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A-CCC > GP-cardio > Flashcards

GP-cardio Flashcards

1
Q

HTN definition

A

Hypertension is the term used to describe high blood pressure.

above 140/90 in the clinical setting, confirmed with ambulatory or home readings above 135/85.

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2
Q

causes of HTN

A
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3
Q

complications of HTN

A
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4
Q

HTN staging

A
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5
Q

investigations nice recommends to all patients with a new diagnosis of HTN

A
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6
Q

NICE flow chart for diagnosis of HTN and deciding who to treat

A
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7
Q

lifestyle advice for HTN

A

Lifestyle advice should not be forgotten and is frequently tested in exams:
* a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
* caffeine intake should be reduced
* the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight

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8
Q

who do you treat for HTN/requirements

A
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9
Q

drug treatment flow chart for HTN

A
  • angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
  • for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor

when at 4th stage before seeking soecilaist advice first, check for:
* confirm elevated clinic BP with ABPM or HBPM
* assess for postural hypotension.
* discuss adherence

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10
Q

blood pressure targets in HTN

A
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11
Q

Spironolactone and thiazide like diuretics SE

A
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12
Q

hypertensive emergency definition and management

A
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13
Q
  • Examples of ace inhibitors, beta blockers, alpha blockers, CCB, thiazide like diuretics, ARB and potassium sparing diuretics
A
  • A – ACE inhibitor (e.g., ramipril)
  • B – Beta blocker (e.g., bisoprolol)
  • C – Calcium channel blocker (e.g., amlodipine)
  • D – Thiazide-like diuretic (e.g., indapamide)
  • ARB – Angiotensin II receptor blocker (e.g., candesartan)
  • Alpha blocker: doxazosin
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14
Q

AF definition

A

Atrial fibrillation (AF) is a condition where the electrical activity in the atria of the heart becomes disorganised, leading to fibrillation (random muscle twitching) of the atria and an irregularly irregular pulse.

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15
Q

The overall effects of atrial fibrillation are:

A
  • Irregularly irregular ventricular contractions
  • Tachycardia (fast heart rate)
  • Heart failure due to impaired filling of the ventricles during diastole
  • Increased risk of stroke
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16
Q

The most common causes of atrial fibrillation

A

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I– Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

Alcohol and caffeine are lifestyle causes worth remembering.

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17
Q

AF presentation

A

Patients are often asymptomatic, and atrial fibrillation is an incidental finding. It may be diagnosed after a stroke.

Patients may present with:

  • Palpitations
  • Shortness of breath
  • Dizziness or syncope (loss of consciousness)
  • Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
  • Chest pain

The key examination finding is an irregularly irregular pulse

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18
Q

There are two differential diagnoses for an irregularly irregular pulse:

A

Atrial fibrillation
Ventricular ectopics

Ventricular ectopics disappear when the heart rate gets above a certain threshold. Therefore, a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.

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19
Q

Types of AF

A
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20
Q

AF investigations

A

ECG and if needed echo

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21
Q

ECG findings in AF

A

Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm

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22
Q

When is an ECHO needed to investigate AF?

A

An echocardiogram may be required to investigate further in cases of:

Valvular heart disease
Heart failure
Planned cardioversion

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23
Q

Paroxysmal AF definition: what further investigations can they have?

A
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24
Q

Valvular AF definition

A
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25
Q

Two key principles when treating AF

A
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26
Q

How does rate control work?

A

rate control: accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function

Rate control aims to get the heart rate below 100 and extend the time during diastole for the ventricles to fill with blood.

