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Medicine > CVS > Flashcards

CVS Flashcards

1
Q

CVS causes of Syncope

A
  1. Arrhythmia (Brady/Tachy)
  2. Mechanical (LV obs, AS, HOCM)
  3. Vasovagal (Neurocardiogenic)
  4. Orthostatic (Drug, elderly)
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2
Q

Anti-arrhythmic agent classes

A

1: Na channel blocker
2: BB
3: K channel blocker (e.g. Amiodarone)
4. CCB
5. Other: Digoxin, Adenosine

For AF,
1,3 = Rhythm control
2,4 = Rate control

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3
Q

Angina drugs

A

Sublingual nitrates (If infrequent angina)
BB (1st line)
CCB (if coronary spasm)

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4
Q

After PCI give what drugs

A

Antiplatelets

  • Aspirin
  • Clopidogrel
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5
Q

Features not suggestive of Myocardial ischemia

A
  1. Pleuritic pain (Sharp/Knifelike pain provoked by respiration/cough)
  2. Primary/Sole location of discomfort @ middle/lower abdomen
  3. Pain localized to 1 tip of finger (particularly @ LV apex, costochondral junction)
  4. Pain reproduced by movement/palpation of chest wall/arms
  5. Pain lasting for few seconds or less
  6. Pain that is of maximal intensity at onset
  7. Pain radiating to LLs
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6
Q

IE prophylaxis in

A
  1. Previous IE
  2. Prosthetic valve
  3. Congenital heart disease
    Cyanotic congenital heart disease that has not been fully repaired; or First 6 months after full repair; or with residual defects after surgery
  4. Heart transplant with valvulopathies
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7
Q

Troponin increased in

A
  1. Renal dysfunction
  2. Post-procedure, e.g. Cardioversion, catheter ablation, PCI
  3. Non-coronary related: Myocarditis, PE, acute/chronic LVF, septic shock, arrhythmias
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8
Q

Anti-ischemic therapy for ACS

A
  1. Bed rest, ECG/BP monitor
  2. Oxygen (4-8L/min if <90 SaO2)
  3. Nitrates (Sublingual or IV; note for BP cuz it is vasodilator)
  4. Morphine
  5. Oral BB/CCB
  6. Atropine if bradycardia or vagal reaction
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9
Q

Absolute CI to anticoagulant

x4

A
  1. Active bleeding
  2. Severe bleeding diathesis
  3. Severe thrombocytopenia
  4. Recent neurosurgery, ocular surgery (exclude cataracts), intracranial bleed
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10
Q

NYHA functional classification

New York Heart Association

A

Patient symptoms: Class 1-4

  1. No limitation of physical activity
  2. Slight limitation, comfortable at rest
  3. Marked limitation, comfortable at rest
  4. Unable to carry on physical activities without discomfort, HF symptoms at rest

Objective assessment: Class A-D
A. No objective evidence of CVS disease. No Sx, no physical limitation
B. Objective evidence of mild CVS disease. Mild Sx, slight limitation. Comfortable at rest
C. Objective evidence of moderately severe CVS disease. Marked limitation. Comfortable at rest
D. Objective evidence of severe CVS disease. Severe limitations. Sx at rest

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11
Q

S/S of Left HF

A

Symptoms

  1. SOB OE
  2. Nocturnal cough
  3. Orthopnea / PND
  4. Palpitation
  5. Dizziness / Pre-syncope

Signs

  1. Tachycardia
  2. Lung crepitations
  3. S3 +/- S4
  4. Cardiomegaly
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12
Q

S/S of Right HF

A

Symptoms

  1. Ankle swelling
  2. Abd distension

Signs

  1. Bilateral pitting ankle edema
  2. Hepatomegaly
  3. Pleural effusion
  4. Elevated JVP
  5. Hepatojugular reflux
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13
Q

Norvasc

A

Amlodipine

CCB

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14
Q

ECG lead positions o’clock

A

Lead 1: 3 o’clock (0)
Lead 2: 5 o’clock (60)
Lead 3: 7 o’clock (120)

aVR: 10 o’clock (-150)
aVL: 2 o’clock (-30)
aVF: 6 o’clock (90)

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15
Q

ECG Lead corresponding part

A

23F –> Inferior
1L56 –> Lateral
12 –> Septal
34 –> Anterior

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16
Q

WPW ECG features

A
  1. Short PR interval (<0.12s) N=0.12-0.2
  2. ?Wide QRS
  3. Delta waves after P wave –> slurred upstroke
  4. Secondary ST / T wave abnormality?

