cardio conditions Flashcards

1
Q

define an abdominal aortic aneurysm (AAA)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

epidemiology of AAA

A

M>F, more common elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

risk factors of AAA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

presentation of AAA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

investigations for AAA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

comps of AAA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define acute pericarditis

A

inflammation of the pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

epidemiology of acute pericarditis

A

80-90% idiopathic
M>F
younger>older

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

risk factors for acute pericarditis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

differential diagnosis for acute pericarditis

A

MI
pneumonia
pulmonary embolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

management of acute pericarditis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

complications of acute pericarditis

A

pericardial effusion
cardiac tamponade
chronic constrictive pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

define aortic dissection

A

tear in the intima of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

epidemiology of aortic dissection

A

M>F, 50-70 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

risk factors for aortic dissection

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
differential diagnosis for aortic dissection
MI, cardiac arrest, pericarditis
26
management of aortic dissection
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
27
complications of aortic dissection
aortic regurgitation MI stroke renal failure cardiac tamponade haemorrhage and shock
28
define aortic regurgitation
leakage of blood into L ventricle during diastole due to ineffective closing of the aortic valve cusps
29
epidemiology of aortic regurgitation
M>F 40-60 yrs
30
causes of aortic regurgitation
rheumatic heart disease infective endocarditis- causes valvular damage connective tissue disorders eg, Marfan's, Ehlers-Danos congenital
31
pathology of aortic regurgitation
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
32
presentation of aortic regurgitation
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
33
investigations for aortic regurgitation
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
34
differential diagnosis for aortic regurgitation
mitral regurgitation aortic stenosis infective endocarditis
35
management of aortic regurgitation
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)
36
complications of aortic regurgitation
heart failure pulmonary oedema & cardiogenic shock
37
define aortic stenosis
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
38
congenital causes of aortic stenosis
congenital bicuspid aortic valve, congenital aortic stenosis
39
risk factors for aortic stenosis
>60 yrs hypertension hypercholesterolaemia smoking diabetes rheumatic heart disease
40
pathology of aortic stenosis
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
41
presentation of aortic stenosis
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
42
investigations for aortic stenosis
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
43
differential diagnosis for aortic stenosis
hypertrophic cardiomyopathy, ischaemic heart disease
44
management of aortic stenosis
surgery if symptomatic lower risk patients= SAVR (surgical aortic valve replacement higher risk patients= TAVI (transcatheter aortic valve implantation
45
complications of aortic valve stenosis
heart failure sudden cardiac death infective endocarditis ventricular arrhythmia microangiopathic haemolytic anaemia
46
define atrial fibrillation (AF)
supraventricular tachycardia caused by uncoordinated, rapid and irregular atrial activity- results in an irregularly irregular ventricular pulse
47
causes of AF
heart failure hypertension coronary artery disease valvular disease-mitral stenosis cardiac surgery cardiomyopathy idiopathic
48
risk factors for AF
>60 yrs hypertension T2DM heart failure past MI
49
pathology of AF
disorganised electrical activity overrides sinoatrial node activity- causes uncoordinated, rapid and irregular contraction of atria 300-600 bpm
50
presentation of AF
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
51
investigations for AF
ECG= -absent p wave -irregualr R-R intervals -narrow QRS other=FBC clotting profiles, U&Es
52
differential diagnosis
atrial flutter wolff-parkinson-white syndrome atrial tachycardia
53
management of AF
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
54
monitoring for AF
CHA2DS2- VASc score - 2 calculate stroke risk if score= <2, anticoagulant required
55
complications of AF
acute stroke MI congestive heart failure
56
define atrial flutter
macro re-entrant atrial tachycardia caused by organised electrical activity in the atrium with a rate of 250-350 bpm
57
causes of atrial flutter
idiopathic CHD heart failure hypertension COPD pericarditis
58
pathology of atrial flutter
originates from a re-entrant circuit around the tricuspid valve annulus short circuit causes the atria to fire rapidly
59
presentation of atrial flutter
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
