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