Type A: V1 is positive, L side accessory pathway
Type B: V1 is negative, R side accessory pathway

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17
Q

Narrow QRS tachycardia

A

Regular

  1. ST
  2. AT
  3. A flutter
  4. AVRT (P in ST)
  5. AVNRT (P fused with QRS)
Check response with ATP
AVRT/AVNRT --> convert to Sinus rhythm
AT/ST --> no QRS
A flutter --> Slurred
AF --> Dead stroke

Irregular

  1. AF
  2. A flutter with variable block
  3. MAT
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18
Q

Wide QRS tachycardia

A

Regular

  1. VT
  2. SVT + aberrancy

Irregular

  1. AF + aberrancy
  2. Pre-excited AF
  3. Polymorphic VT
  4. Torsades de pointes
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19
Q

LMNOP for Acute pulmonary edema

A 
Lasix
Morphine (may not give now)
Nitroglycerin
O2
Position - sit up (or positive pressure)
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20
Q

CI for nitrates

A

HOCM, constrictive pericarditis

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21
Q

JVP, causes of Cannon A wave

A

Cannon A wave (due to AV dissociation)

  • Complete HB
  • A flu
  • Ventricular pacing, VT
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22
Q

JVP, causes of Giant A wave

A

Giant A wave (due to forceful RA contraction cuz decreased RV compliance)

  • Pul HT
  • PS / TS
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23
Q 
JVP waves
A wave
X descent
C wave
V wave
Y descent
A

A wave

  • RA contraction
  • Before carotid pulse

X descent
- RA relaxation

C wave
- Closure of TV

V wave

  • Filling of RA (during ventricular systole)
  • with TV closed
  • Sync with carotid pulse
  • Giant V wave –> TR

Y descent
- Negative deflection of RA pressure during opening of TV

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24
Q

Parasternal heave causes

A
  1. RV volume overload (ASD, PR, TR)
  2. RV pressure overload (LHF, Pul HT, PS)
  3. LA enlargement
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25
Q

Tx of AF, A Flu, AT

Acute Mx

A

Rate control

  • IV AVN blockers (Diltiazem, Esmolol)
  • IV Digoxin

Rhythm control

  • IV Class 1 AAD
  • IV Amiodarone

Non-pharm
- DC cardioversion

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26
Q

Tx of AF, A Flu, AT

Long term Mx

A

Rate control

  • Oral AVN blockers (Diltiazem, BB)
  • Oral Digoxin

Rhythm control

  • ?Oral Class 1 AAD
  • Oral Amiodarone, Sotalol

Non-pharm

  • Catheter ablation
  • Pacing
  • Surgery
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27
Q

CHA2DS2-VASc score

A

Risk stratification for (non-valvular) AF patients for developing Thromboembolic stroke
Max score = 9
>=2 –> Start Warfarin or NOAC

CHF
HT
Age 75
DM
Stroke
Vascular disease (PAD, MI)
Age 65-74
Sex category (Female)
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28
Q 
ECG area of infarct
Inferior
Lateral
Anteroseptal
Anterolateral
Anterior
RV

HH

A 
Inferior - 2,3,F
Lateral- 1,L,6
Anteroseptal- V1,2,3
Anterolateral- V4,5,6
Anterior- V1-6
RV- V3R, V4R

aVF = Augmented vector foot

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29
Q

Ix for Acute STEMI

HH

A
  1. Serial ECG for 3 days
  2. Serial cardiac injury markers for 3 days (CK-MB, Troponin, Myoglobin)
  3. CXR, CBC, L/RFT, Lipid profile (within 24h)
  4. Clotting profile as baseline for thrombolytic tx
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30
Q

Mx for Acute STEMI

HH

A
  1. Close monitoring, BP/P, I/O q1h; Cardiac monitor
  2. Complete bed rest
  3. O2 by nasal cannula if hypoxic/ HF; routine O2 in first 6h
  4. Treat anxiety by explanation / sedation (Diazepam PO)
  5. Stool softener
  6. Analgesics prn (IV Morphine)
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31
Q

