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Yr 3 ALS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

3 Processes of arteriosclerosis

A
  • Progressive fibrosis of intima
  • Fibrosis and scarring of muscular and elastic media
  • Fragmentation of elastic lamina
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2
Q

Stable angina - definition

A

Triggers known

-Will resolve with GTN and rest

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3
Q

Strongest prediction of long term outcome for ACS and angina

A

-Left ventricular ejection fraction

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4
Q

Gold standard test to examine angina/ACS

A

Angiography - perfusion imaging

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5
Q

Vessel corrolated with worst prognosis

A

LAD

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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

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7
Q

3 pathologies of ACS

A
  • NSTEMI
  • STEMI
  • Unstable angina
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8
Q

Hour rules of MI

A

Patient survives first hour, then sudden cardiac death risk diminishes every subsequent hour

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9
Q

Diagnostic features of ACS

A

2 out of:

  • ECG changes
  • History/symptoms
  • Troponin
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10
Q

Which troponin is best indiactor of myocardial damage

A

Troponin T

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11
Q

ST depression vs elevation

A 
Depression = Icheamia
Elevation = Infarction
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12
Q

3 steps STEMI treatment

A
  • PCI (thrombolyse if unavailable)
  • B-blocker
  • ACEi within 24hrs
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13
Q

Drug treatment of unstable angina

A
  • B-blocker
  • Enoxaparin = inactivates clotting factor Xa
  • Nitrates = IV
  • Clopidogrel (+aspirin)
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14
Q

NHS policy on MI

A

Treat within 36 minutes

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15
Q

Contraindications thrombolysis

A
  • Internal bleeding
  • Pancreatitis
  • Active lung disease
  • Pregnancy
  • Liver disease
  • Varices
  • Head trauma
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16
Q

Becks triad of tamponade (fluid in pericardial space decreasing filling capacity)

A
  • Hypotension
  • Distended neck veins
  • Muffled heart sounds
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17
Q

Pulse paradoxus

A

Fall of systolic BP >10 on inspiration

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18
Q

Mural thrombus after MI

A

Clot over damaged myocardium (can embolise)

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19
Q

Ventricular rupture after MI

A

5-10days after MI can cause tamponade or death

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20
Q

Mitral incompetance after MI

A

Due to damage to papillary muscle

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21
Q

Dresslers syndrome

A

1-3wks after = Autoimmune pericarditis after MI

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22
Q

Viral causes of acute pericarditis

A
  • Coxsackie B

- Echovirus

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23
Q

ECG changes pericarditis

A
  • Saddle shaped
  • Widespread ST elevation

*Pericardial rub

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24
Q

Treat pericarditis - risk of treatment

A
  • NSAIDs
  • Cause
  • Steroids

*Dont use NSAIDs directly after MI as increase rupture risk

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25
Q

Chronic pericarditis (6-12mnths) - pathological changes

A

Thickening of pericardium causes decreased filling = Restritive pericarditis

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26
Q

Endocarditis

  • Commonly affected areas
  • Organisms involved
  • 6 signs (FROM JANES)
A
  • 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
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27
Q

Diagnostics endocarditis

A

+ cultures and echo

-can cause altered platelets

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28
Q

Causes of myocraditis and risk

A
  • Viral: coxsackie
  • Drugs
  • Immune (SLE/IBD/Type 2 diabetes)

-Fulminant HF

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29
Q

ECG changes myocarditis and clinical sign

A
  • S3/4 gallop - think HF
  • High troponin
  • ST depression or elevation
  • Twave inversion
  • AV block
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30
Q

Definitive test myocarditis

A

(Risky) = Biopsy

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31
Q

S1 vs S2 splitting

A 
S1 = RBB
S2 = may be physiological (inspiration) or atrial septal defect
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32
Q

S3 vs S4

A

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

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33
Q

Breathing sounds and when bets to hear murmor

A
  • lEft murmours best on Expiration

- rIght murmours best on Inspiration

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34
Q

Murmours
DAR DSM
SMR SAS

A
  • 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
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35
Q

Most common form of HF and measure

A

Systolic - pump failure (fall ejection fraction)

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36
Q

L vs R HF symptoms

A 
L = pulomary oedema/congestion
R = systemcic oedema, JVP, hepato/splenomegaly
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37
Q

Causes of L-HF

  • Systolic
  • Diastolic
A

SYSTOLIC

  • Ischaemic heart disease
  • Non contractile scare tissue
  • Hypertension
  • Dilated cardiomyopathy

DIASTOLIC

  • Hypertension
  • Aortic stenosis
  • Hypertrophic & Restrictive cardiomyopathy
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38
Q

