Cardiology Flashcards
3 Processes of arteriosclerosis
- Progressive fibrosis of intima
- Fibrosis and scarring of muscular and elastic media
- Fragmentation of elastic lamina
Stable angina - definition
Triggers known
-Will resolve with GTN and rest
Strongest prediction of long term outcome for ACS and angina
-Left ventricular ejection fraction
Gold standard test to examine angina/ACS
Angiography - perfusion imaging
Vessel corrolated with worst prognosis
LAD
2 Mechanisms of treating angina with example drugs
- Increase flow to myocardium - vasodilate = Nitrates
- Decrease cardiac work - B-blockers/Ca-channel blockers
3 pathologies of ACS
- NSTEMI
- STEMI
- Unstable angina
Hour rules of MI
Patient survives first hour, then sudden cardiac death risk diminishes every subsequent hour
Diagnostic features of ACS
2 out of:
- ECG changes
- History/symptoms
- Troponin
Which troponin is best indiactor of myocardial damage
Troponin T
ST depression vs elevation
Depression = Icheamia Elevation = Infarction
3 steps STEMI treatment
- PCI (thrombolyse if unavailable)
- B-blocker
- ACEi within 24hrs
Drug treatment of unstable angina
- B-blocker
- Enoxaparin = inactivates clotting factor Xa
- Nitrates = IV
- Clopidogrel (+aspirin)
NHS policy on MI
Treat within 36 minutes
Contraindications thrombolysis
- Internal bleeding
- Pancreatitis
- Active lung disease
- Pregnancy
- Liver disease
- Varices
- Head trauma
Becks triad of tamponade (fluid in pericardial space decreasing filling capacity)
- Hypotension
- Distended neck veins
- Muffled heart sounds
Pulse paradoxus
Fall of systolic BP >10 on inspiration
Mural thrombus after MI
Clot over damaged myocardium (can embolise)
Ventricular rupture after MI
5-10days after MI can cause tamponade or death
Mitral incompetance after MI
Due to damage to papillary muscle
Dresslers syndrome
1-3wks after = Autoimmune pericarditis after MI
Viral causes of acute pericarditis
- Coxsackie B
- Echovirus
ECG changes pericarditis
- Saddle shaped
- Widespread ST elevation
*Pericardial rub
Treat pericarditis - risk of treatment
- NSAIDs
- Cause
- Steroids
*Dont use NSAIDs directly after MI as increase rupture risk
Chronic pericarditis (6-12mnths) - pathological changes
Thickening of pericardium causes decreased filling = Restritive pericarditis
Endocarditis
- Commonly affected areas
- Organisms involved
- 6 signs (FROM JANES)
- Valves (mostly A & M as high pressure L side, R-side = more common in IV users)
- Staph aureus/strep pneumonia - dental
- Fever
- Roths spots (eyes)
- Oslers nodes
- Murmour
- Janeways lesions
- Anemia
- Nail (Splinter) haemmorhage
- Emoli (systemic!)
- Splenomegaly
Diagnostics endocarditis
+ cultures and echo
-can cause altered platelets
Causes of myocraditis and risk
- Viral: coxsackie
- Drugs
- Immune (SLE/IBD/Type 2 diabetes)
-Fulminant HF
ECG changes myocarditis and clinical sign
- S3/4 gallop - think HF
- High troponin
- ST depression or elevation
- Twave inversion
- AV block
Definitive test myocarditis
(Risky) = Biopsy
S1 vs S2 splitting
S1 = RBB S2 = may be physiological (inspiration) or atrial septal defect
S3 vs S4
S3 = KENTUCKY
-Left ventricular failure, oscillation of blood back and forward between ventricle - normal in young and athletes
S4 = TENNESSEE
-Aortic stenosis/Cardiomyopathy, blood forced against stiff ventricle - never normal
Breathing sounds and when bets to hear murmor
- lEft murmours best on Expiration
- rIght murmours best on Inspiration
Murmours
DAR DSM
SMR SAS
- Early Diastolyic = Aortic regurg, best heard leaning forward, collapsing/bounding/water hammer pulse
- Mid Diastolic = Mitral stenosis
- Pan-Systolic = Mitral Regurg, radiates to axilla + 3rd sound
- Mid/Ejection-systolic = Aortis stenosis, crescendo-decrescendo radiates to axilla. Slow rising pulse
Most common form of HF and measure
Systolic - pump failure (fall ejection fraction)
L vs R HF symptoms
L = pulomary oedema/congestion R = systemcic oedema, JVP, hepato/splenomegaly
Causes of L-HF
- Systolic
- Diastolic
SYSTOLIC
- Ischaemic heart disease
- Non contractile scare tissue
- Hypertension
- Dilated cardiomyopathy
DIASTOLIC
- Hypertension
- Aortic stenosis
- Hypertrophic & Restrictive cardiomyopathy
