Cardio Flashcards

1
Q

The main cause of Coronary artery disease

A

Atherosclerosis

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2
Q

What is the cause of vasospastic angina

A

Cigarette smoking, use of stimulants (e.g., cocaine, amphetamines) or sumatriptan, alcohol, stress, hyperventilation, exposure to cold
There is an association with other disorders involving vasospasms (e.g., Raynaud phenomenon, migraine headaches)

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3
Q

Outline in one sentence treatment approach for

  • mild CHD
  • moderate CHD
  • severe CHD
A

All patients: risk factor reduction and antiplatelet drugs

Mild CHD: pharmacologic therapy

Moderate CHD: consider coronary angiography and percutaneous transluminal coronary angioplasty (PTCA)/percutaneous coronary intervention (PCI)

Severe CHD: coronary angiography and revascularization or coronary artery bypass grafting

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4
Q

What are the 1st line anti-anginal treatment

A

First-line

1) Beta-blockers (except in vasospastic angina): can reduce the frequency of coronary events

2) Nitrates
Can prevent exertional angina
Suitable for relief of acute angina or for long-term treatment

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5
Q

What are the 2nd line anti-anginal treatment

A

CCB

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6
Q

What are the indications for revascularization and what are the 2 techniques

A

Indications

1) In stable angina: activity-limiting symptoms despite optimal medical treatment, contraindications to medical therapy, stenosis of critical (e.g., LCA) or multiple coronary arteries
2) Acute coronary syndrome

Techniques

1) Percutaneous coronary intervention
2) Coronary artery bypass grafting

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7
Q

ACS includes 3 conditions which are

A

1) Unstable angina
2) NSTEMI
3) STEMI

Acute coronary syndrome: suspicion or confirmed presence of acute myocardial ischemia and/or myocardial infarction
Further classified as unstable angina, NSTEMI, and STEMI

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8
Q

What is the difference between occlusions in the 3 difference ACS

A

Unstable angina–> Partial occlusion of coronary vessel → decreased blood supply → ischemic symptoms (also during rest)

NSTEMI–>Classically due to partial occlusion of a coronary artery
Affects the inner layer of the heart (subendocardial infarction)

STEMI–>Classically due to complete occlusion of a coronary artery
Affects full thickness of the myocardium (transmural infarction)

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9
Q

Cardiac biomarkers are seen positive in

A

NSTEMI and STEMI

NOT IN UNSTABLE ANGINA

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10
Q

ECG changes in NSTEMI

A

Normal or nonspecific (e.g., ST depression, loss of R wave, or T-wave inversion)
No ST elevations

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11
Q

ECG changes in STEMI

A

ST elevations (in two contiguous leads) or new left bundle branch block

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12
Q

ECG changes in NSTEMI/unstable angina

A
No ST elevations present
Nonspecific changes may be present.
ST depression
Inverted T wave
Loss of R wave
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13
Q

To remember the ECG leads with maximal ST elevation in anterior MI, think “SAL”

A

SAL”: “Septal (V1–2), Apical (V3–4), Lateral (V5–6).

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14
Q

Troponin which is most sensitive is

A

Troponin T

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15
Q

What is the best test for definitive diagnosis of acute coronary occlusion

A

Coronary angiography

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16
Q

Which artery is the most –> least likely to get occluded(3)

A

left the anterior descending artery
right coronary artery
circumflex artery.

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17
Q

What risk stratification score can be used for unstable angina/NSTEMI

A

TIMI score for unstable angina/NSTEMI

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18
Q

State some cardiac causes of chest pain

A
Pericarditis
Myocarditis
Takotsubo cardiomyopathy
Aortic dissection
Valvular anomaly (e.g., acute mitral regurgitation, aortic regurgitation, aortic stenosis)
Vasospastic angina
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19
Q

State some resp causes of chest pain

A
Pulmonary embolism
Pneumonia
pleuritis
Pneumothorax
Asthma
COPD
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20
Q

State some GIT causes of chest pain

A

Gastroesophageal reflux disease, esophagitis
Boerhaave syndrome, esophageal perforation
Acute gastritis
Mallory‑Weiss syndrome
Dyspepsia, peptic ulcer disease
Acute pancreatitis
Cholelithiasis, cholecystitis, biliary colic

