Cardiology Flashcards
What is angina
due to Myocardial ischaemia, not infarction
tightness/squeezing/heaviness/pan in chest, neck, jaw, arms, shoulder, back
+-diaphoresis/nausea/anxiety
elderly- stomach pain
women- burning/tenderness
what is stable angina
on exertion, emotional stress, heavy meals, cold temps
predictable
coronary stenosis >70%
what is unstable/crescendo angina
large occlusion/plaque rupture
unpredictable, at rest
does not respond to GTN/meds
medical emergency
what is prinzmetal’s angina
‘spasmodic/variant’
pain at rest, suddenonset, rare
can be caused by cocaine
?angina ix
- troponin- normal
- ECG
- angiography
what are the ischaemic changes on an ECG
- could be normal
- ST depression
- ST depression +- T wave inversion during unstable angina attack
- t wave inversion only relevant if in leads with upright QRS
- pathological q waves (q waves in V1-3, >1mm /0.04s wide (one small sq), >2mm/0.08s deep (2 small square), >25% depth of QRS
- poor R wave progression- from V1-V6, R wave should become bigger than s wave
Management of Angina
- Sublingual glyceryl trinitrate (can be used as preventer immediately before activity)
- rapid access chest pain clinic
- 1st line- betablocker- bisoprolol, low dose aspirin
- 2nd line rate limiting- add CCB (verapamil, diltiazem), amlodipine (prinzmetals)
- 3rd line- ivabridine, nicorandil!, ranolazine
- HTN control
lifestyle changes
surgery
- PCI
- coronary bypass
what drug is contraindicated in prinzmetal’s angina
betablocker
what secondary preventative measures can be suggested for angina
- cardiac rehab
- exercise
- stop smoking , drinking, eating badly
psychological support
sx of mi
- sudden, severe crushing central chest pain >20mins - not relieved by nitroglycerin - diaphoresis - radiation to neck, jaw, L arm - impending doom - lightheaded, nauseous, may vomit
What is the pathophysiology of an NSTEMI
- severe stenosis, non occlusive thrombus
- no transmural necrosis
- irreversible injury to myocytes
ECG features of NSTEMI
ST depression
+- T wave inversion (in leads with upright QRS)
pathophysiology of STEMI
- complete thrombus occlusion
- transmural necrosis
- irreversible damage to myocytes
ECG features of STEMI
- ST elevation
- New LBBB (broad QRS >3smalsq with QRS wave pointing down in V1/ ‘W’ QRS in V1)
ix for ?MI
ECG
Trop- 2 samples 30min- 3 hours apart with one >99th centile
Immediate management of MI
A-E
STEMI:
MONA BASH
M- morphine 5-10mh IV plus metoclopramide 10mg IV
O- low flow if sats <90%/pulm oedema
N- Nitrates- IV nitroglycerine or GTN spray
A- antiplatelets- Aspirin 300mg PO plus clopidogrel 300mg PO
B- betablocker oral if no asthma/COPD
A- ACEI within 24hours
S- Statin- artorvo 80mg
H- Heparins LMWH (delta) SC, or fondaparinux SC
PCI-
- if available within 2hrs
- if not- thrombolysis (alteplase)
NSTEMI:- PCI within 72hours
Consider also stool softeners to avoid straining and sedatives
Causes of acute aortic regurg
- infective endocarditis
- ascending aortic dissection (type A)
- congenital
- AS
- Rheumatic fever
- chest trauma
Causes of chronic aortic regurg
- congen
- connective tissue eg marfarn’s
- rheumatic heart disease
- SLE
- HTN
- syphilis, RA, Takayasu’s arteritis
- appetite suppressants
sx of aortic regurg
dyspnoea
PND, orthopnoea
palpitations
murmur heard for aortic regurg including location
decrescedno early diastolic murmur (just after S2)
- at L lower sternal boarder
- if loudest at R sternal border- may suggest arotic root dilatation
- best heard with pt sitting forwards on exp hold
other signs of aortic regurg apart from murmur
- collapsing, wide pulse pressure
- pulsatile nail bed/vulva
- head bobbing in time of pulse
- pulm HTN- SOB, oedema
ix for ?aortic regurg
bloods- FBC, CRP, BNP/ANP
- ECG
- CXR
- echo
tx for aortic regurg
- vasodilators (CCB: nifedipine)
- statin
- betablocker if in HF
- ACEI- improves stroke volume
- surgery- valve replacement
IE prophylaxis (amox/clinda)- not routinely offered anymore
causes of aortic stenosis
- senile calcification
- rheumatic disease
- infective vegetation
- *- SLE
- *- post radiation
- bileaflet valve
