Cardiac Core Conditions Flashcards
What does ACS encompass?
STEMI
NSTEMI
Unstable Angina
How is a STEMI caused?
Atherosclerotic plaques build over years starting
Accumulation of LDL & sat fat in the intima
Adhesion of leukocytes to endothelium leading to foam cell formation.
STEMI=sudden abrupt disruption of a cholesterol laden plaque
Resulting in exposure of substances
Promote platelet aggregation & thrombus formation interrupting blood flow in a coronary artery.
Zone of myocardium supplied by vessel loses its ability to shorten & perform contractile work.
How is an NSTEMI caused?
Acute imbalance between myocardial O2 demand & supply
Most commonly due to reduction in myocardial perfusion.
Type 1 MI= non-occlusive thrombus that develops in a disrupted atherosclerotic plaque.
Plaque rupture w/superimposed non-occlusive thromboembolic event leads to CA obstruction, vasospasm, chronic arterial narrowing, vasculitis, extrinsic factors leading to hypoT, hypoxia, hypoV.
Lack of ST elevation because infarct is not full thickness (not transmural).
How is unstable angina caused?
Fissure in the endothelial lining over a cholesterol plaque
Results in loss of integrity of the plaque cap.
Rupture leads to exposure of the subendothelial matrix elements (collagen) stimulating platelet activation & thrombus formation.
Release of tissue factor directly activates coagulation cascade & promotes formation of fibrin.
Occlusive thrombus can lead to an acute STEMI.
How may an MI present in a diabetic?
Silent atypical infarcts SOB Syncope/coma Hyperglycaemic crisis Acute pulmonary oedema May resemble a stroke
How is a STEMI investigated?
ECG: ST ELEVATION/depression, pathological Q waves, new LBBB, PR elevation/depression Troponin: T= rise 3-12hours post-MI I= 3-12hours Lactate dehydrogenase= 8-12hours Myoglobin= 1-4hours Creatinine Kinase
How is an NSTEMI investigated?
ECG: ST depression, T-wave inversion
Troponin: Increased
How is a STEMI treated?
Morphine Oxygen Nitrates Aspirin 300mg Ticagrolol PCI!! Ideally within 2 hours of symptom onset
What are the complications of a STEMI?
Mitral Regurg: Signs of acute CF (pulmO, hypoT) due to chordal rupture, papillary infarct, LV dilation, diagnosed by ECHO,Tx- urgent surgery & reperfusion
Ventricular Septal rupture: Usually anterior/posterior MI, signs similar to mitral regard, pan-systolic murmur, investigated by ECHO, Tx- urgent surgery to repair defect
Cardiac tamponade & rupture: Cause of sudden death post-MI, ECHO, more common in elderly, hypoT, distended neck veins, muffled heart sounds, Tx- temporary pericardiocentesis but urgent surgery required
Arrhythmia: VF- defibrillator, VT-amiodarone, lignocaine, SVT-AF- beta blockers
Continuing chest pain
Fever
Failure (hypoT, cariogenic shock)
What is the pathophysiology of an aortic dissection?
Occurs following a tear in the intimal layer of the aorta with subsequent anterograde/retrograde flow of blood within the outer 1/3rd of the tunica media.
Thought to occur due to medial degeneration
What are the predisposing factors for an aortic dissection?
HTN!! Marfans/Ehlers-Danlos Bicuspid aortic valve Pregnancy Aortic coarctuation Cocaine abuse Iatrogenic Giant cell arteritis Turner's syndrome
Where do most aortic dissections occur?
Ascending aorta
Due to greater pressure on the aortic wall as it is closer to the LV outflow.
What are the consequences of an ascending aortic dissection?
Haemopericardium (syncope & sudden death)
Right haemothorax
What are the consequences if an aortic dissection occludes blood vessels?
Coronary: STEMI
Common carotids: Stroke
Subclavian: Acute upper limb ischaemia
Coeliac/mesenteric: Ischaemic bowel
What are the signs & symptoms of an aortic dissection
Acute onset pain Interscapular tearing pain Stroke Syncope Congestive HF Haemopericardium: Pulsus paradoxus, faint heart sounds, distended neck veins Pulse deficits of >20mmHg
How is an aortic dissection investigated?
ECG
CXR
TTE/TOE
CT/MRI
How is an aortic dissection managed?
Analgesia
Surgery & stenting
BP control: IV Labetalol
What are SVTs? What are the different types?
Any tachycardia arising from above the bundle of HIS
AF, flutter, AV re-entry, junctional, sinus node re-entry
What are the causes of SVT?
Ectopic pacemaker cells
Re-entry circuits
IHD
Stimulants: OH-, caffeine, cocaine
How are SVTs investigated?
ECG: Narrow QRS
abnormally shaped P-waves
How are SVTs managed?
Adenosine 6mg IV then 12mg in 1-2mins if no effect
Beta blocker/CCB: Diltiazem or Verapamil
Digoxin toxicity: Fab fragments
AT w/block: DC cardioversion
What are the complications of an SVT?
Dilated cardiomyopathy
Resistance to therapy
Congestive HF
What are the 2 types of VT?
Non-sustained: HR >120bpm, lasting for at least 3beats then spontaneously resolves in <30secs
Sustained: HR >100bpm, lasts at least 30secs or requires termination earlier due to harm instability
What are the 2 wave forms VT can take?
Monomorphic: Most frequent post-MI sign of extensive damage
Polymorphic: Uncommon, frequently the result of acute cardiac insult, rapidly deteriorates to VF. Rarely sustained
What are the causes of VT?
Cardiomyopathy Drug induced Myocardium damage secondary to ischaemia MI Congenital
What are the signs & symptoms of VT?
Dizziness/lightheaded SOB & anxious Cold & clammy Chest pain & palpitations CV collapse Profound shock Haem instability: dec consciousness, chest pain, systolic BP <90, HF
How is VT investigated?
ECG: Broad based
Monomorphic: All QRS same rate, shape & size: 120-250bpm, RBBB pattern
Polymorphic: QRS varies from preceding one: 200-250bpm
How is VT managed?
If pulse present DO NOT SHOCK
Mono: DC cardioversion 3 attempts then Amiodarone
Poly: DC cardioversion
Torsades: IV magnesium
What is VF?
Rapid uncoordinated fluttering contractions of the ventricles resulting in loss of synchronisation between HB and pulse beat.
What are the causes of VF?
MI
Ischaemia
Chronic infarction scar
What are the signs & symptoms of VF?
Chest pain
Fatigue
Haemodynamic instability
How is VF investigated?
ECG: Rx MI, Short PR, Prolonged QT interval
Amplitude of wave proportional to oxygen content
Drug & tox screen
Bloods: Cardiac enzymes, electrolytes
How is VF managed?
ACLS protocol for cardiac arrest Oxygen DC cardioversion 2mins/5cycles CPR repeat shock Epinephrine/Adrenaline 1mg every 3-5mins Amiodarone 300mg then 150mg
What is the prognosis for VF?
Depends on time from onset to intervention
4-6mins poor prognosis
VF occurence >48hours post-MI = poor prognosis & inc rate of recurrence
What is the most common cause of pulseless electrical activity?
Hypovolaemia
What is the long-term management post-MI?
2 Platelet agents: Aspirin, Ticagrolol
Statin
Beta blocker
What checks need to be done when starting Amiodarone?
U&Es
TFTs
When should/shouldn’t a patient be shocked in AF?
Y: Haemodynamically unstable
N: AF>2days due to VTE risk (if no anticoagulation given- should be prescribed for 3weeks)
What are the different types of angina?
Stable
Unstable
Variant/ Prinzmental