Causes of R-HF

A
  • L-R shint = increased R pressure
  • Lung disease (cor pulmonale) = increased R pressure

*Increased R pressure causes hypertrophy then failure

39
Q

How does HF cause arrhythmia

A

Stretched myocytes become irritated causing arrhythmia

40
Q

ABCD of chronic HF and benefits of each drug

A
  • ACEi or ARB - decrease fluid overload
  • B-blockers
  • Ca channel blockers - improve prognosis
  • Diuretics - improve symptoms
41
Q

Manage Acute HF

A
  • Stabilise diuretic and ventilate

- Start ACEi and B-blocker

42
Q

What causes acute on chronic HF and whats the biggest sign of decompensation

A
  • Acute event (MI, Infection, arrhythmia, electrolyte imbalance)
  • Pulmonary oedema
43
Q

What valves are in each side of the heart

A 
L = MA
R = TP
44
Q

Aortic valve disease

  • Type of valve
  • Disease pathophysiology
A

Aortic = tricuspid
-Stenosis = harder to open
Calcification from age, rheumatic fever, anatomical variaton

-Regurg = harder to close
Aortic root dilation, ideopathic, dissection, endocarditis

45
Q

Mitral valve disease

  • Type of valve
  • Disease pathophysiology
A

Mitral = Bicuspid

  • Both stenosis and regurg = rheumatic fever
  • High risk AF
46
Q

Which valvular pathology is most common

A

Mitral regurgitation

47
Q

Diagnostics valvular disease

+ specific tests to look at extent

A
  • Echo
  • Ecg
  • Angiogram
  • Stress test - determines extent
48
Q

Nitrates

  • 2 examples
  • MOA
  • Main problem
A
  • GTN and isorbide trinitrate
  • Metabolised to NO group, alter CAMP, decrease intracellular Ca and vasodilation
  • Tolerance
49
Q

Clopidogrel

  • MOA
  • SE
  • Contraindication
A
  • Prodrug, inhibits ADP receptor = activates platelets
  • Bleeding, thrombotic thrombocytopenic purpura
  • PPI
50
Q

Thrombolytics

  • 3 examples
  • MOA
  • Limitation
A
  • Alteplase, Tenecteplase, Streptokinase
  • Converts plasminogen to plasmin = degrades fibrin thrombus
  • Streptokinase Ab present in blood and cant be used again for a year
51
Q

Parenteral analogues

  • 2 examples
  • MOA
  • Antidote
  • How is does calculated
  • Contraindications
A
  • Heparin and Daltaparam (low mol weight H)
  • Binds to antithrombin AIII - inhibits factor Xa
  • protamine sulfate
  • by weight
  • renal failure
52
Q

NOACs

  • 3 examples and their MOA
  • Benefit and risk
A
  • 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
Q

Warfarin

  • MOA
  • Factors affectes
  • Big contraindications
A
  • Vitamin K antagonist via reductase
  • Depletes factors II, VII, IX, X
  • Pregnancy, macrolides, the pill, alcohol
54
Q

2 main treatments for AF

  • MOA
  • SE
  • Contraindications
A

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
Q

Diuretics

  • types (examples)
  • MOA and site
  • SE
A

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
Q

Major risk of spironalactone

A

Hyperkalemia

57
Q

Contraindications of Thiazide diuretics (one drug and a conditions LAG)

A
  • Lithium
  • Addisons
  • Gout
58
Q
  • Which B-Blocker isnt cardioselective

- Which has the fastest effect (twice daily dose as opposed to once)

A
  • Propanolol

- Metoprolol

59
Q

Arterial Ca channel blockers (examples)

  • Effect
  • SE
A
  • Amlodipine/Felodopine
  • L-channels in vasculature = dilation
  • Vasodilatory = flushing, snycope
60
Q

Cardiac Ca channel blockers (examples)

  • Effect
  • SE
A
  • Verapamil/Diltiazem
  • Decreases cardiac contractility
  • Contraindicated B-blockers - bradycardia
61
Q

SE and 2 biggest risks of using ACEi

A
  • Cough
  • HF (with diuretics)
  • Nephrotoxic = AKI
62
Q

ARB

  • 2 examples
  • MOA
  • 3 SE
A
  • Losartan/Candesartan
  • Inhibits Ang2
  • Teratogenic/hyperkalemia/renal failure contraindication
63
Q

Alpha blockers

  • 1 cardiac example
  • MOA
  • SE
A
  • Doxazosin
  • Alpha-1 specific, decreases inostiol phosphate, vasodilate
  • Dry mouth, hypotension, floppy iris syndrome
64
Q

