Cardiology Flashcards

1
Q

What is chronic mesenteric ischemia ?

A

Intestinal angina. Narrowing of the mesenteric blood vessels by atherosclerosis. This results in intermittent abdominal pain, when the blood supply can not keep up.

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2
Q

What triad of symptoms are involved in chronic mesenteric ischemia ?

A
  • Central colicky abdominal pain after eating lasting 1-2 hours.
  • Weight loss due to food avoidance
  • Abdominal bruit
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3
Q

What is the gold standard diagnostic investigation for chronic mesenteric ischemia ?

A

CT angiography

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4
Q

How is chronic mesenteric ischemia managed non surgically ?

A
  • Reduction of modifiable RF (CV RF)
  • Secondary prevention (Statins and antiplatelet to break down clots)
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5
Q

How is chronic mesenteric ischemia managed surgically ?

A

Per-cutaneous mes-enteric artery stenting or open surgery

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6
Q

What is acute mesenteric ischemia ?

A

Typically caused by a rapid blockage in blood flow through the SMA. This is usually caused by a thrombus that has developed inside the artery or an embolus from another site

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7
Q

What is one of the major risk factors for acute mesenteric ischemia ?

A

AF - Due to thromboembolic mobilizing down the aorta to the SMA

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8
Q

What are the presenting symptoms of acute mesenteric ischemia ?

A
  • Acute
  • Non specific abdominal pain that is disproportionate to examination findings.
  • Nausea and vomiting
  • Guarding
  • Pain is disproportionate to exam finding
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9
Q

What are some of complications of acute limb ischemia ?

A

Include shock, peritonitis and sepsis, necrosis and perforation

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10
Q

How is acute bowel ischemia diagnosed ?

A

Contrast CT angiography

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11
Q

What will be present on blood tests in acute mesenteric ischaemia?

A
  • High lactate
  • Metabolic acidosis
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12
Q

How is acute mesenteric ischemia managed ?

A

Patients need surgery in order to remove the necrotic bowl and to remove or bypass the blood vessel. Patients have a very high mortality rate.

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13
Q

What diagnostic criteria defines a STEMI ?

A
  • Complete occlusion
  • Cardiac chest pain
  • ST elevation
  • Raised troponin
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14
Q

What diagnostic criteria defines an NSTEMI ?

A
  • Abnormal ECG (Non ST )
  • Raised troponin
  • Incomplete occlusion/stenosis
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15
Q

What diagnostic criteria defines unstable angina ?

A
  • Cardiac chest pain
  • Abnormal/normal ECG
  • Normal troponin
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16
Q

How does ACS typically present ?

A
  • Central/LS sudden crushing chest pain
  • Can radiate to the arm, neck and jaw
  • Nausea, sweating, clamminess, SOB, vomiting/syncope
  • Constant pain
  • Often very severe

Patients may also have epigastric pain, SOB, confusion, syncope and palpitations.

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17
Q

What group of patients are less likely to suffer from pain during an MI ?

A
  • Diabetics and the elderly. Females are also likley to present atypically
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18
Q

When should troponin be taken (time frame) in context of an MI ?

A

Levels typically increase 3 hours after MI begins. If mildly raised, patients will often need a 6-12 hour repeat test.

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19
Q

What is the most important initial investigation in an MI ?

A
  • ECG
  • STEMI - Troponin is not needed = Immediate PCI
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20
Q

What does ST elevation in Leads II,III and aVF indicate ?

A

RCA (Inferior infarc)

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21
Q

What does ST elevation in Leads V1-4 indicate ?

A

LAD infarc

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22
Q

What does ST elevation in leads 1, aVL and depression in v1-3 indicate ?

A

Left circumflex infarc (posterior)

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23
Q

What is the initial management for STEMI before a PCI ?

A

M - IV morphine for pain and vasodilation.

O - O2 therapy

A - Loading dose PO aspirin 300mg

N - Sublingual GTN

C - Clopidogrel.

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24
Q

What is the gold standard of treatment for a patient with STEMI ?

A

Primary PCI

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25
Q

When can a PCI be given in a STEMI ?

A

within 12 hours of the onset of pain and are less than 2 hours since first medical contact

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26
Q

What is the diagnostic criteria for NSTEMI ?

A

A diagnosis needs two of the following.

  1. Cardiac chest pain
  2. Newly abnormal ECG with non ST elevation
  3. Raised troponin.
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27
Q

How is an NSTEMI INITIALLY managed ?

A

O - Targeted o2 therapy

A - Loading dose PO of aspirin 300mg and fondaparinux

N - Sublingual GTN

M - IV morphine

A - Antithrombin therapy like LMWH or fondaparinux (If immediate angiogram).

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28
Q

What should be given if a patients 6 month risk of mortality is low in unstable angina?

A

Prasugrel or ticagrelor

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29
Q

What should be given to patients if there 6 month risk of mortality is high following ACS ?

A

PO clopidogrel 300mg

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30
Q

How is unstable angina managed ?

A

Aspirin.

Fondaparinux in patients where they are due to undergo angiography.

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31
Q

What medications should be given to a patient post MI ?

A
  1. A - Aspirin 75mg OM
  2. A - Antiplatelet clopidogrel 75mg OD or ticagrelor 90mg OD.
  3. A - Ace inhibitor (Ramipril)
  4. B - BB like bisoprolol
  5. S - Statin (Atorvastatin 80mg ON)

ECO and cardiac rehabilitation

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32
Q

What is Dressler’s syndrome ?

A

Post MI pericarditis. Patients present with a persistent fever and pleuritic chest pain 2-3 weeks post MI and symptoms generally resolve within a couple of days.

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33
Q

What is the management of Dressler’s syndrome ?

A

High dose aspirin.

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34
Q

If a patient presents with chest pain less then 10 days post MI, what is the most useful diagnostic blood test to rule out an MI ?

A

If a patient presents with chest pain less than 10 days post MI, the most useful blood test is CK-MB. This remains elevated only up to 4 days post MI.

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35
Q

In acute mesenteric ischemia, what is the most common site of occlusion ?

A

SMA

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36
Q

What should be excluded in all patients with abdominal pain and AF ?

A

Acute mesenteric ischemia

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37
Q

1st line diagnostic criteria for patient with acute limb ischemia ?

A

CT abdomen

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38
Q

Normal serum lactate levels ?

A

Lactate (plasma): 0.5 – 2.2 mmol/L

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39
Q

What are defining features of stable angina ?

A
  • Constriction like pain in the chest/neck/arm/jaw
  • Brought on by physical activity
  • Alleviated by rest or GTN within minutes

2/3 can indicate atypical angina pain.

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40
Q

What is the gold standard of investigation for stable angina ?

A

CT coronary angio

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41
Q

When is CT coronary angio CI ?

A

Renal impairment as the contrast can cause contrast induced nephropathy. In this case, myocardial perfusion imaging would be used.

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42
Q

What is the first line of management for stable angina ?

A
  • Conservative management, modification of RF for CV disease
  • GTN
  • BB

OR

  • Rate limiting CA channel blocker like Diltiazem or veramapril.
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43
Q

Would you give a BB or a rate limiting Ca channel blocker in stable angina in a patient with asthma ?

A

CA channel blocker as BB is CI

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44
Q

What is it important to tell patients who have recently started on GTN spray ?

A

When starting GTN, patients should be informed of the side effects (headaches, flushing, dizziness) and to take another dose if the pain has not subsided after 5 minutes. Importantly, emergency help should be sought if the pain has not subsided after 2 doses of GTN as this may indicate acute coronary syndrome.

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45
Q

What is the second line of treatment for patients with stable angina ?

A
  • BB AND long acting dihydropyridine Ca channel blocker (Amlodipine or felodipine)
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46
Q

What are the indications for CABG in patients with stable angina ?

A
  • Their symptoms are not satisfactorily controlled on optimal medical treatment AND
    • There is complex 3 vessel disease or
    • There is significant left main stem stenosis
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47
Q

What is RSHF caused by and how ?

A

Respiratory disease. Pulmonary hypertension causes the right ventricle being unable to efficiently pump blood.

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48
Q

What is the most common cause of right sided heart failure ?

A

COPD.

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49
Q

What are some causes of right sided heart failure ?

A
  • COPD
  • PE
  • ILD
  • Cystic fibrosis
  • Primary pulmonary hypertension
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50
Q

How does right sided heart failure present ?

A
  • Often patients in early stages are asymptomatic.
  • Most common is SOB
  • Peripheral edema
  • Increased SOB on exertion
  • Syncope
  • Chest pain
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51
Q

What will be present on examination in patients with right sided heart failure ?

A
  • Hypoxia
  • Cyanosis
  • Raised JVP
  • Peripheral odema
  • Pan systolic murmur ( tricuspid regurgitation)
  • Hepatomegaly
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52
Q

What murmur will be present in right sided heart failure ?

A

Pan systolic (Tricuspid regurgitation)

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53
Q

How is right sided heart failure managed ?

A
  • Management of the underlying cause.
  • Most patients are on long term oxygen therapy.
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54
Q

What is myocarditis ?

A

Myocarditis - Inflammatory disease of the myocardium. Myopericarditis if the pericardium is also inflamed

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55
Q

What are the clinical features of myocarditis ?

A
  • Cardiac type chest pain
  • Fatigue
  • Symptoms of heart failure
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56
Q

What would be present on examination in a patient with myocarditis ?

A
  • Signs of heart failure
  • S3 and S4 gallops
  • Pericardial rub if pericarditis is associated.
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57
Q

What are the ECG changes associated with myocarditis ?

A

Non specific ST segment and T wave changes. Ectopic beats and arrhythmias can also be present.

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58
Q

Apart from ECG findings, what else would be present on investigation in patients with acute myocarditis ?

A
  • ECHO can reveal ventricular dysfunction if present.
    • Troponin enzymes can be markedly elevated
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59
Q

What is the gold standard investigation of myocarditis ?