Absolute CI of Fibrinolytic therapy

A
  1. Previous intracranial hemorrhage, other strokes or CVA within 3m; except acute ischemic stroke within 4.5h
  2. Known malignant intracranial neoplasm (primary or met)
  3. Known structural cerebrovascular lesion e.g. AVM
  4. Active bleeding or bleeding diathesis (exclude menses)
  5. Suspected aortic dissection
  6. Sig. closed head or facial trauma within 3m
  7. Intracranial or intraspinal surgery within 2m
  8. Severe uncontrolled HT (unresponsive to emergency tx)
  9. For streptokinase, prior tx within previous 6m
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32
Q

Relative CI for Fibrinolytic therapy

A
  1. Severe uncontrolled HT on presentation (>180/110)
  2. Hx of chronic, severe, poorly controlled HT
  3. Prior ischemic stroke >3m or known intracerebral pathology not covered in absolute CI
  4. Traumatic/prolonged CPR (>10min)
  5. Oral anticoagulant therapy
  6. Major surgery <3wk
  7. Non-compressible vascular punctures
  8. Recent internal bleeding (within 2-4wk)
  9. Preg
  10. Active PU
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33
Q

Causes of HF

A
  1. Myocardial disease
    - CAD +/- ischemic CMP
    - HT heart disease
    - Idiopathic CMP (hypertropic, dilated, restrictive)
    - Other CMP - alcoholic, chemo
  2. Valvular disease
    - Aortic / Mitral valve disease (due to rheumatic / degenerative heart disease)
  3. Pericardial disease
    - Constrictive pericarditis
    - Pericardial effusion
  4. Pul vascular disease
    - Pul thromboembolism
    - Primary pul HT
  5. Congenital anomalies
    - Cyanotic heart disease (R to L shunt)
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34
Q

Cause of constrictive pericarditis (wiki)

A
  1. TB
  2. Post-MI
  3. Infection (virus, fungus etc.)
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35
Q

Framingham criteria

for HF

A

2 major or 1 major + 2 minor

Major

  1. Orthopnea/PND
  2. Venous distension
  3. Crackles
  4. Cardiomegaly
  5. APO
  6. Elevated JVP
  7. Hepatojugular reflux
  8. LOW in response to tx

Minor

  1. Ankle edema
  2. Noctural cough
  3. Exertional dyspnea
  4. Hepatomegaly
  5. Pleural effusion
  6. Tachycardia (>120)
36
Q

Killip classification

Function + classes

A

To stratify severity of LV dysfunction
To determine clinical status of post-MI patients

Class 1: No rales, no S3
Class 2: Rales <50% lung field or Presence of S3
Class 3: Rales >50%: pulmonary edema
Class 4: Cardiogenic shock

37
Q

CXR findings in Acute HF

A
  1. Upper lobe diversion (Cephalization; indicates pul venous HT)
  2. Kerley B lines
  3. Pul alveolar edema (Batwing appearance)
38
Q

BNP

A

Brain natriuretic peptide

39
Q

Mx of Acute HF

A

General measures

  1. Complete bed rest
  2. O2
  3. Low salt diet
  4. Fluid restriction

If BP stable,

  1. IV Frusemide
  2. IV nitrate
  3. Morphine
If BP unstable,
1. Inotropes: Dopamine, Dobutamine
--> if still not stabilized or refractory APO -->
Intra-aortic balloon pump
ECMO

Monitor BP/p, I/O, SpO2, JVP, clinical state
Ventilatory support if desat / exhaustion / cardiogenic shock
1. Non-invasive cPAP
2. Intubation, mechanical ventilation

40
Q

Initial Ix for HF

A
  1. Urine x protein, glucose, blood, microscopy
  2. CBC
  3. RFT: Serum K, Ca, PO4, Creatinine, urea
  4. FG
  5. TSH
  6. ECG
  7. CXR
  8. BNP or pro-BNP
41
Q

Drugs for HF

A
  1. Diuretics + ACEI + BB
  2. If still NYHA Class 2-4 –> Add MR antagonist
  3. If LVEF <= 35% + SR + HR >=70 –> Add Ivabradine
  4. Still NYHA 2-4 and LVEF <=35% –> If QRS >=120ms –> CRT-P/D
  5. If QRS <120 –> ICD
  6. If still NYHA 2-4 –> Consider Digoxin and/or H-ISDN (hydralazine/isosorbide dinitrate)
    If End stage, consider LVAD (LV assist device) and/or transplant
42
Q

