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ΩΩ 2a Bateman - Systems Based > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

HOW CAN ISCHAEMIC HEART DISEASE OCCUR?

A
  1. Reduced blood flow to the heart muscle (clot or atheroma)
  2. Increased distal resistance (LV hypertrophy)
  3. Reduced O2 carrying capacity (anaemia) or availability (hypoxia)
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2
Q

What are some risk factors for IHD?

Modifaible and non-modifiable?

A

MODIFIABLE

Smoking.
Diabetes
Hypertension.
Hypercholesterolaemia.
Sedentary lifestyle

Non-modifiable

Gender.
Family history.
Personal history.
Age.

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3
Q

WHAT IS ANGINA?

A

Chest pain brought on either:

By exertion which resloves with rest

Or at rest

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4
Q

What are the different types of angina?

A

Stable angina

Unstable angina

Decubitus angina (precipitated by lying flat)

Variant (Prinzmetal’s) angina: caused by coronary artery spasm.

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5
Q

What are the causes of angina?

A

Atheroma

Anaemia

Spasm

Tachycardia

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6
Q

What are the symptoms of angina?

A

Chest pain/discomfort.

Heavy, central, tight, radiation to arms, jaw, neck.

Precipitated by exertion.

Relieved by rest or GTN within 5 mins

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7
Q

What are the tests for stable angina?

A

ECG
Pathological Q waves in particular, LBBB, and ST-segment and T wave abnormalities (for example, flattening or inversion).

Bloods
May show anaemia

CXR
May show increased heart size and pulmonary vessels

Angiogram
Gold standard, shows luminal narrowing

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8
Q

What are the management options for stable angina pectoralis?

A

Drugs
Glyceryl Trinitrate (SL) (GTN Spray)
Aspirin to prevent clots
Statin to lower cholesterol

BB (atenolol)/CCB (verapamil/diltiazem)
BB + CCB (nifedipine), OR monotherapy + long-acting nitrate/ivabradine/nicorandil/ranolazine
Can use BB + CCB + 3rd Drug whilst waiting for PCI/CABG

Percutaneous Intervention (PCI)

Coronary Artery Bypass Graft (CABG)

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9
Q

WHAT IS ACUTE CORONARY SYNDROME PATHOLOGY?

A

Plaque rupture, thrombosis, and inflammation.

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10
Q

What are the different acute coronary syndomes?

A

Unstable angina

(NSTEMI) Non-Q wave infarction, ST depression and T wave inversion

(STEMI) Q wave infarction, ST elevation

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11
Q

What are the different ECG changes for ACS?

A

STEMI
ST elevation and tall T waves, may be a new LBBB in larger MIs (STEMI)

NSTEMI
A retrospective diagnosis, will see ST depression

Ischaemia
ST depression and T wave flattening

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12
Q

WHAT IS UNSTABLE ANGINA?

A

An acute coronary syndrome (ACS) that is defined by the absence of biochemical evidence of myocardial damage

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13
Q

What is the clinical classification of unstable angina?

A

Cardiac chest pain at rest.

Cardiac chest pain with crescendo pattern.

New onset angina.

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14
Q

What are the test for unstable angina?

A

FBC
Anaemia aggravates it

Cardiac enzymes
Excludes infarction

ECG
When in pain shows ST depression

Coronary angiography

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15
Q

What is the treatment for unstable angina?

A

Anti-platelet agents e.g. Clopidogrel
Anti-coagulants e.g. Heparin, Warfarin
Break up any clots and stop new ones from forming.

Nitrates

B-blockers

Calcium antagonists (if B-blocker contraindicated)

CABG and PCI

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16
Q

WHAT IS A MYOCARDINAL INFARCTION?

A

Plaque rupture leads to a clot forming which then occludes one of the coronary arteries causing myocardial cell death and inflammation.

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17
Q

What are the symptoms of a myocardial infarction?

How long does it need to last to be an MI?

A

Acute central chest pain radiating to jaw or shoulder

Lasting >20 mins

Nausea

SOB

Palpitations

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18
Q

What are the signs of a myocardial infarction?

A

Clammy and pale

4th heart sound

Pansystolic murmur

May later develop peripheral oedema

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19
Q

What are the tests for a MI?

A

ECG: Classically, hyperacute (tall) T waves, ST elevation or new LBBB occur within hours of transmural infarction.
T wave inversion and development of pathological Q waves follow over hours to days.

CXR:
Cardiomegaly, pulmonary oedema, or a widened mediastinum

Blood
FBC, U&E, glucose, lipids.

Cardiac enzymes
Troponin
Creatine kinase
Myoglobin

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20
Q

What is the initial management for a MI?

A

Morphine

—Oxygen

—Nitrates

—Aspirin (or Clopidogrel if aspirin is contraindicted)

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21
Q

What is the management after a MI?

For ST evelation and non ST elevation?

A

—ST elevation MI
If within 2 hours and ST elevation on ECG then PCI is preferred option.
Beta blocker IV.
ACE inhibitor
Clopidogrel.

—Non ST elevation MI
Beta blocker IV.
Antithrombotic; fondaparinux.
High risk of bleeding; angiography, clopidogrel and aspirin
—Low risk of bleeding; ticagralor, clopidogrel.

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22
Q

What are the complications of MI?

A
  1. Cardiac arrest; cardiogenic shock; LVF.
  2. Unstable angina
  3. Bradycardias or heart block.
  4. Tachyarrhythmias
  5. Pericarditis
  6. DVT & PE
  7. Systemic embolism
  8. Cardiac tamponade
  9. Mitral regurgitation
  10. Ventricular septal defec
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23
Q

What is Dressler’s syndrome?

A

Recurrent pericarditis
pleural effusions
fever
anaemia and ESR increase

1–3 wks post-MI

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24
Q

WHAT IS SHOCK?

A

Circulatory failure resulting in inadequate organ perfusion

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25
Q

What is shock defined as?

A

Low BP

Evidence of tissue hypoperfusion.

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26
Q

What does a patient in shock look like?

A

Skin is pale, cold, sweaty and vasoconstricted

Pulse is weak and rapid

Pulse pressure reduced, MAP may be maintained

Urine output reduced

Confusion, weakness, collapse, coma

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27
Q

What is the main cause of injury from shock?

A

Prolonged hypotension can lead to life threatening organ failure

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28
Q

What are the different types of shock?

