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Phase 2a > cardio conditions > Flashcards

cardio conditions Flashcards

1
Q

define an abdominal aortic aneurysm (AAA)

A

dilation of abdominal aorta, >50%
usually diameter >3cm

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2
Q

epidemiology of AAA

A

M>F, more common elderly

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3
Q

risk factors of AAA

A

increasing age
M
atheroscelrosis
obesity
hypertension
diabetes
connective tissue disorder
family history

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4
Q

pathology of AAA

A

degradation of tunic media + adventitia= vessel dilation & loss of structural integrity
- mechanical stress on weakened tissue = dilation and rupture
-dilation of vessels disrupts laminar flow
AAA most commonly forms below level of renal arteries

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5
Q

presentation of AAA

A

asymptomatic
Sxs of rupture:
palpable, pulsatile abdo mass
tachy + hypotension
abdo pain
bruising
severe epigastric pain
hypovelemic shock

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6
Q

investigations for AAA

A

abdo ultrasound- >3cm/ ruptures= immediate management
CT angiogram

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7
Q

management of AAA

A

ruptured= urgent surgical repair using either open or EVAR (endovascular aneurysm repair)

unruptured= sympto- urgent surgical repair
asympto- surveillance + risk management

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8
Q

comps of AAA

A

AAA rupture
thromboembolism
fistula
abdo compartment syndrome
prog= 80 % mortality if ruptured

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9
Q

define acute pericarditis

A

inflammation of the pericardium

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10
Q

epidemiology of acute pericarditis

A

80-90% idiopathic
M>F
younger>older

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11
Q

causes of acute pericarditis (6)

A

viral- aka enteroviruses eg mumps, HIV, coxsackievirus = most common
TB
rheumatoid arthritis
uraemia secondary 2 kidney disease
Dressler syndrome- past MI inflammation
hypothyroidism
malignancy

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12
Q

risk factors for acute pericarditis

A

male
20-50 years
past MI
bacterial/viral infections
trauma

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13
Q

pathology of acute pericarditis

A

inflammation= narrowed pericardial space
inflamed layers rub against each other - increasing inflammation
pericardial effusion since serous pericardium can’t remove fluid quick enough
effusion due to xtra fluid needed 2 compensate for friction
severe effusion=cardiac tamponade

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14
Q

presentation of acute pericarditis

+ECG changes

A

sudden, sharp, severe & pleuritic chest pain
- pain is relieved sitting forward, worse when lying flat
pericardial rub- squeaky sound when patient leans forward, listen @ sternal edge

dyspnoea
hiccups due to irritated phrenic
tachycardia
tachypnoea
fever

ECG changes= saddle shape + concave ST elevation, PR depression

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15
Q

investigations for acute pericarditis

A

ECG- saddle shape & concave ST elevation, PR depression, T wave flattening
chest xray-water bottle hear
echocardiogram- effusion
bloods (increased WCC + ESR)
other= serum troponin

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16
Q

differential diagnosis for acute pericarditis

A

MI
pneumonia
pulmonary embolus

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17
Q

management of acute pericarditis

A

sedentary activity until symptoms + ECG/CRP improve
1 NSAID/aspirin + colchicine (antinflammatory)

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18
Q

complications of acute pericarditis

A

pericardial effusion
cardiac tamponade
chronic constrictive pericarditis

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19
Q

define aortic dissection

A

tear in the intima of the aorta

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20
Q

epidemiology of aortic dissection

A

M>F, 50-70 yrs

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21
Q

pathology of aortic dissection

A

tear in the intima of the aorta- this causes blood to flow into new, false channel between tunica intima & tunica media
blood spreads thru false channel & can occlude flow thru branches of aorta

type A- tear in ascending aorta before brachiocephalic
type B - tear in descending aorta after L subclavian

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22
Q

risk factors for aortic dissection

A

HYPERTENSION
smoking
family history
trauma
obesity + sedentary lifestyle
connective tissue disorders
narrowing of aorta
pregnancy

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23
Q

presentation of aortic dissection

A

sudden + severe ripping/tearing chest pain
syncope
musc weakness
diff in BP between arms- >10mmHg
tachy + hypotension
diastolic murmur
radial pulse deficit
focal neurological deficit’s
inter scapular pain

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24
Q

Investigations for aortic dissection

A

1st- ECG, ST depression
chest x-ray (widened mediastinum)
TTE echocardiogram

gold = contrast enhanced CT angiogram
other= transoesophageal echocardiogram

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25
Q

differential diagnosis for aortic dissection

A

MI, cardiac arrest, pericarditis

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26
Q

management of aortic dissection

A

Type A- urgent open surgical reapir/stenting
beta blocker eg IV labetalol

Type B- conservative management (bed rest + analgesia
beta blocker eg IV labetalol
TEVAR (thoracic endovascular aortic repair

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27
Q

complications of aortic dissection

A

aortic regurgitation
MI
stroke
renal failure
cardiac tamponade
haemorrhage and shock

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28
Q

define aortic regurgitation

A

leakage of blood into L ventricle during diastole due to ineffective closing of the aortic valve cusps

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29
Q

epidemiology of aortic regurgitation

A

M>F
40-60 yrs

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30
Q

causes of aortic regurgitation

A

rheumatic heart disease
infective endocarditis- causes valvular damage
connective tissue disorders eg, Marfan’s, Ehlers-Danos
congenital

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31
Q

pathology of aortic regurgitation

A

as blood leaks from aorta into L ventricle- L vent blood vol increases, therefore stroke vol increases + systolic BP increases

during diastole- lower blood vol in atria
high systolic + low diastolic pressure= hyperdynamic circulation

overtime- increases in blood vol in L vent cause it to undergo eccentric ventricular hypertrophy

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32
Q

presentation of aortic regurgitation

A

bounding pulse/waterhammer pulse
wide pulse pressure
de musset’s= head bobbing with each beat due to severe bounding pulses
Quincke’s sign= pulsation of capillary beds in finger nails die to bounding pulses
Austin Flint murmur= rumbling diastolic murmur, fluttering of mitral valve due to regurgitant streams
LV hypertrophy seen on imaging

dyspnoea
chest pain
palpitations
syncope

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33
Q

investigations for aortic regurgitation

A

1st- ECG,(non spec ST/T wave changes) chest x-ray= cardiomegaly + enlarged aortic root

gold= echocardiogram- can see origin of regurgitant jet & its width, detection of aortic valve pathology & compensatory changes eg LV hypertrophy & function

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34
Q

differential diagnosis for aortic regurgitation

A

mitral regurgitation
aortic stenosis
infective endocarditis

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35
Q

management of aortic regurgitation

A

aortic valve replacement surgery (SAVR) if symptomatic or asymptomatic with ejection fraction >50%
if unsuitable can use TAVI (transcatheter aortic valve implantation)

vasodilators eg ACE inhibitors, ramipril (sympto only)