CRT-P and CRT-D

A

Cardiac Resynchronization Therapy Pacemaker (CRT-P)

Cardiac Resynchronization Therapy Defibrillator (CRT-D)

43
Q

Causes of AF

A
  1. HT heart disease ?HF?
  2. MI
  3. Valvular heart disease: MS/MR
  4. Alcohol
  5. Hyperthyroidism
  6. Drugs, Theophylline, caffeine
  7. OSA

RB

  1. Mitral valve disease
  2. IHD
  3. Thyroid heart disease
  4. Alcohol
  5. HT
44
Q

Causes of ST elevation in ECG

A
  1. AMI (Convex STE; Hyperacute T wave)
  2. Ventricular aneurysm
  3. LVH
  4. Acute pericarditis (Diffuse concave STE, not in aVR)
  5. Early repolarization
  6. LBBB
  7. ICH
45
Q

Indication of Fibrinolytic therapy

A
  • AMI (Pain + ST elevation in 2 contiguous chest leads)
  • Time of onset of pain <12 hrs
  • Absence of CI: Bleeding tendency, cardiogenic shock, recent head injury, stroke
46
Q

Indication for pacemaker insertion

A
  1. Symptomatic bradycardia with 2nd degree AV block
  2. Asymptomatic 3rd degree AV block with cardiomegaly or LV dysfunction
  3. Exercise-induced 2nd or 3rd degree AV block in the absence of ischemia

Symptomatic bradycardia
Mobitz type II, Intermittent/Continuous 3rd AVB

47
Q

1st / 2nd / 3rd degree HB

A

1st degree
- Prolong PR interval (>200ms)

2nd degree type 1 (aka Wenckebach’s phenomenon)

  • Disease of AVN
  • Progressive prolonged PR interval until P wave is not conducted
  • Longest immediately before dropped (missed) QRS
  • Shortest immediately after dropped QRS
  • Ventricular escape beats (after P waves failed to reach ventricles)
  • usu asymptomatic

2nd degree type 2

  • Disease of distal conduction system (His-Purkinje)
  • No progressive lengthening of PR interval
  • “all or nothing” phenomenon whereby the His-Purkinje cells suddenly and unexpectedly fail to conduct a supraventricular impulse
  • No pattern to the conduction blockade, or alternatively there may be a fixed relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

*high degree: P:QRS 3:1 or higher

3rd degree

  • Junctional rhythm or ventricular escape rhythm
  • P waves may be buried
48
Q

Cause of Increased/Decreased JVP

WCS

A
  1. RHF
  2. Constrictive pericarditis
  3. Tricuspid disease
  4. SVCO

Decreased
1. Dehydration, hypovolemia

49
Q

SE of Amiodarone

A
  1. ILD
  2. Hypothyroidism (Hyper also possible)
  3. ?Liver toxicity
50
Q

HACEK group

A 
Haemophilus
Aggregatibacter (prev aka Actinobacillus)
Cardiobacterium
Eikenella
Kingella
51
Q

Modified Duke’s criteria

A

Modified Duke Criteria:
Pathologic Criteria: Microorganisms demonstrated in Vegetation
Pathologic lesions confirmed by Histology

Clinical Criteria: 2 Major, 1 Major + 3 Minor, 5 Minor

Major Criteria:

  1. Blood Culture showing persistent bacteremia of typical organisms (≥2/3)
    • S. viridans, S. bovis, HACEK group, S. aureus, Enterococci without a primary focus
  2. Evidence of endocardial involvement (with +ve Echo)
    • Moving Masses, Abscess, New Valvular Regurgitation, Prosthetic Valve Dehiscence

Minor Criteria:
1. Predisposing Cardiac lesions or Main-lining Addicts
2. Other Echo features of Endocarditis
3. Atypical Organisms in Blood Culture
4. Fever >38°C
5. Immune Complex disease: GN, Osler Node, Roth’s Spot, RF
6. Embolic phenomenon: Arterial Emboli, Septic Pulmonary infarcts, (Mycotic aneurysm),
(ICH), Conjunctival Hemorrhage, Janeway lesions

52
Q

ACEI

A

For HT, HF

SE

  • Dry cough
  • HyperK
  • Postural hypotension
53
Q

BB

A

For

  1. Angina
  2. MI
  3. HF (start in low dose then increase)
  4. HT – not 1st line now
  5. Arrhythmia (BB is Class 2 anti-arrhythmic)
  6. Thyrotoxicosis (Propranolol; block peripheral conversion of T4 to T3)
  7. Anxiety
  8. Glaucoma (Timolol)