sx aortic stenosis
SAD- syncope, angina, dyspnoea
- Palpitations
- sudden death
murmur heard in aortic stenosis
- crescendo/decrescendo ejection systolic murmrur
- high pitched
- heard over 2nd ICS R sternal boarder
signs of aortic stenosis other than murmur
- LVHF- PND, orthopnea, cyanosis, cough
- heaves
- low vol, slow rising, narrow pulse pressure
- carotid bruits
- pulm HTN- oedema
Ix for ?aortic stenosis
ECG
echo
cardiac catheter to assess value gradient and LV function
ECG findings in aortic stenosis
- p-mitrale- p waves look like M /bifid/notched (LA enlargment)
LVH- - ST depression
- t wave inversion
- LBBB
- left axis deviation
- SV1 + RV6 = >35mm (ie 35/5= 7 bigger squares)
aortic valve stenosis grading
mild >1.5cm
mod 1-1.5cm
severe <1cm
tx aortic stenosis
ACEI, betablockers if mild
balloon valvuloplasty
Valve replacement
IE prophylaxis - amox (S viridans)- not currently recommended
What is stage 2 of atherosclerosis formation
Intermediate lesions
from foam cells, T lymphocytes, plts, extracellular fluid
What is stage one of atherosclerosis formation
fatty streaks
What is stage 3 of atherosclerosis formation
Impedes blood flow, sometimes ruptures, fibrous cap
What is stage 4 of atherosclerosis formation
plaque grows and recede due to digestion by inflammatory markers
what are cardiomyopathies
myocardium is structurally and functionally abnormal without coronary disease, HTN, valvular or congenital heart disease
What types of cardiomyopathies are there
- hypertrophic
- dilated
- arrythmogenic
- restrictive
- unclassified
What causes myocarditis
- Viruses- adeno, COVID-19, hep B/C, parvo, HSV, HIV, EBV
- Bacteria- Staph, Strep, Lyme
- *- Parasites- toxoplasmosis
- Fungi- candida, aspergillus, histoplasmosis
- *- Meds- CT, Abx, Antiepileptic, cocaine
- *- radiation
- *- heavy metal and CO poisoning
- electric shock
- autoimmune- lupus, vasculitis, sarcoidosis, IBD, MG, polymyositis
- *- thyrotoxicosis
sx and signs of myocarditis
asx
- chest pain
- SOB
- viral sx
- fatigue
signs:
- arrhythmias
- oedema
- hypotension
children: fever, syncope, dyspnoea, high RR, tachy/arrhythmias
ix for ?myocarditis
ECG
- ST elevation or depression
- T wave inversion
- atrial arrhythmias
- AV block
bloods
- leukocytosis may be present
- UE
- *- CK (muscle damage)
- trop raised
- ESR CRP
- LFT
- *CXR
- normal silhouette
- pleural effusion
- interstitial and alveolar oedema
Viral serology
***Endomyocardial biopsy (gold standard)
Cardiac MRI
Management of myocarditis
- ITU- ventilation
- mechanical support devices
- severe with hypotension- parenteral inotropes (phosphodiesterase inhibis- milrinone; beta adrenergic rec agonists- DA, dobutamine, adrenaline)
- anticoag if AF
- steroids if giant cell
- limit activity for several months
What is hypertrophic cardiomyopathy
- usually inherited
- LVH is stiff
- impaired diastolic filling due to small volume chambers
- mitral - regurg
- can also create turbulent flow- clot risk
sx hypertrophic cardiomyopathy
- muscle grows during growth, so sx stable in adulthood but gets worse during childhood and when elderly (thickened heart becoming stiffer)
- asx
- sx worse after alcohol
- dyspnoea
- chest pain, palpitations (arrhythmias)
- syncope
- sudden death- ventricular outflow obstruction
signs of hypertrophic cardiomyopathy
- forceful apex
- pansystolic murmur at apex- mitral regurg
ix for ?hypertrophic cardiomyopathy
- Transthoracic echocardiogram - diagnostic
- ECG - LVH- ST changes, T wave inversion, axis deviation
- CXR- increased heart size
- MRI
- cardiac catheter
- endomyocardial biopsy to exclude other causes of LH eg amyloidosis
tx hypertrophic cardiomyopathy
- amiodarone, beta blockers, verapamil (CCB)- improves cardiac filling
- AF- anticoag
- *- implantable cardioverter defib
- cardiac ablation
- surgical myectomy to relieve outflow LV
- heart transplant if HF
- genetic counselling
what is dilated cardiomyopathy
ventricular chamber enlargement and contractile dysfunction with normal LV wall thickness
causes of dilated cardiomyopathy
- idiopahic- most common
- genetic
- substance misuse- alcohol, cocaine!
