedocarditis
CT disorders- marfan syndrome, ehlers danlos syndrome

101
Q

early diastolic soft murmur

A

aortic refurgitation

102
Q

aortic regurgitiation murmur and other s and s and casues and results in

A

early diastolic soft murumur
collpasing pulse as the pusle disappears as the blood flows back into the ventricles

results in heart failure as getting back log of blood and reduced ejection fraction
casues:
idiopathic age related weakess
ct disorders
marfans
ehlers danlos

103
Q

reguritation aortic and mitral have incommon

A

both resultin heart failure as getting back log in heart as blood comes backin
so have reducedejection fraction
casuses that are the same are CT disorders- marfans and ehlers danlos syndorme and idiopahtic age related weakenss

104
Q

ejection systolice high pitch

A

aortic stenosis - sound like jet of water

105
Q

aortic stenosis mrumur
other features and casues

A

ejection systolic- like jet of water as systole speed is slowwest at start and end so crescendo- decrescendo in character -
radiate to carotids slow risjing pulse and narrow pulse pressure
exertional synco[e as diff to maintain good flow to the brain

casues:
idiopahthic age related calcifications
rheumatic heart disease

106
Q

exertional syncope can be casued by which murmur

A

aortic stenosis

107
Q

collapsing pulse means whcih murmur

A

aortic regurigtation

108
Q

radiate to carotits murmur

A

aortic stensois

109
Q

aortic stensois
aortic regurg
mitral regiug
mitral stneosis
their murmur sounds

A

aortic stenosis= ejection sysstolic, high pitch (caortid radite)
mitral regurgitation= pan systolic high ptich (radiate to axilla)

aortic regurgitation= early diastolic soft (collasping pulse)
mitral stensois = mid diastolic, low pithc (malar flush and AF)

110
Q
A
111
Q

asses murmur

A

script
site
character
radiation
intensisty
pitch- velocity- low=low
high=hgih
timing- systolic/diastolc

112
Q

TAVI what scar

A

access to femoral artery

113
Q

lateral throactomy scar

A

mitral valve replaced

114
Q

life span bioprsotheitc and mechanical

A

bioprosthetic- 10 yrs
mechanical over 20

115
Q

whcih valve needs life long anticoagulant

A

mechanical

116
Q

what anticoagulant is used in life long anticoaggualtion for mechanical heart valves

A

warfarin
INR 2.5-3.5

117
Q

INR for warfarin for pt with mechanical heart valve

A

2.5-3.5

118
Q

click replaces S1 means which vlave repalced

A

click replaces S1= metallic mitral valve

119
Q

click repelaces S2 means whic valve repalced

A

click replaces S2= metallic aortic valve

120
Q

complications of mechanical heart valves

A

thrombus- hence neeing lifelong warfarin as anticoagulant
infective endocarditis
hameolyisis resulting in anemia due to blood churning in the valve

121
Q

what orgnaisms casue infective endocarditits in mechanical heart valves

A

gram postitve cocci
enterococcus
streptococcus
staphylococcus

122
Q

looking at QRS complex what need note

A

width
height
morphology

123
Q

what should width of QRS complex be

A

no more than 3 small squares - less than 0.12 seconds = narrow = supraventricular in origin

broad complex= more than 3 small squares.

124
Q

broad QRS complex could mean what

A

abnormal depolarsation sequence
eg. bundle branch block

125
Q

RBBB

A

V1= M
V6=W
raches lbb normally then once left depolasrisedthen goes round to right so have two r peaks due to delyas

126
Q

casues of RBBB

A

can be physiological
lung:
COPD
PE
Cor pulmonale
heart muscle disease
congential
MI

127
Q

LBBB

A

V1=W
V6=M
rach rbb and cant go down hiss to lef tso right depolasrises then oes round to left so two r peaks as not at same time