A

endomyocardial biopsy via cardiac catheterization however carries its own risks as an invasive procedure

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60
Q

How is myocarditis managed (including viral)?

A
  • Addressing the underlying cause and supportive management
  • Patients may need vasopressors (used to increase BP) need ICU monitoring.
  • Viral - Corticosteroids
  • Advice after recovery is that patients should be advised to limit activity for a few months
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61
Q

Myocarditis and STEMI can present similarly with raised troponin, chest pain and ST changed in ECG. How can you tell the difference ?

A

In Myocarditis, ST changes are likely to be widespread throughout the leads, whereas in a stemi, they are more likely to be isolated to certain leads.

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62
Q

What is one of the risks of atrial fibrillation ?

A

Clots can become emboli and can cause ischemic stroke.

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63
Q

How does atrial fibrillation present ?

A
  • Palpitations
  • SOB
  • Syncope
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64
Q

What type of pulse do patients with AF have ?

A

Irregularly irregular

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65
Q

What two conditions have an irregularly irregular pulse and how do they present ?

A
  • AF and ventricular ectopic
    ANYONE with this pulse should have an Ecg. In ventricular ectopics, they disappear before the HR gets over a certain threshold.
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66
Q

How does AF present on an ECG ?

A
  • Absent P waves
  • Narrow complex QRS tachycardia
  • Irregularly irregular ventricular rhythm
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67
Q

What is valvular AF ?

A

Patients with AF that have moderate or severe mitral stenosis or a mechanical heart valve, and that itself has lead to the AF.

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68
Q

What are some of the main causes of AF ?

A

AF effects mrs SMITH

  • Sepsis
  • Mitral valve pathology
  • Ischemic heart disease
  • Thyrotoxicosis
  • Hypertension
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69
Q

What are the two main things to control in AF ?

A

Rate and rhythm control

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70
Q

All patients with AF should have rate and rhythm control unless ….

A
  • There is reversible cause for their AF
  • Their AF is of new onset (within the last 48 hours)
  • Their AF is causing heart failure
  • They remain symptomatic despite being effectively rate controlled
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71
Q

What is the first line of treatment for rate control in AF ?

A
  • First line is BB (Atenolol 50-100mg OD)
  • CA channel blocker like Diltiazem (not used in HF)
  • Digoxin is used in sedentary patients as it needs monitoring and there is a risk of toxicity.
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72
Q

How is rhythm controlled in AF ?

A

Single cardioversion

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73
Q

When is immediate cardioversion indicated ?

A

if AF has been present for less than 48 hours and severely hemodynamically unstable

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74
Q

When is delayed cardioversion indicated ?

A

if the AF has been present for more than 48 hours and the patient is stable. The patient should be anticoagulated for at least 3 weeks before. The patient should have rate control whilst waiting for cardioversion.

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75
Q

What should all patients have before delayed cardioversion for rhythm control ?

A

Anticoagulation at least three weeks before.

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76
Q

What drugs are used in pharmacological cardioversion in AF ?

A

Flecainide or amiodarone (structural heart disease)

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77
Q

What is electrical cardioversion ?

A

Rapidly shock the heart back into sinus rhythm. The patient is usually sedated/GA and a defib is used

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78
Q

What is first line of treatment for long term rhythm control in AF ?

A
  • BB first line
  • Dronedarone - Maintaining normal rhythm where patients have successful cardioversion
  • Amiodarone is used in patients with heart failure or LVD.
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79
Q

What scoring system is used to determine if patients with AF require anticoagulation ?

A

CHA2DS2-VASc

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80
Q

What CHA2DS2-VASc score indicates anticoagulation in AF

A

More than 1

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81
Q

what does the CHA2DS2-VASc score stand for ?
NOTE - used to assess the risk of heart failure in patients with Af

A
  • CCongestive heart failure
  • HHypertension
  • A2Age >75(Scores2)
  • DDiabetes
  • S2Stroke or TIA previously(Scores2)
  • VVascular disease
  • AAge 65-74
  • SSex (female)
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82
Q

What is Warfarin ?

A

Vitamin K antagonist and prolongs PT time

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83
Q

What is INR score used for ?

A

INR is used to assess how anticoagulated a patient is. It measures how the PT time of the patient compares with that of the PT time in a normal healthy adult.

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84
Q

How to interpret INR scores ?

A
  • INR 1 = Normal PT time
  • INR 2 = PT time 2x that of healthy adult (2x as long to form a blood clot.
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85
Q

What is the target INR for AF ?

A

2-3

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86
Q

What are some of the negatives of warfarin use ?

A
  • Warfarin requires close monitoring of patients INR and dose adjustments to keep within range.
  • Target INR for AF = 2-3
  • INR of warfarin is effected by foods that contain vitamin K like green veg, and those that affect p450 like cranberry juice, alcohol and antibiotics.
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87
Q

What is the reverser for warfarin ?

A

Vitamin K

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88
Q

Why are DOACs used rather than warfarin in AF anticoagulation ?

A
  • Apixaban (2D), dabigatran (2D) Rivaroxaban (OD)
  • Short half lives
  • Advantages include - No monitoring is needed, no major interactions.
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89
Q

What tool is used when determining the risk of bleeding in patients on anticoagulation ?

A

orbit tool or HAS - BLED.

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90
Q

What does HAS-BLEED stand for (one year risk of bleeding in atrial fibrillation)?

A
  • H–**Hypertension
  • A–**Abnormal renal and liver function
  • S–**Stroke
  • B–**Bleeding
  • L–**Labile INRs (whilst on warfarin)
  • E–**Elderly
  • D–**Drugs or alcohol
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91
Q

What are the possible complications of persistent hypertension ?

A
  • Increased risk of morbidity and mortality from all causes
  • Heart failure
  • Renal failure
    -CAD
  • Stroke
  • Peripheral vascular disease.
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92
Q

What tool is used in patients to assess CV risk factors ?

A

QRISK

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93
Q

What tests should be conducted in people with hypertension to assess for end organ damage ?

A

Also assess for end organ damage including urine dip, blood glucose, RFT, fundoscopy and ECG for LVH.

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94
Q

When is pharmacological management indicated in patients with hypertension ?

A

Over stage 2 hypertension (140> syst AND 90> DIA) Or Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10%

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95
Q

Before pharmacological intervention in hypertension, what are some of the methods of managing a patient with hypertension ?

A
  • Weight loss
  • Healthy diet (reduce salt and saturated fats)
  • Reduce alcohol and caffeine
  • Reduce stress
  • Stop smoking
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96
Q

What is the first line of treatment of hypertension in a patient under 55, Caucasian with hypertension or a patient with Type 2 diabetes ?

A

ACE inhibitor like Ramipril. If unable to tolerate ARB like candesartan

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97
Q

What is one of the common well known side effects of Ramipril ?

A

It causes a DRY cough

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98
Q

What is the first line of treatment for a patient with hypertension over 55 years old or with African/Caribbean ethnicity?

A

CA channel blocker like amlodipine

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99
Q

What is the second line of treatment for hypertension ?

A

Add in the opposing drug

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100
Q

What is the third line of treatment for hypertension ?

A

Add thiazide-like diuretic(e.g. Indapamide)

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101
Q

What is the fourth stage of treatment for hypertension in patients with hyperkaliemia ?

A
  • If blood potassium <4.5mmol/L then addSpironolactone
  • If >4.5mmol/Lincrease thiazide-like diuretic dose
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102
Q

What is one of the side effects of amlodipine (ca channel blocker) and what should you do if a patient cannot tolerate it ?

A

Peripheral edema. If cannot be tolerated, take an ACE inhibitor instead.

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103
Q

What is the defining ECG feature of first degree heart block ?

A

PR interval > 200ms (5MM)

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104
Q

What are some of the causes of 1st degree heart block ?

A
  • High vagal tone (Athletes)
  • Acute inferior MI
  • Hyperkaliemia
  • Drugs - BB, Digoxin, cholinesterase inhibitors.
  • Prolonged PR - RCAD

Caused by prolongation of electrical activity through the AV node.

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105
Q

How is 1st degree heart block managed ?

A
  • Does not need managed as benign
  • Any underlying pathological findings should be reversed
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106
Q

What is the defining ECG features of Mobitz type 1 (Second degree heart block) ?

A
  • Lengthening PR intervals that eventually results in a dropped beat where the P wave fails to conduct QRS.
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107
Q

What are some of the causes of second degree heart block ( morbitz type 1 ) ?

A
  • Inferior MI
  • Drugs like BB/Ca channel blockers and digocin
  • Professional athletes
  • Myocarditis
  • Cardiac surgery
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108
Q

What is the defining features in ECG in type 2 (Morbitz type 2 ) heart block ?

A
  • Constant PR interval
  • Intermittent unconducted P waves.
  • Usually a conduction system failure
  • usually in a pattern 2:1/3:1 ect
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109
Q

How is second degree heart block (Mobitz type 1 ) managed ?

A
  • Usually does not require treatment if asymptomatic.
  • If symptomatic - ECG monitoring, exclusion of any drugs and atropine if bradycardia
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110
Q

What is the definitive management of third degree heart block ?

A

Permanent pacemaker

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111
Q

What are some of the causes of Type 2 (Morbitz type 2 ) heart block ?

A
  • Anterior MI
  • Surgery (Mitral valve repair)
  • Inflammatory/autoimmune - RHD, SLE, SSM
  • Fibrosis
  • Sarcoidosis, haemochromatosis
  • BB, CA channel blockers, amiodarone, digoxin.
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112
Q

What is the definitive management of Type 2 (Morbitz type 2 ) heart block ?

A

Permanent pacemaker

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113
Q

What are the defining ECG features of third degree heart block ?

A

ECG shows dissociation between the P waves and the QRS complexes.

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114
Q

What are some of the possible causes of third degree heart block ?

A

Can be caused by a combination of BB and Ca channel blockers. In conjunction can cause AV block.

Donepezil used in Alzheimer’s can cause complete heart block.