SE:

  1. Bradycardia
  2. Acute HF
  3. Heart block
  4. Fatigue
  5. Bronchoconstriction
  6. Cold extremities
  7. Nightmare
  8. Impotence
54
Q

3 BBs for HF

MBC

A
  1. Carvedilol
  2. Bisoprolol
  3. Metoprolol
55
Q

Aldosterone antagonist

A
  1. Spironolactone
  2. Eplerenone

SE

  • HyperK
  • Gynecomastia
  • Eple: reduce mortality in MI+HF; less hormonal SE
56
Q

Nitrates

A

Venous vasodilation

↑Supply
- Dilate coronary arteries
- Redistribute blood flow from pericardial to endocardial sites
↓Demand
- ↓Preload
- ↓LV size & LV pressure by reducing BP

Sublingual nitrate: rapid absorption + short acting
- Mononitrates are active without undergoing first pass in liver (unlike Dinitrate) –> bioavailability more predictable

SE

  1. Syncope and Hypotension, esp when with cerebral vascular disease (∵↓Preload and Afterload)
  2. Reflex tachycardia
  3. Headache, flushing
  4. CI in HOCM, constrictive pericarditis
  5. If take Sidenafil (Viagra)威而鋼 –> will result in prolonged hypotension
57
Q

Hydralazine

A

Arterial vasodilation –> Decrease afterload

SE

  1. Tachycardia, headache
  2. Increase baro-reflex –> tachycardia + increase CO –> cause MI
58
Q

Predisposing factors for IE

A
  • Shunts (Congenital, post-surgical, e.g. VSD, PDA, AV fistula)
  • Valvular (MR > MS, AR > AS, prosthetic, IV drug addicts)
59
Q

RFs for IHD

A

Modifiable

  1. HT
  2. HC
  3. DM
  4. Obesity
  5. Waist-to-hip ratio
  6. Smoking
  7. Sedentary lifestyle, poor nutrition

Non-modifiable

  1. FH of CVS disease
  2. Gender (M>F)
  3. Age
60
Q

CCB

A

Selectively block Ca channel during phase 2 action potential
Tissue specific Ca channels
- AV node, SA node
- Vascular and intestinal smooth muscle
- Myocardium (high dose): negative inotropic effect

Action in angina

  • ↑Supply: Dilate coronary a.
  • ↓Demand: Lowers BP
  • Don’t use Nifedipine - short acting; reflex tachycardia may cause angina
  • Verapamil and Diltiazem has additional rate slowing effect

2nd generation CCB (Amlodipine, Felodipine, Isradipine, Lacidipine)

  • All are dihydropyridine derivatives
  • Comparing to Nifedipine
  • Longer acting (taken once daily)
  • Less reflex tachycardia and edema
  • Less negatively inotropic as it is vascular selective

SE

  1. Flushing
  2. Edema
  3. Headache
  4. Palpitations
  5. Negative inotropic effects
  6. Bradycardia (Verapamil, Diltiazem)

For Angina,

  • Nifedipine (short acting) should not be used
  • CCB is useful for vasospasm, concomitant HT
  • Often combined with BB
  • Useful for concomitant HT
61
Q

Choice of drugs for Angina

A

Infrequent angina –> Sublingual nitrates

BB is 1st line cuz of proven effect in CAD, indicated in HT

CCB esp when coronary spasm is present, often combined with BB

62
Q

Indications for coronary angiogram / revascularization

A
  1. Medically refractory angina / ACS
  2. Most patients within 1 day after thrombolysis, and for those with post-infarct ischemia
  3. Prognostically significant ischemia:
    1. 1 Exercise test: significant ST depression at low workload
    2. 2 Stress thallium suggestive of large amount or multiple areas of myocardium at risk
    3. 3 Poor ventricular function with ischemia
  4. Concomitant cardiac surgery (e.g. Valve operation)
  5. For other patients an initial aggressive medical therapy is an option
63
Q

Drug tx for secondary prevention of ACS

A

Antiplatelet therapy

  • Aspirin
  • Clopidogrel when Aspirin is not tolerated (hypersensitivity, GI intolerance)
  • Combined Aspirin + Clopidogrel or other ADP antagonist up to 12 months after NSTE-ACS/PCI

