Cardiology Flashcards
(93 cards)
1
Q
3 Processes of arteriosclerosis
A
- Progressive fibrosis of intima
- Fibrosis and scarring of muscular and elastic media
- Fragmentation of elastic lamina
2
Q
Stable angina - definition
A
Triggers known
-Will resolve with GTN and rest
3
Q
Strongest prediction of long term outcome for ACS and angina
A
-Left ventricular ejection fraction
4
Q
Gold standard test to examine angina/ACS
A
Angiography - perfusion imaging
5
Q
Vessel corrolated with worst prognosis
A
LAD
6
Q
2 Mechanisms of treating angina with example drugs
A
- Increase flow to myocardium - vasodilate = Nitrates
- Decrease cardiac work - B-blockers/Ca-channel blockers
7
Q
3 pathologies of ACS
A
- NSTEMI
- STEMI
- Unstable angina
8
Q
Hour rules of MI
A
Patient survives first hour, then sudden cardiac death risk diminishes every subsequent hour
9
Q
Diagnostic features of ACS
A
2 out of:
- ECG changes
- History/symptoms
- Troponin
10
Q
Which troponin is best indiactor of myocardial damage
A
Troponin T
11
Q
ST depression vs elevation
A
Depression = Icheamia Elevation = Infarction
12
Q
3 steps STEMI treatment
A
- PCI (thrombolyse if unavailable)
- B-blocker
- ACEi within 24hrs
13
Q
Drug treatment of unstable angina
A
- B-blocker
- Enoxaparin = inactivates clotting factor Xa
- Nitrates = IV
- Clopidogrel (+aspirin)
14
Q
NHS policy on MI
A
Treat within 36 minutes
15
Q
Contraindications thrombolysis
A
- Internal bleeding
- Pancreatitis
- Active lung disease
- Pregnancy
- Liver disease
- Varices
- Head trauma
16
Q
Becks triad of tamponade (fluid in pericardial space decreasing filling capacity)
A
- Hypotension
- Distended neck veins
- Muffled heart sounds
17
Q
Pulse paradoxus
A
Fall of systolic BP >10 on inspiration
18
Q
Mural thrombus after MI
A
Clot over damaged myocardium (can embolise)
19
Q
Ventricular rupture after MI
A
5-10days after MI can cause tamponade or death
20
Q
Mitral incompetance after MI
A
Due to damage to papillary muscle
21
Q
Dresslers syndrome
A
1-3wks after = Autoimmune pericarditis after MI
22
Q
Viral causes of acute pericarditis
A
- Coxsackie B
- Echovirus
23
Q
ECG changes pericarditis
A
- Saddle shaped
- Widespread ST elevation
*Pericardial rub
24
Q
Treat pericarditis - risk of treatment
A
- NSAIDs
- Cause
- Steroids
*Dont use NSAIDs directly after MI as increase rupture risk
25
Chronic pericarditis (6-12mnths) - pathological changes
Thickening of pericardium causes decreased filling = Restritive pericarditis
26
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
27
Diagnostics endocarditis
+ cultures and echo
| -can cause altered platelets
28
Causes of myocraditis and risk
- Viral: coxsackie
- Drugs
- Immune (SLE/IBD/Type 2 diabetes)
-Fulminant HF
29
ECG changes myocarditis and clinical sign
- S3/4 gallop - think HF
- High troponin
- ST depression or elevation
- Twave inversion
- AV block
30
Definitive test myocarditis
(Risky) = Biopsy
31
S1 vs S2 splitting
```
S1 = RBB
S2 = may be physiological (inspiration) or atrial septal defect
```
32
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
33
Breathing sounds and when bets to hear murmor
- lEft murmours best on Expiration
| - rIght murmours best on Inspiration
34
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
35
Most common form of HF and measure
Systolic - pump failure (fall ejection fraction)
36
L vs R HF symptoms
```
L = pulomary oedema/congestion
R = systemcic oedema, JVP, hepato/splenomegaly
```
37
Causes of L-HF
- Systolic
- Diastolic
SYSTOLIC
- Ischaemic heart disease
- Non contractile scare tissue
- Hypertension
- Dilated cardiomyopathy
DIASTOLIC
- Hypertension
- Aortic stenosis
- Hypertrophic & Restrictive cardiomyopathy
38
Causes of R-HF
- L-R shint = increased R pressure
- Lung disease (cor pulmonale) = increased R pressure
*Increased R pressure causes hypertrophy then failure
39
How does HF cause arrhythmia
Stretched myocytes become irritated causing arrhythmia
40
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
41
Manage Acute HF
- Stabilise diuretic and ventilate
| - Start ACEi and B-blocker
42
What causes acute on chronic HF and whats the biggest sign of decompensation
- Acute event (MI, Infection, arrhythmia, electrolyte imbalance)
- Pulmonary oedema
43
What valves are in each side of the heart
```
L = MA
R = TP
```
44
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
45
Mitral valve disease
- Type of valve
- Disease pathophysiology
Mitral = Bicuspid
- Both stenosis and regurg = rheumatic fever
- High risk AF
46
Which valvular pathology is most common
Mitral regurgitation
47