Can be caused by Lyme disease

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115
Q

What are the clinical features of third degree heart block ?

A
  • Syncope or cardiac arrest
  • Severe Bradycardia
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116
Q

What are the two shockable rhythms ?

A
  • Ventricular tachycardia (Without a pulse)
  • Ventricular fibrillation

Make sure look over structures on notion

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117
Q

What are the key ECG features of ventricular fibrillation ?

A
  • Randomized waveform.
  • Hill like structure
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118
Q

What are the two non shockable rhythms ?

A
  • Pulseless electrical activity (Apart from VF/VT)
  • Asystole
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119
Q

How are non shock-able rhythms managed (like flat line or pulse less electrical activity)?

A
  • CPR
  • Adrenaline 1mg IV
  • Adrenaline 1mg IV every 3-5 mins during 2 alternate loops of CPR
  • NO SHOCK
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120
Q

What is the characteristic shape of atrial flutter on ECG ?

A
  • Narrow QRS
  • Sawtooth pattern
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121
Q

What are some of the causes of atrial flutter ?

A
  • COPD
  • Obstructive sleep apnoea
  • PE
  • Pulmonary hypertension
  • IHD
  • Valvular heart disease (Mitral stenosis)
  • Sepsis
  • Alcohol
  • Cardiomyopathy
  • Thyrotoxicosis
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122
Q

What are some of the symptoms of atrial flutter ?

A
  • Can be asymptomatic
  • Palpitations
  • Dizziness
  • Chest pain
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123
Q

How is atrial flutter managed in hemodynamically stable patients ?

A
  • Rate control with BB and Ca channel blockers
    Direct current synchronized cardioversion
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124
Q

How is atrial flutter managed in hemodynamically unstable patients ?

A

managed with direct current synchronised cardioversion

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125
Q

What are signs of haemodynamic instability ?

A

shock
syncope
chest pain
pulmonary odema

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126
Q

What are the ecg features of wolff parkinson white syndrome ?

A
  • shortened pr interval
  • delta waves
  • widened qrs
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127
Q

what are the symptoms of wolff parkinson white syndrome ?

A
  • can be asymptomatic
  • palpitations
  • dizziness
  • SOB
  • tachycardia
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128
Q

what is the definitive treatment of WPW syndrome ?

A

radiofrequency ablation of the accessory pathway

  • vagal moves can be trialled
  • amiodarone can be trialled for rate and rhythm control
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129
Q

what drugs are CI in WPW syndrome ?

A
  • Digoxin and Veramapril.
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130
Q

what is the management of WPW syndrome in unstable patients ?

A

urgent DC cardioversion.

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131
Q

What is torsades de pointes ?

A

polymorphic ventricular tachycardia

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132
Q

what are the characteristic ECG changes in TDP ?

A
  • twisting isoelectric line
  • prolonged QTc interval
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133
Q

What can cause TDP ?

A
  • Toxins - Clarithromycin/mycin suffix (Antibiotic) , anti arrhythmic TCAs ect
  • Anti psychotics like haloperidol. Patients will have a PMH of schizophrenia and often new commencement of a drug.
  • Inherited - Congenital long QT syndromes
  • Ischemia
  • Myocarditis
  • Mitral valve prolapse
  • Electrolyte abnormalities (Hypokalaemia and hypocalcaemia like in acute pancreatitis )
  • SAH
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134
Q

How is TDP managed in haemodynamially stable patients ?

A
  • IV magnesium sulphate 2g over 10 minutes
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135
Q

How is Tosades de pointes managed in non haemodynamically unstable patients ?

A

DC cardioversion

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136
Q

What are ventricular ectopics ?

A

Ventricular ectopic are premature ventricular beats that are often caused by random electrical discharges from outside the atria. Patients often complain of random and brief palpitations

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137
Q

How to ventricular ectopics present on and ECG and how are they managed ?

A

They present as abnormal QRS complexes on a background of a normal ECG. In normal healthy patients, treatment is not needed.

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138
Q

What are some of the common causes of bradycardia ?

A
  • Hypothyroidism
  • Electrolyte abnormalities
  • BB overdose
  • Ca channel overdose
  • Sinus/AV node abnormalities
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139
Q

What is the initial management of bradycardia ?

A
  • Iv atropine (500 mcg) after assessment via ABCDE and can be given up to 3mg in boluses.
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140
Q

What are the indications for treatment of bradycardia ?

A

If a patient presents with symptomatic bradycardia (adverse effects e.g syncope)

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141
Q

If a patient presents with bradycardia as a result of BB overdose, what is the recommended treatment ?

A
  • Glucagon before transcutaneous pacing
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142
Q

What is the acronym to remember the main causes of heart fail

A

HIGH VIS

Hypertension
Infection/immune states
Genetic
Heart attack

Volume overload
Infiltration
Structural

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143
Q

What are the main presenting features of chronic heart failure ?

A
  • Dyspnoea on exertion
  • Fatigue
  • Orthopnoea (pillows to reduce symptoms)
  • PND - attacks of severe SOB in the night relieved by sitting up.
  • Nocturnal cough with or without characteristic - Pink frothy sputum
  • Reduced appetite
  • Pre syncope/syncope
  • PMH - HTN - CAD - valvular heart disease (common causes)
  • FHX - Cardiomyopathy or CAD
  • CHF - RF like smoking, excess alcohol and rec drug use
  • DHX - Ca antagonists, antiarrhythmics, cytotoxic medication and BB.
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144
Q

What are the three most memorable symptoms of heart failure ?

A
  • Orthopnoea (pillows at night)
  • PND - attacks of SOB in the night relieved by sitting up
  • Pink frothy sputum
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145
Q

What is present on cardiovascular examination in a patient with heart failure ?

A
  • Raised JVP
  • Hypotension
  • LVH - displaced apex beat
  • Tachycardia at rest
  • Gallop rhythm on auscultation (pathognomic in CHF)
  • Pedal and ankle odema
  • Narrow pulse pressure
  • Murmurs associated with valvular heart disease - Ejection systolic murmur in aortic stenosis.
    P pulmonary - Tall, peaked P waves on ECG trace and reflects right atrial enlargement in right sided heart failure.
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146
Q

What rhythm is charachteristic of chronic heart failure on auscultation ?

A
  • Gallop rhythm
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147
Q

What murmur is associated with valvular heart disease ?

A

ejection systolic murmur

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148
Q

What examination findings are found in patients with CHF on resp examination ?

A
  • Tachypnoea
  • Bibasal end inspiratory crackles and wheeze on auscultation of the lung fields - pul odema
  • Reduced air entry and stony dullness to percussion (pleural effusion)
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149
Q

What are signs on auscultation of a patient with pleural effusion ?

A

reduced air entry

Stony dullness to percussion

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150
Q

What is present on ECG in a patient with CCF ?

A
  • Tachycardia
  • AF
  • LAD - LVH
  • Lead 1 is +, lead 2 and 3 and avf is negative
  • Prolonged PR due to AV block
    -Q waves due to previous MI
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151
Q

How does LVH present on ECG ?

A

+ in L1
_ in L 2,3 and avf

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152
Q

What is NT- Pro BNP and when is it measured ?

A

Should be measured in all patients presenting with symptoms and clinical signs of heart failure to inform the type and urgency of ECHO.

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153
Q

What NTP - ProBNP levels indicate ECHO and ugent review ?

A

NT-proBNP level >2000 ng/L – refer urgently for specialist assessment and transthoracic echocardiography within 2 weeks

NT-proBNP level 400-2000ng/L – refer routinely for specialist assessment and transthoracic echocardiography within 6 weeks

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154
Q

What electrolyte abnormality should be monitored in CHF ?

A

Hyponatraemia due to fluid overload

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155
Q

What imaging should all patients with suspected heart failure have ?

A

ECHO

Cardiac MRI is the gold standard investigations when assessing ventricular mass, volume and wall motion. It is typically used when ECHO has provided inadequate views.

CXR

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156
Q

What are the signs of HF on CXR ?

A
  • Alveolar oedema (bat wing opacification)
  • Kerley B lines
  • Cardiomegaly
  • Dilated upper lobe vessels
  • Effusions
    Fluids in the horizontal fissure
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157
Q

What is left ventricular ejection fraction ?

A

LVEF is the percentage of blood that enters the left ventricle in diastole that is subsequently pumped out in systole.

measured using ECHO

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158
Q

How is HF managed non pharmacologically ?

A

Lifestyle management

  • Fluid and salt restriction
  • Regular excersise
  • Smoking cessation
  • Reduced alcohol intake
  • Vaccination for influenza and pneumococcal disease
  • Medication review for medications that can make HF worse, Ca channel blockers, TCA, lithium, NSAIDS, cox-2 inhib ect
  • Monitoring
  • Management of co-morbidities
  • CAD - may be prescribed statins and aspirin.
  • AF
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159
Q

What EF is considered heart failure ?

A

Below 55 percent

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160
Q

What is the role of furosemide in heart failure ?

A

Furosemide - increase NA excretion and reduce cardiac afterload (note, monitor renal function)

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161
Q

When are ACE inhibitors indicated in heart failure ?

A
  • All patients withCHFand areduced ejection fraction(≤40%) should be commenced on anACE inhibitorunless contraindicated (pril)
  • ACE inhibitors have been shown toimprove ventricular functionandreduce mortality.
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162
Q

When are ARBs like candesartan indicated in HF ?

A

ARB like candesartan should be prescribed as an alternate to ACE inhib if not tolerated due to cough ect

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163
Q

What are the CI for ACE inhibitors ?

A

Contraindications
include a history of angioedema, bilateral renal artery stenosis, hyperkalaemia (>5 mmol/L), severe renal impairment (serum creatinine >220 μmol/L) and severe aortic stenosis.

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164
Q

When are BB indicated in heart failure ?

A

BB should be prescribed in all patients with LVEF less than 40 and symptomatic heart failure. Bisproprolol.

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165
Q

What are the contraindications for BB ?