Causes of R-HF
- L-R shint = increased R pressure
- Lung disease (cor pulmonale) = increased R pressure
*Increased R pressure causes hypertrophy then failure
How does HF cause arrhythmia
Stretched myocytes become irritated causing arrhythmia
ABCD of chronic HF and benefits of each drug
- ACEi or ARB - decrease fluid overload
- B-blockers
- Ca channel blockers - improve prognosis
- Diuretics - improve symptoms
Manage Acute HF
- Stabilise diuretic and ventilate
- Start ACEi and B-blocker
What causes acute on chronic HF and whats the biggest sign of decompensation
- Acute event (MI, Infection, arrhythmia, electrolyte imbalance)
- Pulmonary oedema
What valves are in each side of the heart
L = MA R = TP
Aortic valve disease
- Type of valve
- Disease pathophysiology
Aortic = tricuspid
-Stenosis = harder to open
Calcification from age, rheumatic fever, anatomical variaton
-Regurg = harder to close
Aortic root dilation, ideopathic, dissection, endocarditis
Mitral valve disease
- Type of valve
- Disease pathophysiology
Mitral = Bicuspid
- Both stenosis and regurg = rheumatic fever
- High risk AF
Which valvular pathology is most common
Mitral regurgitation
Diagnostics valvular disease
+ specific tests to look at extent
- Echo
- Ecg
- Angiogram
- Stress test - determines extent
Nitrates
- 2 examples
- MOA
- Main problem
- GTN and isorbide trinitrate
- Metabolised to NO group, alter CAMP, decrease intracellular Ca and vasodilation
- Tolerance
Clopidogrel
- MOA
- SE
- Contraindication
- Prodrug, inhibits ADP receptor = activates platelets
- Bleeding, thrombotic thrombocytopenic purpura
- PPI
Thrombolytics
- 3 examples
- MOA
- Limitation
- Alteplase, Tenecteplase, Streptokinase
- Converts plasminogen to plasmin = degrades fibrin thrombus
- Streptokinase Ab present in blood and cant be used again for a year
Parenteral analogues
- 2 examples
- MOA
- Antidote
- How is does calculated
- Contraindications
- Heparin and Daltaparam (low mol weight H)
- Binds to antithrombin AIII - inhibits factor Xa
- protamine sulfate
- by weight
- renal failure
NOACs
- 3 examples and their MOA
- Benefit and risk
- Riveroxiban = Direct factor Xa inhibitor
- Apixaban = Direct factor Xa inhibitor = AF used
- Dabigatron = Direct thrombin inhibitor
-Wider therapeutic index than warfarin but no antidotes
Warfarin
- MOA
- Factors affectes
- Big contraindications
- Vitamin K antagonist via reductase
- Depletes factors II, VII, IX, X
- Pregnancy, macrolides, the pill, alcohol
2 main treatments for AF
- MOA
- SE
- Contraindications
Amiodarone
- Membrane stabiliser - Na/Ca/Alpha-receptors
- Lung/Ears/Thyroid/Liver toxic
- Digoxin
Digoxin
- Na+K+atpase, increases Na = -chrono +iono
- Narrow therapeutic index
Diuretics
- types (examples)
- MOA and site
- SE
THIAZIDES - bendroflumathiazie, indepamide, metolazone
- Na+Cl- symporter DCT
- Electrolyte disturbances
LOOP - Furosemide and Bumetanide
- Na+K+Cl in THICK A loop Henle
- Electrolyte disturbance and otoxic, renal failure with NSAIDs and ACEi
K+ SPARING
- Amiloride = Na+ resorption in DCT
- Spironalactone = Aldosterone receptor antagonist
- Contraindicated with any drugs that affect RAAS
Major risk of spironalactone
Hyperkalemia
Contraindications of Thiazide diuretics (one drug and a conditions LAG)
- Lithium
- Addisons
- Gout
- Which B-Blocker isnt cardioselective
- Which has the fastest effect (twice daily dose as opposed to once)
- Propanolol
- Metoprolol
Arterial Ca channel blockers (examples)
- Effect
- SE
- Amlodipine/Felodopine
- L-channels in vasculature = dilation
- Vasodilatory = flushing, snycope
Cardiac Ca channel blockers (examples)
- Effect
- SE
- Verapamil/Diltiazem
- Decreases cardiac contractility
- Contraindicated B-blockers - bradycardia
SE and 2 biggest risks of using ACEi
- Cough
- HF (with diuretics)
- Nephrotoxic = AKI
ARB
- 2 examples
- MOA
- 3 SE
- Losartan/Candesartan
- Inhibits Ang2
- Teratogenic/hyperkalemia/renal failure contraindication
Alpha blockers
- 1 cardiac example
- MOA
- SE
- Doxazosin
- Alpha-1 specific, decreases inostiol phosphate, vasodilate
- Dry mouth, hypotension, floppy iris syndrome
Statins MOA
HMG-coenzyme A reductase inhibitor, fall in hepatic cholesterol synthesis