A

Hypovolaemic shock

Cardiogenic shock

Distributive shock
Septic shock
Analphylactic shock
Neurogenic shock

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29
Q

WHAT IS HYPOVALEMIC SHOCK?

A

Low circulating blood volume

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30
Q

What can cause hypovalemic shock?

A

Loss of blood
Acute GI bleeding
Trauma
Ruptured AA
Loss of fluid
Dehydration
Burns

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31
Q

How do you treat hypovalaemic shock?

A

Identify and treat underlying cause.

Raise the legs.

Give fluids

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32
Q

WHAT IS CARDIOGENIC SHOCK?

When can it occur?

A

Cardiogenic shock is a state of inadequate tissue perfusion primarily due to cardiac dysfunction.

—May occur suddenly or after progressively worsening heart failure

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33
Q

What are some causes of cardiogenic shock?

A
  1. MI
  2. Arrhythmias
  3. PE
  4. Tension pneumothorax
  5. Cardiac tamponade
  6. Myocarditis
  7. Endocarditis
  8. Aortic dissection
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34
Q

What are the symptoms for cardiogenic shock?

A

Low BP

High HR

High RR

Confusion

Pallor

Clammy

Pale peripheries

Reduced urine output

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35
Q

What are the investigations for cardiogenic shock?

A

ECG
Tachycardic
Blood pressure
Low
JVP pressure
RAISED

U&E, troponins/cardiac enzymes,

ABG

CXR

Echocardiogram

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36
Q

What is the management of cardiogenic shock?

What do you need to monitor?

A

Treat the cause

Oxygen

Diamorphine IV for pain and anxiety

Correct arrhythmias, U&E abnormalities or acid–base disturbance

—Monitor CVP, BP, ABG, ECG, urine

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37
Q

WHAT IS SEPSIS?

A

Sepsis exists when a systemic inflammatory response is associated with an infection

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38
Q

What is septic shock?

A

Septic shock exists when sepsis is complicated by persistent hypotension unresponsive to fluid resuscitation

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39
Q

What are the risk factors for septic shock?

A

Age

Diabetes mellituis (DM)

Immunocompromised

Alcoholics

Burns

IVDU

Pregnancy

Catheter

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40
Q

What are the symptoms for septic shock?

A

Low BP

High HR

Low sats (O2)

High resp rate (RR)

Lactate >2

Unresponsive

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41
Q

What are the investigations for septic shock?

A

Cultures (2 peripheral blood, plus urine/sputum/CSF)

LACTATE

ABG and BP

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42
Q

What is the treatment for septic shock?

A

OXYGEN

FLUIDS (check BP and ABG)

IV ANTIBIOTICS
(Tacozin and gentamicin, and vancomycin)

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43
Q

WHAT IS ANAPHYLATIC SHOCK?

A

Intense allergic reaction.

Massive release of histamine and other vasoactive mediators causing haemodynamic collapse.

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44
Q

What type of hypersensitivity is anaphylatic shock?

A

Type-I IgE-mediated hypersensitivity reaction.

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45
Q

What are some causes of anaphylatic shock?

A
  1. Drugs, eg penicillin, and contrast media in radiology
  2. Latex
  3. Stings, eggs, fish, peanuts, strawberries, semen (rare)
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46
Q

What are the signs and symptoms of anaphylatic shock?

A
  1. Itching
  2. Sweating
  3. Diarrhoea and vomiting
  4. Erythem
  5. Urticaria
  6. Oedema
  7. Wheeze
  8. Laryngeal obstruction
  9. Cyanosis
  10. Tachycardia
  11. Hypotension
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47
Q

What is the management of anaphylatic shock?

A
  1. Oxygen
  2. Remove the cause
  3. Adrenaline IM - 500 micrograms - 1 in 1000
    Repeated every 5 minutes if necessary
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48
Q

WHAT IS NEUROGENIC SHOCK?

A

Distributive

Disruption of the autonomic pathways within the spinal cord

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49
Q

What can cause neurogenic shock?

A

Spinal cord injury

Epidural

Spinal anaesthesia

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50
Q

What are the investigations for neurogenic shock?

A

Cold and clammy suggests cardiogenic shock or fluid loss.

Warm and well perfused, with bounding pulse points to septic shock.

Any features suggestive of anaphylaxis—history, urticaria, angio-oedema, wheeze?

CVS: usually tachycardic and hypotensive.

JVP or central venous pressure: If raised, cardiogenic shock likely.
Check abdomen: Any signs of trauma, or aneurysm? Any evidence of GI bleed?

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51
Q

What are the treatment options for neurogenic shock?

A

Dopamine and vasopressin (ADH).

Atropine is administered for slowed heart rate.

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52
Q

What organs are at risk of shock?

A

Kidneys - Acute tubular necrosis

Lung – Acute Respiratory Distress Syndrome (ARDS) (or “shock lung”)

Heart – myocardial ischaemia and infarction

Brain – confusion, irritability, coma

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53
Q

WHAT IS ACUTE RESPIRATORY DISTRESS SYNDROME?

A
  1. Increase in alveolar permeability
  2. Fluid accumilation in the alveoli
  3. Not associated with cardiac causes
  4. Impaired oxygenation
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54
Q

What are some causes of ARDS?

A
  1. Infection: sepsis, pneumonia
  2. Massive blood transfusion
  3. Trauma
  4. Smoke inhalation
  5. Acute pancreatitis
  6. Cardio-pulmonary bypass
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55
Q

What are the clinical features of ARDS?

A
  1. Dyspnoea
  2. Elevated respiratory rate
  3. Bilateral lung crackles
  4. Low oxygen saturations
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56
Q

What are the investigations for ARDS?

A
  1. Chest x-ray
  2. ABG
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57
Q

What is the management for ARDS?

A
  1. ITU - Oxygenation/ventilation to treat the hypoxaemia
  2. General organ support e.g. vasopressors as needed
  3. Treatment of the underlying cause e.g. antibiotics for sepsis
  4. Certain strategies such as prone positioning and muscle relaxation have been shown to improve outcome in ARDS
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58
Q

WHAT DOES CARDIOMYOPATHY REFER TO?

A

Primary heart muscle disease – often genetic.

Three types.

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59
Q

WHAT IS HYPERTROPHIC CARDIOMYOPATHY?

https://www.youtube.com/watch?v=8RnkKB8xvwA

A

Heart muscle becomes thick, heavy and hypercontactile.

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60
Q

What is Hypertrophic cardiomyopathy (HCM) caused by?