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21
Q

State derm and MSK causes of chest pain

A

costochondritis and herpes zoster

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22
Q

State some psych causes of chest pain

A

Anxiety
Depression
Stimulant drug use (e.g., cocaine)

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23
Q

MONA for ACS, but can we give all of these drugs to all the patients

A

Primary interventions of MI treatment include “MONA”: Morphine, Oxygen, Nitroglycerin, and Aspirin. But remember: Morphine, oxygen, and nitroglycerine are not necessarily indicated for every patient

GTN–>Contraindications: inferior wall infarct (due to risk for hypotension), hypotension, and/or PDE 5 inhibitor (e.g., sildenafil) taken within last 24 hours

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24
Q

What is the immediate 1st step of STEMI

A

REVASCULARIZATION

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25
Q

Tell me about emergency coronary angiography

A

Emergent coronary angiography: with percutaneous coronary intervention (PCI)

Preferred method of revascularization

Balloon dilatation with stent implantation (see cardiac catheterization)
Ideally, door-to-PCI time should be < 90 minutes. It should not exceed 120 minutes.

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26
Q

What are the indications for thrombolytic therapy and what are the drugs that can be used

A

Thrombolytic therapy: tPA, reteplase, or streptokinase

Indications:
If PCI cannot be performed < 120 minutes after onset of STEMI
If PCI was unsuccessful
No contraindications to thrombolysis

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27
Q

State some contraindications for thrombolysis

A
Any prior intracranial bleeding
Recent large GI bleeding
Recent major trauma, head injury, and/or surgery
Ischemic stroke within the past 3 months
Hypertension (> 180/110 mm Hg)
Known coagulopathy
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28
Q

Walk me through the STEMI management(eTG)

A
  1. A- Intubate?, B- Ventilate? , C- IV acces/fluids?
  2. MONA
  3. Investigations eg. ECG, Trops
  4. Admit under coronary care unit
  5. MedicateDual antiplatelet therapy- Aspirin + Clopidogrel (Dose of clopidogrel dependant on means of reperfusion therapy used- i.e. lower dose if doing fibrinolytic therapy)
  6. Reperfusion - 2 methods, one must be started within 12 hours post-presentation, because post 12 hours infarction may already be complete. May be considered after 12 hours if there is - 1) Viable myocardium (R wave progression in infarcted leads) 2) Continued ischaemia (Persisting chest pain) 3) Major complications (shock)
    1) PCI- within 90 minutes of presentation
        Pre procedure- Dual Anti-platelet,  Anti-coagulation - Unfractionated heparin/ Enoxaparin (LWMH)
    2) Fibrinolytic therapy - tTPA Alteplase - If known that PCI cannot be performed within 90 mins, start this witin 30 mins.
        Pre procedure- Dual Anti-platelet,  Anti-coagulation - Unfractionated heparin/ Enoxaparin (LWMH)
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29
Q

What is the priority in STEMI and what is the priority in NSTEMI

A

The priority for a STEMI is re-establishing blood flow in the occluded coronary artery (reperfusion), which is achieved with percutaneous coronary intervention or fibrinolytic therapy.

The priority for a NSTEMI is plaque stabilisation and the prevention of coronary occlusion with medical therapy, and, if appropriate (TIMI score >3 –> revascularisation PCI, preferably within 72 hours)

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30
Q

What is the most common causes of IE

A

Staphylococcus aureus (45–65%)

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31
Q

Acute IE is caused by

A

Staphylococcus aureus (45–65%)

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32
Q

Subacute IE is caused by

A

Viridans streptococci

Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves

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33
Q

What is the criteria used for IE

A

Duke’s criteria

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34
Q

Most common cause of IE

A

Staphylococcus aureus (45–65%)

Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)

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35
Q

FROM JANE

A
FROM JANE -
Fever
Roth's spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail bed hemorrhage
Emboli
36
Q