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36
Q

complications of aortic regurgitation

A

heart failure
pulmonary oedema & cardiogenic shock

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37
Q

define aortic stenosis

A

obstruction of blood flow across aortic valve due 2 narrowing, therefore L vent can’t eject blood properly in systole

can be supravavular- fibrous ridge above valve
or subvalvular - fibrous ridge is below valve

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38
Q

congenital causes of aortic stenosis

A

congenital bicuspid aortic valve, congenital aortic stenosis

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39
Q

risk factors for aortic stenosis

A

> 60 yrs
hypertension
hypercholesterolaemia
smoking
diabetes
rheumatic heart disease

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40
Q

pathology of aortic stenosis

A

aortic valve doesn’t fully open:
mechanical stress over time> damages endothelial> calcification + fibrosis=hardens valve & makes it more difficult to open completely

bicuspid valve- 2 leaflets instead of 3, therefore more stress on just 2

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41
Q

presentation of aortic stenosis

A

SAD:
-syncope
-angina
-dyspnoea

ejection click- valve snapping open due 2 high pressure from L vent
ejection systolic crescendo-decrescendo murmur

slow rising carotid pulse + decreased pulse amplitude

soft/ absent 2nd heart sound + prominent S4 heart sound

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42
Q

investigations for aortic stenosis

A

1st- ECG = L vent hypertrophy (deep S waves in V1 & V2, tall R waves in V5 &V6)
chest x-ray (pulmonary congestion)

gold- echocardiogram + doppler= L vent size + function & doppler derived gradient and valve area

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43
Q

differential diagnosis for aortic stenosis

A

hypertrophic cardiomyopathy, ischaemic heart disease

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44
Q

management of aortic stenosis

A

surgery if symptomatic

lower risk patients= SAVR (surgical aortic valve replacement
higher risk patients= TAVI (transcatheter aortic valve implantation

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45
Q

complications of aortic valve stenosis

A

heart failure
sudden cardiac death
infective endocarditis
ventricular arrhythmia
microangiopathic haemolytic anaemia

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46
Q

define atrial fibrillation (AF)

A

supraventricular tachycardia caused by uncoordinated, rapid and irregular atrial activity- results in an irregularly irregular ventricular pulse

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47
Q

causes of AF

A

heart failure
hypertension
coronary artery disease
valvular disease-mitral stenosis
cardiac surgery
cardiomyopathy
idiopathic

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48
Q

risk factors for AF

A

> 60 yrs
hypertension
T2DM
heart failure
past MI

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49
Q

pathology of AF

A

disorganised electrical activity overrides sinoatrial node activity- causes uncoordinated, rapid and irregular contraction of atria
300-600 bpm

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50
Q

presentation of AF

A

irregular pulse
tachycardia
palpitations
ECG- no p waves & narrow QRS
apical pulse> radial rate
irregularly irregular ventricular contractions
thromboembolism

asymptomatic
chest pain
palpitations
dyspnoea
fainting

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51
Q

investigations for AF

A

ECG=
-absent p wave
-irregualr R-R intervals
-narrow QRS

other=FBC
clotting profiles, U&Es

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52
Q

differential diagnosis

A

atrial flutter
wolff-parkinson-white syndrome
atrial tachycardia

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53
Q

management of AF

A

haemodynamically unstable- direct current cardioverison, shocks AF to sinus rhythm

haemodynamically stable- rate control beta blockers (bisoprolol, metoprolol) or CCB (verapmil/diltiazem) + digoxin
rhythm control w electrical or pharmacological (flecainide)
cardio version + precardioversion anticoagulant

long term= catheter ablation

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54
Q

monitoring for AF

A

CHA2DS2- VASc score - 2 calculate stroke risk
if score= <2, anticoagulant required

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55
Q

complications of AF

A

acute stroke
MI
congestive heart failure

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56
Q

define atrial flutter

A

macro re-entrant atrial tachycardia caused by organised electrical activity in the atrium with a rate of 250-350 bpm

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57
Q

causes of atrial flutter

A

idiopathic
CHD
heart failure
hypertension
COPD
pericarditis

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58
Q

pathology of atrial flutter

A

originates from a re-entrant circuit around the tricuspid valve annulus
short circuit causes the atria to fire rapidly

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59
Q

presentation of atrial flutter

A

ECG=
flutter waves, saw tooth pattern (F waves)
often 2:1 block (2 p waves for every QRS
tachycardia (above 150bpm)

palpitations
dyspnoea
chest pain
dizziness
syncope
fatigue

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60
Q

investigations for atrial flutter

A

ECG= saw tooth pattern (flutter waves)
2:1 block (2 P waves for every QRS

other= FBC

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61
Q

differential diagnosis for atrial flutter

A

AF, atrial tachycardia

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62
Q

management of atrial flutter

A

haemodynamically unstable-= DC cardio version
haemodynamically stable=
1. rate control (beta blocker) + anticoagulant
2. electrical cardio version
3. pharmacological cardioversion

ongoing- catheter ablation 2 remove faulty electrical pathway

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63
Q

monitoring of atrial flutter

A

CHA2SD2-VASc for stroke risk

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64
Q

define bundle branch block

A

a block in the conduction of one of the bundle branches- therefore the ventricles don’t receive impulses @ the same time

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65
Q

causes of RBBB

A

pulmonary embolism
ischemic heart disease
atrial or ventricular septal defect

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66
Q

causes of LBBB

A

ischemic heart disease
valvular disease
cardiomyopathy
cardiac surgery

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67
Q

pathology of RBBB

A

depolarisation only occurs through the LBB, LV depolarises normally
RV walls eventually depolarised by LBB in slower + less effective pathway
creates= second R wave in V1 + slurred S wave (V5-6)

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68
Q

pathology of LBBB

A

depolarisation only occurs in RBB, RV depolarises normally
LV walls eventually depolarised by RBB in slower + less effective pathway
creates= second R wave in V6 + slurred S wave (V1-2)

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69
Q

presentation of BBB

A

asymptomatic
syncope

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70
Q

investigations for BBB

A

William marrow

RBBB: MaRRoW
M in V1
W in V6 (slurred S)
wide QRS

LBBB: WiLLiaM
W in V1 (slurred S)
M in V6
wide QRS

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71
Q

management of BBB

A

usually no treatment

treat hypertension, pacemaker, cardiac resynchronisation therapy (CRT)

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72
Q

define cor pulmonale

A

right sided heart failure caused by respiratory disease

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73
Q

causes of cor pulmonale

A

COPD
pulmonary embolism
interstitial lung disease
cystic fibrosis
primary pulmonary hypertension

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74
Q

pathology of cor pulmonale

A

increased pressure + resistance in the pulmonary arteries (pulmonary arteries)= R vent unable to effectively pump blood out of vent + into pulmonary arteries - leads to back pressure of blood in R atrium + vena cava + systemic venous system

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75
Q

presentation of cor pulmonale

A

shortness of breath
peripheral oedema
chest pain
hypoxia
cyanosis
raised JVP
3rd heart sound
murmurs
hepatomegaly
syncope