128
Q

casues of LBBB

A

always pathological
STEMI wih CP= MI
conduction system degeneration
myocardial issues:
sichemia heart disease
cardiomyopahty
vavlular heart disease

129
Q

whats bifascicular block

A

the left bundle branch then splits into anterior and posterior fasciles cus more mass on the left
bifascicular block = RBBB +block of one of the fasciles of the left bundle branch

130
Q

trifascualr block

A

bifascular block + 3rd degree heart block

131
Q

tall QRS complex means what

A

ventricualr hypertrophy or tall/slim person

132
Q

whats electrical albicans and casue

A

changes in height of the QRS
biggest casue is a big pericardial efusion as the ehart swings in the fluid

133
Q

morphology QRS- Q wave abnormality is what

A

delta wave- sign that the ventricles are being activated earlier than normal from a point distant to the AV node. The early activation then spreads slowly across the myocardium causing the slurred upstroke of the QRS comple
delta wave + tachycardia = WPW
= slurred upstroke of the QRS complex

134
Q

R wave should change how over the V leads

A

R wave smallest in V1 and largest V6

135
Q

when does the S wave becomesmaller than the R wave

A

S>R wave should swap to R>S wave in V3/V4

136
Q

if theres poor progressision of the R wave so that the S wave is still bigger than the R wave in v5 +v6 (r should become bigger than s wave at v3/v4)
what does this mean

A

poor progression of te R wave so that S>R in V5+V6 could mean previous MI or jsut that leads not on right places cus large person

137
Q

atrial fibrillation

A

disorganised electrical activity that overides the SAN
lack of coridoanted atria contraction
leads to irregular conduction of electrical impulses to ventricles

138
Q

key features of AF

A

irregularyl irregular ventricular contractions
no p waves
tahcycarda
can result in heart failure as got poor filling of the ventricles during diastole = lost the 25% of active diastole- where the atria contract

risk of ischemic stroke

139
Q

casues of af

A

vavlular af - pt with AF whi have mod/sever emitral stenosis / mechanical vavle = the mitral stenosis of the left atrium strecthes the cells apart so conduction and electrical acitivity of the cells becomes disorganised

mitral regurg can have same effect

non valvular AF= pts without valvular pathology

mrs SMITH:
sepsis= systemic inflamamtion, increase stress hormones, ANS dysfucntion. volume shifts
mitral valve pathollogy
Ischemic heart disease - damage cells and so damag ethe conduction pathways
thryotoxicosis- increase metabolsim, increase SNS
hypertension=dilates l atria strethcing the cells apart and fibrois of tissue=> decreased intercellular coupling

140
Q

presentation of AF

A

often asymptomatic
syncope- dizzy and faint
SOB
palpitations
symtpoms of associated conditions eg. sepsis, stroke, thryotoxicosis
irrregularly irregular pulse

141
Q

absent p waves
irregulary irregular
narrow QRS complex
tachycardia maybe

A

AF
or
ventricular ecoptics

142
Q

differentiate between AF and ventricualr ectopics

A

ECG
ventricular ecoptics goes when hr over a certain threshold
HR regular during exericse= ventricualr ectopics

143
Q

ECG AF

A

absent p waves
cant comment on pr interval
irregularly irregular
tachycardia maybe
narrow QRS complex - under 3 little squares- normal

144
Q

treatment of AF

A

rate or rhythma control
and do CHA2DS2 VAS to see if anticoagulate - if 1 consider antocoag
if over 1 anticoagulate

rate control = first line unless:
new onset AF- within 48hrs
remain symptomatic depsire rate control used
reversible causes
af casuing heart fialure

for RATE control:
beta blocker first line- atenolol- not sotalol
CCB- dilitazem- not in heart failure
digoxin- only in sedentary people and need monitoring due to toxicity

