Cardiology Flashcards
what is the ratio of chest compressions to ventilation in adults?
30:2
what is adrenaline given in a VT/VT cardiac arrest?
once chest compressions have restarted after the third shock an then every 3-5 mins (during alternate cycles of CPR)
what are the 2 shockable rhythms?
pulseless VT
VF
what happens if a cardiac arrest happens in a cardiac monitored patient?
do up to 3 quick successive ‘stackd’ shocks, rather than 1 shock followed by CPR
what is done in asystole/pulseless electrical activity?
adrenaline 1mg asap
following successful resuscitation, what oxygen sats should be given?
94-98%
to address potential harm caused by hyperoxaemia
what are reversible causes of cardiac arrest?
4T’s and 4H’s
Thrombosis
Tension pneumothorax
Tamponade
Toxins
Hypoxia
Hypovolaemia
Hyperkalaemia, hypoglycaemia, hypocalcaemia
Hypothermia
adrenaline dose in a cardiac arrest?
cardiac arrest: 10ml 1:10,000 IV or 1ml of 1:1000 IV
adrenaline dose in anaphylaxis?
anaphylaxis: 0.5ml 1:1,000 IM
how does adrenaline work?
responsible for the fight or flight response
released by the adrenal glands
acts on α 1 and 2, β 1 and 2 receptors
acts on β 2 receptors in skeletal muscle vessels-causing vasodilation
increases cardiac output and total peripheral resistance
causes vasoconstriction in the skin and kidneys causing a narrow pulse pressure
actions of adrenaline on adrenergic receptors?
inhibits insulin, stimulates glucagon secretion
lots more actions to raise blood glucose
what is brugada syndrome?
inherited cardiovascular disorder which may present with sudden cardiac death
AD inheritance
ECG changes in brugada syndrome?
convex ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
partial right bundle branch block
Ix of brugada syndrome?
ECG changes more apparent following administration of flecainide or ajmaline
mx of brugada syndrome?
implantable cardioverter-defibrillator
what is syncope?
transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery
features of syncope?
trigger- emotion, pain, exercise
prodrome- feeling faint, dizzy, nausea, visual disturbance
pallor
near immediate complete recovery
types of syncope?
reflex syncope (neural mediated) orthostatic syncope cardiac syncope
causes of reflex syncope
vasovagal - emotion, pain, stress
situational- micturition, sneeze etc
carotid hypersensitivity- e.g. shaving, tight collar
causes of orthostatic syncope?
insufficient of baroreceptors causes autonomic dysfunction
types of orthostatic syncope?
primary autonomic failure- PD, lewy body dementia
secondary autonomic failure- diabetic retinopathy, amyloidosis, uraemia
drug-induced- diuretics, alcohol, vasodilators
volume depletion- haemorrhage, diarrhoea
exercise-induced
causes of cardiac syncope?
arrhythmias e.g. sick sinus syndrome, SVT, VT
structural- valvular, MI, hypertrophic obstructive cardiomyopathy
others e.g. PE
questions to ask in a syncope history (5Cs and 5Ps)
5Ps- precipitant, prodrome, palpitations, post-event phenomena
5Cs- colour, convulsions, continence, cardiac problems, family history of cardiac death
Ix of syncope?
CV examination postural BP (fall in SBP by >20 or DBP by >10 is considered diagnostic) ECG/2hr ECG Carotid sinus massage Tilt table test
mx of syncope?
if CV cause -> refer (24 hours)
if epilepsy suspected -> refer (2 weeks)
if uncomplicated- arrange ECG within 3 days and reassure and advice of avoiding triggers
if affecting QOL -> offer referral for tilt table test to assess whether syncope is accompanied by a severe cardioinhibitory response
name some genetic causes of primary cardiomyopathy?
1) hypertrophic obstructive cardiomyopathy- leading cause of death in young athletes
- usually due to a mutation in the gene encoding B-myosin heavy chain protein
2) Arrhythmogenic right ventricular dysplasia- RV myocardium is replaced by fatty and fibrofatty tissue. 50% have mutation encoding for components of desmosome.
