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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Troponin limits?

A

When higher than 99%of a reference population- note that 1% does not have ACS so this test is good for those with a high pre test probability!

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2
Q

Which troponins are used for diagnosing ACS?

A

Cardiac troponins I and T
(cTnI and cTnT)
These are high sensitivity tests, of course at the expense of specificity.
Note: cTnC is also expressed in skeletal muscle, whereas I and T are specific to cardiomyocytes

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3
Q

Cause of raised troponins?

A 
Any sustained or transient ischemic/inflammatory damage to the myocardium:
ACS
Heart failure/Cardiomyopathies
Myocarditis 
Tacchyarrythmias
Pulmonary embolism,severe pulmonary hypertension
Renal failure
Sepsis,critical illness
Extensive burns
Stroke and SAH
INFILTRATIVE DISEASES EG AMYLOIDOSIS 
Cardio toxic drugs 
And.....
Healthy individuals after strenuous exercise
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4
Q

Pattern of troponin changes suggesting MI?

A

They rise within a few hours of MI, and continue to rise before falling again. Raised levels Last 4-7 days (cTnI) and 10-14days (cTnT). Serial testing is most useful to diagnose MI, as there are other causes of raised troponins which don’t rise characteristically like MI.
Typically test 6 hours later, but with latest troponins can do 2-3hourly testing.

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5
Q

Cardiac causes of CP?

A

Myopericarditis
MI
Cardiac rupture
Aortic dissection

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6
Q

Chest pain aetiologies

A
  1. Cardiac (MI,myopericarditis,rupture,aortic dissection,/stent thrombosis)
  2. Respiratory (pneumonia/pleurisy, pneumothorax,PE)
  3. GI(reflux disease +/- perforation)
  4. Oesophagus(spasm)
  5. Musculoskeletal/costrochondritis(#)
  6. Other (shingles, panic attack)
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7
Q

Metformin contraindications?

A

Renal function: (risk of lactic acidosis!)

Excreted really. Small risk of lactic acidosis .03/1000, 50% fatal. Assess renal fx before starting + monitor.

IV contrast can lead to lactic acidosis. Stop before and for 48 hours after if renal fx proven normal.

Stop with any NBM procedures. Any hypoxia States like acute MI, CHF.

Suspect if any sudden deterioration, stop metformin and assess for lactic acidosis.

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8
Q

Diabetics should be on glycemic control and????

A

ACEi

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9
Q

Acute MI auscultatory findings?

A

Added heart sounds: S3 and/or S4 (gallop rhythms) Kentucky Tennessee respectively

Paradoxical splitting of S2 (reflects LBBB)

Murmurs:
1. MR (papillary muscle dysfunction or rupture or mitral annular dilatation)

  1. Ventricular septal rupture (midsternal border holo systolic loud often with thrill)
  2. Ventricular rupture - 2-12 days post. Loud systolic +thrill. Cardiac tamponade and rapid detoriaration are the consequence.
  3. New aortic regurgitation (aortic dissection)
  4. Pericardial friction rub (sliding contact of inflammation roughened surfaces) in 20% at some stage, most commonly 2-4days post MI

Note: bell is for low pitched, diaphragm for higher.
S3/S4 are low pitched.
S3 normal in young fit people but abnormal over 40years. (Rapid filling causing oscillation of blood in (stiff) ventricle or tensing of chordae tendinae when rapidly filling and expanding ventricle)
S4 atrial contraction causing vibrations of LV muscle, MV apparatus and blood mass
S2 physiological splitting with inspiration due to decrease intrathoracic pressure causing increased time needed for pulmonary pressure to exceed RV (AVclosure precedes PV)
Paradoxical split-present at rest, disappears on inspiration. AS. LBBB. LVF.

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10
Q

Metoclopramide

A

Antiemetic, helps delayed gastric emptying (gastro paresis) by relaxing pyloric sphincter and increasing gut peristalsis

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11
Q

Duride

A

Isosorbide mononitrate ISMN

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12
Q

Cartia or cartia XT

A

Cartia = aspirin

Cartia XT = Extended release Diltiazem (heart and vessels CCB)

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13
Q

Verapamil

A

Similar to diltiazem - CCB with heart and vessel action

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14
Q

Surgical sieve

A 
Metabolic
Autoimmune
G
Infectious
Cancer
A
Drugs
Degenerative
I
Trauma 
I
Vascular
Endocrine
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15
Q

beta blocker contraindications

A

Asthma/COPD
Heart failure/cardiogenic shock
2/3rd degree heart block or severe bradycardia,
PR>.24msecs, HR

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16
Q

Valves affected in IE?