RHYTHM control:
use if reverisble casue
new onset within 48hrs
af causing heart failure
rate control used by still symptomatic

cardioversion or long term medicaion rythm control;
cardioverson can have electrical or pharmacological - can do immediate = if onset less than 48hrs or if haemodynamically unstable
or
delayed cardioversion- be on anticoagulant for at least 3 weeks as oonce back into normal rythm thrombus can dislodge and cause ischemic stroke

electricla- sedation/GA, defib
pharmacological:
flecanide
or
amiodarone if structual abnormalities of heart

long term med rhtym control:
beta blockers- first line
dronedarone - used second- mainitna normal rythm once had cardioversion
amiodarone - in pts with heart failure or left ventricular dysfucntion

145
Q

which drug use for pharmacolgical cardioversion of AF

A

flecanide
or
amiodarone if structurla abnomalities of heart

146
Q

rate control of AF

A

beta blockers- 1st
CCB- diltazem but not if heart fialure
digoxin- only sedentary people and need monitor

147
Q

long term medical rythm control

A

beta blockers first line
dronedarone - second line to maitnatin a normal ryhthm after cardioversion
amiodarone - in pts with heart failure/ left ventricular dysfunction

148
Q

paraoxysmal AF

A

AF comes and goes and doesn’t last more than 48 hrs

149
Q

tramtent of paroxysmal AF

A

do CHA2DS2 VAS - see if need anticoagulation
may have pill pocket rx- when feel it take flecanide - not if got atrial flutter as can casue 1:1 av conduction and cause significat tachycardia

  • need to know when symtpoms coming on
    need to understand when to take it
    not have any structual underlying abnomalitites of heart
150
Q

INR aim for pts on warfarin for af

A

2-3

151
Q

when to anticoagulate soemone with AF

A

do CHA2DS2 VAS score- if 1 consider antocoag
if over 2 anticoagulate

can do orbit score- risk of major bleed on anticoagulate

152
Q

warfarin or DOAC AF

A

warfarin inr need 2-3
avoid green leafy veg and cranberries and alcholol as got vit k in = issues
if needed can revers giving pt vitamin K
interactions with CYP450 as metabolise dusing it.
need monitor INR

DOAC- apizaban, rivaroxaban, dabigatran
dont need monitor
no reverse for it but shorter t 1/2 than warfarin of 7-15hrs (apixaban 12)
no major interactions
equal to warfarin to prevent stoke in AF
equal to warfarin at risk of bleeding

153
Q

CHA2DS2 VASc score

A

1- consider anticoagualtion for pt with AF
over 1 anticoagulate
congestive heart fialure
hypertnesion
age- over 75 score 2
diabetes
stroke / TIA previous score 2
vascualr disease
age 65-74
sex- female

154
Q

ORBIT

A

used to se risk of major bleed on antigoagulant
75 or over
bleeding hx
GFR under 60
rx with antiplatlet agents
Hb

155
Q

contraindications for pacemaker insitu

A

MRI scans
Electircal intervention- TENS machine
- diathermy in surgery

156
Q

indications for pacemaker

A

symptomatic bradycardia
severe heart failure- use biventricular pacemaker
hypertrophic obstructive cardiomyopathy -ICD
mobitz type 2 AV block
3rd degree heart block

157
Q

single chamber pacemaker

A

leads in one chamber- r atroum or L ventricle
R atroum= issue with SAN and av conduciton is normal

in L ventricle- issue with av conduction so stimulate ventricles directly

158
Q

dual chamber pacemaeker

A

leads in L ventricle and R atrium
allows synchornisation contraction of atria and ventricles

159
Q

biventricular pacemaker

A

triple chamber
in R atrium and L ventricle and R ventricles
used in heart fialure
all contract same time to optomise heart function
also called cardiac resynchornisation therpay pace maker - CRT

160
Q

implantable cardioverter defibrillator

A

monitors HR and then apply a defib shock to cardioverte pt back to sinus rythm if identifies a shcokable arrythmia