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76
Q

investigations for cor pulmonale

A

1st=
ABG (hypoxia + hypercapnia)
spirometry
chest CT
echocardiogram

gold= right heart catheterisation

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77
Q

management of cor pulmonale

A

treat symptoms + underlying cause
long term O2 therapy
treat heart failure
venesection (reduces RBCs) if haemltocrit >55
consider heart-lung transplantation in young patients

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78
Q

complications of cor pulmonale

A

tricuspid regurgitation
hepatic congestion
cardiac cirrhosis
death

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79
Q

prognosis of cor pulmonale

A

50% 5 year survival

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80
Q

define deep vein thrombosis (DVT)

A

the formation of a blood clot in the deep veins of the leg or pelvis

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81
Q

causes of DVT

A

virchow’s triad: reduced blood flow, endothelial injury, venous stasis

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82
Q

risk factors for DVT

A

virchow’s triad
age, >40 yrs
smoking
drugs: combined contraceptive pill, HRT, tamoxifen
immobility
pregnancy
trauma
malignancy
polycythemia
antiphospholipid syndrome (thrombophilia)

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83
Q

pathology of DVT

A

majority occur in lower legs, below calf- can impede minor veins
more serious occur above calf, can occlude major veins eg superficial femoral, impeding distal flow
thrombus can embolise from deep veins 2 vena cava>R side of heart>pulmonary arteries and cause a pulmonary embolism

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84
Q

presentation of DVT

A

unilateral calf pain, redness and swelling
tenderness
pitting oedema
dilated superficial veins
erythema
cyanosis

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85
Q

investigations for DVT

A

measure circumference of calf 10cm below tibial tuberosity- more than 3cm diff= significant

1st- Wells score 2 calculate DVT risk, scores of ≥ 2= high risk

unlikely DVT- D-dimer test (looks 4 fibrin breakdown products + clotting problems)
if D-dimer raised- order doppler ultrasound of leg

likely DVT- order doppler ultrasound (unable to compress vein= clot)

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86
Q

management of DVT

A

1st- DOAC anticoagulation: apixaban or rivaroxaban

long term: LWMH (low molecular weight heparin)
DOAC (direct oral anticoagulants)/warfarin
compression stockings
treat underlying cause

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87
Q

prevention of DVT

A

compression stocking
calf exercises during periods if immobilisation
LMWH

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88
Q

define heart block

A

AV involves partial or complete interruption of impulse transmission from atria to ventricles

types:
1st degree
2nd degree Mobitz type1
2nd degree Mobitz type 2
3rd degree (complete)

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89
Q

causes of heart block

A

1st degree: AV blocking drugs, beta blockers, CCB,, digoxin
2nd degree Mobitz type 1: AV blocking drugs, inferior MI
2nd degree Mobitz type 2: drugs MI rheumatic fever
3rd degree: MI, hypertension, structural heart defect

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90
Q

risk factors for heart block

A

coronary artery disease
cardiomyopathy
fibrosis

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91
Q

pathology of diff types of heartblock

A

1st; consistent prolongation of PR interval due to delayed conduction via AV node- every P wave followed by QRS

2nd mobitz type 1; progressive prolongation of the PR interval until the atrial impulse isn’t conducted and a QRS is dropped- AVN conduction begins with next beat and sequence repeats

2nd mobitz type 2; consistent prolonged PR interval duration with intermittently dropped QRS complexes due to failure of conduction, PR interval is constant, but every 3rd/4th QRS complex is dropped

3rd (complete); no communication between atria and ventricles due 2 complete failure of conduction. P waves and QRS complexes have no association due to atria and vents functioning independently

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92
Q

presentations of heart block

A

1st= asymptomatic
2nd mobitz type 1= asymptomatic/bradycardia, syncope, irregular pulse
2nd mobitz type 2= palpitations, syncope, regular irregular pulse
3rd= palpitations, syncope, irregular pulse, bradycardia, chest pain, shortness of breath

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93
Q

investigations for heart block

A

ECG:

1st- every P followed by QRS, prolonged PR (>200ms)
regular rhythm

2nd, type 1- progressive lengthening of PR interval until a QRS is dropped + cycle repeats with shorter PR interval, irregular rhythm

2nd, type 2- constant enlarged PR interval, every nth QRS is missing, irregular rhythm

3rd- P waves + QRS complexes= random
PR interval absent due 2 atria-ventricle dissociation

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94
Q

management of heart block

A

1st-
asymptomatic= no treatment
symptomatic= pacemaker

2nd, type 1= asymptomatic= no treatment
symptomatic= pacemaker

2nd, type 2= pacemaker

3rd= IV atropine/isoprenaline + permanent pacemaker

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95
Q

define general heart failure

A

inability of the heart to deliver oxygenated blood to tissues at a satisfactory rate for the tissues metabolic requirements

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96
Q

define systolic heart failure

A

failure of the heart to contract efficiently to eject adequate volumes of blood
ejection fraction= <40%

heart failure w reduced ejection fraction- HFrEF

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97
Q

define diastolic heart failure

A

inability of the ventricles to relax and fill normally- causes increased filling pressures
ejection fraction=>50%

heart failure w preserved ejection fraction- HFpEF

98
Q

define right heart failure

A

inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion

99
Q

define left heart failure

A

inability of left ventricle to pump adequate amount of blood leading to pulmonary circulation congestion and oedema

100
Q

causes of heart failure

A

ischaemic heart disease, hypertension, cardiomyopathy, alcohol excess, valve disease

RHF: pulmonary hypertension, pulmonary embolism, COPD, cor pulmonale

LHF: CAD, valve defect, myocardial infarction, congenital heart defects, arrhythmias

101
Q

risk factors for heart failure

A

older
M>F
obesity
previous MI

102
Q

pathology of heart failure

A

stroke vol requires adequate preload 4 optimal myocardial contractility (Frank-Starling mechanism)+ decreased after load
-reduced cardiac output(heart failure)>decreased preload, decreased contractility, increased afteroad, decreased heart rate

2 maintain CO- compensatory changes needed=
increased SNS (increases HR + contractility
nattriuretic peptide (diuretic, hypotensive, vasodilators)
increased RAAS (increased fluid retention= increased preload)

compensatory mechanisms become exhausted + pathological=
SNS + RAAS also cause vasoconstriction > increases after load + myocardial work> increased cardiac work damages myocytes`. reduces CO= heart failure

103
Q

presentation of LHF

A

pulmonary oedema

LHF: bibasal pulmonary crackles, 3rd & 4th heart sounds, cardiomegaly (displaced apex beat), tachycardia

dyspnoea
orthopnoea
poor exercise tolerance
fatigue
nocturnal cough (pink frothy sputum)
wheeze
cold peripheries