- pregnancy
- **- thyrotoxicosis
- autoimmune- RA, SLE
- phenothiazines
- haemochromatosis,
- sarcoidosis
- **amyloidosis, glycogen storage
- Viruses: HIV, adeno, coxsackie, cytomegalo**
sx and signs of dilated cardiomyopathy
- asx
- stroke
- palpitations
- sudden cardiac death
- HF- oedema, PND, orthopnoea
+- viral prodrome
signs
- arrhythmias
- HF (congestive)- dyspnoea, fatigue, oedema, raised JVP, PE, cardiomegaly, loud S1/S4, pink frothy sputum
- MR- pansystolic
- AR- early diastolic
- fam hx
ix for dilated cardiomyopathy
- diagnosis of exclusion
- CXR- cardiomegaly, pulm oedema
- ECG- LBBB, non specific ST/T wave changes
- echo- dilation of LV cavity
- btype natriuretic peptide
- cardiac catheter
- endomyocardial biopsy- to exclude myocarditis, sarcoidosis, haemochromatosis if clinical supicion
management of dilated cardiomyopathy
- same tx for HF
- titrate all drugs up
- ACEI /ARB
1a. betablocker - add low dose loop (furesomide)
- add mineralocorticoid/aldosterone antag (spironolactone)
- ivabridine
- sacibutril (neprilysin inhib +ARB)
- hydralazine + nitrate
- digoxin
– add anticoag, amiodarone, digoxin if relevant
cardiac resynchronisation
catheter ablation in arrhythmia/vent tachy
LV devices
transplant
What is arrhythmogenic cardiomyopathies
- progressive fatty and fibrous replacement of ventricular myocardium
- leads to arrhythmias
sx arrhythmogenic cardiomyopathies
- arrhythmia- palp, syncope
- sudden cardiac death
- HF in 40s/50s
ix arrhythmogenic cardiomyopathies
ECG- vent arrhythmias with LBBB
- echo, cxr, MRI
- cardiac catheters
- biopsy sometimes
- genetic assessment
tx arrhythmogenic cardiomyopathies
HF tx
- ACEI/ARB
- betablockers
- diuretics
- amiodarone
- anticoag
***- implantable cardioverter defib, pacemakers
ablation
- transplant
Causes of endocarditis
Non infective
- vegetations- plt, immune complexes, cancer cells
Infective-
- Bacterial- Strep viridans, S.aureus, **strep bovis, **enterococci,
- *- Fungal- candida, aspergillus, **histoplasma
RF for infective endocarditis
- skin breaches, IVDU
- immunosupression- diabetes, renal failure
- abnormal valves eg stenostic/regurg, artificial
- hypertophic cardiomyopathy
- hx of IE
- structural heart issues, incl if repaired eg ASD
sx and signs of endocarditis
Infective- sepsis, cough, sore throat, flu-like sx
- chest pain
- abscesses elsewhere
- SOB
- oedema
Signs
- anaemia
- splenomegaly
- new murmur
- Deposits: vasculitis, haematuria, **glomerulonephritis, ***roth spots on fundoscopy
- splinter haemorrhages
- Janeway lesions- soles/palms, not tender
- osler’s nodes- fingers/toes, tender
ix endocarditis
DUKE criteria
- CT/PET
- echo
- blood cultures
- CXR, ECG, MRI
tx of endocarditis
IV/oral abx
- amoxicillin (native valve)- or vanc plus gent
- rifampicin plus gent (prosthetic)
- tx arrhythmias, heart block, HF, stroke, abscess (drain)
- surgery to remove material
- replace valve (if causing HF, unresp to meds, fungal, vegetation >10mm, recurrent embolisation)
NB- IE prophylaxis isnt routinely offered to high risk people anymore, even when undergoing dental procedure- safety net for red flags and inform importance of good oral hygiene
What is rheumatic fever caused by
group A beta haemolytic strep/strep pyogens
sx rheumatic fever
child- sore throat , then 1m later:
- arthritis
- *- carditis- tachy, chest pain, SOB, oedema, fatigue, mitral/aortic regurg, pericardial rub
- chorea- movements of face and upper limbs
- *- SC nodules
- fever
ix ?rheumatic fever
throat swabs
ECG
CXR
doppler echo
tx rheumatic fever
- penicillin
- aspirin
- NSAIDs
- *- diuretics/ACEI and digoxin for HF
- chorea- diazepam
What are the stages of HTN
> 140/90 and 135/85 ambulatory]
1- >140/90
2- >160/100 (home >150/95)
3- >180 or >120
Accelerated- severe with papilloedema/retinal haemorrhage
ix to assess endorgan damage in HTN
12 lead ECG +- ECHO
UE, eGFR, urine dip
Renal USS
fundoscopy
other ix you would do in HTN (apart from assessing end organ damage)
- blood glucose, fasting lipids
could do
- dexamethasone supression test
- 24hour urinary metanephrines (phaeochromocytomas)
- renin/aldoesterone ratio (primary hyperaldoteronism)
causes of secondary HTN
- Cushings
- Renal artery stenosis
- Pheochromocytoma
- primary hyperaloderonism (Conn’s)
- SIADH
- renal disease (PKD, nephritic syndrmoe- IgA, post-strep, HUS, HSP, goodpasture, SLE, vasculitis, IE, Membranoproliferative glomerulonephritis)
Management of HTN
<55yo or diabetic of any age/ethnicity
- ACEI/ARB
> 55yo/Afrocarribean
- CCBs
Then:
- ACEi/ARB + CCB
- add thiazide-like diuretic*****
- alpha blocker (doxasin)
- Beta blocker- bisoprolol
- ACEI and spironolactone (if HF sx)
name some ACEI
-pril
ramipril
lisinopri
enalapril
NB: NOT verapamil
name some ARBs
-sartan
candesartan
losartan
valsartan
name some CCBs
-pine (mostly)
amlodipine felodipine nifedipine verapamil diltiasem
name a thiazide-like diuretics
- indapamide
- bendroflumethiazide
electrolyte SE of spironolactone
hyperkalaemia
cause of the dry cough in ACEI
bradykinin
Pathophysiology of LV impairment
cardiac disorder increases work of LV due to lack of O2 systemically
- LV muscle remodels
- becomes thicker and weaker, leading to dysfunction
- can also occur following an MI
- this is synonymous with HF
symptoms of LV dysfunction/HF
- SOB
- fatigue
- oedema
- Palpitations, chest pain
- *- excessive urination (BP and RAAS)
- dizziness, syncope, nausea
- *- fatigue and weakness
- lack of appetite
signs of LV dysfunction/HF
- orthopnoea, paroxysmal nocturnal dyspnoea
- tachy/bradycardia
- displaced apex
- S3, murmurs, arrhythmias
- Overload: JVP raised, ascites, oedema
- cyanosis
- pink frothy sputum CHF
Ix ?LV dysfunction/HF
- Natriuretic peptide tests— N-terminal prohormone brain natriuretic peptide (NT-proBNP); BNP
- UE, TFT, LFT, lipid, HbA1C, FBC– fatigue, urination
- urinanalysis- urination
- peak flow and spirometry (COPD)
-transthoracic echo- exclude valve disease, assess LV function, shunts
- ECG
- CXR- cardiomegaly, congestion
- exercise tests
- cardiac catheterisation- valve disease
- coronary angio- IHD, angina
why does HF cause polyuria/nocturia
- reduced CO
- reduced renal blood flow, low BP
- RAAS system activated–
- aldosterone increases sodium retention and water retention
- oedema
- at night, the pt lies down, the excessive fluid now returns to the heart
- increased CO
- kidneys perfused
- urination
tx of HF reduced EF
- lifestyle
- offer anticoag if AF present
- do not give adrenaline/stimulants
- avoid CCBs and short acting dihydropyridine agents
1.