Anti-ischemic therapy

  • BB, unless CI
  • ACEI for CHF, LV dysfunction (EF<40%), HT, DM
  • CCB if BB is CI and no HF
  • Nitrates if angina
64
Q

Secondary prevention of ACS

RF control

A
  1. Quit smoking
  2. DM control (HbA1c 6.5)
  3. BP control
  4. Aggressive lipid lowering with statin (and ezetimibe; LDL 1.8)
  5. Diet, weight control
  6. Supplementation: 1g fish oil n-3 poly-unsaturated fatty acids
65
Q

Anti-thrombotic therapy for NSTEMI (Possible/ Likely or Definite / Definite with continuing ischemia or high risk or planned PCI)

A

Possible
1. Aspirin

Likely or Definite

  1. Aspirin +
  2. Clopidogrel or Ticagrelor (loading) +
  3. SC LMWH or IV Heparin or Fondaparinux or Bivalirudin (PCI planned)

Definite with continuing ischemia or high risk or planned PCI

  1. Aspirin +
  2. Clopidogrel or Ticagrelor (loading) or Prasugral (PCI) +
  3. SC LMWH or IV Heparin +
  4. Glycoprotein 2b/3a antagonist: Abciximab (PCI), Tirofiban or Eptifibatide
66
Q

Aims of Tx of NSTEMI

A

Relieve Sx
- Anti-ischemic therapy

Prevent progression and Cx

  • Anti-thrombotic tx
  • Revascularization
67
Q

Anti-ischemic therapy for NSTEMI

A
  1. Bed rest, ECG/BP monitor
  2. O2 if SaO2 <90%
  3. Nitrates (sublingual or IV)
  4. Morphine (IV or SC depends on pain severity)
  5. BB/CCB (Oral; only if no signs of HF)
  6. Atropine (IV; if bradycardia or vagal reaction)
68
Q

Predisposing factors for STEMI

A
  1. Unusual heavy exercise
  2. Emotional stress
  3. Progression from unstable angina
  4. Surgical procedures
  5. Infection (e.g. pneumonia)
  6. Circadian periodicity (Peak incidence @ 0600-1200)
69
Q

DDx for AMI

A
  1. Acute pericarditis
    - Aggravated by RS movement (also lying down), sharp, knifelike
    - Radiates to trapezius ridge
  2. PE
    - Hemoptysis
  3. Aortic dissection
    - Radiates to back, ripping pain, tearing sensation
70
Q

NSTEMI high risk features (consider early PCI)

A
  1. Ongoing or recurrent chest pain
  2. Hypotension and APO
  3. Ventricular arrhythmia
  4. ST segment changes >= 0.1mV; new BBB
  5. Elevated Troponin >0.1mg/mL
  6. High risk score (TIMI, GRACE)
71
Q

Indication of PCI (in STEMI)

A
  1. CI to Lytics
  2. Cardiogenic shock / Unstable hemodynamics
  3. Unclear Dx
  4. Presented 3-12 hours after onset (PCI is better than lytics); Less Cx with late presentation esp stroke
  5. Rescue PCI for failed lytic
72
Q

Oligemic lung fields in CXR

A

PE

73
Q

LMWH

A

Enoxaparin

74
Q

Key pathology in ACS

A

Plaque rupture

75
Q

ECG Dx of AMI (STEMI)

A

ECG Dx of AMI

  1. New STE at J-point (V2-V3: >= 0.2mV in men or >=0.15 in women; Other leads: >=0.1mV)
    * J-point = Point where QRS complex finishes and ST segment starts
  2. New STD, horizontal or down-sloping >=0.05mV in 2 contiguous leads
  3. T inversion >=0.1mV into 2 leads with prominent R wave or R/S ratio >1
76
Q

Complications of AMI

x6

A
  1. HF
  2. Arrhythmias
  3. VSD
  4. MR complicating papillary muscle dysfunction
  5. Pericarditis
  6. Frozen shoulder
77
Q

NOAC

A

Novel oral anticoagulants
e.g.
Direct thrombin inhibitor: Dabigatran
Direct F10 inhibitor: Rivaroxaban, Apixaban