What inheritance is it?

A

Sarcomeric protein gene mutations.

Autosomal dominant inheritance.

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61
Q

What is the epidemology of HCM?

A

Leading cause of death in the young

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62
Q

What is the pathology HCM?

A

Asymmetric septal hypertrophy

Intervenricular septum more than free wall

Take up more room so less filling
More stiff and less compliant

Stroke volume goes down

Heart failure

LV outflow tract (LVOT) obstruction

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63
Q

What type of heart failure if HCM?

A

Diastolic heart failure

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64
Q

What does the obstuction of the ventricular outflow tract cause?

A

Pulling of the mitral valve towards the atrioventricular septum

Venturi effect

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65
Q

What kind of heart sound is heard in HCM? Where is it also seen?

A

Crescendo-decrescendo murmur

Aortic valve stenosis

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66
Q

What are the symptoms of HCM?

A

Sudden death.

Fast arrythmias

Palpitations

Dyspnoea

Dizzy spells or syncope

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67
Q

What are the sings of HCM?

A

—Jerky pulse

Double apex beat

Systolic thrill at lower left sternal edge

Harsh ejection systolic murmur

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68
Q

What are the tests for HCM?

A

Echo
Asymmetrical septal hypertrophy; small LV cavity with hypercontractile posterior wall; midsystolic closure of aortic valve

ECG
LVH; progressive T wave inversion; deep Q waves, AF

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69
Q

What is the treatment for HCM?

A

Beta-blockers or verapamil for angina + SOB.

Amiodarone for arrhythmias (AF, VT) DIGOXIN IS CONTRAINDICATED

Anticoagulate for paroxysmal AF or systemic emboli.

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70
Q

What drug is contraindicated in HCM?

A

Digoxin

Increase contraction force, increase obstruction

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71
Q

WHAT IS DILATED CARDIOMYOPATHY (DCM)?

A

Causes all four chambers of the heart to enlarge

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72
Q

What is Dilated Cardiomyopathy (DCM) often caused by?

A
  1. Alcohol
  2. Increased BP
  3. Haemochromatosis
  4. Viral infection
  5. Autoimmune
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73
Q

What happens in Dilated cardiomyopathy (DCM)?

What type of heart failure is it?

A

Large space, thin walls

Weak contraction

Less blood pumped out in each beat

Biventicular congestive heart failure

Systolic heart failure

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74
Q

What type of heart sound is heard in DCM?

A

Holosystolic murmur

S3 sounds also present, blood slamming into wall in diastole

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75
Q

What are the symptoms of DCM?

A

Fatigue

Dyspnoea

Pulmonary oedema

Right ventricular failure

Emboli

Atrial fibrillation

Ventricular tachycardia

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76
Q

What are the signs of DCM?

A

—Increased pulse

Decreased blood pressure

Increased JVP

Pleural effusion

Oedema

Jaundice, hepatomegaly, ascites

—Displaced diffuse apex beat, S3 gallop

—Mitral or tricuspid regurgitation

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77
Q

What are the tests for DCM?

A

Blood:
Plasma BNP is sensitive and specific in diagnosing heart failure.

CXR:
Cardiomegaly, pulmonary oedema.

ECG:
Tachycardia, non-specific T wave changes, poor R wave progression.

Echo:
Globally dilated hypokinetic heart and low ejection fraction. Look for MR, TR, LV mural thrombus.

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78
Q

What is the treatment for DCM?

A
  1. Stop drinking
  2. Treatment of cardiac failure
    - ACE inhibitors
    - Beta Blockers
    - Diuretics + Digoxin
  3. Anti-arrythmic drugs
    Amiodarone
  4. Cardiac transplantation and cardiomyoplasty
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79
Q

WHAT IS RESTRICTIVE CARDIOPATHY?

A

Heart muscle becomes stiff and less compliant

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80
Q

What diseases commonly cause RCM?

A

Amyloidosis

Familial amyloid cardiomyopathy
Afro-americans

Senile cardiac amyloidosis
Elderly

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81
Q

What are the causes of RCM?

A

Amyloidosis

Sarcoidosis
Collection of immune cells

Haemochromatosis

Radiation

Endocardial fibroelastosis

Loffler endomyocarditis
Eosinophils in lung tissue and heart tissue

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82
Q

What happens in amyloidosis?

A

Proteins that have been misfolded and become insoluble

Deposit in tissue in organs making them become less compliant

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83
Q

What is the pathology of RCM?

A
  1. Heart muscle stays same size
  2. When blood comes in heart doesn’t stretch
  3. Less blood
  4. Less pumped out
  5. = Heart failure
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84
Q

What type of heart failure is RCM?

A

Diastolic heart failure

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85
Q

What are the signs of RCM?

A

These are mainly of right heart failure with increase JVP

Kussmaul’s sign (JVP rising paradoxically with inspiration)

Quiet heart sounds

S3

Diastolic pericardial knock, hepatosplenomegaly, ascites, and oedema.

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86
Q

What are the investigations for RCM?

A

ECG
Low amplitude QRS

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87
Q

What is the treatment for RCM?

A

Treat underlying cause

Heart transplant

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88
Q

What do all cardiomyopathies carry?

A

An arrhythmic risk.

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89
Q

WHAT IS INHERITED ARRHYTHMIA (CHANNELOPATHY) CAUSED BY?

A

Ion channel protein gene mutations.

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90
Q

Which ions are involved with channelopathy?

A

potassium, sodium or calcium channel.

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91
Q

What do channelopathies include?

A

Long QT, short QT, Brugada and CPVT.

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92
Q

What do channelopathies normally present with and what do they have that is normal?

A

Recurrent syncope and have a structurally normal heart.

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93
Q

What is sudden cardiac death in young people normally due to? What disease is it most likely to be?

A

An inherited condition. Cardiomyopathy or ion channelpathy.

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94
Q

What does sudden arrhythmic death syndrome (SADS) usually refer to?

A

Normal heart/arrhythmia.

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95
Q

WHAT IS AN ANEURYSM?

https://www.youtube.com/watch?v=pEOqffiwE7k

A

Abnormal buldge in vessel

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96
Q

What are the risk factors for aneurysms?

A

Male

Over 60

Hypertension

Smoking

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97
Q

What are the typical causes of an anneurysm

A

Atheroma

Trauma

Infection

Connective tissue disorders

Inflammations

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98
Q

What is the pathology of an aneurysm?