- ACEI (ramipril, lisinopril)/ARB (candesartan) AND betablockers (bisop)– 1st line for mortality/morbitiy
- Loop diuretics- 1st line for oedema
- add mineralocorticoid rec antag: spironolactone, eplerenone
- hydralazine with nitrate
- amiodarone, digoxin, ivabradine, sacubitril-valsartan
Surgery-
- valve repair
- LV remodelling
- pacemaker to achieve resync (CRT)
- transplant
Tx of HF with PRESERVED EF
Specialist tx
LTOT not recommended
- loop diuretic
Causes of mitral regurg
- vol overload–> L atrial dilation
- calcification
- infective endocarditis
- mitral prolapse, papillary muscle dysfunction (post MI)
- *- connective tissue
- *- cardiomyopathy
- *- appetite supressants
sx mitral regurg
- palpitations
- SOB/dyspnoea
- fatigue
- HF sx
murmur of mitral regurg
- pansystolic at apex
- heard best with pt rolled on L using bell
- radiation to L axilla
- whistling/high pitched
other signs of mitral regurg apart from murmur
- displaced apex (hypertophic LV)
- AF
- soft S1, split S2 (vol overload)
Ix ?mitral regurg
- FBC, CRP- infection, anaemia
- ECG- AF, LVH (ST wave depression and T wave inversion), p-mitrale (L atrial hypertophy, M p wave)
- CXR- large Left heart, pulm oedema, valve calcified
- ECHO
- catheterisation
tx mitral regurg
- diuretics
- vasodilate- ACEI, hydralazine
- rate- betablocker, CCB (verapamil), digoxin
- surgery - repair/replace
causes of mitral stenosis
- rheumatic fever
- IE
- calcification
sx of mitral stenosis
- progressive dyspnoea
- pulm venous HTN– haemoptysis
- RSHF- oedema, ascites, epistaxis, anorexia
murmur character of mitral stenosis
- low rumbling (low velocity)
- mid diastolic
- heard at apex
- heart best with pt rolling on L at 5th ICS mid clav line
other signs of mitral stenosis
- loud S1
- short S2
- tapping apex beat
- malar flush(pulm system back up– increase n CO2 and vasodilation)
- AF
ix for ?mitral stenosis
ECG- AF, p-mitrale
CXR- pulm congestion. LA big
- ECHO- diagnostic
tx for mitral stenosis
- rate- beta blockers, CCB, digoxin (improves diastolic filling)
- diuretics
- percutaneous valvotomy
- surgery
- IE prophylaxis no longer recommended
what is S1
mitral valve closing
what is S2
aortic valve closing
causes of pericardial effusion
- pericarditis
- myocardial rupture
- aortic dissection
- malignancy
- infection
sx pericardial effusion
- SOB, dyspnoea
- syncope
- chest pain
- nausea, vomiting if viral
signs of pericardial effusion
- S1/2 muffled
- bronchial breathing at L base
Tamponade
- hypotension
- JVP high
- HF
- tachycardia
- hypoperfusion
ix for ?pericardial effusion
- CXR- globular, big heart
- ECG- low V QRS
- echo- echo free zone around heart
- pericardiocentesis
tx of pericardial effusion
- cardiac tamponade- urgent drain of effusion
- pericardiocentesis
- NSAIDs
- pred
- colchicine
- tx cause eg infection, dissection
Classification of pericarditis
- acute (~2w)
- chronic >6w
causes of pericarditis
- idiopathic
- viruses, bacteria, fungi
- autoimmune (SLE, RA)
- CT and RT
- **- hypothyroidism
- **- anorexia nervosa
- **- trauma/surgery
- **- malignancy
sx of pericarditis
- *- hiccups( phrenic nerve runs either side of pericardial sac, irritation)
- *- cough
- central chest pain- worse on insp, lying, improved sitting forwards
- fever, wt loss, joint pain
- *- sight issues
- *- may have sx of tamponade (lightheadedness, chest pain, LoC, syncope)
signs of pericarditis
- pericardial rub
- pericardial effusion on Ix
- cardiac tamponade
Ix ?pericarditis
ECG
- PR depression!!!