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27
Q

NICE guidelines (2021) suggest all patients with AF should have…as first-line, except with:

A

NICE guidelines (2021) suggest all patients with AF should have rate control as first-line, except with:

  • A reversible cause for their AF
  • New onset atrial fibrillation (within the last 48 hours)
  • Heart failure caused by atrial fibrillation
  • Symptoms despite being effectively rate controlled
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28
Q

Options for rate control in AF

A
  • Beta blocker first-line (e.g., atenolol or bisoprolol)
  • Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
  • Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)
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29
Q

Patients presenting with acute AF management

A
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30
Q

In AF Rhythm control may be offered to patients with:

A
  • A reversible cause for their AF
  • New onset atrial fibrillation (within the last 48 hours)
  • Heart failure caused by atrial fibrillation
  • Symptoms despite being effectively rate controlled
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31
Q

Rhythm control aim and how it can be achieved

A

Rhythm control aims to return the patient to normal sinus rhythm. This can be achieved through:

Cardioversion
Long-term rhythm control using medications

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32
Q

Cardioversion options

A

Immediate cardioversion
Delayed cardioversion

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33
Q

Immediate cardioversion is used if the atrial fibrillation is either:

A

Present for less than 48 hours
Causing life-threatening haemodynamic instability

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34
Q

There are two options for immediate cardioversion:

A

Pharmacological cardioversion
Electrical cardioversion

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35
Q

For pharmacological cardioversion, the options are:

A

Flecainide
Amiodarone (the drug of choice in patients with structural heart disease)

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36
Q

How does electrical cardioversion work?

A

Electrical cardioversion aims to shock the heart back into sinus rhythm. It involves using a cardiac defibrillator machine to deliver controlled shocks. This is usually done with sedation or general anaesthesia.

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37
Q

When is delayed cardioversion used as a treatment? how is it carried out?

A

Delayed cardioversion is used if the atrial fibrillation has been present for more than 48 hours and they are stable.
Electrical cardioversion is recommended.

Transoesophageal echocardiography‑guided cardioversion is an option where available.
Amiodarone may be considered before and after electrical cardioversion to prevent AF from recurring.

The patient should be anticoagulated for at least 3 weeks before delayed cardioversion. During the 48 hours before cardioversion, they may have developed a blood clot in the atria, and reverting them to sinus rhythm carries a high risk of mobilising that clot, causing a stroke.
They are rate controlled whilst waiting for cardioversion.

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38
Q

Long-term rhythm control in AF is done with:

A
  • Beta blockers first-line
  • Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion
  • Amiodarone is useful in patients with heart failure or left ventricular dysfunction
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39
Q

Cardioversion management of AF if onset less than 48h

A
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40
Q

Cardioversion management options of AF if onset more than 48h

A
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41
Q

Management of paroxysmal AF

A
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42
Q

When is ablation used for AF? What are the two options for ablation?

A
43
Q

Complications of ablation in AF and success rate

A
44
Q

How is the need for anticoagulation assesses in AF? Name of tool used and scoring

A

The need for anticoagulation should be considered in patients with any history of AF, not just if they are in AF currently, i.e. the following groups should be assessed:
* symptomatic or asymptomatic paroxysmal, persistent or permanent atrial fibrillation
* atrial flutter
* a continuing risk of arrhythmia recurrence after cardioversion back to sinus rhythm or catheter ablation

Remember that if a CHA2DS2-VASc score suggests no need for anticoagulation it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation.

45
Q

Once you start a patient on anticoagulants because of AF, it is important to assess the risk of?

A
46
Q

Anticoagulation options in AF

A

The following DOACs are recommended by NICE for reducing stroke risk in AF:
* apixaban
* dabigatran
* edoxaban
* rivaroxaban

Warfarin is now used second-line, in patients where a DOAC is contraindicated or not tolerated.

Aspirin is not recommended for reducing stroke risk in patients with AF.

47
Q

What is a left atrial appendage occlusion and what is it used for?

A
48
Q

The most common indications for DOACs are:

A
  • Stroke prevention in patients with atrial fibrillation
  • Treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE)
  • Prophylaxis of venous thromboembolism (DVTs and PEs) after a hip or knee replacement
49
Q

DOACS mode of action

A

Apixaban, edoxaban and rivaroxaban are direct factor Xa inhibitors. Dabigatran is a direct thrombin inhibitor.