A

Weakness in vessel wall

Ballooning outwards of vessel wall due to pressure

Laplace’s law causes positive feedback loop

Gives bigger aneurysm

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99
Q

When is an aneurysm official labelled an aneurysm?

A

When the diameter exceeds 1.5 times the normal size

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100
Q

What are the common sites for anneurysms

What are the complications?

A

Common sites Aorta (infrarenal most common), iliac, femoral and popliteal arteries.

Complications Rupture; thrombosis; embolism; fistulae; pressure on other structures.

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101
Q

What are the different types of aneurysms?

A

True aneurysms
Abnormal dilatations that involve all layers of the arterial wall.

THEN EITHER

Fusiform
OR
saccular (Berry aneurysms)

False aneurysms (pseudoaneurysms)
Blood in the outer layer only (adventitia) which communicates with the lumen (eg after trauma).

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102
Q

What happens when an aneurysm explodes?

A

Blood spurts out of the hole

Less blood goes downstream

Ischaemia of downstream cells

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103
Q

What are the symptoms and signs of an abdominal aortic aneurysm?

A

Severe left flank pain
Abdomen
Chest
Lower back
Groin

Pulsating mass with heartbeat

Hypotension

104
Q

What are the diagnosis options for an aneurysm?

A

Often incidental finding

Ultrasound

CT

MRI

105
Q

What are the options for a unruptured anneurysm?

A

Elective surgery

Stenting

106
Q

WHAT IS AORTIC DISSECTION?

https://www.youtube.com/watch?v=AZElPJtyxck

A

Tear in tunica intima, causes blood to pool between intima and media

107
Q

What can cause aortic dissection?

A

Chronic hypetension
Stress
increase blood volume
Coarctation

Weakened aortic wall
Marfan’s
Ehlers-Danlos syndrome
Decrease blood flow to vasa vasorums

Aneurysms

108
Q

Where does aortic dissection normally occur?

A

Within the first 10cm of aorta

109
Q

What can a aortic dissection cause?

A

Blood back up into pericardial space causing
Pericardial temponade

Blood goes out intima and comes back into blood vessel through and hole

Blood flows does the aorta inbetween the layers and puts compression on other arteries
Renal artery
Subclavian artery

110
Q

What are the different types of aortic dissection?

A

Type A (70%) dissections involve the ascending aorta, irrespective of site of the tear,

Whilst if the ascending aorta is not involved it is called type B (30%)

111
Q

What are the symptoms of aortic dissection?

A

Sharp chest pain radiating to back

Weak pulse in downstream artery

Difference in BP between left and right arms

Hypotension

Shock

112
Q

What are the investigations for aortic dissection?

A

CXR
Widend aorta

Transoesophageal echo
True lumen and flase aorta

Angiogram

113
Q

What is the management of aortic dissection?

A

Surgery
Removal of dissected aorta
Blocks entry of blood into wall of aorta
Wall reconstructed with synthetic graft
Stent

Blood pressure meds
Beta Blockers

114
Q

HOW MANY LAYERS IS THE PERICARDIUM? WHAT IS THE STRUCTURE?

A

Two.

Visceral single cell layer adherent to epicardium

Fibrous parietal layer

2mm thick

Acellular collagen and elastin fibres

50ml of serous fluid.

115
Q

What is contained within the pericardium? What is outside?

A

Great vessels lie within the pericardium

Two layers are continuous

Left atrium is mainly outside the pericardium

Parietal layer has fibrous attachments to fix the heart in the thorax.

116
Q

Why is the pericardium important? What is important about the small reserve volume?

A

Restrains the filling volume of the heart.

If the volume is exceeded the pressure is translated to the cardiac chambers.

117
Q

WHAT IS CARDIAC TAMPONADE?

A

Fluid builds up in the pericardium and results in compression of the heart.

118
Q

What is the cause of cardiac tamponade?

A

Any pericarditis

Aortic dissection

MI

Trauma

Trans-septal puncture at cardiac catheterization

Cancer

119
Q

What are the signs of cardiac tamponade?

A

Pulse increase

BP decerease

Pulsus paradoxus

JVP increase

Kussmaul’s sign

Muffled S1 and S2.

120
Q

What is Beck’s triad?

A

Falling BP

Rising JVP

Muffled heart sounds.

121
Q

What are the investigations for cardiac tamponade?

A

Beck’s triad
Falling BP; rising JVP; muffled heart sounds.

CXR
Big globular heart (if >250mL fluid).

ECG
Low voltage QRS ± electrical alternans.

Echo is diagnostic
Echo-free zone around the heart ± diastolic collapse of right atrium and right ventricle.

122
Q

What is the management of cardiac temponade?

A

The pericardial effusion needs urgent drainage

123
Q

What does chronic pericardial effusion have that is unique?

A

Pericardium slowly adapts to the increasing fluid and therefore reduces the effect on diastolic filling of the chambers.

124
Q

WHAT IS PERICARDIAL EFFUSION?

A

Accumulation of fluid in the pericardial sac.

125
Q

What are the causes of pericardial effusion?

A

Any cause of pericarditis.

126
Q

What are the symptoms of pericardial effusion?

A
  1. Dyspnoea
  2. Raised JVP
  3. Bronchial breathing at left base
  4. Look for signs of cardiac tamponade
127
Q

What are the investigations for pericardial effusion?

A

CXR
Enlarged, globular heart.

ECG
Low-voltage QRS complexes and alternating QRS morphologies (electrical alternans).

Echo
Shows an echo-free zone surrounding the heart.

128
Q

What are the management options for pericardial effusion?

A

Treat the cause.

Pericardiocentesis may be diagnostic (suspected bacterial pericarditis) or therapeutic (cardiac tamponade).

129
Q

WHAT IS ACUTE PERICARDITIS?

https://www.youtube.com/watch?v=jqClJsqnFFA

A

Inflammatory pericardial syndrome with or without effusion.

130
Q

What are the causes of pericarditis?

A
  1. Idiopathic.
  2. Viral
    Enteroviruses
    Coxsackie B viruse
    Herpesviruses (EBV, CMV, HHV-6),
  3. Dresseler’s syndrome
    Happens after heart attack
    When an MI happens lots of necrosis
    This also affects the pericardium
  4. Autoimmune
    Rheumatoid arthritis
    Scleraderma
    SLE
131
Q

What is the patholgy of pericarditis?