- ST elevation with concave/saddle shaped
- sinus tachy if acute
- ESR
- trop
- CXR- cardiomegaly
- CT- localised inflammation
tx pericarditis
- NSAIDs/aspirin- 2w- NOT paracetemol!
WITH: Colchicine- take for 3m, decreases recurrence - corticosteroids (pred) if poor response to aspirin/NSAIDs, sometimes given with colchicine, however, encourages recurrence so not used as much
what is an atrial septal defect a remnant of
foramen ovale
what is the function of the foramen ovale
To bypass lungs, valve between R and L atria, creating R to L shunt
Blood oxygenated in placenta 🡪 umbilical vein , return to circulation in portal vein via ductus venosus 🡪 RA 🡪foramen ovale 🡪 LA 🡪LV 🡪aorta and to the body → umbilical artery come off the internal iliacs → placenta
associations of atrial septal defect
foetal alcohol syndrome
down’s
what way does the shunt go in atrial septal defect
L–> R
what is Eisenmenger’s
when the direction of a shunt shifts
the longstanding L to R shunt causes pulmonary HTN
leading to a reversal of the shunt
symptoms of Eisenmenger’s condition
- cyanosis
- syncope
- palpitations
- haemoptysis- pulm HTN
- *- recurrent infections
- *- stroke, gout, gallstones
signs of Eisenmenger’s
- cyanosis
- Clubbing
- HF
- arrhythmias
- bleeding disorders
- iron deficiency, high RBC count (polycythemia)
- poor kidney function
symptoms of atrial septal defect
- acyanotic– L–> R
- DVT, stroke, infarction of spleen, intestine, extremities (turbulence, clot enters systemic blood supply rather than lungs– paradoxical embolism)
- palpitations
- migraine
- pulm HTN (SOB, fatigue)
- Eisenmenger’s– Cyanosis
signs of atrial septal defect
- splitting of S2– due to delayed pulm valve closure due to pulm HTN and increased R heart vol
- soft midsystolic murmur at the upper left sternal border
tx atrial septal defect
- if small- monitor child, spont closure
- surgery- close the hole, if there is L–>R shunt with overload and R heart enlargement
why does a ventricular septal defect occur
- muscular ridge that grows up and the membranous ridge that grows down, fail to fuse
- majority are due to issues with membranous portion
associations with ventricular septal defect
foetal alcohol syndrome
down’s
other cardiac deformities
what way does the shunt go in ventricular septal defect
L to R
signs of ventricular septal defect
pansytolic murmur
Eisenmenger’s- cyanosis
symptoms of ventricular septal defect
- acyanotic
- asx if small
- pulm HTN– SOB, easy tiring
- poor feeding FTT
tx of ventricular septal defect
- surgical closure if sx
what is an atrioventricular defect
- hole in atrial and ventricular septums
direction of shunt in atrioventricular septal defect
L to R
sx of atrioventricular septal defect
- asx (partial, no valve regurg)
Baby:
- breathing issues
- pounding heart, weak pulse
- poor feeding, slow wt gain
- tired
- oedema of legs/abdo
partial- may present as child
- palpitations
- congestive HF- SOB, oedema
- pulm HTN- SOB
signs of atrioventricular septal defect
- systolic ejection murmur
- holosystolic murmur due to left AV valve regurg
ix ?atrioventricular septal defects
- USS
- ECHO
- ECG
tx of atrioventicular septal defect
- repair at about 5yo, sooner if sig
- if complete- do at 4-6m of age
what abnormalities are present in tetralogy of fallot
- stenosis of pulmonary artery
- hypertrophy of RV
- ventricular septal defect
- overriding aorta– arises from both ventricles instead of just L
Direction of shunt in Tetraology of Fallot
Pulm artery not that stenosed:
- L–> R
Pulm artery v stenosed
- R–> L as pressure in R heart is higher than the L
- cyanosis
sx of tetralogy of Fallot
- baby with cyanosis at birth
- clubbing ~2m old
- FFT
Tet spells
- cyanotic spell
- increased O2 demand, increased CO, increased shunt- deox blood into body
- child squats
why does child squat to relieve a Tet spell
- kinks fem arts
- increasing systemic resistance and in LV
- reversing the shunt to the R
- no deox blood now going to body
tx of tet spell
- keep child calm
- O2, Fluid
- betablocker,
- **- Opioids, phenylepinephrine- these increase pulm BF and therefore decrease resistance in R heart
Ix for ?tetralogy of Fallot
- prenatal ECHO
- CXR- boot shaped
tx of tetralogy of Fallot
Within 1st year of life:
- repair VSD
- enlarge pulm artery
- other defects then spontaneously resolve
Staging HF
- no undue dyspnoea from acitvity
- comfortable at rest, dyspnoea ordinary activity
- limiting dyspnoea on ADLs
- dyspnoea at rest, all activities cause discomfort
Monitoring of HF
6 monthly HF monitoring
- functional capacity
- fluid status
- cardiac rhythm
- cognition
- nutritional status