50
Q

Some of the DOACs have agents available to reverse the effects in uncontrolled or life-threatening bleeding:

A

Andexanet alfa (apixaban and rivaroxaban)
Idarucizumab (a monoclonal antibody against dabigatran)

51
Q
  • Warfarin MOA
A

Warfarin is a vitamin K antagonist. Vitamin K is essential for the functioning of several clotting factors. Warfarin blocks vitamin K. It prolongs the prothrombin time, which is the time it takes for blood to clot.

52
Q

how is warfarin monitored?

A

The INR (international normalised ratio) is used to assess how anticoagulated the patient is by warfarin. The INR calculates the patient’s prothrombin time compared with the prothrombin time of an average healthy adult. An INR of 1 indicates a normal prothrombin time. An INR of 2 means the patient has a prothrombin time twice that of an average healthy adult (it takes them twice as long to form a blood clot).

Warfarin requires close monitoring of the INR and frequent dose adjustments to keep the INR in range. It is given once daily, usually around 6 pm when in the hospital, so the INR is available before deciding the dose. The target INR for AF is 2 – 3.

Time in therapeutic range (TTR) refers to the percentage of time that the INR is in the target range. When the INR is too low, the patient is at increased risk of a stroke. When the INR is too high, the patient is at increased risk of bleeding.

53
Q

How is warfarin reversed?

A

Vitamin K can reverse the effects of warfarin in the event of a very high INR or significant bleeding. Warfarin has a half-life of 1-3 days.

54
Q

Chronic heart failure refers to

A

Chronic heart failure refers to the clinical features of impaired heart function, specifically the function of the left ventricle to pump blood out of the heart and around the body.

55
Q

chronic heart failure brief pathophysiology

A

Impaired left ventricular function results in a chronic backlog of blood waiting to flow into and through the left side of the heart. The left atrium, pulmonary veins and lungs experience an increased volume and pressure of blood. They start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema.

56
Q

The ejection fraction is

A

The ejection fraction is the percentage of blood in the left ventricle squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.

57
Q

Heart failure with reduced ejection fraction is

A

Heart failure with reduced ejection fraction is when the ejection fraction is less than 50%.

58
Q

Heart failure with preserved ejection fraction is when

A

Heart failure with preserved ejection fraction is when someone has the clinical features of heart failure but an ejection fraction greater than 50%. This is the result of diastolic dysfunction, where there is an issue with the left ventricle filling with blood during diastole (the ventricle relaxing).

59
Q

causes of chronic heart failure

A

Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
Cardiomyopathy

60
Q

symptoms and signs of chronic heart failure

A
  • signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly
  • weight loss (‘cardiac cachexia’): occurs in up to 15% of patients. Remember this may be hidden by weight gained secondary to oedema
61
Q

Paroxysmal nocturnal dyspnoea (PND) describes the experience that

A

Paroxysmal nocturnal dyspnoea (PND) describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

They may describe having to sit on the side of the bed or walk around the room, gasping for breath. They may feel suffocated and want to open a window to get fresh air. Symptoms improve over several minutes.

62
Q

Establishing a diagnosis of heart failure involves:

A
63
Q

How to interpret a BNP test?
what are the next steps once you get results?

A
64
Q

factors which can alter the BNP levels

A
65
Q

classification system used to grade the severity of symptoms related to heart failure

A
66
Q

The urgency of the referral for chronic heart failure and specialist assessment depends on the NT-proBNP result. According to the NICE guidelines:

A
  • From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
  • Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
67
Q

5 principles of chronic heart failure management,
additional management

A
68
Q

The first-line medical treatment of chronic heart failure, including monitoring investigations

A
69
Q

Additional specialist treatments in patients with chronic heart failure are:

A
70
Q

Procedural and surgical interventions for chronic heart failure

A
71
Q

Angina cause and definition

A

Angina is caused by atherosclerosis affecting the coronary arteries, narrowing the lumen (inside diameter) and reducing blood flow to the myocardium (heart muscle). During times of high demand, such as exercise, there is an insufficient supply of blood to meet the demand. This causes the symptoms of angina, typically constricting chest pain, with or without radiation to the jaw or arms.