A

Fluid and immune cells move from tiny blood cells into the fibrous pericardium

132
Q

What is the clinical presentation of somebody with pericarditis?

A

Fever

Chest pain
Worse with heavy breathing
Better with sitting up and leaning forward

133
Q

What can a clinical diagnosis of acute pericarditis be diagnosed from?

A

2 of 4 of:

  1. Chest pain.
  2. Friction rub.
  3. ECG changes.
  4. Pericardial effusion.
134
Q

What tests can you do to check if somebody has pericarditis?

A
  1. Clinical examination
    Pericardial rub
    Sinus tachycardia
    Signs of effusion (pulsus paradoxus, Kussmauls sign)
  2. ECG
  3. Bloods
    FBC
    Modest increase in WCC, mild lympocytosis
    ESR & CRP
    High ESR may suggest aetiology
    ANA in young females - SLE
    Troponin
    Elevations suggest myopericarditis
  4. CXR
    Silouette
  5. Echocardiogram
135
Q

What does an ECG look like with a patient who has pericarditis?

A

First few weeks
Diffuse ST segment elevation
Decrease PR

After that
T waves flattened

After that
ECG returns back to normal

136
Q

What management can help with pericarditis?

A

Sedentary activity

NSAID
Ibuprofen PO or Aspirin PO

Treat cause

Colchicine
PO limited by nausea and diarrhoea, reduces recurrence.

137
Q

WHAT IS HEART FAILURE?

A

A symptomatic condition where breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output

A state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues

138
Q

How do you calculate cardiac output?

A

CO = HR x SV

139
Q

What is the most common cause of heart failure? What does this usually result from? What are some other causes?

A

Myocardial dysfunction.

IHD.

Hypertension.
Alcohol excess.
Cardiomyopathy.
Valvular.
Endocardial.
Pericardial causes.

140
Q

What is systolic heart failure?

A

Inability of the ventricle to contract normally, resulting in decreaed cardiac output.

Ejection fraction (EF) is <40%

141
Q

What are the causes of systolic heart failure?

A

IHD

MI

Cardiomyopathy.

142
Q

What is diastolic heart failure?

A

Inability of the ventricle to relax and fill normally

Causing increased filling pressures.

EF is >50%.

143
Q

What are the causes of diastolic heart failure?

A

Constrictive pericarditis

Tamponade

Restrictive cardiomyopathy

Hypertension

144
Q

How may left and right sided heart failure occur?

A

Left ventricular failure (LVF) and right ventricular failure (RVF) may occur independently, or together as congestive cardiac failure (CCF).

145
Q

What are some causes of left sided heart failure?

A

Hypertension

146
Q

What are the symptoms of left sided heart failure?

A

Dyspnoea,

Poor exercise tolerance

Fatigue

Orthopnoea

Paroxysmal nocturnal dyspnoea (PND)

Nocturnal cough (±pink frothy sputum)

147
Q

What are some causes of right ventricular failure?

A

LVF, pulmonary stenosis, lung disease.

148
Q

What are the symptoms of right ventricular heart failure?

A

Peripheral oedema (up to thighs, sacrum, abdominal wall),

Ascites

Nausea

Anorexia

Facial engorgement

Pulsation in neck and face (tricuspid regurgitation)

Epistaxis.

149
Q

What tests can you do for heart failure?

A

History and physical examination

Blood Tests
BNP
LFTS, FBC, U&Es, BNP, TFTs

Cardiac enzymes
Creatinine kinase, troponin I, troponin T

CXR

ECG.

Echocardiography

150
Q

What would you see on a chest XR for heart failure?

A

ABCDE

  1. Alveolar oedema
  2. Kerley B lines
  3. Cardiomegaly
  4. Dilated prominant upper lobe vessels
  5. Pleural Effusion
151
Q

What are the systems involved with protection and survival of the heart?

A

The sympathetic system
Increases afterload by causing peripheral vasoconstriction

The renin-angiotensin-aldosterone axis
Salt and water retention
Increases afterload and preload (^ volume and vasoconstriction)

Cardiac changes
Ventricular dilatation
Myocytehypertrophy

152
Q

What does an increase in cardiac norepinephrine produce? What happens in the long term?

A

Increased adrenergic activation

Direct toxicity to myocytes

Increased HR and contractility causing extra strain on heart

Increased vasocontriction, increased afterload, more strain on heart

153
Q

What does angiotensin 2 produce?

A

Increase salt and water retention

Increased preload, extra strain on heart

154
Q

What is the treatment for heart failure?

A

Loop diuretics
Furosemide

ACEi
Lisinopril

Beta blockers
Bisoprolol

Aldosterone antagonists
Spironolactone

Calcium glycoside
Digoxin inhibits Na/K

155
Q

WHAT IS TETRALOGY OF FALLOT?

A
  1. Pulmonary stenosis
  2. RV hypertrophy
  3. Overriding aorta
  4. VSD
156
Q

What are the physiology of Tetralogy of Fallot?

A

The stenosis of the RV outflow leads to the RV being at higher pressure than the left

Therefore blue blood passes from the RV to the LV

The patients are BLUE

Toddlers may squat

157
Q

What is the presentation of infants in tetralogy of Fallot and why?

A

Infants may be acyanotic at birth

Pulmonary stenosis murmur as the only initial finding.

Cyanotic due to decreasing flow of blood to the lungs as well as right-to-left shunt across the VSD.

Toddlers may squat
Typical of TOF, as it increases peripheral vascular resistance and decreases the degree of right to left shunt.

Adult patients are often asymptomatic

158
Q

What are the tests for tetrology of Fallot?

A

ECG
RV hypertrophy with a right bundle-branch block.

CXR
Boot-shaped heart

Echocardiography
Can show the anatomy as well as the degree of stenosis.

159
Q

What is the management of tetrology of Fallot?

A
  1. Surgical repair is often undertaken in two parts
  2. Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm
160
Q

WHAT IS VENTRICULAR SEPTAL DEFECTS?

A

Hole in the connecting venticles

161
Q

What are the different pressures in the ventricles and what is the result in VSD?

A

High pressure LV

Low pressure RV

Blood flows from high pressure chamber to low pressure chamber

Therefore NOT blue

Increased blood flow through the lungs

162
Q

What are the causes of VSD?

A

Congenital

  1. Down’s syndrome
  2. Edward’s syndrome
  3. Patau syndrome
  4. cri-du-chat syndrome

Acquired (post-MI).

163
Q

What are the ventricular septal defects clinical signs?

