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ICC1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Which part of the aorta do the coronary arteries arise from?

A

Ascending aorta

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2
Q

Whqt does the RCA Supply? (6)

A
  1. Right Atrium
  2. Right Ventricle
  3. Interventricular septum
  4. SA node
  5. AV node
  6. Apex of the heart bu giving a right marginal branch.
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3
Q

What does the branch of the LCA that runs along the anterior inter ventricular sulcus supply?

A

That is the left anterior descending artery. It supplies:

  • apical portion of both ventricles
  • gives off 4-6 septal branches supplying interventricular septum.
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4
Q

What artery anastomoses with the RCA and what does it supply?

A

Left circumflex artery. Supplies left atrium and postero lateral surface of the left ventricle

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5
Q

What does ischameia usually present as?

A

PAIN. Usually exertional.
E.g. limb ischameia: limb claudication ( cramping pain when walking)
Myocardial ischemia : chetst pain

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6
Q

What is angina?

A

Episodic clinical syndrome due to transient myocardial ischemia characterized mostly by chest pain with no cardiac tissue damage

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7
Q

Where does anginal pain radiate?

A

Neck, Lower jaw, left shoulder, up to fingers

Could also include the right shoulder

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8
Q

What is stable angina?

A

This occurs when coronary perfusion is impaired by a fixed, stable atheroma. However, no complete vessel blockage.
(This type of angina is usually exertional and predictable)
Basically, it I’ll be felt when someone has an atheroma I’m their coronary’s not causing complete occlusion, however with effort, the chest pain commences

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9
Q

Describe the pain of stable angina

A

Chest heaviness, retrosternal pain.
Radiates to: epigastrium, jaw, neck, shoulder, left arm
Relieved by rest or nitrates
My be accompined with faintness, dsypnea, fatigue

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10
Q

Under what condition is the term acute coronary syndrome applied? What are the 3 types and what are its clinical features?

A

Reduction or complete loss of blood supply to the cardiomyocytes. It is only applied when we suspect myocardial infarction.
NSTEMI, STEMI, unstable angina

Clinical features: 
Breathlesness (tachypnea, tachychardia)
Autonomic symptoms (nausea, dizziness)
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11
Q

What is variable/ prinzmetal’s angina. How does it present on an ECG?

A

Idiopathic angina due go vasopastic coronary vessels.

Usually associated with ST segment elevations

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12
Q

Investigations in CAD?

A

ECG - standard test
First line: CT coronary angiography
Second line: stress echocardium, myocardial perfusion scan (under stress and at rest)
Third line: Invasive coronary angiography

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13
Q

What is the dye used in a myocardial perfusion scan?

A

Thallium IV

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14
Q

What is the medical term for a heart attack?

A

Myocardial infarction

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15
Q

What enzyme is used as a biomarker for MI?

A

Troponin. Increases in levels drastically after a recent MI. Theya re used for routine investigations of acute chest syndrome.

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16
Q

Inheritance pattern of hypertrophic cardiomyopathy?

A

Autosomal dominant

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17
Q

Fever, Murmur, Systemic embolisation.

What do you suspect?

A

Infective endocarditis until proven otherwise.

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18
Q

Most common organism causing infective endocarditis?

A

viridans streptococci

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19
Q

What imaging modality shows the vegetations in infective endocarditis

A

Echo

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20
Q

Consequences of right sided infective endocarditis?

A

pulmonary infiltrates and lung abscesses

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21
Q

What are 3 signs of immune related vasculitis in infective endocarditis?

A

OSLER’S NODES
JANE-WAY LESIONS
SPLINTER HEMORRHAGES

Complexes of antigen and antibody form and deposit in the peripheral vessels

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22
Q

IVDU get endocarditis of which valve and what is the causative organism?

A

Tricuspid, staph aureus

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23
Q

Causative organisms of Prosthetic valve endocarditis?

A

First 6 months
– S. aureus
– Coagulase negative staphylococci e.g. Staphylococcus epidermidis (SE)

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24
Q

Most important investigation of IE?

A

Blood cultures

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25
Q

What may lead to culture negative endocarditis?

A

previous antibiotic therapy
• fastidious streptococci
• HACEK organism ( very difficult to grow)
• Coxiella burnetii (diagnosis only by anti coxiella antibiodies)
•Candida spp.

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26
Q

Investigations of IE?

A 
Echo 
Blood culture 
CBC, U and E, TLC, CRP, ESR
Urine microscopy
Chest x ray
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27
Q

Using duke’s criteria, what is the definitive diagnosis for IE?

A

MAJOR
positive blood cultures or organisms seen at histology
evidence of endocardial involvement – ECHO
new valvular regurgitation

MINOR
• predisposition or I.V. drug abuse
• fever 38
°• vascular ➔ septic pulmonary infarction intracranial haemorrhage
• immunological ➔ glomerulonephritis (microscopic haematuria) Osler’s nodes (tender nodules) Splinters
• serology e.g coxiella antibodies

Definite diagnosis of IE
– 2 major
– 1 major + 3 minor

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28
Q

What are the culprit arteries of anterior/ inferior/ lateral wall MI?