A

include asthma, 2nd or 3rd degree AV block, sick sinus syndrome and sinus bradycardia.

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166
Q

What are the potential complications of heart failure ?

A
  • Arrhythmia - AF and ventricular arrhythmia.
  • Depression and impaired quality of life
  • Loss of muscle mass
  • Sudden cardiac death.
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167
Q

What is the classic triad of symptoms in aortic stenosis, what are some of the other possible symptoms ?

A
  • Syncope
  • Angina
  • Dyspnoea

Also associated with heart failure, excertional dyspnoea and decreased excersise tolerance.

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168
Q

What murmur is heard in aortic stenosis and where ?

A

Ejection systolic murmur that is heard loudest over the aortic area (over the 2nd intercostal space) and radiates to the carotid arteries.

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169
Q

What clinical features are heard in aortic stenosis during clinical examination ?

A

-Ejection systolic murmur heart loudest over the aortic valve and radiates to the carotid artery.
- s2 may be quiet or absent due to radiation to the carotid
- Pulse is slow rising and narrow pulse pressure
- heaving apex beat that is non displaced (LVH)
- Murmur is loudest on expiration and when the patient is sitting forward

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170
Q

What is the first line investigation for aortic stenosis ?

A

ECHO

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171
Q

Apart from ECHO, what are the other investigations in aortic stenosis.

A

CT angio

Cardiac MRI

ECG - to look for LVH.

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172
Q

What is present on ECG in aortic stenosis ?

A

LVH is a common sign of aortic stenosis.

It is commonly diagnosed by the S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm

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173
Q

What are the indications for intervention in aortic stenosis ?

A
  • All patients with symptomatic aortic stenosis
  • Asymptomatic patients with LVEF < 50
  • Asymptomatic patients with an LVEF > 50% who are physically active, and who have symptoms or a fall in blood pressure during exercise testing
  • Asymptomatic patients with an LVEF > 50% who have the following risk factors
    • Aortic valve peak velocity > 5.5m/s
    • Markedly elevated BNP levels without other explanation
    • Severe pulmonary hypertension (pulmonary artery systolic pressure > 60mmHg)
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174
Q

What are the two methods of treatment in aortic stenosis ?

A

SAVR and TAVR

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175
Q

What is the advantages and disadvantages if mechanical heart valves in treating aortic stenosis ?

A

Mechanical - ADV lasts longer and is unlikley to be rejected however patients need warfarin which requires INR monitoring.

176
Q

What are the advantages of biological valves in traeting aortic stenosis

A

Biologics - No anticoagulation is needed but cant be used in the immunosuppressed and is less sustainable.

177
Q

When is a TAVI indicated in aortic stenosis treatment ?

A

A TAVI can be used in patients that are not fit for surgery. Usually patients older than 75, previous heart surgery, frailty, restricted mobility, severe comorbidities ect.

178
Q

How are patients not fit for surgery monitored in aortic stenosis ?

A

Patients that are not fit for surgery, should have regular follow up. Severe every 6 months, every onve 1 year if moderate

179
Q

What is aortic sclerosis ?

A

Aortic sclerosis is an asymptomatic condition that can be incidentally revealed through physical examination or ECHO. It is caused by age related senile degeneration of the valve.

180
Q

What are the classic examination findings or aortic scleorsis ?

A

Classic examination findings are an ejection systolic murmur that does not radiate to the carotids. Cardiovascular examination is normal.

181
Q

How are metallic heart valves anti coagulated ?

A

Warfarin

182
Q

What groups of people is infective endocarditis more common in ?

A
  • IVDU
  • Valve replacement
  • Pacemakers
183
Q

What are the two sub classifications of IE ?

A

Can be classified as left sided which is more common (aortic/mitral) or right sided (pulmonary/tricuspid).

  • Can be prostetic valve, which is more serious with worse prognosis and native valve endocarditis.
184
Q

What three features occur at the same time in IE ?

A
  • Transient bacteraemia
  • Damage to valvular tissue
  • formation of vegetations

Bacteria often enters the bloodstream, often by things like dental infections, IV drug use ect.

185
Q

What groups of people is staph aureus IE more prevalent in ?

A

Endocarditis in patients with prosthetic valves, acute endocarditis and intravenous drug use.

186
Q

What is blood culture negative IE and why is it caused ?

A

No causative organism is found from standard blood culture methods. This is often due to patients having antibiotic therapy prior to blood cultures being taken. You may need serology to identify them.

187
Q

What are some examples of culture negative bacteria in IE ?

A
  • HACEK organisms
  • Coxiella burnetti(Q fever)
  • Chlamydia spp
  • Bartonella spp (trench fever and cat-scratch disease)
  • Legionella
188
Q

What are some of the RF for infective endocarditis ?

A
  • IVDU
  • Invasive procedures like central lines
  • Poor oral hygiene/infections
    _ valvular stenosis or regurgitation
  • Hypertrophic cardiomyopathy
  • Previous infection causing structural damage
189
Q

What are the clinical features of infective endocarditis ?

A
  • Systemic features of infection (fever, malaise, night sweats, weight loss)
  • Anaemia symptoms ( fatigue and SOB)
  • Other symptoms associated with symptoms like emboli and mesenteric ischaemia
190
Q

What is present on examination in patients with infective endocarditis ?

A
    • Fever and tachycardia
    • New or changing heart murmur
    • Splinter haemorrhages
    • Oslers nodes - Tender subcutaneous nodules in the fingers
    • Janeway lesions - Painless erythematous macules on the palms.
    • roth spots
    • Clubbing (late sign)
    • Mild splenomegaly
    • Bi basal lung crepitations (HF in severe cases)
191
Q

What can be present on ECG in patients with IE ?

A

May have first degree heart block, which is a finding of aortic root abscesses, a rare complication of IE ( 5 small boxes = 20s). This measurement should be0.12-0.20 seconds, or 3-5 small squares in duration

192
Q

How long is a normal PR interval ?

A

This measurement should be0.12-0.20 seconds, or 3-5 small squares in duration

193
Q

How are blood cultures collected in IE ?

A

Blood cultures - Should be done ideally prior to starting antibiotic therapy. Three sets of blood cultures at least 30 mins apart from three separate sites.

194
Q

Apart from ECG and BC, what are the other important investigations in IE ?

A
  • Basic obs - Look for signs of infection like fever or tachycardia.
  • Urine dipstick to look for microscopic haematuria.
  • FBC - WCC and HB monitoring
  • CRP and ESR
  • Urea and electrolytes - baseline as well as needed if the patient is going to be starting gentamycin as it is nephrotoxic.
195
Q

What is the first line imaging investigation for IE ?

A

Trans thoracic echo which should be performed as soon as suspected to look for vegetation.

196
Q

What imaging modality is used if transthoracic ECHO is clear in IE ?

A

If ECHO is clear, a transoeophageal ECHO can be arranged.

Patients can also undergo CXR and CT abdomen.

197
Q

What criteria confirms definite endocarditis ?

A
  • Directevidenceof infective endocarditis byhistologyorcultureof organisms (e.g. from a vegetation)
  • TWOmajor criteria
  • ONEmajor +THREEminor criteria
  • FIVEminor criteria
198
Q

What criteria indicate possible endocarditis ?

A
  • ONEmajor andONEminor criterion
  • THREEminor criteria
199
Q

What are the major criteria for IE ?

A

Positive for typical organisms (Strep bovis, Staph aureus, community aquired enterococci)
Persistently positive cultures

Single positive culture for coxiella burnetti

Evidence of endocardial involvement like intra cardiac vegitation, abscess, new valvular regurgitation or new partial dehiscence of prostetic valve.

200
Q

What are the minor criteria for IE ?

A

Risk factors for infective endocarditis (see risk factors section)

Fever > 38oC

Vascular phenomena: septic emboli, Janeway lesions, conjunctival haemorrhage, intracranial haemorrhage

Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots, positive rheumatoid factor

Microbiological evidence: positive blood cultures which do not meet the major criteria

201
Q

What is the mainstay of treatment for IE ?

A

Mainstay - prolonged course of IV antibiotics for at least two weeks before switching to oral preparations

202
Q

How long should antibiotic therapy last in IE with prosthetic valves ?

A

at least 6 weeks

203
Q

How long should antibiotic therapy last in IE with native valves ?

A

2-3 weeks

204
Q

How long should antibiotic therapy last in IE with native valves ?

A

2-3 weeks

205
Q

When should antibiotic courses be started in IE ?

A

Start of antibiotic course is taken from the first day a negative set of blood cultures are taken.

regardless of if antibiotics have been started before

206
Q

When should antibiotic courses be started in IE ?

A

Start of antibiotic course is taken from the first day a negative set of blood cultures are taken.

regardless of if antibiotics have been started before

207
Q

What are the indications for surgery in IE ?

A
  • Heart failure
  • Uncontrolled infection
  • PE and large vegitations
  • Increased PR interval and aortic root abscesses
208
Q

Why can mes-enteric ischaemia be a possible complication of IE ?

A

Mesenteric ischaemia - complication of septic emboli. Gold standard is CT angio

209
Q

Why can mes-enteric ischaemia be a possible complication of IE ?

A

Mesenteric ischaemia - complication of septic emboli. Gold standard is CT angio

210
Q

What are some of the systemic complications of IE ?

A
  • Emboli (e.g. stroke, splenic infarction)
  • Immune complex deposition (e.g. glomerulonephritis)
  • Septicaemia
  • Death
211
Q

What are some of the local complications of IE ?

A
  • Valve destruction
  • Heart failure (secondary to valve regurgitation)
  • Arrhythmias and conduction disorders (e.g. AV block)
  • Myocardial infarction
  • Pericarditis
  • Aortic root abscess
  • Mesenteric ischaemia - complication of septic emboli. Gold standard is CT angio
212
Q

What is high output cardiac failure ?

A

Failure of the heart to generate sufficient CO to meet the metabolic demands of the body. Heart output is normal, but there is an increase in peripheral metabolic demands.

