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2a Bateman - Phase 2a MASTER DECK > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

HOW CAN ISCHAEMIC HEART DISEASE OCCUR?

A

Reduced blood flow to the heart muscle (clot or atheroma)

Increased distal resistance (LV hypertrophy)

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 a QRISK2 score?

A

Predicts risk of CVD in next ten years.

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4
Q

What does QRISK2 take into account?

A

BP

Age

Smoking status

Cholesterol

RA

DM

Anti-hypertensives

BMI

Ethnicity

Measures of deprivation

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5
Q

WHAT IS ANGINA?

A

Presents with chest pain brought on by exertion but rapidly resolves with rest.

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6
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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7
Q

What are the causes of angina?

A

Mostly atheroma

Anaemia

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8
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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9
Q

What are the tests for stable angina?

A

ECG
Usually normal, may show ST depression and T wave inversion.

Bloods
Anaemia

CXR
Check heart size and pulmonary vessels

Angiogram
Gold standard, shows luminal narrowing

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10
Q

What are the management options for angina pectoralis?

A

Aspirin, Statin, Glyceryl Trinitrate (SL)

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

PCI

Surgery (CABG)

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11
Q

WHAT IS ACUTE CORONARY SYNDROME PATHOLOGY?

A

Plaque rupture, thrombosis, and inflammation.

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12
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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13
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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14
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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15
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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16
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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17
Q

What is the treatment for unstable angina?

A

Anti-platelet agents and Anti-coagulants
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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18
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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19
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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20
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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21
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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22
Q

What is the initial management for a MI?

A

Morphine

—Oxygen

—Nitrates

—Aspirin (or Clopidogrel if aspirin is contraindicted)

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23
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; angiography, clopidogrel and aspirin
—Low risk; clopidogrel.

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24
Q

What are the complications of MI?

A

Cardiac arrest; cardiogenic shock; LVF.

Unstable angina

Bradycardias or heart block.

Tachyarrhythmias

Pericarditis

DVT & PE

Systemic embolism

Cardiac tamponade

Mitral regurgitation

Ventricular septal defec

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25
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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26
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.

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27
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)

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28
Q

What are the symptoms of PVD?

A

Cramping pain in calves, thighs and buttocks relieved by rest

Also known as claudication

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29
Q

What are the signs of PVD?

A

Absent pulses

Punched out ulcers

Postural colour change (Buerger’s Test)

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30
Q

What are the tests for PVD?

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

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31
Q

What are the management options for PVD?

A

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

Medications
Anti-platelet, clopidogrel is recommended as 1st line.

Exercise programmes
Reduce claudication by improving blood flow.

PTA or surgery if severely stenosed

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32
Q

What is critical limb ischaemia due to?

A

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

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33
Q

What are the 6 P’s of peripheral limb ischaemia?

A

Pain

Pallor

Pulselessness

Paresthesis

Paralysis

Perishing cold

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34
Q

What are the options for critical limb ischaemia?

A

If not revascularized then lose limb

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35
Q

WHAT IS SHOCK?

A

Circulatory failure resulting in inadequate organ perfusion

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36
Q

What is shock defined as?

A

Low BP

Evidence of tissue hypoperfusion.

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37
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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38
Q

What is the main cause of injury from shock?

A

Prolonged hypotension can lead to life threatening organ failure

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39
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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40
Q

WHAT IS HYPOVALEMIC SHOCK?

A

Low circulating blood volume

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41
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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42
Q

How do you treat hypovalaemic shock?

A

Identify and treat underlying cause.

Raise the legs.

Give fluids

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43
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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44
Q

What are some causes of cardiogenic shock?

A

MI

Arrhythmias

PE

Tension pneumothorax

Cardiac tamponade

Myocarditis

Endocarditis

Aortic dissection

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45
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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46
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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47
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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48
Q

WHAT IS SEPSIS?

A

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

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49
Q

What is septic shock?

A

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

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50
Q

What are the risk factors for septic shock?