60
investigations for atrial flutter
ECG= saw tooth pattern (flutter waves) 2:1 block (2 P waves for every QRS other= FBC
61
differential diagnosis for atrial flutter
AF, atrial tachycardia
62
management of atrial flutter
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
63
monitoring of atrial flutter
CHA2SD2-VASc for stroke risk
64
define bundle branch block
a block in the conduction of one of the bundle branches- therefore the ventricles don't receive impulses @ the same time
65
causes of RBBB
pulmonary embolism ischemic heart disease atrial or ventricular septal defect
66
causes of LBBB
ischemic heart disease valvular disease cardiomyopathy cardiac surgery
67
pathology of RBBB
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)
68
pathology of LBBB
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)
69
presentation of BBB
asymptomatic syncope
70
investigations for BBB
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
71
management of BBB
usually no treatment treat hypertension, pacemaker, cardiac resynchronisation therapy (CRT)
72
define cor pulmonale
right sided heart failure caused by respiratory disease
73
causes of cor pulmonale
COPD pulmonary embolism interstitial lung disease cystic fibrosis primary pulmonary hypertension
74
pathology of cor pulmonale
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
75
presentation of cor pulmonale
shortness of breath peripheral oedema chest pain hypoxia cyanosis raised JVP 3rd heart sound murmurs hepatomegaly syncope
76
investigations for cor pulmonale
1st= ABG (hypoxia + hypercapnia) spirometry chest CT echocardiogram gold= right heart catheterisation
77
management of cor pulmonale
treat symptoms + underlying cause long term O2 therapy treat heart failure venesection (reduces RBCs) if haemltocrit >55 consider heart-lung transplantation in young patients
78
complications of cor pulmonale
tricuspid regurgitation hepatic congestion cardiac cirrhosis death
79
prognosis of cor pulmonale
50% 5 year survival
80
define deep vein thrombosis (DVT)
the formation of a blood clot in the deep veins of the leg or pelvis
81
causes of DVT
virchow's triad: reduced blood flow, endothelial injury, venous stasis
82
risk factors for DVT
virchow's triad age, >40 yrs smoking drugs: combined contraceptive pill, HRT, tamoxifen immobility pregnancy trauma malignancy polycythemia antiphospholipid syndrome (thrombophilia)
83
pathology of DVT
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
84
presentation of DVT
unilateral calf pain, redness and swelling tenderness pitting oedema dilated superficial veins erythema cyanosis
85
investigations for DVT
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)
86
management of DVT
1st- DOAC anticoagulation: apixaban or rivaroxaban long term: LWMH (low molecular weight heparin) DOAC (direct oral anticoagulants)/warfarin compression stockings treat underlying cause
87
prevention of DVT
compression stocking calf exercises during periods if immobilisation LMWH
88
define heart block
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)
89
causes of heart block
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
90
risk factors for heart block
coronary artery disease cardiomyopathy fibrosis
91
pathology of diff types of heartblock
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
92
presentations of heart block
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
93
investigations for heart block
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
94
management of heart block
1st- asymptomatic= no treatment symptomatic= pacemaker 2nd, type 1= asymptomatic= no treatment symptomatic= pacemaker 2nd, type 2= pacemaker 3rd= IV atropine/isoprenaline + permanent pacemaker
95
define general heart failure
inability of the heart to deliver oxygenated blood to tissues at a satisfactory rate for the tissues metabolic requirements
96
define systolic heart failure
failure of the heart to contract efficiently to eject adequate volumes of blood ejection fraction= <40% heart failure w reduced ejection fraction- HFrEF
97
define diastolic heart failure
inability of the ventricles to relax and fill normally- causes increased filling pressures ejection fraction=>50% heart failure w preserved ejection fraction- HFpEF
98
define right heart failure
inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion
99
define left heart failure
inability of left ventricle to pump adequate amount of blood leading to pulmonary circulation congestion and oedema
100
causes of heart failure
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
risk factors for heart failure
older M>F obesity previous MI
102
pathology of heart failure
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
presentation of LHF
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
presentation of RHF
peripheral oedema RHF: raised JVP, hepatomegaly, pitting oedema, weight gain (fluid) ascites nausea anorexia facial engorgement epistaxis
105
investigations for heart failure
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
management of heart failure
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
complications of heart failure
pleural effusion actue kidney injury sudden cardiac death
108
prognosis for heart failure
50% die within 5 years of diagnosis