Extra-cardiac symptoms of IE

  • what are the reasons for extracardiac symptoms
  • state as many as you can
A

These manifestations are mainly caused by bacterial microemboli and/or the precipitation of immune complexes

1) Petechiae; especially splinter hemorrhages (hemorrhages underneath fingernails)
2) Janeway lesions: non-tender, erythematous macules on palms and soles (due to microemboli and microabscesses with neutrophilic capillary infiltration)
3) Osler nodes: painful nodules on pads of the fingers and toes
4) Roth spots: retinal hemorrhages with pale centres

Signs of acute renal injury, including hematuria and anuria

Splenomegaly and possible LUQ pain

Neurological manifestations (e.g., seizures, paresis)

Signs of pulmonary embolism (e.g., dyspnea)

Possible arthritis

37
Q

In IE, which nodules are painful and which are not

A

Osler nodes are painful–>OOOOO

Janeway lesions are not

38
Q

What are the clinical consequences of IE systemically(like you know the pathophysiology, what will happen because of it)

A

Bacterial thromboemboli from bacterial vegetation → vessel occlusion with infarctions
Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes

39
Q

What are the clinical consequences of IE systemically(like you know the pathophysiology, what will happen because of it)

A

Bacterial thromboembolic from bacterial vegetation → vessel occlusion with infarctions
Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes

40
Q

Outline the Duke criteria(Modified)

A

The Duke criteria help to diagnose infective endocarditis.

To confirm the diagnosis, one of the following requirements must be met:

  1. Two major criteria
  2. One major and three minor criteria
  3. Five minor criteria

Major diagnostic criteria
1) Two separate blood cultures positive for typical pathogens
2) Evidence of endocardial involvement in echocardiography
3) A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)
Minor diagnostic criteria
Predisposition: underlying heart disease or IV drug abuse
Fever ≥ 38°C (100.4F)
Vascular abnormalities
Immunologic disorder
Microbiology

41
Q

Outline the Duke criteria(Modified)

A

The Duke criteria help to diagnose infective endocarditis.

To confirm the diagnosis, one of the following requirements must be met:

  1. Two major criteria
  2. One major and three minor criteria
  3. Five minor criteria

Major diagnostic criteria

1) Two separate blood cultures positive for typical pathogens
2) Evidence of endocardial involvement in echocardiography
3) A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient)

Minor diagnostic criteria

1) Predisposition: underlying heart disease or IV drug abuse
2) Fever ≥ 38°C (100.4F)
3) Vascular abnormalities
4) Immunologic disorder
5) Microbiology

42
Q

Which diagnostic test is the most sensitive for IE

A

Only negative findings on transesophageal echocardiography (TEE) can reliably rule out endocarditis, as transthoracic echocardiography (TTE) is not sensitive enough!

43
Q

How many cultures are needed for IE

A

Blood Cultures- 3 sets from separate venepuncture sites

44
Q

IE treatment for-Prosthetic valve

A

vancomycin+flucloxacillin+gentamicin

45
Q

IE treatment for-Native valves

A

benzylpenicillin+flucloxacillin+gentamicin(triple therapy)

46
Q

Life-threatening condition of chest pain-4

A

Myocardial infarction
pulmonary embolism
aortic dissection
pneumothorax

47
Q

ECG right ventricular strain pattern is

A

S1Q3T3 pattern, right bundle branch block.

48
Q

RHD includes 2 conditions what are the (or 2 clinical sequelae)

A

Acute pancarditis as a sequela of GAS infection

Chronic cardiac valvular changes as a complication of acute rheumatic fever

49
Q

Is rheumatic fever associated with strep skin infection

A

Rheumatic fever is not associated with streptococcal skin infections (e.g., erysipelas, impetigo, cellulitis).

50
Q

JONES criteria and CAFEPAL

A

Major criteria
Arthritis (migratory polyarthritis involving primarily the large joints)
Carditis (pancarditis, including valvulitis)
Sydenham chorea (CNS involvement)
Subcutaneous nodules
Erythema marginatum

Minor criteria
Arthralgia
Fever
↑ Acute phase reactants (ESR, CRP)
Prolonged PR interval on the electrocardiogram
51
Q

What must be met in JONES criterion

A

Interpretation: two major OR one major plus two minor criteria are required for diagnosis.