Statins MOA

A

HMG-coenzyme A reductase inhibitor, fall in hepatic cholesterol synthesis

65
Q

Fibrates MOA

A

PPARalpha agonist - decrease in lipid metabolism

66
Q

SE of Fibrates and Statins

-Interactions of statins

A
  • Myalgia (increased by amiodarone)
  • Hepatotoxic

-Fibrates, antibiotics, ca channel blockers

67
Q
  • Brady vs tachycardia

- SVT definition

A
  • Brady = >50 , Tachy>100

- Any tachy above bundle of his mostly considered to be AVNRT or AVRT - all NARROW complex

68
Q

2 Treatment lines for AF

A

1) B-blocker** OR Ca++channel blocker

2) Add Digoxin or Amiodarone

69
Q

Cause of Arial flutter, risk and treatment

A
  • Rentry rhythm
  • Becoming AF
  • Same as AF but shock if haemodynamically unstable
70
Q

AVNRT

  • ECG pattern
  • Patho
  • Epi

-TREAT

A
  • 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
Q

AVRT = Wolf parkinson White

  • ECG pattern
  • Patho

-TREAT

A
  • Short slurred QRS + delta wave (classic sign WPW)
  • Accessory path not in AV node

TREAT

  • Valsalva/Carotid massage
  • Adenosine
  • Cardioversion
72
Q

2 non shockable rhythms

A
  • PEA

- Asystole

73
Q

Ventricular tachys (BROAD)

  • 3 types
  • epi
A

VT

  • often after MI
  • may become VF
  • regular broad QRS

Torsades

  • subtype VT (polymorphic)
  • twisting QRS
  • Mg sulfate + isoprenaline

VF

74
Q

Defib vs cardioversion

A

Defib is not syncronised to peak of QRS (cardioversion) it is shock emergancy at any point of cycle.

75
Q

Difference between VT’s and SVT’s

A

SVT will be affected by carotid sinus pressure (vasalva and massage) VT will not

76
Q

1st degree block

  • ECG changes
  • Patho

HINT: If the R is far from P then you have a first degree

A
  • P far from QRS (prolong PR)

- AV nodal block - often not serious

77
Q

Mobitz 1 (Wenkenbach) block

  • ECG changes
  • Patho

HINT: Longer, longer longer drop then you have a wenkenbach

A
  • Progressive PR length then absent QRS (repeat)

- Disease of AV node

78
Q

Mobitz 2 block

  • ECG changes
  • Patho

HINT: If some P’s dont get through then you have a type 2

A
  • 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
Q

Complete/3rd degree block

  • ECG changes
  • Patho

HINT: If P’s and Q’s dont agree then you have a third degree

A
  • No relationship between P and Q (random PR changes)

- Atrial contraction normal but none is being conducted to ventricles

80
Q

Treatments of blocks

A
  • 1st = none/monitor

- M1/M2/3 = pace

81
Q

R Bundle branch block

  • Ecg
  • Cause
  • Treat
A 
MaRroW
-M in V1
-W in V6
-Atrial sept defect
Treat = monitor and control other pathologies
82
Q

L Bundle branch block

  • Ecg
  • Cause
  • Treat
A 
WiLliaM
-W in V1
-M in V6
-L-sided disease (stenosis, cardiomyopathy, HF)
Treat = Pace if symptomatic
83
Q

Ectopics

  • Atrial
  • Ventricular
A

Occur when P waves or QRS out of sequance = Benign

  • Atrial = abnormal pacemaker stimulus
  • Ventricular = wide QRS, increase with age
84
Q

Which ectopic usually presents with symptoms and what can cause them

A
  • Atrial

- Caffeine/stress/B-blocker/exercise/electrolytes

85
Q

Ventricular extrasystoles

  • Patho
  • Symptoms
  • treat
A

Feeling of a “skipped beat”

  • Premature ventricular contraction initiated from purkinje fibres instead of SAN
  • Symptoms - syncope on exertion
  • Lifestyle changes/antiarrhythmics/ablation
86
Q

What is the span of the normal cardiac axis

A

+90 - -30

87
Q

aVR should always be negative, what are some reasons it could be positive

A
  • Dextrocardia

- Inproperly places leads

88
Q

Pulomary hypertension

  • epi
  • possible cause
  • symptoms
  • x-ray findings
A
  • 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
Q

SE of calcium channel blockers

A

Oedema

90
Q

What is a major complication of mitral stenosis

A

Pulmonary hypertension

91
Q

Principles of treating HTN

A

Increase doses of drugs used to max (eg amlodipine) before begining another drug to reduce polypharmacy

92
Q

Digoxin effect and half life

A

35hr half life taking 5-7days to reach steady state, not a drug for rapid action

93
Q

Drug treatment for HTN (2 arms)

Hint: Caribbean=C

A 
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

Yr 3 ALS (10 decks)

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