- review meds
- renal function
– doo every 2w if any changes
what does HF with preserved EF mean
EF >50%
- diastolic failure, due to inability of ventricle to relax and fill normally
- ie the % of blood pumped out of the LV is still high, but it has filled poorly
- vent hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity
what is HF with reduced EF
- EF <40%
- systolic failure
- inability of the heart contracting normally
- causes: MI, IHD, cardiomyopathy
what does ejection fraction mean
the % of blood pumped out of a filled LV
what is a tachyarrhythmia
> 100bpm
Name some causes of a narrow complex tachyarrhythmia
QRS <120ms/3 small sq
Supraventricular Tachys:
- sinus (regular)
- AF (irreg)
- atrial flutter (reg or irreg)
- wolff-parkinson- white
- AV re-entry
Name some causes of a broad complex tachyarrhythmia
Ventricular tachys:
- monomorphic (reg)
- vent fib
- torsade de pointes
- vent flutter
- any narrow complex causes combined with a block
what is a Supraventricular tachycardia
- arise above the level of the Bundle of His
- encompass regular atrial, irregular atrial and regular atrioventricular tachys
- NARROW QRS
What is a ventricular tachycardia
- tachy originating from the ventricles
- BROAD QRS complex
What is atrial flutter
- SVT
- re-entrant circuit around RA
ECG features of atrial fluuter
- saw-toothed flutter waves inbetween QRSes
- regularly irregular- ratio of flutter waves to QRSes is generally constant
- > 150bpm
- narrow qrs
sx of atrial flutter
- palpitation
- light headedness, syncope
- chest pain
- ## SOB
tx for atrial flutter
- cardioversion if unstable
- beta blockers or diltiazem/verapamil, digoxin for rate control if stable
- NO rhythm control
- LT anticoags
What is atrial fib
- loss of regular and ordered atrial contraction, so ventricle beats irregularly
- atrial depolarisation waves are too fast (>300bpm) for the vent to contract everytime, so only random waves make their way through
causes of atrial fib
MITRAL
- mitral valve regurg/stenosis
- IHD
- Thyrotoxicosis
- Raised BP
- Alcoholism/caffeine
- Lone/idiopathic
TOXIC-
- electrolytes
- Thyrotoxicosis
- Alcohol withdrawal
- *- dehydration
- *- Sepsis
- *- Haemochromatosis
STRETCH
- acute- PE, **MI
- Chronic- valvular (MS, MR), LVH with LA dilatation, AS
RUB
- myocarditis
- pericarditis
- *- tumours
MOST COMMON Mrs SMITH - female **- Sepsis - Mitral valve - IHD - Thyrotoxicosis - HTN
sx of AF
- SOB
- palpitations
- light headedness
ECG features of AF
- no p waves (lead II)
- irregularly irregular
- chaotic, fibrillatory baseline
- random QRS complexes
- narrow QRSes
ix ?AF
- ECG
- trop
- *- TFT, UE
- echo
tx of AF
- tx underlying cause if found
Acute
- haem unstable- electrical cardioversion
- Rhythm- preferable if younger, stable–> flecainide, amiodarone- gve as one off or more LT
- rate control- preference if older, stable
1a. beta blockers
1b. CCB (verapamil, diltiazem)
2. digoxin
Chronic
- just rate control initially as cardioversion and rhythm control risks embolism
- cardiovert/rhythm control only after 3w on anticoag
ANTICOAG
CHADSVASC score:- risk of stroke before starting anticoag
- Male + >=2- DOAC
- consider DOAC if >1 - give warfarin if DOAC is CI (prosthetic heart valve, elderly, renal)
- catheter ablation
name some doacs
rivaroxaban
apixaban
dabigatran
– be careful for renal disease
CI for spironolactone
hyperkalaemia
renal disease
what is the CHA2DS2VASc score
Cong HF- 1
HTN- 1
Age >=75yo- 2
Diabetes- 1
hx of stroke/TIA/VTE- 2
vasc disease (peripheral artery, MI, aprtic plaque)- 1
Age 65-74yo- 1
Sex- female- 1
what is wolff- parkinson-white syndrome
aberrant accessory pathway (bundle of Kent)- congential remnants
- intermittent racing heart rate, sudden onset, can last up to an hour
sx of wolff-parkinson white
- sudden palpitation
- light-headedness/dizziness, syncope
- SOB
- chest pain
- sweating
- fatigue on exertion
- sudden death
ecg features wolff-parkinson white
- sudden onset tachy (irreg)
- delta wave- small p wave then no clear isolelectric PR interval, QRS starts straight after p wave- loos like a swooping up to QRS
management of wolff-parkinson white
Symptomatic:
1. ablation
2 amiodarone, sotalol, flecainide
do NOT use digoxin= is contraindicated in WPW
acute: - narrow QRS, regular
1. vagal maneouvres
2. IV adenosine 6mg, 12mg, 12mg
3. BB/CCB
What is vent fib
ventricular tachy
broad QRS
- chaotic vent acivtity
sx vent fib
- loss of consciousness
- sudden death
management of vent fib/ VT no pulse
ALS algorithm-
- CPR until defib is charged
- 1st shock: give 1 shock if unwitnessed arrest, !3 quick succession shocks if witnessed arrest!