52
Q

Confirmation of GAS infection

A

↑ Antistreptolysin O titer (ASO): antibodies against metabolites of GAS

53
Q

Confirmation of GAS infection can be done through what kind of tests
-what will be an FBC show?

A

↑ Antistreptolysin O titer (ASO): antibodies against metabolites of GAS

Positive rapid streptococcal antigen test or throat culture for GAS

FBC:Normochromic, normocytic anemia of chronic inflammation
Leukocytosis

Echocardiogram (may show mitral or aortic regurgitation)

54
Q

What is the treatment for Acute ARF(eTG)

A
  • IM- Benzathine benzylpenicillin IM, single-dose, then followed by
  • Oral- Phenoxymethylpenicillin for 10 days (need to ensure adherence)
55
Q

What is the treatment for arthritis and fever

A
  • NSAIDs
  • Aspirin

Stop NSAID after the patient has been symptoms free for 1-2 weeks

56
Q

What is the treatment for chorea

A
  • Carbamazepine / sodium valporate
57
Q

How to prevention measure should be taken for ARF

A

Prevention - Antibiotic prophylaxis against GAS infection to prevent recurrence of acute rheumatic fever and development or progression of rheumatic heart disease

  • IM- Benzathine benzylpenicillin IM, every 28 days
58
Q

Erysipelas is caused by

A

Erysipelas is almost always caused by Streptococcus pyogenes (group A streptococcus).

59
Q

Acute pericarditis vs constrictive pericarditis-definition

A

Acute pericarditis is inflammation of the pericardium that either occurs as an isolated process or with concurrent myocarditis.

Constrictive pericarditis is characterized by compromised cardiac function caused by a thickened, rigid, and fibrous pericardium secondary to acute pericarditis.

60
Q

The most common cause of pericarditis

A

Viral

61
Q

Can MI give you pericarditis

A

Yes

Myocardial infarction: pericarditis may occur either within 1–3 days as an immediate reaction (i.e., post-infarction fibrinous pericarditis),

or weeks to months following an acute myocardial infarction (Dressler syndrome).

62
Q

State some of the features of constrictive pericarditis

A

Symptoms of fluid overload (backward failure)

Jugular vein distention, ↑ jugular venous pressure
Kussmaul sign
Hepatic vein congestion → hepatomegaly, painful liver capsule distention, hepatojugular reflux
Peripheral edema or anasarca, ascites with abdominal discomfort

Symptoms of reduced cardiac output (forward failure)

Fatigue, dyspnea on exertion
Tachycardia
Pericardial knock: sudden cessation of the ventricular filling during early diastole that is heard best at the left sternal border
Pulsus paradoxus: ↓ blood pressure amplitude during deep inspiration

63
Q

Pericarditis-ECG-initial stage

A

Stage 1: initial diffuse ST elevations, but ST depression in aVR and V1; PR segment depression

64
Q

Treatment for

1) Acute pericarditis
2) Constrictive pericarditis

A

Acute pericarditis is often self-limiting and resolves within approx. 2–6 weeks.

Treat underlying cause
Restricted physical activity
NSAIDs plus colchicine (alleviates symptoms, reduces rate of recurrence)
Glucocorticoids if NSAIDs are ineffective

Constrictive pericarditis
Treat underlying condition
Symptomatic therapy (manage fluid overload with diuretic therapy)
Pericardiectomy (complete removal of the pericardium)

65
Q

Complication if pericarditis is not treated

A
Constrictive pericarditis(as a complication of acute pericarditis)
Cardiac tamponade
66
Q

Most common causes of myocarditis

  • viral
  • bacterial
A

Coxsackie B1-B5 (picornavirus), parvovirus B19,

β-hemolytic Streptococcus group A (acute rheumatic fever)
Corynebacterium diphtheriae (diphtheria, diphtheria toxin)
67
Q