A

Age

Diabetes mellituis (DM)

Immunocompromised

Alcoholics

Burns

IVDU

Pregnancy

Catheter

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51
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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52
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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53
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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54
Q

WHAT IS ANAPHYLATIC SHOCK?

A

Intense allergic reaction.

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

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55
Q

What type of hypersensitivity is this reaction?

A

Type-I IgE-mediated hypersensitivity reaction.

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56
Q

What are some causes of anaphylatic shock?

A

Drugs, eg penicillin, and contrast media in radiology
Latex
Stings, eggs, fish, peanuts, strawberries, semen (rare)

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57
Q

What are the signs and symptoms of anaphylatic shock?

A

Itching, sweating, diarrhoea and vomiting, erythema, urticaria, oedema

Wheeze, laryngeal obstruction, cyanosis

Tachycardia, hypotension

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58
Q

What is the management of anaphylatic shock?

A

Oxygen

Remove the cause

Adrenaline IM

IV fluids
Chlorphenamine (antihistamine) and hydrocortisone (steroid)

If wheeze, treat for asthma

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59
Q

WHAT IS NEUROGENIC SHOCK?

A

Distributive

Disruption of the autonomic pathways within the spinal cord

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60
Q

What can cause neurogenic shock?

A

Spinal cord injury

Epidural

Spinal anaesthesia

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61
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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62
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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63
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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64
Q

WHAT IS ARDS?

A

Acute Respiratory Distress Syndrome

Impaired oxygenation

Bilateral pulmonary infiltrates

No cardiac failure / normal PAOP

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65
Q

What processes are involved with ARDS?

A

Alveolar capillary membrane injury
Non-cardiogenic pulmonary oedema
Neutrophil influx

Exudative phase

Proliferative phase
Reorganisation of exudates, fibroblast proliferation

Fibrotic phase
Scarring

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66
Q

What are some causes of ARDS?

A

Extrapulmonary Causes

Pulmonary Causes

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67
Q

What are some extrapulmonary causes of ARDS?

A

Extrapulmonary Causes
Shock of any cause
Head injury
Drug reaction
Sepsis

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68
Q

What are some pulmonary causes of ARDS?

A

Pulmonary Causes
Pneumonia
Chemical pneumonitis
Smoke inhalation
Near drowning

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69
Q

WHAT DOES CARDIOMYOPATHY REFER TO?

A

Primary heart muscle disease – often genetic.

Three types.

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70
Q

WHAT IS HYPERTROPHIC CARDIOMYOPATHY?

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

A

Heart muscle becomes thick, heavy and hypercontactile.

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71
Q

What is Hypertrophic cardiomyopathy (HCM) caused by?

What inheritance is it?

A

Sarcomeric protein gene mutations.

Autosomal dominant inheritance.

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72
Q

What is the epidemology of HCM?

A

Leading cause of death in the young

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73
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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74
Q

What type of heart failure if HCM?

A

Diastolic heart failure

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75
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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76
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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77
Q

What are the symptoms of HCM?

A

Sudden death.

Fast arrythmias

Palpitations

Dyspnoea

Dizzy spells or syncope

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78
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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79
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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80
Q

What is the treatment for HCM?

A

Beta-blockers or verapamil for symptoms.

Amiodarone for arrhythmias (AF, VT).

Anticoagulate for paroxysmal AF or systemic emboli.

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81
Q

What drug is contraindicated in HCM?

A

Digoxin

Increase contraction force, increase obstruction

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82
Q

WHAT IS DILATED CARDIOMYOPATHY (DCM)?

A

Causes all four chambers of the heart to enlarge

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83
Q

What is Dilated cardiomyopathy (DCM) often caused by?

A

Alcohol

Increased BP

Haemochromatosis

Viral infection

Autoimmune

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84
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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85
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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86
Q

What are the symptoms of DCM?

A

Fatigue

Dyspnoea

Pulmonary oedema

Right ventricular failure

Emboli

Atrial fibrillation

Ventricular tachycardia

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87
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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88
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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89
Q

What is the treatment for DCM?