A

Large
Pan-systloic murmur varies in intensity
Small breathless skinny baby
Increased respiratory rate
Tachycardia
Big heart on chest X ray

Small
Loud systolic murmur
Thrill (buzzing sensation)
Well grown
Normal heart rate
Normal heart size.

164
Q

What is the treatment for VSD?

A

Large

Require fixing in infancy (PA band, complete repair)

Small

Endocarditis risk

Need no intervention

165
Q

What may VSD lead to?

A

May lead to Eisenmengers syndrome.

166
Q

What is Eisenmengers syndrome?

A
  1. High pressure pulmonary blood flow
  2. Damages to delicate pulmonary vasculature
  3. The resistance to blood flow through the lungs increases
  4. The RV pressure increases
  5. The shunt direction reverses
  6. The patient becomes BLUE.
167
Q

WHAT IS ATRIAL SEPTAL DEFECT?

A

Abnormal connection between the two atria (primum, secundum, sinus venosus)

Common

Often present in adulthood.

168
Q

What are the two types of ASD?

A

Primum: present earlier, may involve AV valves

Secundum: may be asymptomatic until adulthood

169
Q

What is the physiology of atrial septal defects?

A

Slightly higher pressure in the LA than the RA

Shunt is left to right

Therefore NOT blue

Increased flow into right heart and lungs

170
Q

What is the physiology between large and small atrial septal defects?

A

Large
Significant increased flow through the right heart and lungs in childhood
Right heart dilatation
SOBOE
Increased chest infections
If any stretch on the right heart should be closed

Small
Small increase in flow
No right heart dilatation
No symptoms
Leave alone
NB. The shunt on small to moderate sized defects increases with age

171
Q

What are some complications of ASD?

A

Reversal of left-to-right shunt, ie Eisenmenger’s complex.

Paradoxical emboli (vein to artery via ASD; rare).

172
Q

What are the clinical signs of atrial septal defects?

A

Pulmonary flow murmur

Fixed split second heart sound (delayed closure of PV because more blood has to get out)

Big pulmonary arteries on CXR

Big heart on chest X ray

173
Q

What is the treatment of ASD?

A

In children closure is recommended before age 10yrs.

In adults, transcatheter closure is now more common than surgical.

174
Q

WHAT CAN ATRIA-VENTRICULAR SEPTAL DEFECTS INVOLVE?

A

Hole in the centre. Can involve the ventricular septum, the atrial septum, the mitral and tricuspid valves.

175
Q

What is the physiology of atria-ventricular septal defect? For a partial and complete defect?

A

Complete defect –Breathless as neonate –Poor weight gain –Poor feeding –Torrential pulmonary blood flow –Needs repair or PA band in infancy –Repair is surgically challenging

Partial defect –Can present in late adulthood –Presents like a small VSD / ASD –May be left alone if there is no right heart dilatation

176
Q

WHAT IS PATENT DUCTUS ARTERIOSUS?

A

Failure of ductus arterioles to close.

177
Q

What are the clinical signs of ductus arterioles?

A

Continuous ‘machinery’ murmur

If large, big heart, breathless

Eisenmenger’s syndrome
–Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)

178
Q

What is the physiology of patent ductus arterioles with a large and a small?

A

Large –Torrential flow from the aorta to the pulmonary arteries in infancy –Breathless, poor feeding, failure to thrive –More common in prem babies –Need to be closed (surgically) •Small –Little flow from the aorta to Pas –Usually asymptomatic –Murmur found incidentally –Endocarditis risk

179
Q

How do you close the ductus arterioles?

A

Surgical or percutaneous.

Local anaesthetic.

Venous approach.

180
Q

WHAT IS COARCTATION OF THE AORTA?

A

Narrowing of the aorta at the site of insertion of the ductus arterioles.

181
Q

What is the physiology for coarctation of the aorta?

A

Severe
Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair

Mild
Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term

182
Q

What are the clinical signs of coarctation of the aorta?

A
  1. Infancy: heart failure
  2. Adult: hypertension
  3. Radio-femoral delay
  4. Mid systolic murmur, maximal over back
  5. Apical click from the aortic valve
  6. Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
183
Q

What are the long term problems of coarctation of the aorta?

A

Hypertension
Early coronary artery disease
Early strokes
Sub arachnoid haemorrhage

Re-coarctation requiring repeat intervention

Aneurysm formation at the site of repair

184
Q

What is the treatment of coarctation of the aorta?

A
  1. Surgery, or balloon dilatation ± stenting.
185
Q

WHAT IS BICUSPID AORTIC VALVE?

A

Normal AV valves has three cusps.

This has two

186
Q

what are the problems associated with bicuspid AVs?

A

Can be severely stenotic in infancy or childhood

Degenerate quicker than normal valves

Become regurgitant earlier than normal valves

Are associated with coarctation and dilatation of the ascending aorta

187
Q

How can you treat bicuspid aortic valve?

A

Surgery

188
Q

WHAT IS PULMONARY STENOSIS?

A

Narrowing of the outflow of the right ventricle.

Valvar.

Sub valvar.

Supra valvar.

Branch.

189
Q

What are the problems with pulmonary stenosis?

A

Severe
–Right ventricular failure as neonate
–Collapse
–Poor pulmonary blood flow
–RV hypertrophy
–Tricuspid regurgitation

Moderate / mild
–Well tolerated for many years
–Right ventricular hypertrophy

190
Q

What is the treatment for pulmonary stenosis?

A

Treatment
–Balloon valvuloplasty
–Open valvotomy
–Open trans-annular patch
–Shunt (to bypass the blockage)

191
Q

WHAT IS HYPERTENSION?

A

Over 140/90

192
Q

What are the two types of hypertension?

A

Essential hypertension (primary, cause unknown). ~95% of cases.

Secondary hypertension ~5% of cases.

193
Q

What are some causes of secondary hypertension?

A

Renal
CKD

Endocrine disease
Conn’s syndrome

Others
Coarctation, pregnancy

194
Q

What are the tests for hypertension?

A

24hr ambulatory BP monitor

Multiple home BP monitoring

Fundoscopy–in severe HTN
Bilateral retinal haemorrhages
Papilloedema

Overall CVD risk
Fasting glucose
Cholesterol

End Organ Damage
12 lead ECG –past MI, LV hypertrophy
Urine analysis –protein, blood

195
Q

What are some lifestyle to lower blood pressure?

