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SENIOR MEDICINE BLOCK > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

MyocardIal Infarction

What is Acute Coronary Syndrome?

A

Refers to a group of diseases in which **blood flow to the heart **is decreases. Some examples include ST-elevation myocardial infarction, non-ST elevation myocardial infarction, and unstable angina.

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2
Q

Coronary Artery Disease

What is Atherosclerosis, what vessels does it affect and how is it caused?

A

medium and large arteries.** It is caused by chronic inflammation and activation of the immune system in the artery wall.** This causes the deposition of lipids in the artery wall, followed by the development of fibrous atheromatous plaques.**

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3
Q

Coronary Artery Disease

Define Acute Coronary Syndrome. what is formed and what 3 medications are used against it?

A

Acute coronary syndrome (ACS) is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
* When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets.
* This is why antiplatelet medications such as **aspirin, clopidogrel and ticagrelor **are the mainstay of treatment.

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4
Q

Coronary Artery Disease

Name 3 types of ACS?

A
  1. **Unstable angina
  2. ST-elevation myocardial infarction (STEMI)
  3. Non-ST-elevation myocardial infarction (NSTEMI) **
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5
Q

Coronary Artery Disease

Describe the symptoms associated with central constricting chest pain in ACS?

A
  • Pain radiating to the jaw or arms
  • Nausea and vomiting
  • Sweating and clamminess
  • A feeling of impending doom
  • Shortness of breath
  • Palpitations
  • **Symptoms should continue at rest for more than 15 minutes. **
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6
Q

Coronary Artery Disease

What are the ECG changes seen in STEMI and NSTEMI?

A

STEMI:

ST-segment elevation
New left bundle branch block

NSTEMI:

ST segment depression
T wave inversion

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7
Q

Coronary Artery Disease

What are pathological Q waves suggestive of and when do they typically appear?

A
  • deep infarction involving the full thickness of the heart muscle (transmural)
  • typically appear 6 or more hours after the onset of symptoms.
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8
Q

Coronary Artery Disease

Name 4 investigation used for ACS?

A

Troponin
Baseline bloods, including FBC, U&E, LFT, lipids and glucose

Chest x-ray to investigate for pulmonary oedema and other causes of chest pain

Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function

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9
Q

Coronary Artery Disease

Describe how unstable angina is diagnosed when there are symptoms of ACS and the** troponin is normal?**

A

A normal ECG
Other ECG changes (ST depression or T wave inversion)
NSTEMI: Raised troponin with the above

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10
Q

Coronary Artery Disease

Describe the Initial Management of patients presenting with symptoms of ACS?

A

CPAIN:
C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)

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11
Q

Coronary Artery Disease

Describe the Managment of STEMI and describe PCI/Thrombolysis procedure?

A
  • Patients with STEMI presenting within 12 hours of onset should be discussed urgently
  • Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
  • Thrombolysis (if PCI is not available within 2 hours)
  • PCI: Percutaneous coronary intervention (PCI) involves putting a catheter into the patient’s radial or femoral artery (radial is preferred)»> coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography)»>Blockages can be treated using balloons to widen the lumen (angioplasty)»Usually, a stent is inserted to keep the artery open.
  • Thrombolysis involves injecting a fibrinolytic agent»>work by breaking down fibrin in blood clots»significant risk of bleeding» Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
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12
Q

Coronary Artery Disease

Describe the management of NSTEMI and when do you give O2?

A

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)
* Give oxygen only if their saturation drops (less than 95% in someone without COPD).

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13
Q

Coronary Artery Disease

Describe angiography in NSTEMI and what is the GRACE score?

A
  • Unstable patients are considered for immediate angiography, similar to with a STEMI.
  • The GRACE score gives a** 6-month probability of death** after having an NSTEMI.
  • 3% or less is considered low risk
    Above 3% is considered medium to high risk
    Patients at **medium or high risk are considered for early angiography with PCI (within 72 hours). **
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14
Q

Coronary Artery Disease

Describe the medications for secondary prevention in ACS?

A

Medication for secondary prevention can be remembered with the “6 A’s” mnemonic or ABCDE

Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

A- ACE inhibitor
B- Beta Blocker
C-Cholesterol (Statin)
D-Dual Anti-Platelet Therapy
E-Eplerenone (Aldosterone Antagonist)

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15
Q

Coronary Artery Disease

Describe why it is essential to monitor renal function in patients taking ACE inhibitors and Aldoesterone Antagonists?

A
  • spironolactone or eplerenone (aldosterone antagonists) plus an ACE inhibitor or angiotensin receptor blocker carries a risk of fatal hyperkalaemia.
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16
Q

Coronary Artery Disease

Describe 5 complications of an MI?