- resume CPR 2 mins
- rhythm check
- 2nd shock
- CPR 2 mins
- rhythm check
- 3rd shock and give adrenaline 1mg and amiodarone 300mg IV - repeat , giving A + A after 3rd, 5th, 7th, 9th shocks
once stable:
- implantable cardioverter defibrillator inacse occurs again
ecg features of vent fib
wide, irregular QRS
chaotic activity- irreg delfections of varying amplitude
- no ID p waves or QRSses
- rate 150-55bpm
- amplitude deacreases with duration (caorse VF– fine VF– flatline)
What type of tachy is torsades de Points, ecg feature
- polymorphic ventricular tachy
- ECG- twisting of peaks– looks like arctic monkeys album cover
RFs for torsades de point
- *- prolonged QT
- deranged electrolyes
- bradycardia
- HF
- LV hypertorphy
- drugs- cipro, flecainide, fluclonazole, levofloxacin, sotalol
what drugs can prolong the QT interval
- Heart meds- amiodarone, ivadradine
- *- Opioids- apomorphine, methadone
**- kinase inhib (cancers)- bosutinib, dasatinib, encoafenib, levnatinib, sorafenib
Psych
- Mood stabiliser- Lithium
- SSRI- citalopram, venlafaxine
- 1st gen- chlorpromazine, haloperidol, droperidol
- 2nd gen- risperidone
- fluclonazole
- abx- clarithro, erythromycin, levofloxacin
- anti-emetics- ondansetron (serotinergic antag), domperidone (DA antag)
- *- quinine
- sildenafil, vardenafil
management of torsades de point
- self limiting episodes although can turn into VF
- cardioversion if unstable and/or below hasnt worked
- Mg infusion (2g over 10min)
later- LT pacemaker
Algorithm for management of tachyarrhythmias
Unstable
- synchroniced DC shck
- amiodarone 300mg IV over 10-20mins, 900mg over 24hour
Stable - broad irregular QRS escalate polymorphic VT (torsades)- Mg 2g AF with BBB- tx as AF with bb/diltiazem pre-excited AF- amiodarone
- broad regular QRS
VT–amiodarone 300mg 20m, 900mg 24hr
if hx SVT with bundle branch block- vagal/adenosine as below - Narrow irregular QRS
tx as AF- BB/ diltiazem, consider amiodarone, digoxin - Regular narrow QRS-
Vagal maneouvres, adenosine bolus IV 6mg, 12mg, 12mg
– not improves - Atrial flutter– BB
– improves– was reentry SVT
What could a irregular broad QRS tachy be
- AF with bundle branch block
- Polymorphic VT (torsades de point)
- pre-excited AF
- vent fib (no pulse and unconscious)
What could a regular broad QRS tachy be
- vent tachy
- supravent tachys with bundle branch block
What could a irregular narrow QRS tachy be
SVT:
- AF
- atrial flutter
What could a regular narrow QRS tachy be
SVT:s
- Atriovent nodal re-entrant tachy (AVNRT)- mpost common
- atrioventricular reciprocating tachy
- atrial tachy
atrial flutter
What are bradyarrhythmias caused by
- IHD/MI
- drugs eg digoxin
- cardiac surgery
Type of Bradyarrhythmias
- 1st degree
- 2nd degree (mobitz 1/wenckebach, mobitz 2
- 3rd degree
- bundle branch block (L, R)
what is 1st degree heartblock
- normal pattern but PR interval >200ms (5 small sq)
- commonly seen in inferior MI
- often no sx
- should be monitored
what conditions is 1st degree heart block commonly seen in
inferior MI
Symptoms of 1st degree heart block
usually none
management of 1st degree heartblock
monitor
if high grade occurs- stop CCBs and beta blockers
UE for electrolyte imbalances
What is second degree heartblock
- more p waves than QRSes
- regular relationship between the two (can ratio them)
type of 2nd degree heart block
Mobitz 1/wenckebach
- progressively prolonged PR interval until QRS dropped, starts again
Mobitz 2
- PR int. constant but every few beats QRS is dropped - sudden unpredictable drop
what is 3rd degree heart block
no relationship between p waves and QRS- go at own paces, complete dissoc
QRSes- called escape beats, can be as low as 30bpm
Management of second degree heart block
Mobitz 1- consider pacing
Mobitz 2- pacemaker
sx of second degree heart block
often asx
tx of third degree/complete heart block
pacemaker- risk of sudden death
sx of complete heart block
- light-headedness/dizziness
- fatigue
- confusion
- chest pressure/pain
- SOB
What is bundle branch block
disease/lesion causing delay or blockage of conducting pathways
sx of bundle branch block
often asx
light headedness
SOB
Syncope
Types and causes of bundle branch block
LBBB- activation spreads from R-L/front to back
- MI
- HTN
- myocarditis
- cardiomyopathy
RBBB- activation spreads from L-R
- PE, MI, congen structural disease, pulm HTN, myocarditis
ecg features of LBBB
- Broad QRS (>120ms/3 small sq)
- W in V1, M in V6 (WiLLiaM)
- in V1, QRS is pointing down
ECG features of RBBB
- broad QRS (>120ms/3 small sq)
- M in V1, W in V6 (MaRRoW)
- in V1, QRS is pointing up
what does a new LBBB suggest
MI
Management of Bundle branch block
- control HTN
- tx sx of HF (loop diuretics)