A

Usually occurs in already abnormal heart.

Right sided in IV drug users

Usually left in the rest of IE. Most common is mitral prolapse and degenerative mitral and aortic regurgitation

17
Q

Valves affected in rheumatic heart disease?

A

In order of most common to least:

Mitral
Aortic
Tricuspid
Pulmonary

Usually occurs as mitral + 1 or more of
the other 3

Rheumatic heart disease is the predominant cause of mitral stenosis

Stenosis, insufficiency, Mixed insufficiency and stenosis,

18
Q

Overdiuresis causes what?

A

Worsening of renal function - Reduced eGFR, increased creatinine

Hypokalaemia
Hypotension

Potentials toxicity of other agents eg digoxin by decreasing renal function or causing hypokalaemia

Decrease dose of causing renal impairment, if severe impairment then withhold and assess daily, reintroducing at lower doses

19
Q

EGFR and ACEi?

A

?

20
Q

AF MANAGEMENT including FAST AF

90% of clots form in left atrial appendage

A

?

21
Q

Cause of pan-systolic murmurs?

A

Mitral regurg
Tricuspid regurg
VSD
aorto-pulmonary shunts (rare)

22
Q

Causes of ESM?

A 
Flow murmur
Aortic sclerosis
Aortic stenosis(including bicuspid )
Pulmonary stenosis
HOCM
Dilation of aortic root or pulmonary trunk
ASD!
23
Q

Aortic stenosis

A

Male, older, congenital bicuspid valve

High flow through narrowed valve

Sob, lightheaded, syncope, CP, etc

Echo gives flows and area:
>1.5cm2 mild
1-1.5 moderate

24
Q

bumetanide?

A

Loop diuretic

Furosemide, bumetanide

25
Q

Metaolazone

A

Thiazide like diuretic for HTN and CHF, used in combo with loop diuretics in severe CHF

Indapamide

26
Q

Digoxin toxicity?

A

Loss of appetite is first.
Nausea and vomiting.
Reverse tick(not necessarily toxicity)

27
Q

U wave abnormalities?

Note: Normal U Is small, same direction as T, inversely proportional to rate, (seen below 65)

A

Prominent:
>1-2mm or 25% of T Wave
- bradycardia (most common)
- Hypokalaemia
- Drugs eg digoxin and other antiarrhythmics
May also be seen in hypoCa, hypoMa, hypothermia, LVH, HOCM, raised ICP

Inverted:
Specific for heart disease eg 
- cardiomyopathy, 
- valvular disease, 
- CAD, 
- HTN 
- hyperthyroid, 
- congenital heart disease
Also 
- myocardial ischemia - CP! May be the earliest marker and predict >75 LAD or LMCA stenosis and presence of LV dysfunction. Can be the only ECG sign
28
Q

MI with Brady cardia?

A

RCA , supplies most of upper conduction system
ischemia of SA node or increased vagal tone?

Can have heart block too.
LCA (LAD) causes LBBB ??

29
Q

AF causes?

A 
Thyroid
Alcohol/drugs
Heart disease 
Lung disease
Systemic disease (eg infection)
30
Q

ST depression?

A
  • Ischemia (reduced blood flow cf. hypoxia)
  • Subendocardial infarction
  • Digitalis
  • Hypertrophy or bundle branch blocks (discordant with QRS plus T inversion)
31
Q

ST elevation?

A
  • Infarction (acute/recent)
  • pericarditis
  • ventricular aneurysm - ST elevation doesn’t return to baseline with time
  • Brugada syndrome V1-3
  • Hypertrophy/bundle branch block
  • prinzmetal angina (transient, angina without exertion and no infarction)
32
Q

Q wave?

A

Necrosis (Q cf. q)
Normal in some leads due to septal depolarisation from LBB to right (Left and inferior leads)
Bigger than one square in duration, >25% of following R,

33
Q

Posterior infarction?

A
  • Large R wave in V1 or V2 ( usually small-equivalent to a Q)
  • ST depression V1-2
    Other differential is RVH
34
Q

Ecg changes for K+ pathology?

A

HypoK:

  • flat->inverted T
  • prominent U, proportional to severity

Think of T as housing K, big if lots, otherwise smaller

HyperK:

  • wide, flat P, + disappears if extreme
  • wide QRS
  • peaked T
35
Q

ECG for Ca2+ disorders?

A

HypoCa:
- long QTINTERVAL

HyperCa:
- short QT

36
Q

Immediate care in asymptomatic angina?

A

Significant comorbidity eh renal hepatic pulmonary frailty/age haemodynamic instability symptoms with minimal exertion arrythmias

Medicine (8 decks)

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