A

Digoxin

Diuretics

ACE-i

Anticoagulation

Bi-ventricular pacing

Cardiac transplantation.

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90
Q

WHAT IS RESTRICTIVE CARDIOPATHY?

A

Heart muscle becomes stiff and less compliant

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91
Q

What diseases commonly cause RCM?

A

Amyloidosis

Familial amyloid cardiomyopathy
Afro-americans

Senile cardiac amyloidosis
Elderly

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92
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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93
Q

What happens in amyloidosis?

A

Proteins that have been misfolded and become insoluble

Deposit in tissue in organs making them become less compliant

Familial amyloid cardiomyoopathy
Mutant transthyretin protein misfolded and prone to deposit in heart tissue
Normally transport thyroxine and retionol

Senile cardiac amyloidosis
Normal TTR deposits in heart

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94
Q

What is the pathology of RCM?

A

Heart muscle stays same size

When blood comes in heart doesn’t stretch

Less blood

Less pumped out

Heart failure

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95
Q

What type of heart failure is RCM?

A

Diastolic heart failure

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96
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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97
Q

What are the investigations for RCM?

A

ECG
Low amplitude QRS

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98
Q

What is the treatment for RCM?

A

Treat underlying cause

Heart transplant

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99
Q

What do all cardiomyopathies carry?

A

An arrhythmic risk.

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100
Q

WHAT IS INHERITED ARRHYTHMIA (CHANNELOPATHY) CAUSED BY?

A

Ion channel protein gene mutations.

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101
Q

Which ions are involved with channelopathy?

A

potassium, sodium or calcium channel.

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102
Q

What do channelopathies include?

A

Long QT, short QT, Brugada and CPVT.

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103
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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104
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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105
Q

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

A

Normal heart/arrhythmia.

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106
Q

What are common problems to be inherited?

A

Aortic aneurysm or dissection.

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107
Q

WHAT IS AN ANEURYSM?

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

A

Abnormal buldge in vessel

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108
Q

What are the risk factors for aneurysms?

A

Male

Over 60

Hypertension

Smoking

109
Q

What are the typical causes of an anneurysm

A

Atheroma

Trauma

Infection

Connective tissue disorders

Inflammations

110
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

111
Q

When is an aneurysm official labelled an aneurysm?

A

When the diameter exceeds 1.5 times the normal size

112
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.

113
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).

114
Q

What happens when an aneurysm explodes?

A

Blood spurts out of the hole

Less blood goes downstream

Ischaemia of downstream cells

115
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

116
Q

What are the diagnosis options for an aneurysm?

A

Often incidental finding

Ultrasound

CT

MRI

117
Q

What are the options for a unruptured anneurysm?

A

Elective surgery.

Stenting.

118
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

119
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

120
Q

Where does aortic dissection normally occur?

A

Within the first 10cm of aorta

121
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

122
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%)

123
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

124
Q

What are the investigations for aortic dissection?

A

CXR
Widend aorta

Transoesophageal echo
True lumen and flase aorta

Angiogram

125
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

126
Q

WHAT AORTAVASCULAR SYNDROMES ARE THERE?

A

Marfan, Loeys-Dietz, vascular Ehler Danlos (EDS).

127
Q

What are ICCs inheritance?

A

Dominantly with a 50% risk.

128
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.

129
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.

130
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.

131
Q

WHAT IS CARDIAC TAMPONADE?

A

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

132
Q

What is the cause of cardiac tamponade?

A

Any pericarditis

Aortic dissection

MI

Trauma

Trans-septal puncture at cardiac catheterization

Cancer

133
Q

What are the signs of cardiac tamponade?

A

Pulse increase

BP decerease

Pulsus paradoxus

JVP increase

Kussmaul’s sign

Muffled S1 and S2.

134
Q

What is Beck’s triad?

A

Falling BP

Rising JVP

Muffled heart sounds.

135
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.