104
Q

presentation of RHF

A

peripheral oedema

RHF: raised JVP, hepatomegaly, pitting oedema, weight gain (fluid)

ascites
nausea
anorexia
facial engorgement
epistaxis

105
Q

investigations for heart failure

A

1st:
ECG
BNP (brain natriuretic peptide= elevated)- released from myocardial walls under stress
chest x-ray (ABCDE- alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessels, effusions (pleural)

gold: echocardiogram
other= FBC

106
Q

management of heart failure

A

1st= ABAL
A- ACE inhibitor (ramipril)
B- Beta blocker (bisoprolol)
A- aldosterone antagonist (spironolactone)
L- loop diuretic (furosemide)

consider cardiac resynchronsiation therapy
surgery= LVAD, cardiac transplantation

107
Q

complications of heart failure

A

pleural effusion
actue kidney injury
sudden cardiac death

108
Q

prognosis for heart failure

A

50% die within 5 years of diagnosis

109
Q

define hypertension

A

persistent elevation of arterial BP
≥140/90 mmHg in clinic
≥ 135/85 mmHg for ambulatory or home readings

primary or secondary

110
Q

non modifiable risk factors for hypertension

A

age
Family history
ethnicity (afro-caribbean)

111
Q

modifiable risk factors for hypertension

A

obesity
sedentary life style
alcohol excess
smoking
high sodium intake (>1.5g/day)
stress

112
Q

pathology of primary hypertension

A

no known underlying cause- 90-95% of cases
some contributing factors=
-genetics
-excessive SNS activity
-abnoramlities of Na+/K+ membrane transport
-high salt intake
-abnormalities in RAAS

113
Q

pathology of secondary hypertension

A

indicates an unknown underlying cause including:
-renal diseases
-endocrine disorders
-medications (glucocorticoids, contraception)
-pregnancy (pre-eclampsia)

114
Q

presentation of hypertension

A

most often asymptomatic

malignant hypertension- ≥180/120 mmHg
- headache
-visual disturbance
-cardiac symptoms
-oliguria/polyuria

secondary hypertension- signs of the underlying cause eg hyperthyroidism causes weight loss, sweating, palpitations, etc

115
Q

investigations for hypertension

A

measure BP:
stage 1=
≥140/90 - clinic
≥135/85- ABPM

stage 2=
≥160/90-clinic
≥150/95- ABPM

stage 3=
≥180/120- clinic

ambulatory BP- worn 24hrs
other=
fundoscopy (HTN retinopathy
albumin:creatinine ratio(proteinuria)
bloods (HbA1c, GFR, lipids)
ECG

116
Q

management of hypertension

A

1- lifestyle mods
T2DM or <55 yrs= give ACWI eg ramipril
>55 yrs or black/ afro caribbean= CCB (calcium channel blocker) eg amlodipine

2 ACEi + CCB

3 ACEi + CCB + thiazide-like diuretic

  1. if k+ >4.5 add alpha or beta blocker to 1,2 & 3
    if K+ <4.5 add aldosterone antagonist eg spironolactone

other= direct renin inhibitors for patients intolerant to norm antihypertensives

117
Q

monitoring of hypertension

A

measure BP every 5 yrs
more often for patients on borderline of diagnosis (140/90)

118
Q

complications of hypertension

A

CAD
cerebrovascular incident
congestive heart failure
CKD
hypertensive retinopathy

119
Q

define infective endocarditis (IE)

A

infection of heart valves + other endocardial lined structures of the heart (chord tendineae, sites of septal defects etc)

types=
-left sided native (mitral or aortic)
-left sided prosthetic
-right sided
-device related, eg pacemaker, defibrillator

120
Q

epidemiology of infective endocarditis

A

elderly
young IV drug users
congenital heart disease
anyone w prosthetic valve
rheumatic fever
surgery
poor dental hygiene
iv catheter
immunosuppression

121
Q

what causes infective endocarditis

A

bacteria

s.aureus (common in IVDU, T2DM, surgery)-normally acute
s. viridans (poor dental hygiene)-normally subacute
enterococci/s. bovis
HACEK organisms
fungi

122
Q

pathology of infective endocarditis

A

abnormal/damaged endocardium creates turbulent flow- endothelium is damaged> exposes underlying collagen + tissue factor- platelets + fibrin adhere= forms a thrombus (nonbacterial thrombotic endocarditis)
if bacteria attach to thrombus (vegetation)- becomes ineffective endocarditis

123
Q

presentation of infective endocarditis

A

heart murmur- due 2 turbulent blood flow
splint haemorrhages -red lines under nails
Osler’s nodes- painful nodules on fingers/toes
Janeway lesions- painless plaques on palms & soles
Roth’s spots- retinal haemorrhages
fever
weight loss, fatigue
valve disfunction therefore arrhythmia + heart failure
embolism
night sweats

124
Q

investigations for infective endocarditis

A

1st=
inflammatory markers- raised WCC, ESR,CRP
blood cultures (positive)
transthoracic echo- vegetation
FBC- anaemia, neutrophilic
ECG- prolonged PR interval

Duke’s criteria:
needs 2 major OR 1 major & 3 minor OR 5 minor

MAJOR=
positive blood culture organisms typical of IE
evidence of endocardial involvement
MINOR=
risk factors
fever
vascular phenomena
immune phenomena
microbio evidence

other= transoesophageal echo if transthoracic doesn’t show IE

125
Q

management of infective endocarditis

A

1st- IV antibiotics based on cultures via either central line or PICC

s.aureus= beta lactam/vancomycin + rifampicin + gentamicin
s.viridans= beta lactam/vancomycin + gentamicin
s.bovis/enterococci= beta lactam/vancomycin + amino glycoside

surgery 2 remove infective tissue + repair and replace infected valves, remove large vegetations before they embolism

126
Q

complications of infective endocarditis

A

vegetations embolising causing stroke, MI, PE, heart failure, sepsis

regurgitation due 2 damaged valves

127
Q

define mitral regurgitation

A

incompetence of the valve leading to back flow of blood from the LV to LA during systole

128
Q

risk factors for mitral regurgitation

A

F
>age
connective tissue disorders (marfans, Ehlers-danlos)
prior mi
infective endocarditis
rheumatic fever
cardiomyopathies
medications
myxomatous degeneration (floppy valve)

129
Q

pathology of mitral regurgitation

A

mitral valve prolapse=
myxomatous degeneration (weakening of connective tissue)
when high pressure on valve- chordae tendinae are stretched/rupture- leaflet can fold back up into LA

damage to papillary muscles post MI= they can no longer anchor chordae tendinae

L ventricle overload due 2 hypertension
L sided heart failure

130
Q

presentation of mitral regurgitation

A

mid-systolic click (in mitral prolapse)
pan-systolic murmur- leaking of blood in LA
soft S1- incomplete closure of valve
additional S3 sound- rapid filling of dilated vent
apex beat displaced laterally
systolic thrill
tachycardia
signs of heart failure
dyspnoea + orthopnoea due 2 pulmonary hypotension
fatigue + malaise due reduced CO
palpitations
exercise intolerance