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome»post-myocardial infarction syndrome»2 – 3 weeks after an acute myocardial infarction»caused by a localised immune response that results in inflammation of the pericardium, the membrane that surrounds the heart (pericarditis)»presents with pleuritic chest pain, low-grade fever and a pericardial rub on auscultation.can cause a pericardial effusion and rarely a **pericardial tamponade (where the fluid constricts the heart and inhibits function).»>diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).»Management is with NSAIDs (e.g., aspirin or ibuprofen) and, in more severe cases, steroids (e.g., prednisolone). Pericardiocentesis may be required to remove fluid from around the heart, if there is a significant pericardial effusion.**

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17
Q

Coronary Artery Disease

Describe the 4 types of MIs?

A

**Type 1: Traditional MI due to an **acute coronary event
**Type 2: **Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with procedures such as PCI, coronary stenting and CABG

You could remember these with the “ACDC” mnemonic:

Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI**

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18
Q

A 55-year-old obese male presents with aching pain across the lower chest, radiating up into his jaw. The pain started while walking around the supermarket, but did not go away with rest.

An ECG shows normal sinus rhythm with normal ST segments and no T wave inversion.

His past medical history is significant for pre-diabetes. He is prescribed glyceryl trinitrate spray and analgesia.

What is the appropriate pharmacological intervention?

A

All patients with suspect ACS should be given aspirin 300mg-

19
Q

What is the score and medication for Primary Prevention of CVD?

A

Medication for primary prevention is based on the QRISK3 score.
estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years
result is above 1**0%, they should be offered a statin, initially atorvastatin 20mg at night.
**
Atorvastatin 20mg is offered as primary prevention to all patients with:

Chronic kidney disease (eGFR less than 60 ml/min/1.73 m2)
Type 1 diabetes for more than 10 years or are over 40 years

20
Q

Myocardial Infarction

Define MI?

A
  • necrosis of myocardial tissue>following occlusion of a coronary artery and subsequent ischaemia> MI is a major manifestation of coronary heart disease (CHD).
21
Q

Myocardial Infarction

Describe the commonest cause of MI and give 2 types?

A
  • commonest cause of MI is an atheromatous plaque rupturing or eroding in a coronary artery; this causes a coronary thrombus to form, which partially or completely obstructs the artery
  • ST-segment elevation myocardial infarction (STEMI), which is generally caused by complete and persisting blockage of the artery
    Non-ST-segment elevation myocardial infarction (NSTEMI), reflecting partial or intermittent blockage of the artery.
22
Q

MI

Describe 5 complications that can occur after an MI?

A
  • heart failure> acute (within hours, daus due to rupture of papillary msucles and valve incompetence or ventricular septal defect. acute decompensation of Chronic HF and LVSD) or chronic (presents with breathlessness, fatigue and oedema)
  • angina-Post infarction-pain or heaviness in centre of chest
  • Stroke:
  • depression and axniety
  • and sudden death due to another MI or an arrhythmia-due to myocardial ruputre/fatal arrythmia
  • Dresslers: pericarditis post MI (2-4 weeks after an MI with self-limiting febrile illness accompanied with pericardial/pleural pain)
23
Q

MI

Describe the secondary prevention aims for MI?

A
  • cardiac rehabilitation-With exercise component
  • addressing relevant lifestyle risk-factors-Smoking cessation, diet, exercise, losing weight and less alcohol
  • drug treatment-ACE Inhibitor, Beta Blocker, Cholesterol (Statin) and Dual AntiPlatelet
24
Q

Describe 2 drugs that can cause 1st degree heart block?

A

Bisoprolol and Calcium Channel Blockers- they can cause the slowing of conduction through AV node and precipitate 1st degree heart block

25
Q

Cardiac Tamponade

What are the signs for cardiac tamponade which makes up Becks Triad?

A

HQR
H-Hypotension
Q-Quiet Heart Sounds
R- Raised JVP

26
Q

Aortic Dissection

Define Aortic Dissection?

A

Dissection occurs when a tear in the tunica intima of the aorta creates a false lumen whereby blood can flow between the inner and outer layers of the walls of the aorta.

27
Q

Aortic Dissection

Describe risk factors for aortic dissection- HAVCC?

A

H- HTN
A- Amphetamine use
V- Valvular heart disease
C- Cocaine use
C- Connective tissue disorder (Marfans)

28
Q

Aortic Dissection

Describe the classification of aortic dissection and give clinical features and
Signs seen on examination?

A

Stanford classification of aortic dissections

Stanford Type A: Involves the ascending aorta, arch of the aorta
Stanford Type B: Involves the descending aorta to left subclavian

Clinical features

Usually presents in men over the age of 50
Sudden onset ‘tearing’ chest pain or interscapular pain radiating to the back.
It can also present with (depending on how far the dissection extends):
Bowel/limb ischaemia
Renal failure
Syncope

Clinical signs on examination

Radio-radial delay
Radio-femoral delay
Blood pressure differential between arms

29
Q

Aortic Dissection

Describe the investigations used for aortic dissection?