Seen in pregnancy, thiamine deficiency, anaemia, AVN malformation and pagets.

213
Q

What are the clinical features of right sided heart failure ?

A
  • Raised JVP
  • Ascities
  • Fatigue
  • Pitting ankle odema and sacral odema
  • Bilateral pleural effusions
  • Weight gain
  • usually secondary to chronic pulmonary problems like COPD as they cause pulmonary hypo perfusion.
214
Q

What system is used to classify heart failure ?

A

New york heart association classification of heart failure.

  • Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitation or dyspnoea.
  • Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitation and/or dyspnoea.
  • Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
  • Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
215
Q

What is used in the cause of ECHO findings being unremarkable in suspected heart failure ?

A

Cardiac MRI

216
Q

What are the two sub types of heart failure ?

A
  • <40% = heart failure is reduced ejection fraction
  • Greater than 40% but raised BNP = Heart failure with preserved ejection fraction
217
Q

In patients with non EF heart failure, what is the recommended treatment programme ?

A

Furosemide for symptom relief and conservative management of risk factors.

218
Q

What is the first line of treatment for patients with EF heart failure ?

A
  • Furosmide
  • BB
  • ACE (ARB) if not tolerated due to cough.
219
Q

If 1st line therapy has not worked in HF, what else can be used ?

A

If a patient has persistent symptoms and is new york classification 3/4, consider an alternate like aldosterone agonists (spirnolactone)

or ivadarabrine if already on enadebrine

220
Q

How is acute heart failure managed ?

A
  • Sit upright
  • O2 therapy
  • IV furosemide (40mg or more) and fluid balance.
  • SC morphine
221
Q

A 75-year-old female patient is reviewed in the cardiology heart failure clinic. She is being treated with Bisoprolol 10 mg and Ramipril 10 mg in addition to Furosemide 80 mg but she still complains of difficulty with her breathing.

What is the most appropriate escalation of her therapy?

A

Spirnolactone

222
Q

When is an ICD considered in HF ?

A

ICD should be considered in all patients with a reasonable quality of life and poor LVEF despite optimum medical therapy. Also should be considered in patients with previous episodes of VF or VT

223
Q

What is haemochromatosis ?

A

Iron storage disorder that results in excessive total body iron and the deposition of iron in tissues

224
Q

Where does mutation occur in haemochromatosis ?

A

Usually due to mutation in HFE gene on chromosome 6. Autosomal recessive.

225
Q

What are the symptoms of haemochromatosis ?

A
  • Chronic fatigue
  • Joint pain
  • Bronze/slate grey pigmentation.
  • Hair loss
  • Erectile dysfunction
  • Amenorrhoea
  • Cognitive symptoms
226
Q

How is a diagnosis of haemochromatosis made ?

A
  • Main : serum ferritin.
  • Transferrin saturation is helpful in distinguishing between a high ferritin caused by iron overload (high) or due to other causes like inflammation or NAFL.
  • Liver biopsy with perls stain - iron conc in parechymal cells
  • CT abdo and MRI for liver deposits of iron.
227
Q

What are the indications for genetic testing in haemochromatosis ?

A

High serum ferritin and high Transferrin saturation with no other reason = genetic testing

228
Q

What are some of the possible complications of haemochromatosis ?

A
  • T1D
  • Liver cirrhosis
  • Iron deposits in the pituitary and gonads
  • Cardiomyopathy
  • Hepatocellular carcinoma
  • Hypothyroidism
  • Chondrocalcinosis/pseudogout
229
Q

How is haemochromatosis managed ?

A
  • Venesection - removal of blood to decrease total body iron
  • Serum ferritin monitoring
  • Alcohol avoidance
  • Genetic counselling
  • Monitoring and treatment of complications.
230
Q

When is embelectomy indicated in a PE ?

A

Massive PE when thrombolysis is CI

231
Q

What is the first line of treatment in a PE ?

A

DOAC like apixaban

232
Q

When is LMWH used in PE treatment over a DOAC ?

A

used in patients with renal failure in preference to DOAC. This is due to poor renal clearance. Also preferred in patients with a history of cancer

233
Q

What is the treatment of PE in patients that are haemodynamically unstable ?

A

IV ateplase (thrombolysis)

234
Q

what is an absolute CI for thrombolysis ?

A

History of stroke

235
Q

What should the target INR be in patients with VTE occurrence ?

A

2-3 increased to 3-4

236
Q

What does a wells score of more than 4 indicate ?

A

Diagnostic imaging is required. LMWH should be administered if clinical suspicion is high.

PE is very likley

237
Q

What does a wells score of less than 4 indicate ?

A

D dimer should be carried out. PE is less likely

238
Q

What scoring system is used in PE diagnosis ?

A

Wells score

239
Q

What is the gold standard test in diagnosing a PE ?

A

CTPA

240
Q

In a PE, when is V/Q scan preferred to a CTPA ?

A

Pregnancy
Renal impairment
Allergies

241
Q

What are some of the possible CXR findings in a PE ?

A

This is typically normal in PE but possible findings includeFleischner sign
(an enlarged pulmonary artery),Hampton’s hump
(a peripheral wedge shaped opacity), andWestermark’s sign
(regional oligaemia). The chest x-ray is helpful in ruling out differentials (e.g. pneumonia, pneumothorax).

242
Q

What are some of the possible CXR findings in a PE ?

A

This is typically normal in PE but possible findings includeFleischner sign
(an enlarged pulmonary artery),Hampton’s hump
(a peripheral wedge shaped opacity), andWestermark’s sign
(regional oligaemia). The chest x-ray is helpful in ruling out differentials (e.g. pneumonia, pneumothorax).

243
Q

What blood test is used in PE ?

A

D dimer

244
Q

What will be present on ABG in a patient with a PE ?

A

T1RF and or resp alkalosis

245
Q

Why is clotting function important to test in patients with suspected PE ?

A

Important if the patient is started on LMWH or Warfarin

246
Q

What is the classical ECG presentation in PE ?

A

Classic Q3S1T3 sign is only present in 20 percent of presentations. May also be signs of right sided heart strain

Lg S wave in L1

Inverted T wave in L3

Q wave in Lead 3

or can be sinus tachycardia

247
Q

What are some of the common examination findings in a patient with a PE ?

A
  • Tachypnoea
  • Tachycardia (sometimes the only presenting symp)
  • Hypoxia
  • Low grade pyrexia
  • Small - Asymptomatic
  • Large - Hypotension, cyanosis, signs or RSHS
  • Calves - Tenderness that may indicate a DVT
248
Q

What common triad of symptoms are suspicious of a PE ?

A
  • Sudden onset SOB
  • Pleuritic chest pain
  • Haemoptysis
249
Q

What are the five drugs that are commenced post ACS ?

A

Aspirin
Atorvastatin
Bisopolol
Ramipril
Clopidogrel

250
Q

Why is anticoagulation indicated in AF ?

A

Due to the risk of emboli dislodging and causing a stroke.

251
Q

What are the two DD of an irregularly irregular pulse ?

A

AF or ventricular ectopics.

252
Q

What are some of the presenting symptoms of AF ?

A
  • Often incidental
  • SOB
    -Syncope
  • Symptoms of complications - stroke, sepsis or thyrotoxicosis.
253
Q

What is present on an ECG in a patient with AF ?

A
  • Absent P waves
  • Narrow QRS complex tachycardia
  • Irregularly irregular ventricular rhythm.
254
Q

What are the most common causes of atrial fibrillation ?

A

S - sepsis

M - Mitral valve pathology

I - IHD

T - Thyrotoxicosis

H - Hypertension

255
Q

What is the first line of treatment in patients with AF ?

A

First line (rate control - BB like atenolol 50/100mg OD)

Ca channel blocker (not in HF)

Digoxin - Only in sedentary patients.

256
Q

When is cardio-version commenced in new onset AF?

A

Immediate - If AF has been present for less than 48 hours or very haemodynamically unstable.

Delayed - If the AF has been present for more than 48 hours and they are stable. The patient should be anti-coagulated for at least 3 weeks prior to the cardio-version

  • There is a reversible cause for their AF
  • Their AF is of new onset (<48 hours)
  • Their AF is causing heart failure
  • They remain symptomatic despite being effectively rate controlled
257
Q

What is the target INR for warfarin ?

A

2-3

258
Q

What is the antidote for warfarin ?

A

Vitamin K

259
Q

What is a cardiac tamponade ?

A

Cardiac tamponade is where a pericardial effusion is large enough to raise the intra pericardial pressure. This leads to reduced filling during diastole.

260
Q

What are some of the causes of cardiac tamponade ?

A
  • Transudative effusion - CHF or pulmonary hypertension
  • Exudative effusions - (inflammatory ) like in infection, autoimmune and inflammatory conditions, injury to the pericardium (after an MI), uraemia, cancer and certain medications like methotrexate. Rupture of the heart of the aorta can cause rapid onset cardiac tamponade like MI, type A aortic dissection and trauma.
261
Q

How does cardiac tamponade present ?

A

A rapidly collecting effusion with cardiac tamponade can quickly cause haemodynamic compromise and collapse.

Slowly developing, chronic effusions, may initially be asymptomatic. As the pressure rises, symptoms can develop which may include

  • Chest pain
  • SOB
  • Feeling of fullness in the chest
  • Orthopnoea
262
Q

In cardiac tamponade, sometimes the effusion can be big enough to compress the surrounding structures. What are some of these symptoms ?

A
  • Phrenic nerves compression may cause hiccups.
  • Oesophageal nerve may cause dysphagia.
  • Recurrent laryngeal nerve compression - Hoarse voice.
263
Q

What are some of the examination findings seen in cardiac tamponade ?

A
  • Quiet heart sounds
  • Fall in BP on inspiration
  • HYPOTENSION
  • Raised JVP
  • Fever with pericarditis and pericardial rub
264
Q

What is the gold standard of investigation in cardiac tamponade ?