131
Q

investigations for mitral regurgitation

A

1st
ECG- LA enlargement (M shaped P waves)
chest x-ray= LA enlargement, pulmonary oedema in acute

gold= echo
estimation of LA, LV size and function

132
Q

management of mitral regurgitation

A

1st= surgery if symptomatic/ asymptomatic with ejection fraction <60% or LV end-systolic diameter >40mm

surgery = valve repair OR replacement

medication:
BB eg atenolol/calcium channel blockers/digoxin

vasodilators ef ACE inhibits (ramipril or hydralazine)
antigoacualtion for AF
diuretics for fluid overload eg furosemide or spironolactone

cardiac resynchronisation therapy (CRT)

133
Q

complications of mitral regurgitaiton

A

L sided heart failure
AF
infective endocarditis
congestive heart failure

134
Q

define mitral stenosis

A

narrowing of mitral valve orifice, making it difficult for blood to flow from the LA to LV in diastole

135
Q

risk factors for mitral valve stenosis

A

s. pyogenes infection leading 2 rheumatic heart disease
M>F

136
Q

causes of mitral stenosis

A

rheumatic fever- inflammation cause leaflets to fuse together
congenital
mitral annular calcification

137
Q

pathology of mitral stenosis

A

increased vol of blood in LA= higher pressure in LA- causes LA to dilate + allows blood to back up into pulmonary circulation (pulmonary congestion + oedema)
-resulting in pulmonary hypertension & R sided heart failure

as LA dilates- must walls stretch + pacemakers become more irritable - increases risk of AF

138
Q

presentation of mitral stenosis

A

AF
malar flush (due to vasoconstriction responding 2 reduced CO)
sign of right sided heart failure
signs of pulmonary hypertension
loud S1 snap- valve opening under high pressures
dyspnoea
reduced exercise tolerance
haemoptysis- (coughing up blood) due to ruptured bronchial vessels from elevated bronchial pressure
angina
dysphagia- if atria presses on oesophagus
partner syndrome- horse voice due to dilated atria causing left recurrent laryngeal nerve palsy

139
Q

investigations for mitral stenosis

A

1st=
ECG- AF + LA enlargement, M shaped p waves
chest x-ray- LA enlargement
pulmonary vessel congestion

gold=
echo- asses mitral valve mobility, gradient + orifice area, hockey stick shaped mitral deformity

140
Q

treatment for mitral stenosis

A

diuretics 2 relieve LA pressure
BB eg atenolol & digoxin (control heart rate + prolong diastolic filling)
CCB
anticoagulants due to risk of thrombus formation

surgery= mitral balloon valvotomy, valve replacement

141
Q

define an NSTEMI

A

Non-ST-elevated myocardial infarction is part of ACS (acute coronary syndrome)
it is an acute ischaemic event causing myocardial cell necrosis and troponin release

142
Q

non-modifiable risk factors for an NSTEMI

A

age >65 yrs
male
family history
premature menopause

143
Q

modifiable risk factors for an NSTEMI

A

smoking
DM
hyperlipidaemia
hypertension
obesity
sedentary lifestyle
recreational drug use

144
Q

pathology of an NSTEMI

A

atherosclerotic plaque rupture and thrombosis cause partial occlusion to coronary artery> this causes necrosis of cardiac tissue and infarction to sub endothelium

145
Q

presentation of an NSTEMI

A

central, crushing chest pain radiating down arms, jaw & neck - lasts longer than 20 mins + not relieved by rest or GTN spray
impending doom feeling
tachycardia
high/low BP
4th heart sound
signs of heart failure
shortness of breath
sweating/clammy
nausea
palpitations

146
Q

investigations for an NSTEMI

A

1st=
ECG- ST depression, T wave inversion
elevated troponin

other= CT angiography, bloods

147
Q

management of an NSTEMI

A

immediate management= MONA (morphine, oxygen <92%, nitrates, aspirin)

then invasive coronary angiography and PCI

GRACE score- 6 month risk of death or repeat MI after NSTEMI

prevention= aspirin, clopidogrel (antiplatelet), statin (atorvastatin), metoprolol (BB or CBB). ACEi
modify risk factors

148
Q

complications of an NSTEMI

A

heart failure
ruptured infarcted ventricle
rupture interventricular septum
mitral regurgitation
arrhythmias
heart block
post MI pericarditis (Dressler syndrome)

149
Q

define pericardial effusion and cardiac tamponade

A

pericardial effusion= accumulation of fluid in the pericardial sac

cardiac tamponade= the pericardial effusion is large enough to raise the inter-pericardial pressure leading to reduced filling of the ventricles during diastole- resulting in reduced CO in systole

150
Q

causes of cardiac tamponade

A

idiopathic
pericarditis
transudative effusions from increased venous pressure causing restricted drainage of the pericardial space- congestive heart failure, pulmonary hypertension
rupture of heart /aorta causing bleeding in pericardial space eg aortic dissection
malignancy:
-lung
-breast
-haematological
trauma eg knife wound

151
Q

pathology of cardiac tamponade

A

pericardial effusion causes raises interpericardial pressure- compresses chambers of heart= reduced stroke vol + CO
- causes hypotension, heart tries to compensate by beating faster

152
Q

presentation of cardiac tamponade

A

Beck’s triad:
-hypotension
-Kussmaul’s sign: raised JVP & distended jugular veins
-muffled heart sounds

pulses paradoxus: systolic BP reduction of >10mmHg on inspiration

tachycardia
prolonged capillary refill time
cool peripheries

dyspnoea
coughing
chest discomfort
lightheadedness
peripheral oedema
confusion

153
Q

investigations for cardiac tamponade

A

1st=
ECG- electrical alternans (QRS complex varies in amplitude as heart moves in fluid)
chest x-ray- (enlarged globular heart)

gold= transthoracic echo - will show ‘dancing heart’

other=
FBC- raised WBC, raised ESR showing inflammation

154
Q

management of pericardial effusion & cardiac tamponade

A

just pericardial effusion=
treat underlying cause, pericarditis - aspirin NSAIDS, colchicine

drain the effusion- needle pericardiocentesis or surgical drainage

pericardial effusion + cardiac tamponade=
urgent pericardiocentesis (pericardial fluid aspirated to relieve intrapericardial pressure

155
Q

complications of cardiac tamponade

A

cardiac arrest
constrictive pericarditis

156
Q

modifiable risk factors for PAD

A

obesity
diabetes
hypertension
high LDL
smoking

157
Q

pathology of PAD

A

arterial obstruction normally due 2 atherosclerosis/thrombosis> reduced blood supply + ischaemia in lower limbs

when muscle becomes ischaemic- cells release adenosine, causes pain in nearby nerves (lactic acid production also contributes 2 pain)

intermittent claudication: ischaemia in limb during exertion- relieved @ rest
acute limb iscahemia- rapid onset of iscahemia in limb due 2 thrombus blocking blood supply
critical limb ischaemia: blood supply barely adequate to meet metabolic demands of tissue- end stage of PVD, can cause gangrene + complete limb loss