109
define hypertension
persistent elevation of arterial BP ≥140/90 mmHg in clinic ≥ 135/85 mmHg for ambulatory or home readings primary or secondary
110
non modifiable risk factors for hypertension
age Family history ethnicity (afro-caribbean)
111
modifiable risk factors for hypertension
obesity sedentary life style alcohol excess smoking high sodium intake (>1.5g/day) stress
112
pathology of primary hypertension
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
pathology of secondary hypertension
indicates an unknown underlying cause including: -renal diseases -endocrine disorders -medications (glucocorticoids, contraception) -pregnancy (pre-eclampsia)
114
presentation of hypertension
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
investigations for hypertension
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
management of hypertension
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 4. 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
monitoring of hypertension
measure BP every 5 yrs more often for patients on borderline of diagnosis (140/90)
118
complications of hypertension
CAD cerebrovascular incident congestive heart failure CKD hypertensive retinopathy
119
define infective endocarditis (IE)
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
epidemiology of infective endocarditis
elderly young IV drug users congenital heart disease anyone w prosthetic valve rheumatic fever surgery poor dental hygiene iv catheter immunosuppression
121
what causes infective endocarditis
bacteria s.aureus (common in IVDU, T2DM, surgery)-normally acute s. viridans (poor dental hygiene)-normally subacute enterococci/s. bovis HACEK organisms fungi
122
pathology of infective endocarditis
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
presentation of infective endocarditis
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
investigations for infective endocarditis
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
management of infective endocarditis
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
complications of infective endocarditis
vegetations embolising causing stroke, MI, PE, heart failure, sepsis regurgitation due 2 damaged valves
127
define mitral regurgitation
incompetence of the valve leading to back flow of blood from the LV to LA during systole
128
risk factors for mitral regurgitation
F >age connective tissue disorders (marfans, Ehlers-danlos) prior mi infective endocarditis rheumatic fever cardiomyopathies medications myxomatous degeneration (floppy valve)
129
pathology of mitral regurgitation
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
presentation of mitral regurgitation
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
investigations for mitral regurgitation
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
management of mitral regurgitation
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
complications of mitral regurgitaiton
L sided heart failure AF infective endocarditis congestive heart failure
134
define mitral stenosis
narrowing of mitral valve orifice, making it difficult for blood to flow from the LA to LV in diastole
135
risk factors for mitral valve stenosis
s. pyogenes infection leading 2 rheumatic heart disease M>F
136
causes of mitral stenosis
rheumatic fever- inflammation cause leaflets to fuse together congenital mitral annular calcification
137
pathology of mitral stenosis
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
presentation of mitral stenosis
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
investigations for mitral stenosis
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
treatment for mitral stenosis
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
define an NSTEMI
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
non-modifiable risk factors for an NSTEMI
age >65 yrs male family history premature menopause
143
modifiable risk factors for an NSTEMI
smoking DM hyperlipidaemia hypertension obesity sedentary lifestyle recreational drug use
144
pathology of an NSTEMI
atherosclerotic plaque rupture and thrombosis cause partial occlusion to coronary artery> this causes necrosis of cardiac tissue and infarction to sub endothelium
145
presentation of an NSTEMI
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
investigations for an NSTEMI
1st= ECG- ST depression, T wave inversion elevated troponin other= CT angiography, bloods
147
management of an NSTEMI
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
complications of an NSTEMI
heart failure ruptured infarcted ventricle rupture interventricular septum mitral regurgitation arrhythmias heart block post MI pericarditis (Dressler syndrome)
149
define pericardial effusion and cardiac tamponade
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
causes of cardiac tamponade
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
pathology of cardiac tamponade
pericardial effusion causes raises interpericardial pressure- compresses chambers of heart= reduced stroke vol + CO - causes hypotension, heart tries to compensate by beating faster
152
presentation of cardiac tamponade
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
investigations for cardiac tamponade
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