ECG abnormalities- V1-V3, typically T wave inversion, epsilon wave (terminal notch in QRS complex)
mx of Arrhythmogenic right ventricular dysplasia?
sotalol, catheter ablation, ICD
name some acquired causes of primary cardiomyopathy?
- peripartum cardiomyopathy- typically develops between last month of pregnancy and 5 months post-partum. More common in older women, greater parity and multiple gestations
- takotsubo cardiomyopathy- ‘stress’ induced cardiomyopathy i.e. family member has just died. Transient, apical ballooning of the myocardium
name some mixed causes of primary cardiomyopathy?
- dilated cardiomyopathy- alcohol, coxsackie B virus, doxorubicin, post partum hypertension
- restrictive cardiomyopathy- amyloidosis, post-radiotherapy, Loeffler’s endocarditis
causes of secondary cardiomyopathy?
- infective
- infiltrative- amyloidosis
- storage- haemochromatosis
- toxicity- doxorubicin, alcoholic cardiomyopathy
- inflammatory sarcoidosis
- endocrine- DM, thyrotoxicosis, acromegaly
- neuromuscular- Friendreich’s ataxia, DMD, myotonic dystrophy
- nutritional deficiency- thiamine
- autoimmune- SLE
signs and symptoms of dilated cardiomyopathy?
acute pulmonary oedema
systemic or pulmonary emboli
congestive cardiac failure (exertional dyspnoea, orthopnoea, PND, fatigue, RUQ pain)
Ix of dilated cardiomyopathy?
ECHO
ECG- sinus tachycardia, AF
CXR- heart failure signs
tx of dilated cardiomyopathy?
diuretics ACEi BB aldosterone antagonists antiarrhythmic agents anticoagulation cardiac resynchronisation therapy, ICDs cardiac transplantation
what is the most common cause of cardiac death in the young?
hypertrophic obstructive cardiomyopathy
what is hypertrophic obstructive cardiomyopathy?
AD disorder of muscle tissue caused by defects in the genes encoding contractile proteins-> most commonly B-myosin heavy chain protein or myosin binding C protein
features of hypertrophic obstructive cardiomyopathy?
often asymptomatic
exertional dyspnoea, angina, syncope
arrhythmias, HF, sudden death
jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur increases with Valsalva manoeuvre and decreases on squatting
associations with hypertrophic obstructive cardiomyopathy
Friedreich’s ataxia
Wolff-Parkinson white
ECHO findings of hypertrophic obstructive cardiomyopathy?
mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
ECG findings of hypertrophic obstructive cardiomyopathy?
LVH
non- specific ST segment and T-wave abnormalities, progressive T-wave inversion may be seen
Deep Q waves
AF
mx of hypertrophic obstructive cardiomyopathy?
Amiodarone Beta blockers or verapamil for symptoms Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis
what is Friedreich’s ataxia?
AR
GAA repeat in X25 gene on chromosome 9
onset age 10-15 years
features of Friedreich’s ataxia?
gait ataxia, kyphoscoliosis, absent ankle jerks/extensor plantars, cerebellar ataxia, optic atrophy, spinocerebellar tract degeneration
differentials of chest pain?
ACS pneumothorax PE pericarditis dissection aortic aneurysm GORD MSK pain shingles
features of MI?
sudden onset, central crushing chest pain
may radiate into neck and down left arm
signs of autonomic dysfunction- sweating, nausea, pale
what is an NSTEMI?
partial thickness necrosis of the myocardium
ST changes- ST depression, T-wave inversion or no changes
no troponin rise
ECG features of previous MI?
pathological Q waves
what is a STEMI?
full thickness necrosis of myocardium
hyper acute T waves are often first sign
ST elevation- >0.2mV in men and >0.15mV in women in leads V2-V3 and/or >0.1 in other leads
name some cardiac enzymes?
Troponin T- rises at 4-6 hours, peaks at 12-24, normal at 7-10 days CK-MB- returns to normal after 2-3 days CK AST LDH
false positives of troponin T?
-itis e.g pericarditis, myocarditis
trauma to heart
CKD
sepsis
medical mx of MI?