A

Anterior/ septal Wall infarction: Occlusion in left anterior descending branch of LCA

Lateral wall infarction: Occlusion in Left Circumflex artery of LCA

Inferior wall infarction: Occlusion in right coronary artery

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29
Q

Investigations in MI? (4)

A

ECG: look for ST segment and T wave changes

Cardiac biomarkers: troponin, CKMB

Echo: Detect the territory of infarction, Detect acute MI complications, Evaluate the LV function

Coronary angiography: (Diagnostic and Therapeutic) Coronary arteriography should be considered with a view to revascularization.

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30
Q

State which leads correspond to which part of the heart affecting which artery

A

ANTERIOR VIEW: V3,V4 = LAD
SEPTAL: V1, V2 = LAD
INFERIOR: aVF, lead II, lead III = RCA
LATERAL: V5, V6, lead I, avL

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31
Q

Complications of MI?

A
  1. Dressler’s syndrome: post MI pericarditis (low grade fever, pleuritic chest pain)
  2. Cardiac tamponade: Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid in the pericardial space resulting in reduced ventricular filling and subsequent hemodynamic compromise
    The condition is a medical emergency, the complications of which include pulmonary edema, shock, and death (CHAMBERS DONT FILL PROPERLY, LESS C.O., HYPOTENSION)
  3. Mural thrombus: thrombus stuck to heart wall
32
Q

Treatment of MI?

A
  1. Reperfusion therapy:
    PCI should be done if it can be done within 120mins.
    If not, we give thrombolytic therapy until we can do PCI.
  2. Pain and hypoxia management:
    Opiates and oxygen
  3. DRUGS (aspirin, ace inhibitors, ARBS, b blockers, statins
33
Q

In acute heart failure, what is a staple treatment?

A
  • DIURETICS - 40mg furosemide
  • vasodilators to decrease preload and after load.
  • Nitrates are potent venodilators. These agents decrease preload and therefore decrease LV filling pressure and relieve dyspnea.
  • the most common route of administration in acute heart failure is IV
  • Sodium nitroprusside is a potent, primarily arterial, vasodilator that causes a very efficient afterload reduction and decrease of intracardiac filling pressures
34
Q

Clinical picture of heart failure?

A

Exertional Dyspnoea
• Orthopnoea
• PND
• Pink frothy sputum
• Features suggestive of underlying cause: e.g. Chest Pain
• Tachypnoea / Tachycardia
• Bilateral crackles, wheeze (cardiac asthma)
• Evidence of Cardiac congestive failure : JVP, pitting ankle oedema

35
Q

Treatment of HF?

A

Treatment outline Emergency Management
• Hospitalization
• High flow oxygen 100%
Reduction of Pre load & After load
• IV Loop diuretic Frusemide 40 mg
• IV nitrates (Glyceryl trinitrate) infusion
• Morphine IV 5 mg for pain control if present Non Invasive ventilation

36
Q

Most important cause of heart failure?

A 
Coronary artery disease. 
Other causes:
Valvular heart disease
Atrial fibrillation
Hypertension
 Acute kidney disease
37
Q

What is the GRACE score?

A

risk of mortality after ACS.

High grace score is more than 140

38
Q

4 causes of life threating chest pain?

A

MI
PE
Tension pneumothorax
Aortic dissection

39
Q

Investigations of heart failure

A

ECG, Echo, coronary angiography to exclude coronary artery disease

40
Q

Why is the p wave biphasic in V1?

A

Early right atrial forces are directed anteriorly, giving rise to an initial positive deflection; these are followed by left atrial forces travelling posteriorly, producing a later negative deflection.

41
Q

What does a bundle branch block look like on ECG?

A

Wide QRS on V1,V2, V5,V6

42
Q

Which valvular abnormality causes an impalpable apex?

A

TR

43
Q

Which valvular abnormality causes an haemoptysis?

A

Mitral stenosis

44
Q

Main clinical presentation of:

AS, MS, AR, MR, TS, TR

A

AS: Angina, syncope, dyspnea
MS: Cough, hemoptysis, dyspnea,
AR, MR: Dyspnea
TR, TS: Lower limb edema, ascites

45
Q

Most common valvular abnormality associated with AF?

A

Mitral stenosis

46
Q

No.1 cause of congestive heart failure?

A

Coronary artery disease.

47
Q

Which valvular heart disease has a “slapping” apex?

A

Mitral Stenosis

48
Q

Which valvular heart disease causes apex to shift outwards and downwards?

A

MR, AR

49
Q

Tapping/ slapping apex?

A

MS

50
Q

Peripheral signs of AR?

A

Corrigan sign (prominent carotid pulsations) and waterhammer pulse (felt radial and ulnar pulsation in forearm).

51
Q

How do we decide if we can perform balloon valvuloplasty on a stenotic mitral valve or not?