Diagnostics valvular disease
| + specific tests to look at extent
- Echo
- Ecg
- Angiogram
- Stress test - determines extent
48
Nitrates
- 2 examples
- MOA
- Main problem
- GTN and isorbide trinitrate
- Metabolised to NO group, alter CAMP, decrease intracellular Ca and vasodilation
- Tolerance
49
Clopidogrel
- MOA
- SE
- Contraindication
- Prodrug, inhibits ADP receptor = activates platelets
- Bleeding, thrombotic thrombocytopenic purpura
- PPI
50
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
51
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
52
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
53
Warfarin
- MOA
- Factors affectes
- Big contraindications
- Vitamin K antagonist via reductase
- Depletes factors II, VII, IX, X
- Pregnancy, macrolides, the pill, alcohol
54
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
55
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
56
Major risk of spironalactone
Hyperkalemia
57
Contraindications of Thiazide diuretics (one drug and a conditions LAG)
- Lithium
- Addisons
- Gout
58
- Which B-Blocker isnt cardioselective
| - Which has the fastest effect (twice daily dose as opposed to once)
- Propanolol
| - Metoprolol
59
Arterial Ca channel blockers (examples)
- Effect
- SE
- Amlodipine/Felodopine
- L-channels in vasculature = dilation
- Vasodilatory = flushing, snycope
60
Cardiac Ca channel blockers (examples)
- Effect
- SE
- Verapamil/Diltiazem
- Decreases cardiac contractility
- Contraindicated B-blockers - bradycardia
61
SE and 2 biggest risks of using ACEi
- Cough
- HF (with diuretics)
- Nephrotoxic = AKI
62
ARB
- 2 examples
- MOA
- 3 SE
- Losartan/Candesartan
- Inhibits Ang2
- Teratogenic/hyperkalemia/renal failure contraindication
63
Alpha blockers
- 1 cardiac example
- MOA
- SE
- Doxazosin
- Alpha-1 specific, decreases inostiol phosphate, vasodilate
- Dry mouth, hypotension, floppy iris syndrome
64
Statins MOA
HMG-coenzyme A reductase inhibitor, fall in hepatic cholesterol synthesis
65
Fibrates MOA
PPARalpha agonist - decrease in lipid metabolism
66
SE of Fibrates and Statins
-Interactions of statins
- Myalgia (increased by amiodarone)
- Hepatotoxic
-Fibrates, antibiotics, ca channel blockers
67
- 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
68
2 Treatment lines for AF
1) B-blocker** OR Ca++channel blocker
| 2) Add Digoxin or Amiodarone
69
Cause of Arial flutter, risk and treatment
- Rentry rhythm
- Becoming AF
- Same as AF but shock if haemodynamically unstable
70
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
71
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
72
2 non shockable rhythms
- PEA
| - Asystole
73
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
74
Defib vs cardioversion
Defib is not syncronised to peak of QRS (cardioversion) it is shock emergancy at any point of cycle.
75
Difference between VT's and SVT's
SVT will be affected by carotid sinus pressure (vasalva and massage) VT will not
76
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
77
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
78
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
79
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
80
Treatments of blocks
- 1st = none/monitor
| - M1/M2/3 = pace
81
R Bundle branch block
- Ecg
- Cause
- Treat
```
MaRroW
-M in V1
-W in V6
-Atrial sept defect
Treat = monitor and control other pathologies
```
82
L Bundle branch block
- Ecg
- Cause
- Treat
```
WiLliaM
-W in V1
-M in V6
-L-sided disease (stenosis, cardiomyopathy, HF)
Treat = Pace if symptomatic
```
83
Ectopics
- Atrial
- Ventricular
Occur when P waves or QRS out of sequance = Benign
- Atrial = abnormal pacemaker stimulus
- Ventricular = wide QRS, increase with age
84
Which ectopic usually presents with symptoms and what can cause them
- Atrial
| - Caffeine/stress/B-blocker/exercise/electrolytes
85
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
86
What is the span of the normal cardiac axis
+90 - -30
87
aVR should always be negative, what are some reasons it could be positive
- Dextrocardia
| - Inproperly places leads
88
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
89
SE of calcium channel blockers
Oedema
90
What is a major complication of mitral stenosis
Pulmonary hypertension
91
Principles of treating HTN
Increase doses of drugs used to max (eg amlodipine) before begining another drug to reduce polypharmacy
92
Digoxin effect and half life
35hr half life taking 5-7days to reach steady state, not a drug for rapid action
93
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
```