A

Gold standard investigation (ECHO)

Fluid analysis to determine the underlying cause

265
Q

What is a TIA ?

A

Symptoms of a stroke that resolve within 24 hours. Ischaemia without infarction. Often precede a full stroke.

266
Q

What is a cresendo TIA ?

A

Two or more TIAs in a week. This carries a risk of developing into a stroke.

267
Q

How are TIAs managed ?

A
  • Aspirin 300mg daily.
  • Secondary prevention for CVD.
  • 24 hours to see stroke specialist.
268
Q

How does a stroke commonly present ?

A
  • Sudden weakness of limbs
  • Sudden facial weakness
  • Sudden onset dysphasia (speech disturbance)
  • Sudden onset visual or sensory loss
269
Q

What tool is used in screening stroke symptoms ?

A

ROSIER TOOL (stroke is likely in patients with a score over 0 )

270
Q

What are the risk factors for stroke ?

A
  • CVD like angina, PVD or MI
  • Previous stroke or TIA
  • AF
  • CAD
  • Hypertension
  • Smoking and diabeties
  • Vasculitis
  • Combined contraceptive pill
271
Q

How is a stroke immediately managed ?

A
  • Admit to a specialist stroke centre
  • Exclude hypoglycaemia
  • CT brain
  • Aspirin 300mg STAT and continue for 2 weeks.
272
Q

How is a stroke managed in a specialist centre ?

A
  • Thrombolysis with ateplase can be used after CT brain has excluded intracranial haemorrhage.
  • Thombectomy can be offered if an occlusion is confirmed on imaging. Not used after 24 hours of the symptoms starting.
  • Diffusion weighted MRI
  • Carotid USS for carotid stenosis
  • Endarterectomy to remove plaques or carotid stenting.
273
Q

What is the secondary prevention of stroke (medical, interventional and conservative) ?

A
  • Clopidogrel 75mg OD
  • Atorvastatin 80 mg (not straight away)
  • Carotid endererectomy or stenting in patients with CAD
  • Treat modifiable RF like hypertension and diabeties.
  • Stroke rehabilitation if needed.
274
Q

What is pulmonary hypertension ?

A

Pulmonary hypertension is increased resistance and pressure of the blood in the pulmonary arteries.

275
Q

What effect does pulmonary hypertension have on the heart ?

A

Causes right sided heart strain and right ventricular hypertrophy.

276
Q

What are some of the causes of pulmonary hypertension ?

A
  • LSHF
    COPD
    PVD
    sarcoidosis, SLE
    Can be primary
277
Q

What are some of the signs of pulmonary hypertension ?

A
  • SOB is the main presenting symptoms
  • Syncope
  • Tachycardia
  • Hepatomegaly
  • peripheral odema.
  • Raised JVP.
278
Q

What will be present on ECG in right sided heart strain (like in pulmonary hypertension ? )

A

Shows right sided heart strain (
seen as larger R waves on the right sided chest leads (V1-3) and S waves on the left sided chest leads (V4-6), RAD and RBBB.

279
Q

What will be present on investigation in right sided heart strain ?

A

CXR will show right ventricular hypertrophy and dilated pulmonary arteries.
Raised NT-proBNP and ECHO will show raised pulmonary artery pressure

280
Q

How is primary pulmonary hypertension managed ?

A
  • IV prostanoids like epoprostenol
  • Endothelin receptor antagonists like macitentan
  • Phosphodiesterase 5 inhib like sidenafil
281
Q

How is secondary pulmonary hypertension managed ?

A

managing the underlying cause like PE or SLE.

282
Q

What are some of the causes of pericarditis ?

A
    • Infective causes - Viruses (HIV, coxsackie ect)
    • Bacteria - Staphylococcus, pneumococcus, streptococcus, TB ect
    • Malignant causes (lung, breast and hodgkin lymphoma)
    • Cardiac causes (HF), dresslers syndrome.
    • Drugs and toxin causes
    • Radiation
    • Rheumatological disease like SLE, RA ect
    • Renal failure
    • IBD ect
283
Q

What are some of the clinical features of pericarditis ?

A
  • Pleuritic chest pain - worse on lying flat
  • Fever
  • Pericardial friction rub
  • ECG changes (saddle shaped ST elevation, PR depression)
  • Raised troponin
284
Q

What are some of the ECG changes in pericarditis ?

A
  • 1-3 weeks: normalisation of ST changes, T wave flattening
  • 3-8 weeks: flattened T waves become inverted
  • 8+ weeks: ECG returns to normal

Saddle shaped ST elevation and PR depression

285
Q

How is pericarditis diagnosed ?

A
  • ECG
  • Troponin
  • ECHO
  • Angiogram - Normal coronary arteries that excludes an MI
286
Q

What is the first line of treatment in viral or idiopathic pericarditis ?

A

Exercise restriction and NSAIDS. Colchicine in patients with hepatic or renal impairment.

287
Q

What is the first line of treatment in non viral pericarditis or patients with viral pericarditis unable to tolerate NSAIDS ?

A

Corticosteroids

288
Q

What is bacterial pericarditis treated with ?

A

Bacterial causes are treated with intravenous antibiotics and pericardiocentesis if purulent exudate present.

289
Q

What are some of the possible complications of pericarditis ?

A

Although rare, cardiac tamponade and pericardial effusion. Long term, patients may develop constrictive pericarditis.

290
Q

What is constrictive pericarditis ?

A

Due to fibrosis and constriction of the tissues surrounding the heart

291
Q

What are the features of constrictive pericarditis ?

A
  • Raised JVP
  • Kussmaul’s sign (paradoxical rise in JVP with inspiration),
  • Pulsus paradoxus (drop in cardiac output on inspiration)
  • Heart sounds may also be quiet (if pericardial effusion also present)
  • Third heart sound (S3) may be present (due to rapid early diastolic ventricular filling).
292
Q

What is an important change in ECG during pericarditis ?

A

Saddle ST changes - Widespread ST elevation and PR depression

293
Q

What is the first line of treatment in a patient with massive PE and risk of bleeding ?

A

IV heparin. DOAC inidcated in a small PE

294
Q

What medication is used in cardiac arrest after failure of DC cardioversion/adrenaline ?

A

Amiodarone

295
Q

In severe supraventricular tachycardia, adenosine 6mg is indicated. When is this not indicated and what should be given instaid ?

A

Asthmatics
veramapril 2.5mg-5mg

296
Q

When is atropine indicated ?

A

In bradycardia

297
Q

What are the symptoms of digoxin toxicity ?

A

Abdo pain
Nausea and vomiting
Arrhythmia
Yellow green visual disturbance

298
Q

How long does new onset AF last so it qualifies for rhythm control without delay ?

A

48 hours

299
Q

What ECG features are present in Ventricular tachycardia ?

A

Tachycardia (>100 beats per minute), plus
Absent P waves, plus
Monomorphic regular broad QRS complexes (>120 ms).

300
Q

Changes in which leads are seen in an inferior STEMI/NSTEMI (RCA)

A

Leads 2,3 and aVF

301
Q

When is electrical cardioversion inidcated in atrial fibrillation ?

A

New onset Af where there is a heart rate 120 or over ?

302
Q

What is indicated in aortic dissection where the patient is heamodynamically stable ?

A

CT angio

303
Q

What is a common cause of AF ?

A

Alcohol

304
Q

what does a globular apperance of the heart indicate ?

A

Pericardial effusion

305
Q

What does ST elevation in leads 2,3 and avf indicate ?

A

RCA infarct. Inferior

306
Q

What is an atrial myxoma and what are the common signs ?

A

Tumour of the cardiac atria usually in the left atria

Patients with a history of AF, dyspoea and high cholesterol make this more likley

307
Q

A patient with a recent history of bleeding and need for blood transfusion has a PE. What is the most important initial treatment of the PE and why ?

A

Iv heparin. This is because of its short half life and reversibility. Alteplase/DOACs are usually used in a PE.

Heparins features if also why patients are often changed to heparin before surgery, as it can be turned on and off in theory.

308
Q

An 80 year old patient presents with non ischaemia related bradycardia. What is the initial management ?

A

IV atropine sulfate.

309
Q

What is mecklers triad ?

A

Three symptoms that can indicate oesophageal rupture. These include

  • Neck emphysema
  • Vomiting
  • Severe chest pain.
310
Q

What does a pan systolic murmur indicate ?

A

Mitral regurgition

311
Q

Why can mitral regurgitation occur after an MI ?

A

Due to rupture of the papillary muscles.

312
Q

How is supra ventricular tachycardia with no adverse features managed initially (like WPW) ?

A

Vagal menouvures

313
Q

How is bradycardia with no adverse features managed ?

A

Make sure to look for any other potential causes

314
Q

How would bradycardia as a result of hypothyroidism present (symptoms) ?

A

Depression, consipation and lethargy

315
Q

What is present on ECG in hypothermia ?

A

J waves/osbourne waves

316
Q

What medications can increase QT interval and hence cause torsades de pointes ?

A

Macrolide antibiotics like arithromycin as well as ondansetron and some antidpressants/antipsychotics.

317
Q

What is the most common viral cause of myocarditis ?

A

Coxsackie B virus

318
Q

What is the initial step when managing asymptomatic AF (assess and manage) ?

A

Chadsvasc score and anti-coagulating with DOAC. If patients heart rate is under 80, there is no need for rate control with BB or CA channel blocker

319
Q

What are the CI for the use of a DOAC in anti-coagulating in AF ?

A
  • Mechanical heart valves
  • Stage 4/5 CKD.
320
Q

What is cardiomyopathy ?

A

Structural or functional abnormality of the myocardium without CAD, hypertension, valvular or congenital heart disease.

321
Q

What is dilated cardiomyopathy ?

A

Dilation and poor contraction of either the left ventricle or both of the ventricles (EF less than 40 percent). Most common

322
Q

What are some of the causes of dilated cardiomyopathy ?