A

CT angiography of chest, abdomen and and pelvis is used to diagnose dissection but other investigations can suggest the diagnosis and/or its complications:
CT angiopgraphy: False lumen is a key finding

ECG - May show ischaemia in specific territories if dissection extends into coronary arteries.
Echocardiogram - May demonstrate pericardial effusion and aortic valve involvement.
Chest x-ray - May show a widened mediastinum
Bloods:
Troponin may be raised
D-dimer may be positive

30
Q

Aortic Dissection

Describe the initial and definitive management of Aortic Dissection, what is the prognosis?

A

Initial management

Resuscitation if necessary
Cardiac monitoring
Strict blood pressure control (e.g. IV metoprolol infusion/labetalol- target systolic of 100-200

Definitive management

Depends on the type of dissection

Type A: Usually requires surgical management (e.g. aortic graft)
Type B: Normally managed conservatively with blood pressure control (Reduce BP with IV labetalol). If there is evidence of end organ damage then endovascular/open repair may be performed.

Prognosis

Prompt diagnosis and treatment is required as rupture carries an 80% mortality rate.

31
Q

Aortic Dissection

Describe a key finding suggestive of aortic dissection on CT angiography?

A

FALSE LUMEN IN ASCENDING AORTA

32
Q

Aortic Dissection

Describe the complications of a backward and forward tear for aortic dissection?

A

Backwards: aortic incompetence/regurgitation
inferior MI (RCA)
Forwards: unequal arm pulses and BP/Stroke/renal failure

33
Q

Pericarditis

Describe the ECG finding seen with patients presenting with acute pericarditis?

A

SADDLE-SHAPED ST ELEVATION

34
Q

Pericarditis

Define and give causes of acute pericarditis?

A

Define: inflammation of pericardial sac- lasting for <4-6 weeks
Causes:
1. Viral infections
2. TB
3. Uraemia
4. Post-MI (early: 1-3 days- fibrinous pericarditis) and late: weeks to months- autoimmune pericarditis-Dresslers Syndrome)
5. radiotherapy
6. Connective tissue disorfers (SLE/RA)
7. hypothyroidism
8. malignancy-lung and breast
9. trauma

35
Q

Pericarditis

Describe the key clinical features of acute pericarditis?

A
  1. Chest pain: pleurtic-often relieved by sitting forwards
  2. Non productive cough, dyspnoea and flu-like symptoms
  3. pericardial rub
36
Q

Pericarditis

Describe the investigations carried out for pericarditis?

A
  1. ECG Changes: global/widerspread so not territories seen in ischaemic events» saddle shaped ST elevation» PR depression (most specific ECG marker)
  2. Transthoracic echocardiography
  3. Bloods: inflammatory markers/30% may have raised troponin
37
Q

Angina Pectoris

Describe the drug management of stable angina?

A
  • all patients should receive aspirin and a statin in the absence of any contraindication
  • * sublingual glyceryl trinitrate to abort angina attacks
  • NICE recommend using either a **beta-blocker or a calcium channel blocker first-line **based on ‘comorbidities, contraindications
  • if a calcium channel blocker is used as monotherapy a **rate-limiting one such as verapamil or diltiazem
    **
  • if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
  • remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
  • if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa
    if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs:
  • a long-acting nitrate
  • ivabradine
  • nicorandil
  • ranolazine
    *
38
Q

Angina Pectoris

Describe Nitrate tolerance in angina pectoris?

A
  • many patients who take nitrates develop tolerance and experience reduced efficacy
  • NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to *minimise *the development of nitrate tolerance
39
Q

Mitral Valve Disease- Stenosis

Describe what is mitral stenosis?

A
  1. Obstruction of blood flow across the mitral valve from LA to LV- increase in pressure within LA, Pulmonary vasculature and RS of heart
40
Q

Mitral Valve Disease- Stenosis

Describe the causes of Mitral Stenosis?

A
  1. Rheumatic heart disease (rheumatic fever)
  2. Infective Endocarditis
41
Q

Mitral Valve Disease- Stenosis

Describe the features of mitral stenosis?

A
  1. dyspnoea: increased left atrial pressure-pulmonary venous HTN
  2. haemoptysis: due to pulmonary pressures and vascular congestion>pink frothy sputum to sudden haemorrhage secondary to rupture of thin-walled and dilated bronchial veins
  3. mid-late diastolic murmur (best heard in expiration)
  4. loud S1> opening snap
    indicates mitral valve leaflets are still mobile
  5. low volume pulse
  6. malar flush» red discolouration of upper cheeks and nose» back pressure of blood into pulmonary system>rise in CO2 and Vasodilation
  7. atrial fibrillation
    secondary to ↑ left atrial pressure → left atrial enlargement» electrical disruption> fibrillation

Features of severe MS:
1. Length of murmur increases
2. opening snap comes closer to S2

42
Q
A
42
Q
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42
Q

Mitral Valve Disease- Stenosis

What investigations can be carried out for Mitral Stenosis?

A
  1. C-XRAY: L atrial enlargement
  2. Echocardiography

SENIOR MEDICINE BLOCK (16 decks)

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