management of pericardial effusion & cardiac tamponade
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
complications of cardiac tamponade
cardiac arrest constrictive pericarditis
156
modifiable risk factors for PAD
obesity diabetes hypertension high LDL smoking
157
pathology of PAD
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
presentation of PAD
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
what is buerger's test for PAD
raise foot= pale put foot down= blue (deoxy blood returns to foot)> then dark red (reactive hyperaemia)
160
investigations for PAD
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
management of PAD
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
define a pulmonary embolism
obstruction to the pulmonary vasculature, secondary to an embolus
163
what 3 things make up Virchow's triad
reduced blood flow endothelial injury hypercoagulability
164
risk factors for pulmonary embolism
virchow's triad: -venous stasis -vascular injury -hypercaogulability (pregnant, COPD, malignancy, oestrogen therapy, thrombophilia- predispose to clots eg antiphospholipid syndrome)
165
pathology of a pulmonary embolism
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
presentation of a pulmonary embolism
hypoxia + cyanosis DVT (swollen calf) sudden, onset pleuritic chest pain dyspnoea fever tachypnoea + tachycardia crackles hypotension elevated JVP haemoptysis syncope
167
investigations for a pulmonary embolism
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
management of pulmonary embolism
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
complications of a pulmonary embolism
pulmonary infarction cor pulmonale sudden death if both pulmonary arteries blocked resp alkalosis cardiac arrest
170
define angina pectoris (stable angina)
central crushing chest pain due to decreased coronary artery blood flow causing oxygen supply/demand mismatch in exertion
171
causes of angina pectoris
narrowing of coronary artery by atherosclerosis rare= reduced O2 carrying capacity (anaemia), peripheral resistance (LV hypertrophy), coronary artery spasm
172
non-modifiable and modifiable risk factors for angina pectoris
non-modifiable: age gender- M>F race modifiable= diabetes hypertension obesity high LDL smoking
173
pathology of angina pectoris
narrowing of coronary arteries from atherosclerotic plaques reduces blood flow- on exertion, higher O2 demand that cannot be met > myocardial ischaemia> angina
174
explain the stages of the formation of an atherosclerotic plaque
* 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
presentation of pectoris angina
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
investigations for angina pectoris
1st= ECG (normal) gold= CT angiography (presence of luminal narrowing & plaques other= echocardiogram, exercise tolerance test, invasive angiography, bloods, lipid profile, HbA1c
177
management of angina pectoris (need to check this)
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
complications of angina pectoris
MI chronic heart failure stroke
179
define a STEMI
ST elevated myocardial infarction (part of ACS) ischaemic event leading 2 death of heart tissue + troponin release
180
non-modifiable + modifiable risk factors for STEMI
non-modifiable= age gender- M>F race modifiable= hypertension diabetes obesity high LDL smoking
181
pathology of STEMI
atherosclerotic plaque rupture + thrombosis= complete occlusion of coronary artery leading 2 transmural injury and myocardial infarction
182
presentation of STEMI
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
investigations for STEMI
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
management of STEMI
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
complications of a STEMI
heart failure rupture of infarcted vent rupture of inter ventricular septum heart block arrhythmias mitral regurgitation post MI pericarditis (dressler's syndrome)
186
define unstable angina
myocardial ischaemia at rest or on minimal exertion with the absence of myocardial injury -not relieved with GTN spray or rest
187
presentation of unstable angina
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
investigations for unstable angina
1st= history, ECG (sometimes ST depression and T wave inversion) biomarkers- NO TROPONIN other = CT angiography
189
management of unstable angina
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
(yellow) define atriotentricular node re-entry tachycardia (AVNRT)
tachycardia due to the presence of 2 functionally and anatomically distinct conduction pathways in the AV node
191
causes of AVNRT
cardiomyopathy iscchaemic heart disease hyperthyroidism cocaine excess alcohol
192
pathology of AVNRT
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
presentation of AVNRT
tachycardia (140-280bpm) paroxysmal attacks (sudden onset/offset palpitations) neck pulsation chest pain shortness of breath fatigue + weakness
194
investigations for AVNRT
1st= ECG - p waves included in QRS complex, narrow QRS followed by T wave repeated
195
management of AVNRT
1st= vagal manoeuvres (valsalva, carotid sinus massage) 2nd= IV adenosine prevention= BB, CCB, flecainide
196
what is coarctation of the aorta
narrowing of the aorta at the site of the insertion of the ductus arteriosus