A

Stop smoking

Low-fat diet

Reduce alcohol and salt intake

Increase exercise

Reduce weight if obese

196
Q

What do you give for hypertension if they are over 55 or afro-carribean?

A

Calcium channel blocker

Amlodipine

Nifedipine

Verapamil

197
Q

What do you give for hypertension if they are below 55 and not afro-carribean?

A

ACE inhibitor

Ramapril
Peridopril

OR

Angiotensin receptor blocker

Candesartan
Valsartan

198
Q

What do you give them if their drug doesn’t work?

A

The other one

199
Q

What do you give them if all their drugs don’t work?

A

Thiazide like diuretic

Chlorothiazide

Hydrocholrothiazide

200
Q

How can renal artery stenosis cause hypertension?

A

Less blood flow to kidneys

Secretes Renin

More water and salt retention

Higher BP

201
Q

What is a pheochromocytoma? How does it cause hypertension?

A

Tumour on adrenal glands

Constantly produce catecholamines (e.g. adrenaline)

Increase heart rate and peripheral vascular resistance

Increase BP

202
Q

How does cushing’s cuase hypertension?

A

Enhances adrenalines effect on blood vessels to constrict them

Also can act as a mineralacorticoid (aldosterone)

Increase BP

203
Q

How does Conn’s syndrome cause hypertension?

A

High aldosterone

Increased sodium and water retention

Increased BP

204
Q

WHAT IS AORTIC STENOSIS?

A

Hardening of the aorta

205
Q

What is the cause of aortic valve stenosis

A
  1. Congenital bicuspid valve
  2. Degenerative calcification
  3. Rheumatic Heart disease
206
Q

What is rheumatic heart disease?

A

Fusion of cusps.

207
Q

How does a person with aortic stenosis present?

A

Syncope

Angina

Dyspnoea

Sudden death

208
Q

What physical signs would you hear on aortic stenosis?

A
  1. Narrow pulse pressure
    • ​​Slow rising carotid pulse (pulsus tardus)
    • & decreased pulse amplitude (pulsus parvus)
  2. Heart sounds
    • ​​Soft or absent second heart sound, S4 gallop due to LVH.
  3. Ejection systolic murmur
    • Crescendo-decrescendo character.
209
Q

What tests would you do for someone with aortic stenosis?

A

Echocardiography

Two measurements obtained are:
Left ventricular size and function: LVH, Dilation, and EF
Doppler derived gradient and valve area (AVA).

ECG

CXR –LVH, calcified aortic valve

210
Q

What is the management for aortic stenosis?

A

General:
Fastidious dental hygiene / care
Consider IE prophylaxis in dental procedures

Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS

Surgical Replacement: Definitive treatment

TAVI – Transcatheter Aortic Valve Implantation

211
Q

WHAT IS MITRAL VALVE REGURGITATION?

A

Definition: Backflow of blood from the LV to the LA during systole

Mild (physiological) MR is seen in 80% of normal individuals.

212
Q

What are the aetiologies of chronic mitral valve regurgitation?

A

Myxomatous degeneration (MVP)

Ischemic MR

Rheumatic heart disease

Infective Endocarditis.

213
Q

What is the pathophysiology of mitral valve regurgitation?

A

Pure Volume Overload

Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility

Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.

Progressive left ventricular volume overload leads to dilatation

214
Q

What are the symptoms of mitral valve regurgitation?

A

Mainly asymptomatic

Exertion dyspnoea –exercise intolerance

Palpitations

Fatigue

215
Q

What are the signs of mitral valve regurgitation?

A

Pansystolic murmur at apex radiating to axilla

Soft S1

Displaced hyperdynamic apex

216
Q

What do imaging studies for mitral regurgitation show?

A

ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR

CXR: LA enlargement, central pulmonary artery enlargement.

ECHO: Estimation of LA, LV size and function. Valve structure assessment TOE v helpful

217
Q

What are the medications/management for MR?

A

Vasodilator –ACEi, hydralazine

Rate control for AF –BB, CCB, Digoxin

Anticoagulant for AF and flutter

Diuretics –to control symptoms

Surgery for deteriorating symptoms –aim to replace valve

218
Q

What are the indications for surgery of severe MR?

A

ANY Symptoms at rest or exercise with (repair if feasible)

Asymptomatic:
If EF <60%, LVESD >45mm
If new onset atrial fibrillation/raised PAP.

219
Q

WHAT IS AORTIC VALVE REGURGITATION?

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps.

220
Q

What is the cause of AR?

A

Bicuspid aortic valve

Rheumatic

Infective endocarditis.

221
Q

What is the pathophysiology of AR?

A

Combined pressure AND volume overload

Compensatory Mechanisms: LV dilation, LVH

Progressive dilation leads to heart failure

222
Q

What are the symptoms of aortic valve regurgitation?

A

Exertional dyspnoea

Orthopnoea

Paroxysmal nocturnal dyspnoea

223
Q

What are the signs or aortic regurgitation?

A

Collapsing (water hammer) pulse
Wide pulse pressure
Displaced hyperdynamic apex beat
Early diastolic murmur

Notable eponyms
Corrigans sign (ear movements)
De Musset’s sign (head movements)
Duroziez’s sign (Femoral artery murmur)
Austin flint murmur (cardiac apex murmur)
Traube’s sign (pistol shot over femoral)

224
Q

What would cardiac tests show you for AR?

A

CXR
Cardiomegaly

ECHO
LV dilation and hypertrophy

225
Q

What is the management for AR?

A

Vasdilators
ACEi only if symptomatic or HTN

Surgical
Replace valve before LV dysfunction

226
Q

WHAT IS MITRAL VALVE STENOSIS?

A

Obstruction of LV inflow that prevents proper filling during diastole

227
Q

What is the aetiology of mitral valve stenosis?

A

Rheumatic heart disease

Infective endocarditis

Mitral annular calcification.

228
Q

What is mitral valve stenosis pathophysiology?

A

LA dilation incerease pulmonary congestion (reduced emptying)

Increased Transmitral Pressures
Leads to left atrial enlargement and atrial fibrillation.

Right heart failure symptoms: due to Pulmonary venous HTN

229
Q

What are the symptoms of mitral valve stenosis?

A
  1. Dyspnoea
  2. Fatigue
  3. Palpitations
  4. Chest pain
230
Q

What are the signs in mitral valve stenosis?