161
Q

what see on ECG if pt got pacemaker

A

vertical line either before p wave +/ QRS= pacemaker intervention cpmplex on all leads

162
Q

line before p wave

A

lead in atria

163
Q

line before QRS

A

lead in ventricle

164
Q

line before p wave or QRS what type pacemaker

A

single chamber pacemaker

165
Q

line before p and QRS what type pcemaker

A

dual chamber pacemaker

166
Q

treatment of symptomatic bradycardia

A

atropine

167
Q

what can you hear on asucultation of the heart in acute left sided heart fialure sometimes

A

S3

168
Q

triad of symtpoms for right sided heart failure

A

ankle oedmea
raised JVP
hepatomegaly

169
Q

what ECG change can be seen eith PE

A

RBBB

170
Q

what can casue pulsus paradoxus

A

= bp falls on inspiration (radial pulse will be harder to feel too)
anything that when breathe in air in so makes any pressure on the heart worse so harder to pump blood out:
cardiac tamponade
massive pericardial effusion
acute asthma
congestiv eheart fialure
COPD
pericarditits
tnesion pneumothroax

171
Q

ACEi contraindicated in what

A

pregnancy

172
Q

ECG bifasciular block

A

left axis deviation
RBBB

173
Q

pt has bp 180/120 or more. what do

A

asses for organ damage- fundocopy eg.
if got orgna damage start on meds
if not organ damage then repeat clinic bp readining within 7 days to see if they do have this ht

if they have:
retina haemoorhage/papilloedema
or
life threatening symtoms
or
suspect phaecromocytoma
then refer same day speciaslt

174
Q

statins must be temporaily held when starting what type of antibiotcs

A

macrolide eg. clarithromycin due to increased risk of rhabdomyolysis

175
Q

side efect of thiazide like diuretics

A

hypercalcaemia
= Stones Kidney or biliary stones
Bones Bony pain
Groans Abdominal pains
Thrones Constipation or frequent urination
Tones Muscle weakness and hyporeflexia
Psychiatric moans Depression, anxiety, confusion

176
Q

whats the cardiac arrest rhythms

A

shockable - VF, VT
non shockable- PEA, asytole

177
Q

treatment for any form tachycardia in unstable patient

A

3 shocks
consider amidodarone IV

178
Q

narrow complex tachycardias

A

AF
Atrial flutter
SVTs

179
Q

treatment summary for tachycardias narrow complex- stable

A

AF= rate control w/ beta blockers/ CCB (diltazem/verapamil)

atrial flutter = rate control w/ beta blocker

SVT= vagal mouveres then adenosine

180
Q

treatmnet for stbale broad complex tachycardia

A

VT/unclear= amiodarone IV

known SVT with BBB = treat as normal svt

irregular then may be a version of AF- go get advice

181
Q

whats atrial flutter

A

re entrant rhyty,s in either atrium
self perpetuating loop due to extra pathway

atri contract 300bpm
due to longer refractory period in ventricles- AVN- every second lap goes into the ventriclaes = 150bpm ventricular contraction

saw tooth appearance = lots of p waves

182
Q

asscoaited conidtions with atrial flutter

A

hyperthryoidism= thryortoxicosis
ischemic heart disease
cardiomyopathy
hypertension

183
Q

treatment for atrial flutter

A

rate control- beta blocker
/ cardioversion
treat underlying casue
radiofrequency ablation of the re entrant rhyth,
anti coag based on CHA2DS2VASc score

184
Q

casue of supraventricular tachycardias

A

electrical signal re entering the atria from the ventricles
ventricles–> atria–> AVN–> vetricular contraction –> atria
(normally doesnt go back to atria)

paroxysmal svt= svt reoccurs and remits in pt over time

185
Q

types of SVT

A

atrioventricualr nodal re entrant tachycardia= re entry point is back through the AVN

atrioventricular re entrant tachycardai= re entry point id an accesorry pathyway eg. WPW

atrial tachycarida= electrical signal originates not from SAN=> no caused by the rentry from vetricles