- cardiac resynch therapy pacemaker- bivent
What are ventricular ectopics
- extra QRS complexes
- very common, mostly benign
presentation of ventricular ectopic
- palpitations
- feeling of heart missing a beat, or “thud”
Management of ectopics
- if many- can lead to myocardial strain (>=5% ectopics)
- catheter ablation
Management algorithm for badycardias
If unstable/risk of asystole (mobitz II/complete block, ventricular pause >3s, recent asystole):
- atropine 500mcg IV
No response to above:
- repeat atropine 500mcg until max dose of 3mg
OR
- TC pacing with opioid
OR
- adrenaline 2-10mcg/min infusion (6mg adrenaline in 500mL saline at 10-50ml/hour)
- Isoprenaline
- consider LT pacemaker or implantable cardioverter defib
What is cardiogenic shock
Circulatory failure resulting in inadequate organ perfusion
- <90mmHg systolic or MAP <65mmHg, with evidence of hypoperfusion
- caused by pump failure
causes of cardiogenic shock
- ACS
- dysrhythmias
- valve
- tension PTX
- tamponade
presentation of cardiogenic shock
- cold, clammy
- tachycardic
- low BP
- confusion, decreased GCS
- poor prognosis
name the acyanotic heart defects
L to R shunts
- VSD
- ASD
- PDA
- AV canal/AVSD
Name the cyanotic heart defects
R to L
- any acyanotic defects that have switched due to increased pulm BP (Eisenmenger’s)
The 4 T’s
- Transposition of the great arteries
- Tetralogy of Fallot
- *- Truncus arteriosus
- *- Tricuspid abnormalities
- *- Total anomalous pulmonary venous connection
- Tons of others
- *(pulmonary atresia, hypoplastic L heart, coarctation of aorta)
ecg characteristics of digoxin toxicity
- *- downsloping ST depression!
- *- inverted T waves
- short QT interval (<2 bigger squares from begginning of Q and end of T)
arrhythmias
- SVT
- slow AF
- VT
- sinus brady
- AV block
what should pts be taking after PCI for STEMI
- dual antiplt
- betablocker
- ACEI
- statin
what drug class worsens psoriasis
beta blocker
ecg features of PE
- sinus tachy
- RBBB
- R axis deviation
- RV strain- t wave inversion in V1-4
______________ - SI, QIII, TIII- deep S wave lead I, q wave in III, inverted T in III (classic but present in only 20% of cases, not specific)
- AF, flutter
- non specific ST changed (50%) incl depression
what time of day should you take statins
last thing in evening
SE of nicorandil (angina medication after CCB, BB havent worked)
GI ulceration:
if this occurs discontinue the medication immediately
also GI perf/haemorrhage/fistula/abscess
what route should you ogive medications in ALS if IV access cannot be obtained?
Intraosseous
a single episode of AF o warrants what
anticoagulation with CHA2DS2VASc and/or HASBLED/ORBIT scores done prior
CHA2DS2VASc-
- 0 - “low” risk and may not require anticoagulation;
- a 1 score is “low-moderate” risk and should consider antiplatelet or anticoagulation
- score 2 or greater is “moderate-high” risk and should otherwise be an anticoagulation candidate.
DOACs are now theoretically preferred over warfarin (in exam qs), although in practice not rly lols ok - maybe due to warfarin being better on kidneys and also has reversal agent
is statin safe in preg
no- stop it
definition of orthostatic hypotension
3-2-1 drop
- after 3 mins of standing!
- drop in BP S of at least 20mmHg
- and/or drop in BP D of at least 10
ECG characteristics of hypokalaemia
- u waves (small deflections immediately after T wave, usually in same direction as T wave)
- QT interval prolongation (>2 big sq from beginning of Q to end of T)
ECG characteristics of hypercalcaemia
- shortened QT interval
- J waves- positive deflection immediately after QRS)
ECG characteritics of hyperkalaemia
- tall tented twaves
- flattened p waves
- PR prolongation >(5ss)
- broad QRS
ECG changes in wolff parkinson white
- delta waves (slurred upstroke to QRS)- make QRS look wide at base
- short PR interval (<3ss)
SE warfarin
haemorrhage
teratogenic, ok in breast feeding
skin necrosis
purple toes
what antianginal do pts build up a tolerance to
standard release isosorbide
what cardiac conitions have a double pulse (bisferiens)
- arotic regurg
- aortic stenosis
- HOCM
how do you tx pda
indomethacin or ibuprofen
given to the neonate
inhibits prostaglandin synthesis
if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
what heart defect may occur within the first week of an MI
- VSD
new pansystolic murmur, HF- orthopnoea, SOB
what additional drug should be considered in a pt who needs CPR with a hx of PE
alteplase
what is ebstein’s anomaly, signs
congen cardiac abnormality
- low insertion of the tricuspid valve
- large RA and small RV
- tricuspid incompetence
- assoc with Li exposure in utero
signs
- cyanosis
- pansystolic murmur
- RBBB- split S1 and S2