136
Q

What is the management of cardiac temponade?

A

The pericardial effusion needs urgent drainage

137
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.

138
Q

WHAT IS PERICARDIAL EFFUSION?

A

Accumulation of fluid in the pericardial sac.

139
Q

What are the causes of pericardial effusion?

A

Any cause of pericarditis.

140
Q

What are the symptoms of pericardial effusion?

A

Dyspnoea

Raised JVP

Bronchial breathing at left base

Look for signs of cardiac tamponade

141
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.

142
Q

What are the management options for pericardial effusion?

A

Treat the cause.

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

143
Q

WHAT IS ACUTE PERICARDITIS?

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

A

Inflammatory pericardial syndrome with or without effusion.

144
Q

What are most cases of pericarditis?

A

Idiopathic.

145
Q

What are the viral (common) causes of acute pericarditis?

A

Enteroviruses
Coxsackie B viruse

Herpesviruses (EBV, CMV, HHV-6),

146
Q

What is a syndrome assocaiated with pericarditis?

A

Dresseler’s syndrome

Happens after heart attack

When an MI happens lots of necrosis
This also affects the pericardium

147
Q

What is uremic pericarditis?

A

Blood levels of urea and nitrogen get high

Due to kidney problems

Iritate serous pericardium

Secrete thick pericardial fluid
Full of fibrin strands and white blood cells

Wall of pericarditis gets a buttered bread apperance

148
Q

What autoimmune disease are associated with pericarditis?

A

Rheumatoid arthritis

Scleraderma

SLE

149
Q

What is the patholgy of pericarditis?

A

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

150
Q

What happens when the serous pericardium becomes more and more fibrous?

A

Hard for the heart to expand and relax

Stroke volume goes down

Heart rate goes up

151
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

152
Q

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

A

2 of 4 of:

Chest pain.

Friction rub.

ECG changes.

Pericardial effusion.

153
Q

What is the differential diagnosis of pericarditis?

A

Pneumonia
Pleurisy
Pulmonary embolus
Chostocondritis
Gastro-oesophageal reflux
Myocardial ischaemia/infarction.
Aortic dissection

154
Q

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

A

Clinical examination
Pericardial rub
Sinus tachycardia
Fever
Signs of effusion (pulsus paradoxus, Kussmauls sign)

ECG

Bloods

CXR
Silouette

Echocardiogram

155
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

156
Q

What would blood tests show in tests of pericarditis?

A

FBC
Modest increase in WCC, mild lympocytosis

ESR & CRP
High ESR may suggest aetiology
ANA in young females - SLE

Troponin
Elevations suggest myopericarditis

157
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.

158
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

159
Q

How do you calculate cardiac output?

A

CO = HR x SV

160
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.

161
Q

What is systolic heart failure?

A

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

Ejection fraction (EF) is <40%

162
Q

What are the causes of systolic heart failure?

A

IHD

MI

Cardiomyopathy.

163
Q

What is diastolic heart failure?

A

Inability of the ventricle to relax and fill normally

Causing increased filling pressures.

EF is >50%.

164
Q

What are the causes of diastolic heart failure?

A

Constrictive pericarditis

Tamponade

Restrictive cardiomyopathy

Hypertension

165
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).

166
Q

What are some causes of left sided heart failure?

A

Hypertension

167
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)

168
Q

What are some causes of right ventricular failure?

A

LVF, pulmonary stenosis, lung disease.

169
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.

170
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

171
Q

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

A

ABCDE

Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated prominant upper lobe vessels
Pleural Effusion

172
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

173
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

174
Q

What does angiotensin 2 produce?

A

Increase salt and water retention

Increased preload, extra strain on heart

175
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

176
Q

WHAT IS TETRALOGY OF FALLOT?

A

Pulmonary stenosis

RV hypertrophy

Overriding aorta

VSD

177
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

178
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

179
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.

180
Q

What is the management of tetrology of Fallot?