Clinical features of myocarditis

A
  • Often asymptomatic
  • Preceding (1–2 weeks) flulike symptoms
  • Fatigue, weakness, dyspnea
  • Cardiac arrhythmias: often sinus tachycardia; palpitations or syncope
  • Chest pain: indicates pericardial involvement (perimyocarditis)
  • Acute decompensated congestive heart failure with dilated cardiomyopathy
  • Cardiogenic shock in fulminant cases

Auscultation findings

1) systolic murmurs
2) Heart failure → S3 (and S4) gallops
3) Pericarditis → pericardial friction rub

68
Q

Complications of myocarditis

A

1) Progression to dilated cardiomyopathy
2) Heart failure or sudden cardiac death
3) Acute and/or persistent arrhythmias

69
Q

Pericardial effusion

A

Pericardial effusion is the acute or chronic accumulation of fluid in the pericardial space (between the parietal and the visceral pericardium) and is often associated with a variety of underlying disorders.

70
Q

Pericardial effusion and cardiac tamponade symptoms and signs

A
  • Usually initially asymptomatic
  • Shortness of breath, especially while lying down (orthopnea)
  • Beck’s triad
    1) Hypotension
    2) Muffled heart sounds
    3) Distended neck veins
  • Tachycardia, pulsus paradoxus
  • Retrosternal chest pain
  • Apical impulse difficult to locate or nonpalpable
  • Pallor, cold sweats
  • Symptoms of left heart failure and symptoms of right heart failure
  • Cardiogenic shock, asystole
71
Q

Beck’s triad

A
  • Beck’s triad
    1) Hypotension
    2) Muffled heart sounds
    3) Distended neck veins–>Due to elevated jugular venous pressure.
72
Q

CXR in pericardial effusion shows

A

CXR: enlarged cardiac silhouette, clear lungs, in severe cases a globular “water bottle-shaped” heart contour (water bottle sign)

73
Q

Treatment for pericardial effusion and cardiac tamponade

1) Depends on
2) What is the treatment for those approaches

A

Unstable –> Pericardial fluid drainage: ultrasound-guided pericardiocentesis or surgical drainage

Stable–> underlying cause

74
Q

What are the causes of pericardial effusion and cardiac tamponade

A

Hemopericardium

  1. Cardiac wall rupture (e.g., the complication of myocardial infarction)
  2. Chest trauma
  3. Aortic dissection
  4. Cardiac surgery (e.g., heart valve surgery, coronary bypass surgery)

Serous pericardial effusion

  1. Idiopathic
  2. Acute pericarditis (especially viral, but also fungal, tuberculous or bacterial)
  3. Malignancy
  4. Poststernotomy syndrome
  5. Uremic
  6. Autoimmune disorders
  7. Hypothyroidism
75
Q

Most common cause of syncope

A

Vasovagal

76
Q

State the types of syncope

A

1) Cardiac–>Arrhythmogenic syncope and CVD syncope
2) Reflex/vasovagal
3) Orthostatic syncope (postural hypotension)

77
Q

Which two investigations do all syncope patients get

A

ECG (for all patients!)

CBC (↓ serum Hb)

78
Q

What are the life-threatening conditions you should rule out in syncope

A

It is important to rule out life-threatening causes of syncope such as pulmonary embolism, hemorrhage, or serious cardiac conditions!

79
Q

DDx for syncope

A
Seizure	
Vertebrobasilar insufficiency	
Craniocerebral injury--> TBI
Heatstroke	
Panic attacks(Hyperventilation)
80
Q

State some common causes of syncope

A
Vasovagal
Arrhythmias
Dehydration 
Drugs--> new drug started?
Intoxication
Hypoglycemia
81
Q

Bilateral edema of the leg mainly points to a diagnosis of

A

Cardiac failure

82
Q

Generalized peripheral pitting edema with swelling of the eyelids indicates

A

Hypoalbuminemia (e.g., in nephrotic syndrome)

83
Q

Non-pitting edema suggests

A

lymphatic disorders and thyroid conditions.

84
Q

What are the 4 internal edema

A

Interstitial pulmonary edema
Cerebral edema
Ascites
Pleural effusion

85
Q

Cause of edema in the CHF

A

↑ Pc due to venous congestion (e.g., congestive heart failure)