Morphine- 2.5-10mg IV PRN
O2 (if sats <94%)
GTN- 2 puffs
Aspirin 300mg
perform an ECG but don’t delay transfer to hospital
dual antiplatelet therapy- aspirin and clopidogrel/ticagrelor
unfractionated heparin if going to have PCI
when to refer for chest pain?
onset <12 hours with abnormal ECG-> emergency admission
onset 12-72 hours ago-> refer for same day assessment
onset >72 hours ago -> perform ECG and troponin before deciding on action
surgical intervention for MI?
PCI within 120 mins (if onset <12 hours ago)
thrombolysis if PCI can’t be done within 120 mins (and onset <12 hours ago)
CABG
types of thrombolysis?
tissue plasminogen activator, tenecteplase, alteplase
what needs to be done after thrombolysis?
ECG within 90 mins to seen if there has been a >50% resolution in the ST elevation
(if there has not been adequate resolution then rescue PCI)
risks of thrombolysis?
reocclusion
intracranial haemorrhage
infection
bleeding
how to thrombolytics work?
plasminogen to form plasmin, which degrades fibrin and so breaks up the thrombi
what class of drug is clopidogrel and ticagrelor?
P2Y12-receptor antagonist
CI to thrombolysis?
active internal bleeding recent haemorrhage, surgery or trauma coagulation and bleeding disorders intracranial neoplasm stroke <3 months aortic dissection recent head injury pregnancy severe hypertension
secondary prevention of MI?
DAPT- aspirin plus ticagrelor, clopidogrel, prasugrel ACEi Beta-blocker Statins aldosterone antagonist if MI plus HF
lifestyle- diet, exercise, sex after 4 weeks of uncomplicated MI
complications of MI?
cardiac arrest cardiogenic shock chronic HF arrhythmias pericarditis aneurysms left ventricular wall rupture
what are the primary and secondary prevention doses of statins?
primary- 20mg
secondary- 80mg
how does aspirin work?
antiplatelet
inhibits COX which in turn inhibits production of thromboxane A2
reduces platelets ability to aggregate
what is the GRACE score?
a risk stratification tool used for an NSTEMI to decide upon further management
high risk= coronary angiography during admission
low risk= coronary angiography at a later date
what is the pathophysiology of ACS?
Atherosclerosis in coronary arteries -> gradual narrowing and reduced O2 reaching myocardium -> plaque rupture causes occlusion and ischaemia of myocardium
unmodifiable risk factors for IHD?
increasing age
male
FH
modifiable risk factors for IHD?
smoking DM Hypertension hypercholesterolaemia obesity
ECG changes and coronary territories?
anterior- V1-V4 (LAD)
inferior- II,III,aVF (right coronary)
lateral- I, V5-6 (left circumflex)
features of typical angina?
1) constricting discomfort in the front of the chest, or in the neck, shoulders, jaw and arm
2) precipitated by physical exertion
3) relieved by rest or GTN in about 5 minutes
features of atypical and non-anginal pain?
2 features- atypical
0/1 feature- non-anginal chest pain
mx of stable angina?
Attacks- GTN spray
1st line -beta blocker or CCB
if using CCB on its own- use rate-limiting e.g. verapamil or diltiazem
if using BB and CCB, use long-acting dihydropyridine e.g. nifedipine
If still symptomatic on BB and CCB-> only add third drug whilst waiting for PCI or CABG
if can’t tolerate CCB and BB- add long-acting nitrate e.g ivabradine, nicorandil or ranolazine
SE of CCBs?
headache
flushing
ankle oedema
SEs of BBs?
bronchospasm
fatigue
cold peripheries
sleep disturbances
SEs of nitrates?
headache
postural hypotension
tachycardia
SEs of nicorandil?
headache
flushing
anal ulceration
what is nicorandil?
potassium channel activator
causes of acute pericarditis?
viral infections- coxsackie virus, EBV, influenza, HIV TB uraemia trauma post MI connective tissue disease hypothyroidism malignancy
features of acute pericarditis?
pleuritic chest pain relieved by sitting forwards non-productive cough dyspnoea flu-like symptoms pericardial rub tachypnoea tachycardia
ECG changes of acute pericarditis?
saddle-shaped ST elevation
PR depression