186
Q

ECG of SVT

A

p waves buried in QRS normally - so dont see p waves
normally narrow QRS complex
tachycardia
regular

may see the p wave just after the qrs or in or v rarely before

187
Q

acute managment of SVT if stbale

A

continous ECG monitoring
valsava manouvere- blow hard agasint resitance
then
carotid sinus massafe - one side
then
adenosine (alternative is verampil)
then
direct cardioversion f above all fails

188
Q

how does adenosine work in managment of SVT and cousnelling pt on it and CI

A

CI= asthma, copd, heart failure, heart block, severe hypertension

slows cardiac contraction through AVN = resets back to sinus rythma

need rapid bolus to ensure reaches the heart enoguh with impact to interpurt the pathyway => have a breif period of asytole/ bradycarida

warn pt of feeling scary dyng feeling/impending doom

fast iV bolus in large proximal cannula= grey in antercubital fossa
6mg then 12mg then 12mg if dont have imporvmanet after each one

189
Q

long term managment for pt woth paroxysmal SVT

A

have recurrig and remiting episodes of SVT

meds= b blockers, ccb, amiodarone
radiofrequency ablation

190
Q

wolf parkinson white syndrome

A

extra electrical pathyway connecting ventricles and atria- pathyway called bundle of kent
so once in ventricles it goes back to atria and keeps casuing re entry of electical activity so casues tachycardia and its above the ventricles so its called svt

191
Q

treatment of WPW

A

radiofrequency ablation of accesory pathway

192
Q

ECG shw for WPW

A

short PR - les than 3 small squares (not normal)
wide QRS- over 3 small squares (not nomral)
delta wave- surred upstroke of QRS
tachycardia cus its a form of SVT

193
Q

whta should not be given to patient who has WPW who also have AF/ flutter

A

antiarythmic meds in patient with WPW and atrial fibrillation/ flutter shouldnt be fiven
this is becasue the meds encouarge conudction through the acesory pathyway and so then can get a chaotic atrial activity and casue a polymorphic wide complex tachycardia

194
Q

what are arrhythmias

A

interuption f the normal electical signals that coordiante the contraction of the heart muscle

195
Q

whats radiofrequency ablation

A

cath lab
catheter in femoral vein
xray guided
test singlas
heat applied to remove source of arrhtymia- the extra pathyway eg.

196
Q

when can radiofrequecy ablation be used

A

AF
atrial flutter
WPW
SVT

197
Q

short PR
wide QRS
tachycardia
delta wave

A

WPW

198
Q

whats torsades de pointes

A

polymorphic (multiple shape) VT
normal VT but height of QRS vomplect is smaller then gets bigger etc

occurs in prolonged QT interva
get prolonged repolarasiation of the muscles after the heart contraction
the long waiting time means that get random spontaneous depolarisation in some areas of te heart myocytes

depolarisation spreads through the ventricles and leads to ventricular contraction prior to proper repolarisation (so some arnt able to contract so have smaller contraction and then bigger when all cells involved i think)

199
Q

torsades de pointes can progress to what

A

VT

200
Q

casyes of torsade de pointes

A

prolonged QT

201
Q

QRS complex get bigger then shorter then bigger
looks ike VT

A

torsades de points

202
Q

casues of prolonged QT

A

long QT syndrome= congenital
meds= antipsycotics, citalopram, felcanide, sotalol, amiodarone, macrolide abx

electroyle= hypomagensia, hypo calcaemia, hypocalaemia

203
Q

meds that casue prolonged QT

A

antipscyotics
felcanide
sotolol
macrolide abx
citalopram
amiodarone

204
Q

casues of rpolonged qt that are elecrtorylte disturbances

A

hypocalcameia
hypomageasmiea
hypokalameia

205
Q

manage acute torsade de pointes

A

correct casue
Mg infusion - eve in mg is normal
defib if progress to VT

206
Q

long term managment of prolonged QT

A

avoid meds that casue prolonged QT
correct electryolte disrubances
b BLOCKERS- not sotalol- cus casues prolonged QT
pace maker/ implanaable defib