A

Malar flush on cheeks

Low volume pulse

Tapping, non displaced apex beat

Rumbling mid-diastolic murmur

Loud opening S1

231
Q

What tests can you do on mitral valve stenosis and what will they show?

A

ECG
May show atrial fibrillation and LA enlargement

CXR
LA enlargement and pulmonary congestion
Occasionally calcified

MV ECHO
The GOLD STANDARD for diagnosis
Asses mitral valve mobility, gradient and mitral valve area

232
Q

How would you manage a patient with mitral valve stenosis?

A

If in AF, rate control

Anticoagulatewith warfarin

Diuretics

Percutaneous mitral balloon valvotomy

233
Q

WHAT IS INFECTIVE ENDOCARDITIS?

A

Infection of heart valve/s or other endocardial lined structures within the heart.

234
Q

What is the most causative organism in infective endocarditis?

A

Staph aureus - MOST COMMON and in IVDU or prosthetic valves

Strep viridans

Staph epidermis - prosthetic valves

235
Q

What are the different types of infective endocarditis?

A

Left sided native IE (mitral or aortic) Left sided prosthetic IE Right sided IE (rarely prosthetic as rare to have PV or TV replaced) Device related IE (pacemakers, defibrillators, with or without valve IE Prosthetic; can be Early (within year) or Late (after a year) post op Each type can have different presentations, pathogens and outcomes.

236
Q

How do you catch infective endocarditis?

A

Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected. Introduce infectious material into the blood stream or directly onto the heart during surgery Have had IE previously

237
Q

Who does infective endocarditis affect?

A

the elderly (in an ageing population) the young i.v. drug abusers the young with congenital heart disease. Anyone with prosthetic heart valves.

238
Q

What is the clinical presentation of infective endocarditis?

A

Depends on site, organism, etc Signs of systemic infection (fever, sweats, etc) Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction Valve dysfunction; heart failure, arrythmia

239
Q

How do you diagnose somebody with infective endocarditis?

A

2 Major Criteria Bugs grown from blood cultures evidence of endocarditis on echo, or new valve leak 5 Minor Criteria Predisposing factors Fever Vascular phenomena Immune phenomena Equivocal blood cultures. Definite IE 2 major, 1 major+3 minor, 5 minor Possible IE 1 major, 1 major+3 minor, 5 minor.

240
Q

What test can you do for infective endocarditis?

A

ECG (ischemia or infarction, new appearance of heart block) Transthoracic echo (TTE). Safe, non-invasive, no discomfort, often poor images so lower sensitivity. Transoesophageal (TOE/TEE). Excellent pictures as long as you don’t mind having a big tube pushed down your throat. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration. Easiest if ventilated (but never ventilate just for TOE)

241
Q

What are some peripheral stigmata of infective endocarditis?

A
  1. Petechiae 10 to 15%
  2. Splinter hemorrhages
  3. Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
  4. Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
  5. Roth spots on fundoscopy.
242
Q

How can you diagnose infective endocarditis?

A
  1. Blood cultures
  2. Echo
  3. Urine - microscopic haematuria and proteinuria are common
243
Q

How can you treat infective endocarditis?

A

Native valve endocarditis (NVE):

  1. IV amoxicillin + gentamicin
  2. If penicillin allergic: IV vancomycin

Prosthetic valve endocarditis:

  1. IV vancomycin, gentamicin + rifampacin
244
Q

When do you operate on somebody with infective endocarditis?

A

the infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall) complications (aortic root abscess, severe valve damage to remove infected devices (always needed) to replace valve after infection cured (may be weeks/months/years later To remove large vegetations before they embolise

245
Q

WHAT IS PERIPHERAL VASCULAR DISEASE?

https://www.youtube.com/watch?v=rTbIazck7rk&t=229s

A

Blood vessels outside of your heart and brain to narrow, block, or spasm.

246
Q

What are the three patterns of disease seen in PVD?

A
  1. Intermittent cludication
  2. Critical limb ischaemia
  3. Acute limb-threatening ischaemia
247
Q

What is the classification of PVD called?

What do the numbers mean?

A

—Fontaine

—1 Asymptomatic

—2 Intermittent claudication

—3 Ischaemic rest pain

—4 Ulceration/gangrene (critical ischaemia)

248
Q

What is claudication?

A

Intermittent claudication is a cramp-like, muscular pain in the calf, brought on by exercise and relieved only by rest.

249
Q

What are the symptoms of claudication?

A

Intermittent claudication: aching or burning in the leg muscles following walking

Patients can typically walk for a predictable distance before the symptoms start

Usually relieved within minutes of stopping

Not present at rest

250
Q

What are the investigations for claudication?

A

ABPI
Normal is 1-1.2; PAD is 0.5-0.9 gangene<0.5

Colour Duplex USS
Quick and non-invasive, can show vessels and blood flow within them

MR/CT angiography
Identify stenosesand quality of vessels.

Blood tests
Raised CK-MM, shows muscle damage

251
Q

What is the management for claudication?

A

Medications
1st line - Clopidogrel

Risk factor modification
Quit smoking, treat HTN, lower cholesterol, improve DM control, lower fat diet.

Exercise programmes
Reduce claudication by improving blood flow.

PTA or surgery if severely stenosed

252
Q

WHAT IS CRITICAL LIMB ISCAHEMIA?

A

Critical limb ischaemia results from severe peripheral arterial disease

253
Q

What are the symptoms of critical limb ischaemia?

A

Pale

Pulseless

Painful

Paralysed

Paraesthetic

‘Perishing with cold’

254
Q

What are the investigations for ctitical limb ischaemia?

A

Handheld arterial Doppler examination.

If Doppler signals are present, an ankle-brachial pressure index (ABI) should also be obtained.

255
Q

What is the management for critical limb ischaemia?

A

Initial management

  • ABC approach
  • Analgesia: IV opioids are often used
  • IV unfractionated heparin is usually given to prevent thrombus propagation
  • Vascular review

Definitive management:

  • Intra-arterial thrombolysis
  • Surgical embolectomy
  • Angioplasty
  • Bypass surgery
  • Amputation: for patients with irreversible ischaemia
256
Q

What is critical limb ischaemia due to?

A

May be due to a thrombosis (in ‘vasculopaths’), emboli, graft occlusion or trauma

257
Q

What drugs cuase prolongation of QT interval?

A

Amiodarone

Tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)

Methadone

Erythromycin

Haloperidol

Ondanestron

ΩΩ 2a Bateman - Systems Based (11 decks)

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