A
  • Post MI (ischaemic heart disease)
  • Haemochromatosis
  • Hypertension
  • Congenital/ genetic/congenital
  • Thyrotoxicosis
323
Q

What are some of the symptoms of dilated cardiomyopathy ?

A
  • Exertional dyspnoea
  • Orthopnoea
  • PND
  • Peripheral odema
  • Arrhythmias
  • SCD
  • Conduction disturbances
    Symptoms of heart failure
324
Q

What are some of the examination findings in a patient with dilated cardiomyopathy ?

A
  • Displaced apex beat
  • S3 gallop rhythm
  • Murmur (mitral regurgitation) - systolic murmur
  • Signs of HF (odema/hepatomegaly/ascites/raised JVP)
325
Q

How is dilated cardiomyopathy treated ?

A

Diagnostic - ECHO

326
Q

What is the first line of treatment for dilated cardiomyopathy ?

A

ACE inhib as they narrow blood vessels and increase blood pressure. Decrease risk of heart failure

327
Q

What is hypertrophic cardiomyopathy ?

A

Genetic condition characterised by left ventricular hypertrophy. Arises as a result of a mutation in one of the myocyte sarcomere genes like myosin and troponin. Most inheritance develops during childhood and adolescent period, however genetic variation means some late onset disease does occur.

328
Q

What is the most common cause of sudden cardiac death in young people ?

A

Hypertrophic cardiomyopathy

329
Q

What are some of the symptoms of hypertrophic cardiomyopathy ?

A
  • Most are asymptomatic
  • First presentation - Presyncope/syncope or sudden death
  • Some may experience excertional dyspnoea, fatigue or chest pain
330
Q

What are some of the consequences of hypertrophic cardiomyopathy ?

A
  • Left ventricular outflow tract obstruction
  • Diastolic dysfunction
  • Ischaemia
  • Mitral regurgitation
331
Q

What are some of the signs on examination of hypertrophic cardiomyopathy ?

A
  • Jerky pulse
  • Double apex beat
  • Harsh Ejection systolic murmur
  • Apical thrill.
332
Q

What are some of the ECG signs of hypertrophic cardiomyopathy ?

A
  • Abnormal Q waves
  • Deep inverted T waves
  • LVH - V1-V3 have a large downwards deflection due to the direction of the depolarisation. Further to travel due to the increased thickness of the ventricular wall.
333
Q

How is hypertrophic cardiomyopathy diagnosed ?

A

ECHO

334
Q

What is restrictive cardiomyopathy ?

A

Non dilated, non hypertrophied ventricles with impaired ventricular filling

335
Q

What are some of the causes of restrictive cardiomyopathy ?

A
  • Familial
    AMyloidosis
    Diabetic cardiomyopathy
    Radiotherapy/chemotherapy
336
Q

What are some of the clinical features of restrictive cardiomyopathy ?

A
  • Heart failure
  • Similar to constrictive pericarditis
  • 75 percent of patients have associated atrial fibrillation
337
Q

How does restrictive cardiomyopathy as a result of amyloidosis present ?

A

Results in amyloid protein deposition in tissues in the body. Can lead to restrictive cardiomyopathy that appears sparkling on ECHO. Also causes arrhythmia’s and conduction disturbances. Heart failure symptoms.

338
Q

What are the common causes of CCF ?

A

LV pathology. Impaired function results in chronic backlog of blood waiting to flow into the heart. Vasculature begins to leak fluid.

339
Q

What is ejection fraction ?

A

Percentage of blood in the left ventricle that is squeezed out with each ventricular contraction.

340
Q

What is HF with preserved EF ?

A

a patient has the clinical features of heart failure, but EF is more than 50 percent. Usually due to an issue with diastolic dysfunction.

341
Q

What is HF with reduced EF ?

A

HF symtpoms where the EF is less than 50 percent

342
Q

What are the main causes of CCF ?

A
  • IHD
  • Valvular heart disease like in AS
  • Hypertension
  • Arrhythmias like AF
  • Cardiomyopathy.
343
Q

How does CCF present ?

A
  • Breathlessness worse on excertion
  • Cough - may produce frothy white/pink sputum
  • Orthopnoea - Breathless when lying flat. Patients will often lie with multiple pillows.
  • PND
  • Peripheral odema
  • Fatigue.
344
Q

What are the signs on examination in CCF ?

A
  • Tachycardia
  • Tachypnoea
  • Hypertension
  • Murmurs - As
  • Third heart sound
  • Bilateral bibasal crackles (wet sounding on auscultation) indicating pulmonary odema.
  • Raised JVP
  • Peripheral odema.
345
Q

What murmur can be heard in CCF ?

A

Ejection systolic in AS

346
Q

What specific blood test is used in heart failure ?

A

NT-proBNP

347
Q

What classification is used in determining severity of heart failure and what are the categories ?

A
  • New york association classification
    -Class 1 - No limitation on activity
  • Class 2 - Comfortable at rest, symptomatic ordinary with activity
  • Class 3 - Comfortable at rest but symptomatic with any activity
  • Class 4 - Symptomatic at rest.
348
Q

What NT-Pro BNP levels warrant referral to cardiology urgently ?

A
  • From 400 – 2000 ng/litreshould be seen and have an echocardiogramwithin 6 weeks
  • Above 2000 ng/litreshould be seen and have an echocardiogramwithin 2 weeks
349
Q

How is CCF managed medically ?

A
  • ACE inhib like ramipril. ARB can be given if not tolerated. (ARB not given to patients with valvular heart disease)
  • BB like bisoprolol
350
Q

When are aldosterone antagonists used in CCF ?

A

when symptom are not controlled with A/B like spirinolactone. Used when there is reduced EF and symptoms not controlled by the above.

351
Q

What blood levels should be monitored in CCF ?

A

ACE inhib and aldosterone antagonists can derange U and Es hence should be monitored. Renal function should be monitored. Hyperkalaemia risk.

352
Q

What blood levels should be monitored in CCF ?

A

ACE inhib and aldosterone antagonists can derange U and Es hence should be monitored. Renal function should be monitored. Hyperkalaemia risk.

353
Q

What electrolyte imbalance is there a risk of when treating CCF with ACE inhib and aldosterone antagonists ?

A

Hyperkalaemia.

354
Q

How is CCF managed non pharmacologically ?

A
  • Lifestyle interventions like management of CVD, smoking, diet ect.
355
Q

What surgical inteventions can occur in CCF ?

A
  • TAVI in underlying heart disease
  • Implantable cardioverter defib in patients with ventricular tachycardia/VF
  • Heart transplants in patients with severe disease
356
Q

When is cardiac re-synchronisation therapy used in CCF ?

A

Used in HF with an EF of less than 35 percent. Synchronises the contractions in the chambers to optomise heart function.

357
Q

What is the first line of anti-coagulation in patients post AF ?

A

Riveroxaban

358
Q

How are patients with haemochromatosis monitored during venesection treatment ?

A

Transferrin sats and serum ferittin measured

359
Q

What is the main cause of death in young patients with hypertrophic obstructive cardiomyopathy ?

A

Ventricular arrhythmia

360
Q

What is present on ECG in patients with HOCM ?

A

LVH

361
Q

What conditions is HOCM associated with (arrhythmias ) ?

A

WPWS
Friedchrichs ataxia

362
Q

What are the symptoms of WPW syndrome ?

A
  • Palpitations
  • Chest pain
  • SOB
  • Syncope.
363
Q

What is the pathophysiology of WPW syndrome ?

A

Syndrome caused by congenital accessory conducting pathway between the atria and ventricles, causing AV re entry tachycardia.

364
Q

What are the signs of WPWS on ECG ?

A
  • Short PR interval (normal PR interval 0.12-0.2 seconds), one large square = 0.2 seconds
  • Wide QRS complex with a delta wave
  • LAD (most of the time if a problem with the right sided accessory pathway)
  • RAD (most of the time if a problem with left sided pathway)
365
Q

What are the associations with WPWS ?

A
  • HOCM (hypertrophic obstructive cardiomyopathy)
  • Mitral valve prolapse
  • Ebsteins anomaly
  • Thyrotoxicosis
  • Secundum ASD
366
Q

What are the prominant features in type A WPWS ?

A

Type A (left sided pathway) - RAD and dominant R wave in V1

367
Q

What are the prominant features in type B WPWS ?

A

Type B (right sided pathway) - LAD no dominant R wave in V1

368
Q

What is the definative treatment of WPWS ?

A

Radio-frequency ablation of the accessory pathway

369
Q

What is the definative treatment of WPWS ?

A

Radio-frequency ablation of the accessory pathway

370
Q

What are some of the medical therapies that can be used in WPWS ?

A

Sotalol, amiodarone, flecainide

371
Q

When is solatol CI in WPWS ?

A

not used if there is co-existing AF, as may cause VF

372
Q

What are the shock-able rhythms ?

A

VF and pulseless VT

373
Q

What are the non shockable rhythms ?

A

Asystole and PEA

374
Q

What are the ALS guidelines in shock-able rhythms ?

A

Start CPR and get IV access
Single shock, followed by 2 mins of CPR/if known patient, up to three shocks.
1mg adrenaline after third shock
Give adrenaline 1mg every 3-5 mins
Amiodarone 300mg after the third shock.
Further 150mg of amiodarone should be give after 5 shocks have been administered.

375
Q

What are the ALS guideleines for non shock-able rhythms (PEA and asystole) ?

A

Start CPR and get IV access.
Adrenaline 1mg as soon as possible

Give adrenaline 1mg every 3-5 mins

376
Q

How are patients who are in Cardiac arrest due to a PE managed ?

A

Thrombolytic can be given if a PE is suspected. CPR should be continued for 60/90 mins.

377
Q

What is a pericardial effusion ?

A

Pericardial effusion - Excess of fluid accumulates around the pericardial sac.

378
Q

What types of fluid can accumulate in a pericardial effusion ?