Fibrates MOA
PPARalpha agonist - decrease in lipid metabolism
SE of Fibrates and Statins
-Interactions of statins
- Myalgia (increased by amiodarone)
- Hepatotoxic
-Fibrates, antibiotics, ca channel blockers
- Brady vs tachycardia
- SVT definition
- Brady = >50 , Tachy>100
- Any tachy above bundle of his mostly considered to be AVNRT or AVRT - all NARROW complex
2 Treatment lines for AF
1) B-blocker** OR Ca++channel blocker
2) Add Digoxin or Amiodarone
Cause of Arial flutter, risk and treatment
- Rentry rhythm
- Becoming AF
- Same as AF but shock if haemodynamically unstable
AVNRT
- ECG pattern
- Patho
- Epi
-TREAT
- Pwave immediatly following QRS - may be hidden inside
- Regular
- Rentry path at AV node
- Most common SVT, Women 3:1
TREAT
- Valsalva/Carotid massage
- Adenosine
- Cardioversion
AVRT = Wolf parkinson White
- ECG pattern
- Patho
-TREAT
- Short slurred QRS + delta wave (classic sign WPW)
- Accessory path not in AV node
TREAT
- Valsalva/Carotid massage
- Adenosine
- Cardioversion
2 non shockable rhythms
- PEA
- Asystole
Ventricular tachys (BROAD)
- 3 types
- epi
VT
- often after MI
- may become VF
- regular broad QRS
Torsades
- subtype VT (polymorphic)
- twisting QRS
- Mg sulfate + isoprenaline
VF
Defib vs cardioversion
Defib is not syncronised to peak of QRS (cardioversion) it is shock emergancy at any point of cycle.
Difference between VT’s and SVT’s
SVT will be affected by carotid sinus pressure (vasalva and massage) VT will not
1st degree block
- ECG changes
- Patho
HINT: If the R is far from P then you have a first degree
- P far from QRS (prolong PR)
- AV nodal block - often not serious
Mobitz 1 (Wenkenbach) block
- ECG changes
- Patho
HINT: Longer, longer longer drop then you have a wenkenbach
- Progressive PR length then absent QRS (repeat)
- Disease of AV node
Mobitz 2 block
- ECG changes
- Patho
HINT: If some P’s dont get through then you have a type 2
- Extra p waves as some are not being conducted down to ventricles = occasional missing QRS. PR interval = regular
- Every qrs may have 2/3 p’s
Complete/3rd degree block
- ECG changes
- Patho
HINT: If P’s and Q’s dont agree then you have a third degree
- No relationship between P and Q (random PR changes)
- Atrial contraction normal but none is being conducted to ventricles
Treatments of blocks
- 1st = none/monitor
- M1/M2/3 = pace
R Bundle branch block
- Ecg
- Cause
- Treat
MaRroW -M in V1 -W in V6 -Atrial sept defect Treat = monitor and control other pathologies
L Bundle branch block
- Ecg
- Cause
- Treat
WiLliaM -W in V1 -M in V6 -L-sided disease (stenosis, cardiomyopathy, HF) Treat = Pace if symptomatic
Ectopics
- Atrial
- Ventricular
Occur when P waves or QRS out of sequance = Benign
- Atrial = abnormal pacemaker stimulus
- Ventricular = wide QRS, increase with age
Which ectopic usually presents with symptoms and what can cause them
- Atrial
- Caffeine/stress/B-blocker/exercise/electrolytes
Ventricular extrasystoles
- Patho
- Symptoms
- treat
Feeling of a “skipped beat”
- Premature ventricular contraction initiated from purkinje fibres instead of SAN
- Symptoms - syncope on exertion
- Lifestyle changes/antiarrhythmics/ablation
What is the span of the normal cardiac axis
+90 - -30
aVR should always be negative, what are some reasons it could be positive
- Dextrocardia
- Inproperly places leads
Pulomary hypertension
- epi
- possible cause
- symptoms
- x-ray findings
- rare often fatal disease of small vessels often affecting women
- ideopathic
- cyanosis/sob/pain/fatigue/oedema
- often clear lungs but central “pruned” vessels and big pas
SE of calcium channel blockers
Oedema
What is a major complication of mitral stenosis
Pulmonary hypertension
Principles of treating HTN
Increase doses of drugs used to max (eg amlodipine) before begining another drug to reduce polypharmacy
Digoxin effect and half life
35hr half life taking 5-7days to reach steady state, not a drug for rapid action
Drug treatment for HTN (2 arms)
Hint: Caribbean=C
Under 55 with HTN 1-ACE or ARB 2-Add Ca channel blocker 3-Add thiazide diuretic 4-Add spironalactone
55+ or Afro/carribean 1-Ca channel blocker 2-Add ACE or ARB 3-Add thiazide diuretic 4-Add spironalactone