158
Q

presentation of PAD

A

fontine classification:

stage1- aysmptomatic, lack of palpable pulse

stage2- intermittent claudication
-aching/burning leg muscles relieved w rest
the 6 Ps= pain, pale, pulseless, perishing cold,paraesthesia, paralysis
-ankle brachial pressure index <0.9

stage 3- critical limb ischaemia
-rest pain (relived by dangling leg over bed @ night)
-imminent risk of limb loss

stage 4- tissue loss
ulceration or gangrene

159
Q

what is buerger’s test for PAD

A

raise foot= pale
put foot down= blue (deoxy blood returns to foot)> then dark red (reactive hyperaemia)

160
Q

investigations for PAD

A

1st ankle-brachial pressure index (0.5-0.9= mild PAD, <0.5= severe PAD)

fontaine classification
1 asymptomatic
2 intermittent claudication
3 ischaemic rest pain
4 ischaemic ulcers eg gangrene

gold= CT angiogram 2 show occlusions

other= duplex ultrasound (shows speed + vol of blood flow)

161
Q

management of PAD

A

intermittent claudication: risk factor management (smoking, excercise, statins, anti platelet-aspirin eg clopidogrel)

chronic limb ischaemia : risk factor management, revascularisation surgery (stenting & angioplasty, vein bypassing), amputation if severe

acute limb ischaemia: urgent surgery (end-vascular thrombolysis, endarterectomy, bypass surgery) amputation

162
Q

define a pulmonary embolism

A

obstruction to the pulmonary vasculature, secondary to an embolus

163
Q

what 3 things make up Virchow’s triad

A

reduced blood flow
endothelial injury
hypercoagulability

164
Q

risk factors for pulmonary embolism

A

virchow’s triad:
-venous stasis
-vascular injury
-hypercaogulability (pregnant, COPD, malignancy, oestrogen therapy, thrombophilia- predispose to clots eg antiphospholipid syndrome)

165
Q

pathology of a pulmonary embolism

A

clot forms> increased pressure on vein causes it 2 break free (thromboembolus)- travels 2 lungs + becomes stuck
- decreased blood flow2 lung tissue = V/Q mismatch

can cause cor pulmonate due 2 increased pulmonary resistance

166
Q

presentation of a pulmonary embolism

A

hypoxia + cyanosis
DVT (swollen calf)
sudden, onset pleuritic chest pain
dyspnoea
fever
tachypnoea + tachycardia
crackles
hypotension
elevated JVP
haemoptysis
syncope

167
Q

investigations for a pulmonary embolism

A

1st=
Wells score (risk of DVT or PE)
1. <4 =unlikely PE, order D-dimer (looks for fibrin breakdown products & clotting problems)
2. >4= likely PE, order CT pulmonary angiogram

gold= CT pulmonary angiogram 2 get direct visual of thrombus in pulmonary artery

other=
ECG- sinus tachycardia, S1Q3T3 pattern= cor pulmonale, T wave inversion in Lead III

V/Q scan
ABG- low O2, low CO2

168
Q

management of pulmonary embolism

A

prevention=
compression stockings, frequent calf exercises, prophylactic treatment w low molecular weight heparin (LMWH)

massive PE=
thrombolysis (alteplase/streptokinase)- fibrinolytic medication 2 rapidly dissolve clots

non massive PE=
LMWH, DOAC or warfarin

169
Q

complications of a pulmonary embolism

A

pulmonary infarction
cor pulmonale
sudden death if both pulmonary arteries blocked
resp alkalosis
cardiac arrest

170
Q

define angina pectoris (stable angina)

A

central crushing chest pain due to decreased coronary artery blood flow causing oxygen supply/demand mismatch in exertion

171
Q

causes of angina pectoris

A

narrowing of coronary artery by atherosclerosis

rare= reduced O2 carrying capacity (anaemia), peripheral resistance (LV hypertrophy), coronary artery spasm

172
Q

non-modifiable and modifiable risk factors for angina pectoris

A

non-modifiable:
age
gender- M>F
race

modifiable=
diabetes
hypertension
obesity high LDL
smoking

173
Q

pathology of angina pectoris

A

narrowing of coronary arteries from atherosclerotic plaques reduces blood flow- on exertion, higher O2 demand that cannot be met > myocardial ischaemia> angina

174
Q

explain the stages of the formation of an atherosclerotic plaque

A
  • High levels of cholesterol damages endothelium.
  • LDLs pass in and out of the arterial wall in excess and accumulate in it, and there is undergoes oxidation and multiplies, leading to inflammation
  • The inflammation releases chemoattractants, which attracts Macrophages try to break down, LDLs, turning into foam cells, which produce a LIPID CORE/FATTY STREAK
  • This inflammatory reaction leads to tissue repair, so the smooth muscle proliferates forming a fibrous cap that encloses the lipid core.
175
Q

presentation of pectoris angina

A

angina precipitated by exertion, heavy meals, cold weather & emotion
-cause central crushing chest pain which can radiate to jaw, neck, arms > relieved with GTN spray/ 5 min rest

dyspnoea
nausea
sweating
syncope

176
Q

investigations for angina pectoris

A

1st=
ECG (normal)

gold= CT angiography (presence of luminal narrowing & plaques

other= echocardiogram, exercise tolerance test, invasive angiography, bloods, lipid profile, HbA1c

177
Q

management of angina pectoris (need to check this)

A

immediate symptomatic relief= GTN spray

anti-anginal medication:
1st- BB or non hydropyridine CCB (amlodipine)
2nd- BB + non hydropyridine CCB
3rd- add additional anti-anginal med
eg. nitrates, ivabradine,nicorandfil, ranolazine

revascularisation:
PCI (percutaneous coronary intervention)
CABG (coronary artery bypass graft)

secondary prevention:
lifestyle changes
aspirin + a statin
ACE inhibitor (angina + diabetes)

178
Q

complications of angina pectoris

A

MI
chronic heart failure
stroke

179
Q

define a STEMI

A

ST elevated myocardial infarction (part of ACS)
ischaemic event leading 2 death of heart tissue + troponin release

180
Q

non-modifiable + modifiable risk factors for STEMI

A

non-modifiable=
age
gender- M>F
race

modifiable=
hypertension
diabetes
obesity
high LDL
smoking

181
Q

pathology of STEMI

A

atherosclerotic plaque rupture + thrombosis= complete occlusion of coronary artery leading 2 transmural injury and myocardial infarction

182
Q

presentation of STEMI

A

central crushing chest pain radiating down arms jaw and neck- not relieved by rest or GTN spray
persists >20mins
impending doom feeling
tachycardia
high/low BP
4th heart sound
sweating
dyspnoea
fatigue
palpitations