78
Q

HT crisis Mx

HH

A
  1. Always recheck BP at least twice
  2. Look for target organ damage (neurological, cardiac)
  3. Complete bed rest, low salt diet (NPO in HT emergency)
  4. BP/P q1h or more frequently, monitor I/O (Close monitoring in CCU/ICU with intra-arterial line in HT emergency)
  5. CBC, R/LFT, cardiac enzymes, aPTT/PT, CXR, ECG,
    urine x RBC and albumin
  6. Aim: Controlled reduction (Rapid drop may ppt CVA / MI)

Target BP
Chronic HT, elderly, acute CVA 170-180 / 100
Previously normotensive, postcardiac/vascular surgery 140 / 80
Acute aortic dissection 100-120 SBP

  1. If HT urgency,
    - Use oral route, BP/P q15 mins for 1h
    - Continue taking usual anti-HT if already taking
    - Not prev on anti-HT or failure of control for 4-6 hrs:
    Oral Metoprolol/ Labetalol
    Oral Captopril (if pheo suspected)
    Long acting CCB (Isradipine/Felodipine)
    If not volume depleted, Lasix in renal insufficiency
    - Aim: Decrease BP to 160/110 over several hours
  2. HT emergency (aka Malig HT)
    - Labetalol IV
    - Nitroprusside IV infusion (protect from light by wrapping)
    - Hydralazine IV (avoid in AMI, dissecting aneurysm)
    - Phentolamine IV (for catecholamine crisis)
  3. Notes on specific clinical conditions
    - APO -Nitroprusside/nitroglycerin + loop diuretic, avoid
    diazoxide/hydralazine (increase cardiac work) or Labetalol and BB in LV dysfunction
  • Angina or AMI - Nitroglycerin, nitroprusside,
    labetalol, CCB (Diazoxide or hydralazine CI)
  • Increase in sympathetic activity (clonidine withdrawal,
    pheochromocytoma, autonomic dysfunction (GBS/post spinal cord injury), sympathomimetic drugs
    (phenylpropanolamine, cocaine, amphetamines, MAOI or
    phencyclidine + tyramine containing foods) –>
    Phentolamine (non-selective AB), Labetalol (AB+BB) or Nitroprusside (Nitrate)
    BB is CI (further rise in BP due to unopposed alpha-adrenergic vasoconstriction)
  • Aortic dissection - aim: ↓systolic pressure to 100-120mmHg and ↓cardiac contractility
    Nitroprusside + Labetalol / Propanolol IV
  1. Look for causes of HT crisis, e.g. renal artery stenosis
79
Q

PE ECG

A

S1Q3T3

Large S wave in Lead 1
Q wave in Lead 3
Inverted T wave in Lead 3
==> indicate acute right heart strain

80
Q 
Palpitation types
1 Rapid fluttering
2 Flip-flopping
3 Intermittent forceful beats
4 Irregular pounding in neck 
5 Regular pounding in neck (Frog sign)
A

Rapid fluttering
- ST, SVT, AF, AFL, VT

Flip-flopping
- PVCs, PACs

Intermittent forceful beats
- PVCs

Irregular pounding in neck
- AV dissociation: PVCs, VT, CHB

Regular pounding in neck
- SVT

81
Q

Palpitation types
6 Young age of onset
7 Sudden onset
8 Gradual onset

A

Young
- SVT

Sudden
- AVNRT, AVRT, VT

Gradual
- AT, ST

82
Q 
Palpitation types
9 Respond to vagal maneuvers, positional changes
10 Syncope
11 At night in bed
12 During exercise
A

Respond to vagal / position
- AVNRT, AVRT

Syncope
- VT, SVT, CHB

At night in bed
- PACs, PVCs, AF

During exercise
- SVT, AF, VT (structurally normal heart)

83
Q

Causes of Bil ankle edema

WCS (Siu)

A
  1. RHF
  2. Chronic renal failure
  3. Hypoalbuminemia (cirrhosis, proteinuria)
  4. Drug (CCB: Nifedipine)
  5. Immobility
  6. Local obs

1,2 also increase JVP

84
Q

Digoxin SE

A

Paroxysmal atrial tachycardia with AV block
i.e. PAT w/ AV block

MCQ: Atrial tachycardia with variable block

85
Q 
Adrenocepter action (a, b1, b2)
WCS
A

Alpha: Vasoconstriction
Beta-1: Heart muscle contractility, rate
Beta-2: Bronchial and vascular smooth muscle

Medicine (9 decks)

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