A

Presence of Opening snap in patients with MS means that the mitral valve is pliable and feasible for balloon valvuloplasty. Heavy calcification of the mitral valve in patients with MS can results in muffled S1. So, presence of muffled S1 and absence of opening snap in patient with severe MS means that this patient mostly will need surgical mitral valve replacement (rather than balloon valvuloplasty

52
Q

How do we describe the character of valvular heart diseases?

A

Stenotic lesion are harsh in character except MS and TS which are rumbling , while Regurgitant lesions are usually soft in character (could be harsh)

53
Q

How does the apex shift with TR?

A

OUTWARDS ONLY, NOT DOWNWARDS

with evidence of left parasternal, epigastric and pulmonary pulsation

54
Q

Peripheral signs of TR?

A

Systolic expansion of the neck veins and congested tender hepatomegaly

55
Q

TR vs MR?

A

If the maximal intensity of the murmur is heard over the apex and the murmur increases in left lateral position and radiate to the axilla, it is MR murmur. While if the maximal intensity of the murmur is heart over the tricuspid area and the murmur increases with inspiration, it is TR murmur)

56
Q

In cases of cardiomyopathies, how do we know if the cardiac infiltration is with muscle or amyloid tissue? (Like I’m restrictive cardiomyopathy)

A

Cardiac MRI.

57
Q

Symptoms of obstructive type of hypertrophic cardiomyopathy?

A 
DIASTOLIC DYSFUCNTION: DIASTOLIC HEART FAILURE 
Mimic AS (dyspnea, syncope, fatigue, dizziness) because septal enlargement causing obstruction of the left ventricular outflow tract, leading to low cardiac output
58
Q

Describe the murmur of HCM and how rid different to the murmur of AS

A

Ejection systolic murmur over the second aortic area in HCM
AS: FIRST AORITC AREA
not radiating to the carotid in HCM
RADIATING TO THE CAROTID IN AS
murmur increases with Valsalva or standing, decreases with squatting in HCM
ONLY INCREASES WITH LEANING FORWARD IN AS

59
Q

Treatment of HCM

A

Septal myectomy, alcohol septal ablation ,
BETA BLOCKERS: bisoprolol /metoprolol, or
calcium channel blockers such as verapamil or diltiazem (negative inotropic effect) .

60
Q

Findings on echo for HCM?

A 
LVH (deep q waves V1,V2-V5,V6)
Atrial enlargement (leads II and V1
61
Q

Write down the classes of anti-arrhythmic drugs

A

Class I: Na+ channel blockers (procainamide)
Class II: B blockers (propranolol, atenolol)
Class III: K+ channel blockers (Amiodarone)
Class IV: Ca2+ channel blockers (Verapamil, Dilitazem)
Class V: Unidentified (Adenoisn, digoxin)

62
Q

Findings on an echo of HCM?

A

Asymmetrical septal hypertrophy (ASH) or Systolic anterior motion(SAM) of anterior mitral valve leaflet

63
Q

What cardiomyopathy has an Epsilon wave on ECG?

A

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/ARVC):fibrofatty infiltration of RV

64
Q

State a few drugs that may cause hypertension

A

NSAID, steroids, oral contraceptive pills, nasal decongestant, anabolic steroids

65
Q

First line for LDL reduction?

A

Statin. (Ezetimibe).

66
Q

Describe the events of an aortic dissection

A

sudden severe acute chest pain, tearing in nature, radiating to inter-scapular region, with unequal pulse and BP , murmur of AR, wide mediastinum in CXR, Dilated aortic root in Echo, dissection flap in CT aortography

67
Q

In which patients should we suspect aortic dissection if they present with acute chest pain?

A
  • In patients with aortopathy such as Marfan syndrome or smoker with uncontrolled hypertension
  • If there is concomitant chest pain &neurological symptoms or chest pain with lower limb ischemia
68
Q

Difference between type A and type B aortic dissection?

A

Type A: involving ascending aorta, retrosternal pain

Type B: involving descending aorta, interscapular pain.

69
Q

What valvular abnormality is associated with aortic dissection?

A

AR

70
Q

ECG results of acute pericarditis?

A

widespread ST elevation &PR segment depression, except AVR which will show ST depression and PR segment elevation ,

71
Q

Acute pericarditis echo?

A

pericardial effusion

72
Q

Treatment of pericarditis?

A

bed rest, NSAIDs and colchicine

73
Q

Treatment of tamponade?

A

Urgent pericardiocentesis

74
Q

How do we diagnose tamponade

A

Diagnosis of tamponade is mainly clinical:

  • beck’s triad(high JVP, hypotension and muffled heart sounds)
  • pulsus paradoxus: Pulsus paradoxus refers to an exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg
  • Kussmaul sign (inspiratory filling of neck veins)
  • Echo(Pericardial effusion +Diastolic RV collapse)
  • electrical alternans in ECG
75
Q

Main presentation of constrictive pericarditis?

A

dyspnea , ascites and lower limb edema , Pericardial knock

76
Q

CT and MRI results of constrictive pericarditis?

A

pericardial calcification in CXR and pericardial thickening in cardiac MRI or CT

ICC1 (4 decks)

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