72
Q

Stable angina definition

A

Angina is “stable” when symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN).

73
Q

Unstable angina definition

A

It is “unstable” when the symptoms appear randomly whilst at rest. Unstable angina is a type of acute coronary syndrome (ACS) and requires immediate management.

74
Q

angina investigations

A
75
Q

There are five principles of management for angina

A

There are five principles of management. You can remember this with the “RAMPS” mnemonic:

R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention

Referrals are usually sent to the rapid access chest pain clinic (RACPC).

76
Q

Medical management of stable angina including side effects and patient instructions on how to take them

A
77
Q

Surgical management of stable angina

A
78
Q

Types of surgical scars you can get following surgeries to treat angina:

A
79
Q

ACS cause

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.

80
Q

ACS: 3 types

A

Unstable angina
ST-elevation myocardial infarction (STEMI)
Non-ST-elevation myocardial infarction (NSTEMI)

81
Q

The right coronary artery supplies which parts of the heart?

A

The right coronary artery (RCA) curves around the right side and under the heart and supplies the:

Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area

82
Q

left coronary artery branches and which part of the heart they supply

A

The left coronary artery becomes the:

  • Circumflex artery
  • Left anterior descending (LAD)

The circumflex artery curves around the top, left and back of the heart and supplies the:

  • Left atrium
  • Posterior aspect of the left ventricle

The left anterior descending (LAD) travels down the middle of the heart and supplies the:

  • Anterior aspect of the left ventricle
  • Anterior aspect of the septum
83
Q

ACS presentation

A

Acute coronary syndrome typically presents with central, constricting chest pain.

The chest pain is often associated with:

  • 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.

84
Q

A silent myocardial infarction is when…
Patients with…are particularly at risk of silent MIs.

A

A silent myocardial infarction is when someone does not experience typical chest pain during acute coronary syndrome. Patients with diabetes are particularly at risk of silent MIs.

85
Q

ECG changes in STEMI

A

STEMI:

ST-segment elevation (in correpsonding area of ischemia)
New left bundle branch block (in hours)

hyperacute (tall) T waves T wave inversion & pathological Q waves follow (over hrs to days)

86
Q

NSTEMI ECG changes

A

NSTEMI:

ST segment depression
T wave inversion

87
Q

Pathological Q waves on ECG suggest..

A

Pathological Q waves suggest a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

88
Q

simplified correlation between ECG changes and coronary territories:

A
89
Q

diagnosis and investigations for ACS

A
90
Q

classification of ACS: how to differentiate between the 3 types

A
91
Q

first line management of ACS

A

also perform an ECG

When the patient is pain-free, but the pain occurred within the past 72 hours, they need to be referred to the hospital for same-day assessment, usually to be seen by the medical team in the Ambulatory Care Unit (depending on local pathways). They may require emergency admission if there are ECG changes or complications (e.g., signs of heart failure).

92
Q

management of STEMI

A

or clopidrogrel instead of aspirin and pasugrel

93
Q

Management of NSTEMI

A
94
Q

Scoring used to determine decision about angiography in NSTEMI

A
95
Q

Ongoing management in ACS including medication used in secondary prevention

A
96
Q

The complications of a myocardial infarction

A

The complications of a myocardial infarction can be remembered with the “DREAD” mnemonic:

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

97
Q

Dressler’s syndrome cause, presentation, management

A
98
Q

RF for cardiovascular disease

A
99
Q

Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk:

A

Diabetes
Hypertension
Chronic kidney disease (CKD)
Inflammatory conditions, such as rheumatoid arthritis
Atypical antipsychotic medications

100
Q

End result of atherosclerosis

A

Angina
Myocardial infarction
Transient ischaemic attacks
Strokes
Peripheral arterial disease
Chronic mesenteric ischaemia

101
Q

Primary prevention of cardiovascular disease

A
102
Q

Statins: MOA, monitoring investigations, side effects and interactions

A
103
Q

which CCB should be initiated for black patients to control HTN

A

nifedipine and NOT veramipil

A-CCC (9 decks)

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