197
causes of coarctation of the aorta
congenital malformation Turner's syndrome
198
pathology of coarctation of the aorta (infant +adult form)
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
presentation of coarctation of the aorta
hypertension Diff upper body and lower body BP diminished pulse in Lower extremities tachypnoea bruits over scapulae & back systolic ejection murmur
200
investigations for coarctation of the aorta
1st- chest x-ray (rib notching ECG- L vent hypertrophy gold= echo (narrowing in aorta, pressure gradient across narrowing
201
management of coarctation of the aorta
surgical repair of stenting prostaglandin E to keep ductus arteriosus open while awaiting surgery
202
define dilated cardiomyopathy
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
causes of dilated cardiomyopathy
genetic (autosomal dominant- Duchenne muscular dystrophy) alcohol thyroid dsiorder ischaemic heart disease infection
204
pathology of dilated cardiomyopathy
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
presentation of dilated cardiomyopathy
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
investigations for dilated cardiomyopathy
ECG= tachycardia, LBBB, T wave inversion, Q waves chest x-ray= enlarged heart gold -echo= dilated heart + low ejection fraction
207
management of dilated cardiomyopathy
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
define hypertrophic cardiomyopathy
cardiomyopathy = group of mycocardium diseases affecting heart's mechanical/electrical function hypertrophic CM= L vent hypertrophy causing obstruction to the outflow tract
209
causes of hypertrophic cardiomyopathy
genetic autosomal domination mutation In sarcomere proteins troponin T, beta-myosin
210
risk factors for Hypertrophic cardiomyopathy
family history of HCM Friedreich's ataxia
211
pathology of hypertrophic cardiomyopathy
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
presentation of hypertrophic cardiomyopathy
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
investigations for hypertrophic cardiomyopathy
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
management of hypertrophic cardiomyopathy
1st= BB/CCB (dilimiazem/verapamil) - (no digoxin as contraindications) anti-arrhythmic meds eg amidarone anticoagulation prevention= implantable cardioverter-defib
215
define restrictive cardiomyopathy
scar tissue replaces the normal heart muscle and the ventricles become rigid so don't contract properly
216
cause of restrictive cardiomyopathy
idiopathic granulomatous diseases (amyloidosis, sarcoidosis) end-myocardial fibrosis
217
pathology of restrictive cardiomyopathy
restricted ventricles = decreased vol > bi-atrial enlargement rigid fibrous myocardium fills poorly + contracts poorly causing decreased CO
218
presentation of restrictive cardiomyopathy
3rd + 4th heart sounds signs of heart failure: -dyspnoea -fatigue -peripheral oedema -increased JVP -hepatomegaly ascites
219
investigations for restrictive cardiomyopathy
1st= ECG- low amplitude QRS chest x-ray echo- thickened vent walls, atria & septa gold= cardiac catheterisation
220
management of restrictive cardiomyopathy
no direct treatment -treat underlying cause -heart transplant
221
define tetralogy of Fallot
congenital cardiac malformation with 4 existing pathologies: 1. vent septal defect 2. overriding aorta 3. pulmonary valve stenosis 4. right ventricular hypertrophy
222
describe the 4 four pathologies of congenital cardiac malformation
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
presentation of Tetralogy of Fallot
cyanosis systolic ejection murmur Tet spells (R 2 L shunt temporarily worsened) tachypnoea clubbing poor feeding, poor weight gain squatting posture reduced SpO2
224
investigations for Tetralogy of Fallot
1st= chest x-ray- boot shaped heart due 2 RV thickening gold= echo (shows blood flow route) other= hyporexia test
225
management of tetralogy of Fallot
full surgical repair within 2 years of life
226
define Wolff-Parkinson-White syndrome (AVRT)
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
pathology of AVRT
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
presentation of AVRT
palpitations tachycardia dizziness dyspnoea ECG: short PR interval, wide QRS, slurred upstroke of QRS complex=delta wave
229
investigations for AVRT
ECG= short PR interval wide QRS slurred upstroke of QRS complex= delta wave
230
management of AVRT
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
RED= define atrial septal defect
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
brugada syndrome
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
long QT syndrome
ventricular tachyarrhythmia characterised by prolonged QT interval on ECG >480ms syncope, palpitaions correct electrolyte disturbances + remove causative factors, BB, pacemaker, implantable defib
234
patent ductus arteriosus
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
prinzmetal angina
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
rheumatic fever
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
torsades de pointes
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
ventricular ectopics
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
ventricular septal defect
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