A
  • Transudate (low protein content)
  • Exudates (high protein content)
  • Blood
  • Pus
  • Gas (bacterial infections)
379
Q

What types of fluid can accumulate in a pericardial effusion ?

A
  • Transudate (low protein content)
  • Exudates (high protein content)
  • Blood
  • Pus
  • Gas (bacterial infections)
380
Q

What is cardiac tampoade ?

A
  • pericardial effusions is large enough to raise the Intra pericardial pressure. This increased pressure squeezes on the heart and affects its ability to function. This means there is decreased filling of the heart in diastole and decreased CO in systole. Emergency requiring draining.
381
Q

What are the causes of transudative effusions ?

A

Increased venous pressure can reduce drainage from the pericardial cavity - (congestive heart failure and pulmonary hypertension)

382
Q

What are the causes of transudative effusions ?

A

Increased venous pressure can reduce drainage from the pericardial cavity - (congestive heart failure and pulmonary hypertension)

383
Q

What are the causes of exudative effusions ?

A

Inflammatory - (pericarditis) like in infection (TB, HIV, Coxsackievirus, epstein barr virus), SLE/RA, injury to the pericardium like MI, open heart surgery or trauma, uraemia secondary to renal impairment, cancer and some medications like methotrexate.

384
Q

What complication can rupture of the heart/aorta cause ?

A

(MI/Trauma/Aortic dissection type A) can cause bleeding into the pericardial cavity resulting in a rapid onset cardiac tamponade.

385
Q

How will a rapid effusion causing cardiac tamponade present ?

A

haemodynamic compromise and collapse.

386
Q

How will a pericardial effusion/cardiac tamponade present ?

A
  • Chest pain
  • SOB
  • A feeling of fullness in the chest
  • Orthopnoea
  • Compression of phrenic nerve - Hiccups
  • Oesophageal compression - dysphagia
  • Recurrent laryngeal - hoarse voice.
387
Q

What will be present on examination in patients with pericardial effusion ?

A
  • Quiet heart sounds
  • Pulsus paradoxux - abnormally large fall in BP on inspiration, when palpating the pulse
  • Hypotension
  • Raised JVP
  • Fever/pericardial rub in pericarditis.
388
Q

What is the investigation of choice in pericardial effusion ?

A

ECHO

389
Q

What will be investigated on fluid analysis in patients with pericardial effusion ?

A

protein, bacterial culture, viral PCR, cytology and tumour markers.

390
Q

What are the two main methods of treatment in pericardial effusion ?

A

Treatment of the underlying cause and drainage of the effusion where required

Inflammatory causes ( like pericarditis) - aspirin, NSAIDs, colchicine and steroids.

Drainage - Needle pericardiocentesis (echo guided) and surgical drainage.

391
Q

What will be present on CXR in patients with pericardial effusion ?

A

globular appearance, flattening of the upper heart borders.

392
Q

What surgical options can be used in treating pericardial effusion ?

A

Pericardial window - Surgical procedure where a portion of the pericardium is removed creating a window or a fistula, this allows fluid to drain from the pericardial cavity into the into the pleural/peritoneal cavity.

In recurrent cases, a pericardiectomy can be performed (surgical removal of the pericardium).

393
Q

What is the definition of malignant hypertension ?

A

BP over 180/120 with retinal haemorrhages or papilloedema (swelling of the optic disc due to raised ICP)

394
Q

What is the immediate management of malignant hypertension in primary care (GP) ?

A
  • Same day referral
  • Fundocopy examination
  • Monitor for any side effects. Confusion, HF, suspected ACS or AKI - End organ damage.
395
Q

What IV medical options can be used to reduce BP in malignant hypertension ?

A
  • Sodium nitroprusside
  • Labelatol
  • GTN
  • Nicardipine.
396
Q

What is acute LVF ?

A

Acute event results in the left ventricle being unable to move blood efficiently through the left side of the heart and into the systemic circulation.

Pulmonary odema occurs due to backlog of blood in the pulmonary vascularure, leading to SOB and reduced oxygen saturation.

397
Q

What is acute LVF usually a result of ?

A

Decompensated CHF

398
Q

What are some of the possible triggers of acute LVF ?

A
  • Iatarogenic (agressive IV fluid in frail elderly patient)
  • MI
  • Arrhythmias
  • Sepsis
  • Hypertensive emergency.
399
Q

ACute desaturating patient with SOB ?

A

Acute left ventricular failure and pulmonary oedema are common in the acute hospital setting. When a nurse asks you to review a breathless and desaturating patient, ask yourself how much fluid that patient has been given and whether they will be able to cope with that amount. For example, an 85 year old patient with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturation. This is a common scenario, and a dose of IV furosemide can work like magic to clear the excess fluid and resolve the symptoms.

400
Q

What will be present on ABG in acute left ventricular failure ?

A

Type 1 respiratory failure

401
Q

What are the symptoms of acute left ventricular failure ?

A
  • Acute SOB made worse by lying flat and improves on sitting up
  • T1 RF
  • Cough with frothy white or pink sputum
  • Looking and feeling unwell.
402
Q

What are the signs on examination in acute left ventricular failure ?

A
  • Raised RR
  • Tachycardia
  • Reduced o2 sats
  • 3rd HS
  • Bilateral basal crackles (wet)
  • Hypotension in severe cases.

There all may also be signs of the precipitating cause, chest pain in an MI, fever in sepsis and palpitations with arrhythmia’s.

Patients may also have RSHF - raised JVP and peripheral odema.

403
Q

What will be abnormal on blood tests/ECHO in left ventricular failure ?

A
  • BNP will be raised
  • ECHO - EF can measure LVF. Below 50 is abnormal
404
Q

What will be present on CXR in acute left ventricular failure ?

A

Cardiomegaly, upper lobe diversion (increased prominence and diameter of the upper lobe vessels), bilateral pleural effusions, fluid in the interlobular fissures and fluid in the septal lines (kerley lines)

405
Q

What is the basic management of acute left ventricular failure ?

A
  • SSit up
  • OOxygen
  • DDiuretics
  • IIntravenous fluids should bestopped
  • UUnderlying causes need to be identified and treated (e.g., myocardial infarction)
  • MMonitor fluid balance
406
Q

What is the most common site effected in IE as a result of IVDU ?

A

Tricuspid valve

407
Q

What is a side effect of propanolol but not atenolol ?

A

Cool peripheries (atenolol not as it is a cardioselective BB). Propanolol can be used in things like anxiety management

408
Q

What is the stepwise management of SVT (narrow complex tachycardia) ?

A

vagal manoeuvres
IV adenosine 6mg –> 12mg –> 18mg
Electrical cardioversion

PREVENTIVES (BB and radiofrequency ablation)

409
Q

When is an SAVR used in comparison to a TAVR

A

SAVAR in patients that are a good candidate for surgery i.e no co-morbidities like no and fit and healthy.

TAVAR - More co-morbidities/frail and elderly.

410
Q

What is the first line management of heart failure ?

A

BB and ACE inhib

411
Q

How is warfarin managed in major bleeding ?

A

Stop the Warfarin, IV vitamin K 5mg and PT complex concentrate

412
Q

What is the primary dose of statin and when is it indicated?

A

20 mg OD

T1DM, QRISK score > 10 or CKD > egfr 60

413
Q

What is the secondary dose of statin and when is it indicated ?

A

80 Mg OD
IHD, CVD or PAD.

414
Q

Tosades de pointes is caused by a prolonged QT interval. What can cause a prolonged QT interval ?

A

Long QT syndrome (an inherited condition)
Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia

415
Q

Intraventricular septal rupture is a side effect of an MI, what are the signs of this ?

A

New pan systolic murmur and new AHF.

416
Q

What is the antidote for chronic mitral regurgitation ?

A

Glucagon

417
Q

What is a long QT ?

A

more than 450 ms (more than 2 large squares)

418
Q

What are the main causes of long QT syndrome ?

A
  • Drugs - Amiodarone (slow down the heart), TCAs, antiotics like flucanazole, erythromycin ect. Hypo (electrolyte abnormalities)
  • Myocardial disease
419
Q

What are the important investigations in long QT syndrome ?

A
  • Electrocardiogram +/- 24 hour tape.
  • ECHO for structural heart disease
  • Genetic testing if required
420
Q

What is the management of long QT syndrome ?

A
  • BB
  • Cardiac pacing
  • Manage the underlying cause
  • Implantation of ICD.
421
Q

What is rheumatic fever ?

A

Complication of streptococcus infection (typically laryngitis) and patients present 2-4 weeks post infection

422
Q

What marker will be raised in sted in strep infection ?

A

ASOT

423
Q

What is the management of rheumatic fever ?

A
  • STAT dose of IV benzylpenicillin with a 10 day course of phenoxymethylpenicillin to follow
  • Analgesia for arthritic symptoms like arthritis
  • Glucocorticoids if carditis is suspected.
424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

424
Q

What are the signs of right sided heart failure ?

A

Pulmonary congestion (SOB/orthopnoea/PND and nocturnal cough and bi-basal auscultation of lungs)

Systemic hypo-perfusion - Cyanosis, increased capillary refil time and hypotension.

425
Q

What are patients with anorexia nervosa at a higher risk of develooping CV ?

A

Loss of cardiac muscle and hence mitral valve prolaps

426
Q

What is present on examination in mitral valve prolapse ?

A

Pan systolic murmur and click

427
Q

All patients with anorexia nervosa as an inpatient in hospital should have an ECG. What are the cardica symptoms in a patient with anorexia nerveosa?

A

Bradycardua, hypotension and prolonged QT interval. There can be loss of cardiac muscle causing mitral valve prolapse (mitral valve prolapse and click)

428
Q

What is used in BB overdose ?

A

Glucagon and atropine can be used in haemodynamically unstable patients

429
Q

In patients with suspected IE and no findings on TTE, what is the next most suitable method of imaging ?

A

PET CT

430
Q

What medications used in heart failure cause hyperkalaemia.?

A

ACE inhibitors and spirinolactone as well as enephelrone