183
Q

investigations for STEMI

A

1st + gold= ECG- ST elevation in anterolateral leads, after some time- T wave inversion, deep broad Q waves, LBBB

biomarkers- troponin elevated

other= CT angiography, bloods

184
Q

management of STEMI

A

acute treatment= MONA (morphine, O2 <92%, nitrates, aspirin)

primary PCI if available within 12 hours of symptoms , if unavailable, fibrinolysis 2 breakdown clot eg alteplase

secondary prevention= aspirin, anti platelet eg clopidogrel, statin eg atorvastatin, metoprolol (BB OR CCB), ACEi
modify risk factors

185
Q

complications of a STEMI

A

heart failure
rupture of infarcted vent
rupture of inter ventricular septum
heart block
arrhythmias
mitral regurgitation
post MI pericarditis (dressler’s syndrome)

186
Q

define unstable angina

A

myocardial ischaemia at rest or on minimal exertion with the absence of myocardial injury
-not relieved with GTN spray or rest

187
Q

presentation of unstable angina

A

central crushing pain radiating to arms, neck and jaw- not relieved by GTN spray or rest
persists longer than 20 mins
crescendo chest pain

sweating
dyspnoea
nausea
syncope
palpitations

188
Q

investigations for unstable angina

A

1st= history, ECG (sometimes ST depression and T wave inversion)
biomarkers- NO TROPONIN

other = CT angiography

189
Q

management of unstable angina

A

immediate= MONA

GRACE score (6 month risk of death or repeat MI after NSTEMI)

prevention:
aspirin, antiplatelet eg clopidogrel, statin eg atorvastatin, metoprolol (BB OR CCB), ACEi
modify risk factors

high risk= angiography + PCI

190
Q

(yellow) define atriotentricular node re-entry tachycardia (AVNRT)

A

tachycardia due to the presence of 2 functionally and anatomically distinct conduction pathways in the AV node

191
Q

causes of AVNRT

A

cardiomyopathy
iscchaemic heart disease
hyperthyroidism
cocaine
excess alcohol

192
Q

pathology of AVNRT

A

electrical signal re-enters the atria from the ventricles through the AV node
-once signal back in atria, travels thru AV node + causes another ventricular contraction

creates a self-perpetuating loop w no end point= fast + narrow QRS complex tachycardia

193
Q

presentation of AVNRT

A

tachycardia (140-280bpm)
paroxysmal attacks (sudden onset/offset palpitations)
neck pulsation
chest pain
shortness of breath
fatigue + weakness

194
Q

investigations for AVNRT

A

1st= ECG
- p waves included in QRS complex, narrow QRS followed by T wave repeated

195
Q

management of AVNRT

A

1st= vagal manoeuvres (valsalva, carotid sinus massage)
2nd= IV adenosine

prevention= BB, CCB, flecainide

196
Q

what is coarctation of the aorta

A

narrowing of the aorta at the site of the insertion of the ductus arteriosus

197
Q

causes of coarctation of the aorta

A

congenital malformation
Turner’s syndrome

198
Q

pathology of coarctation of the aorta
(infant +adult form)

A

infant form=
ductus arterioles still open
- due 2 low pressure in aorta below constriction, blood moves through ductus arteriosus into aorta, bypassing pulmonary arteries> causes cyanosis as deoxygenated blood travels into systemic circulation

adult form=
no patent ductus arteriosus
- pressure = high upstream of coarctation + low downstream of coarctation

therefore increased pressure in upper extremities + head
decreased bp in lower extremities

199
Q

presentation of coarctation of the aorta

A

hypertension
Diff upper body and lower body BP
diminished pulse in Lower extremities
tachypnoea
bruits over scapulae & back
systolic ejection murmur

200
Q

investigations for coarctation of the aorta

A

1st- chest x-ray (rib notching
ECG- L vent hypertrophy

gold= echo (narrowing in aorta, pressure gradient across narrowing

201
Q

management of coarctation of the aorta

A

surgical repair of stenting
prostaglandin E to keep ductus arteriosus open while awaiting surgery

202
Q

define dilated cardiomyopathy

A

cardiomyopathy= group of myocardial diseases that affect the affect the mechanical and electrical function of the heart

dilated cardiomyopathy= walls of the chambers of the heart are dilated, thick muscle wall stretches- becoming thinner + weaker therefore contractions are weaker

203
Q

causes of dilated cardiomyopathy

A

genetic (autosomal dominant- Duchenne muscular dystrophy)
alcohol
thyroid dsiorder
ischaemic heart disease
infection

204
Q

pathology of dilated cardiomyopathy

A

ventricular enlargement and poor contraction
dilation of the ventricle disrupts the heart’s ability to contract leading 2 progressive heart failure
-there is diffuse interstitial fibrosis and systolic dysfunction between the ventricles

205
Q

presentation of dilated cardiomyopathy

A

heart failure presentation:
-dyspnoea
-fatigue
-peripheral oedema
-raised JVP

larger heart on imaging
systolic murmur due 2 regurgitation
S3 gallop
arrhythmia
low BP
chest pain

206
Q

investigations for dilated cardiomyopathy

A

ECG=
tachycardia, LBBB, T wave inversion, Q waves
chest x-ray= enlarged heart
gold -echo= dilated heart + low ejection fraction

207
Q

management of dilated cardiomyopathy

A

bed rest
diuretics - 4 oedema
BB- control HR
ACE inhibitors- dilate vessels 2 improve blood flow
anticoag- due 2 increased thrombus risk
ICD- (implantable cardioverter defibrillator for high risk arrhythmia patients)
LVAD (L vent assist device)

xtreme= heart transplant

208
Q

define hypertrophic cardiomyopathy

A

cardiomyopathy = group of mycocardium diseases affecting heart’s mechanical/electrical function

hypertrophic CM= L vent hypertrophy causing obstruction to the outflow tract

209
Q

causes of hypertrophic cardiomyopathy

A

genetic autosomal domination mutation In sarcomere proteins troponin T, beta-myosin

210
Q

risk factors for Hypertrophic cardiomyopathy

A

family history of HCM
Friedreich’s ataxia

211
Q

pathology of hypertrophic cardiomyopathy

A

L vent hypertrophy caused by genetic dysfunction of sarcomere proteins
consequences of L vent hypertrophy=
-walls take up more room- less room 4 blood
-walls are more stiff+ less compliant so can’t stretch 2 fill w more blood
> therefore SV + CO reduced

hypertrophy also leads to abnormal Mitral valve which obstructs L vent outflow tract

212
Q

presentation of hypertrophic cardiomyopathy

A

ejection-systolic murmur- crescendo-decrescendo character due 2 blood flow thru obstructed L vent outflow tract
bifid pulse
S4 sound
arrhythmias

sudden death
chest pain
palpitations
syncope
dyspnoea

213
Q

investigations for hypertrophic cardiomyopathy

A

1st= ECG
-can see LVH from progressive T wave inversion
-deep Q waves
-ST depression

chest x-ray= cardiomegaly
echo= L vent hypertrophy, asymmetrical septal hypertrophy

other= genetic testing

214
Q

management of hypertrophic cardiomyopathy

A

1st= BB/CCB (dilimiazem/verapamil) - (no digoxin as contraindications)

anti-arrhythmic meds eg amidarone
anticoagulation

prevention= implantable cardioverter-defib

215
Q

define restrictive cardiomyopathy

A

scar tissue replaces the normal heart muscle and the ventricles become rigid so don’t contract properly