207
Q

what are ventricular ectopics

A

premature ventricualr beats casued by random electircal discharges from outside the atria
random breif palpations

ECG shows indv random abnormal broad QRS complez n a background of a normal ECG

208
Q

whats bigeminy

A

v frequent ectopics- happen after every sinus beat (p, qrs then ectopic then again )

209
Q

patient has ectopic then sinus then ecopi then sinus. whats this

A

bigeminy

210
Q

abnormal broad complex, random
normal ecg othersie

A

ventricualr ectopics

211
Q

treatment of ventricular ectopics

A

bloods- see if anemia, electrylte disrubances, thryoid
reassure and dont treat if healthy person
get advice if pt has another ehart condition/ other fesatures eg. cp, syndope, fam hx of abrupt death, murmur

212
Q

which heart blocks are at risk of asytolw

A

mobitz type 2 and thrid degree ehart blco k

213
Q

first degree heart block

A

fixed prolonged PR interval - no isses with QRS

214
Q

mobitz type 1

A

progressviely prolonged PR interval and then eventually a QRS is dropped
= eventuallt rhe atrial impulse is not conducted so have drop of QRS

215
Q

mobitz type 2

A

fixed PR (can be normal or prolonged i thin)
have p wave marching on through same distance in between each p wave = fixed p wave and then will get intermittend drop of QRS
can have 3:1 block so every 3rd the qrs is dropeed

216
Q

fixed PR (can be normal or prolonged i thin)
have p wave marching on through same distance in between each p wave = fixed p wave and then will get intermittend drop of QRS
can have 3:1 block so every 3rd the qrs is dropeed

A

mobitz type 2

217
Q

progressviely prolonged PR interval and then eventually a QRS is dropped
= eventuallt rhe atrial impulse is not conducted so have drop of QRS

A

mobitx type 1

218
Q

fixed prolonged PR interval

A

first degree heart block

219
Q

no relationship between p and QRS

A

third degree heart block

220
Q

third degree heart block

A

no relationshiop between p and qrs. each are regular

221
Q

treatment for bradycarda and AVN block

A

stabe = observe
unstable or are at risk of asytole (mobitx type 2, 3rd degree heart block or had previous asytole):
atropine 500mcg IV

if dont imporve then atropine 500mcg IV - can repeat up to 6 doses
try pther inotropes- noradrenalin
treasncutaenous cardaic pacing - defib

222
Q

if high risk of asytole in bradycardia and AVN block rx

A

temporay transvenous cardiac pacing
permanent imlantable pacemaker

223
Q

vomiting, thoracic pain, subcutaneous emphysema. It commonly presents in middle aged men with a background of alcohol abuse.

A

boehaaeve sydnrome

224
Q

proximal aortic dissectin

A

An inferior myocardial infarction and AR murmur should raise suspicions of an ascending aorta dissection rather than an inferior myocardial infarction alone. Also the history is more suggestive of a dissection. Other features may include pericardial effusion, carotid dissection and absent subclavian pulse.

225
Q

cardiac tamponade becks triad

A

Beck’s triad of falling BP, rising JVP and muffled heart sound is characteristic of cardiac tamponade

226
Q

STEMI treatment

A

1-2-12 Rule for STEMI’

1 → Primary PCI is the #1 choice for STEMI if available.
2 → If transport to a PCI center takes more than 2 hours (120 minutes), opt for thrombolysis.
12 → For symptom onset within the last 12 hours, primary PCI is still an option even if thrombolysis was given.

227
Q

PT with heart failure with reduced ejection fraction has high bp
rx

A

beta blocker and acei first line

Medicine (11 decks)

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