216
Q

cause of restrictive cardiomyopathy

A

idiopathic
granulomatous diseases (amyloidosis, sarcoidosis)
end-myocardial fibrosis

217
Q

pathology of restrictive cardiomyopathy

A

restricted ventricles = decreased vol > bi-atrial enlargement
rigid fibrous myocardium fills poorly + contracts poorly causing decreased CO

218
Q

presentation of restrictive cardiomyopathy

A

3rd + 4th heart sounds

signs of heart failure:
-dyspnoea
-fatigue
-peripheral oedema
-increased JVP
-hepatomegaly

ascites

219
Q

investigations for restrictive cardiomyopathy

A

1st=
ECG- low amplitude QRS
chest x-ray
echo- thickened vent walls, atria & septa

gold=
cardiac catheterisation

220
Q

management of restrictive cardiomyopathy

A

no direct treatment

-treat underlying cause
-heart transplant

221
Q

define tetralogy of Fallot

A

congenital cardiac malformation with 4 existing pathologies:
1. vent septal defect
2. overriding aorta
3. pulmonary valve stenosis
4. right ventricular hypertrophy

222
Q

describe the 4 four pathologies of congenital cardiac malformation

A
  1. ventral septal defect allows blood to shunt between ventricles
  2. overriding aorta=entrance to the aorta is placed further to the R than normal, above the VSD- therefore when the R vent contracts greater proportion of deoxygenated blood enters aorta
  3. pulmonary stenosis= creates resistance against blood flow from the R vent- creates R 2 L shunt, therefore deoxygenated blood enters L vent and systemic circualtion
  4. increased strain on the R vent trying 2 pump against resistance cause hypertrophy
223
Q

presentation of Tetralogy of Fallot

A

cyanosis
systolic ejection murmur
Tet spells (R 2 L shunt temporarily worsened)
tachypnoea
clubbing
poor feeding, poor weight gain
squatting posture
reduced SpO2

224
Q

investigations for Tetralogy of Fallot

A

1st=
chest x-ray- boot shaped heart due 2 RV thickening
gold= echo (shows blood flow route)

other= hyporexia test

225
Q

management of tetralogy of Fallot

A

full surgical repair within 2 years of life

226
Q

define Wolff-Parkinson-White syndrome (AVRT)

A

AVRT= atrioventricular re-entry tachycardia
-there is an accessory pathway for impulse conduction caused by a congenital connection between the atria and ventricles- not through the AV node

caused by congenital abnormality

227
Q

pathology of AVRT

A

an accessory pathway between atria and ventricles allows electrical conduction 2 bypass the AV node so that the ventricles and stimulated prematurely > leads 2 double exciting of the ventricles

secondary pathway in AVRT= bundle of Kent, since conduction not regulated by AV node

228
Q

presentation of AVRT

A

palpitations
tachycardia
dizziness
dyspnoea
ECG: short PR interval, wide QRS, slurred upstroke of QRS complex=delta wave

229
Q

investigations for AVRT

A

ECG=
short PR interval
wide QRS
slurred upstroke of QRS complex= delta wave

230
Q

management of AVRT

A

1st= vagal manoeuvre 2 slow heart: valsalva manoeuvre, carotid sinus massage

2.if unsuccessful give IV adenosine 2 slow conduction thru heart- 6mg then 12mg

3.cardioversion Long term- catheter ablation (remove faulty electrical pathway

231
Q

RED= define atrial septal defect

A

abnormal connection between the 2 atria
congenital - down syndrome, foetal alcohol syndrome
small = asymptomatic
large= significant inc in blood flow thru RH & lungs

ECG= tall p waves showing R atrial enlargement
chest x-ray shows enlarged heart + pulmonary arteries
echo 4 shunt visuals

will need surgical closure if closure isn’t spontaneous

232
Q

brugada syndrome

A

sodium channelopathy causing dangerously fast arrhythmias

gene mutation

syncope, palpitations, dyspnoea, chest pain

ECG= coved ST elevation in chest leads V1-3

manage with implantable cardiac defib

233
Q

long QT syndrome

A

ventricular tachyarrhythmia characterised by prolonged QT interval on ECG >480ms

syncope, palpitaions

correct electrolyte disturbances + remove causative factors, BB, pacemaker, implantable defib

234
Q

patent ductus arteriosus

A

ductus arteriosus fails to close at birth
congenital/premature

large= cont machine like murmur, cardiomegaly, pulmonary hypotension, poor feeding, failure 2 thrive

chest x ray 4 cardiomegaly
ECG- deep Q waves + r waves= L atrial enlargement
echo 2 see shunt/ventricle hypertrophy

spontaneous/surgical closure
indomethacin (prostaglandin inhibitor) may close PDA

235
Q

prinzmetal angina

A

angina due 2 coronary artery spasm + narrowing

no correlation w exertion

central crushing pain @ rest- resolved w GTN spray
dyspnoea, sweating, nausea
ECG- ST elevated during acute episode
biomarkers= not elevated

coronary angiography

use GTN spray 1st, other = CCB + long acting nitrates
reduce risk factors

236
Q

rheumatic fever

A

systemic infection from Group A beta-haemolytic streptococcus- mainly s.pyogenes

antibodies against streptococcus bacteria also attack body tissues (rheumatic heart disease)

murmur, pericardial rub, jerky movements, pink rings/rash on torso & limbs

diagnose using JONES criteria & FEAR

ESR/CRP= raised ECG= prolonged PR
throat swab 4 antistreptococcal antibodies

treat w antibiotics- IV benzylpenicillin then phenoxymethicillin for 10 days

237
Q

torsades de pointes

A

polymorphic ventricular tachycardia- QRS amplitude varies
long QT interval
-will either terminate spontaneously + revert back 2 sinus rhytmn or progress into ventricular tachycardia

palpitations, dizziness, syncope, tachycardia

correct electrolyte imbalance or remove cause
Mg infusion
defib if V-fib occurs

238
Q

ventricular ectopics

A

premature ventricular beats caused by random electrical discharges from the ventricles before an electrical impulse can be made by the atrium

random brief palpitations, abnormal beat, syncope

ECG= individual random, abnormal, broad QRS complexes

self-monitoring, BB OR CCB
ablation 2 stop normal signals

239
Q

ventricular septal defect

A

congenital abnormal connection between the 2 ventricles

congenital- Down’a, Turner’s

small VSD= asymptomatic
large= exercise intolerance, harsh pansystolic murmur , breathless, poor feeding, high pulmonary blood flow,

chest x ray 4 pulmonary plethora, cardiomegaly
echo- shows stunting across VSD

small= no treatment
large= surgical repair

240
Q
A

Phase 2a (12 decks)

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