A

Surgery

181
Q

WHAT IS VENTRICULAR SEPTAL DEFECTS?

A

Hole in the connecting venticles

182
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

183
Q

What are the causes of VSD?

A

Congenital

Acquired (post-MI).

184
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.

185
Q

What is the treatment for VSD?

A

Large

Require fixing in infancy (PA band, complete repair)

Small

Endocarditis risk

Need no intervention

186
Q

What may VSD lead to?

A

May lead to Eisenmengers syndrome.

187
Q

What is Eisenmengers syndrome?

A

High pressure pulmonary blood flow

Damages to delicate pulmonary vasculature

The resistance to blood flow through the lungs increases

The RV pressure increases

The shunt direction reverses

The patient becomes BLUE.

188
Q

WHAT IS ATRIAL SEPTAL DEFECT?

A

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

Common

Often present in adulthood.

189
Q

What are the two types of ASD?

A

Primum: present earlier, may involve AV valves

Secundum: may be asymptomatic until adulthood

190
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

191
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

192
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).

193
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

194
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.

195
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.

196
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

197
Q

WHAT IS PATENT DUCTUS ARTERIOSUS?

A

Failure of ductus arterioles to close.

198
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)

199
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

200
Q

How do you close the ductus arterioles?

A

Surgical or percutaneous.

Local anaesthetic.

Venous approach.

201
Q

WHAT IS COARCTATION OF THE AORTA?

A

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

202
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

203
Q

What are the clinical signs of coarctation of the aorta?

A

Right arm hypertension

Bruits (buzzes) over the scapulae and back from collateral vessels

Murmur

204
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

205
Q

What is the treatment of coarctation of the aorta?

A

Surgery, or balloon dilatation ± stenting.

206
Q

WHAT IS BICUSPID AORTIC VALVE?

A

Normal AV valves has three cusps.

This has two

207
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

208
Q

How can you treat bicuspid aortic valve?

A

Surgery

209
Q

WHAT IS PULMONARY STENOSIS?

A

Narrowing of the outflow of the right ventricle.

Valvar.

Sub valvar.

Supra valvar.

Branch.

210
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

211
Q

What is the treatment for pulmonary stenosis?

A

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

212
Q

WHAT IS HYPERTENSION?

A

Over 140/90

213
Q

What are the two types of hypertension?

A

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

Secondary hypertension ~5% of cases.

214
Q

What are some causes of secondary hypertension?

A

Renal
CKD

Endocrine disease
Conn’s syndrome

Others
Coarctation, pregnancy

215
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

216
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

217
Q

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

A

Calcium channel blocker

Amlodipine

Nifedipine

Verapamil

218
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

219
Q

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

A

The other one

220
Q

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

A

Thiazide like diuretic

Chlorothiazide

Hydrocholrothiazide

221
Q

How can renal artery stenosis cause hypertension?

A

Less blood flow to kidneys

Secretes Renin

More water and salt retention

Higher BP

222
Q

What is a pheochromocytoma? How does it cause hypertension?

A

Tumour on adrenal glands

Constantly produce catecholamines

Increase heart rate and peripheral vascular resistance

Increase BP

223
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

224
Q

How does Conn’s syndrome cause hypertension?

A

High aldosterone

Increased sodium and water retention

Increased BP

225
Q

WHAT IS AORTIC STENOSIS?

A

Hardening of the aorta

226
Q

What is the normal aorta valve area?

A

3-4 cm2

227
Q

When do aortic stenosis symptoms occur?

A

When the valve area is 1/4th of normal.

228
Q

What are the different types of aortic stenosis?

A

Supravalvular

Subvalvular

Valvular.

229
Q

What can congenital aortic stenosis occur with?

A

Unicuspid, bicuspid and tricuspid valve.

230
Q

What is the cause of aortic valve stenosis

A

Congenital bicuspid valve

Degenerative calcification

Rheumatic Heart disease

231
Q

What is rheumatic heart disease?

A

Fusion of cusps.

232
Q

How does a person with aortic stenosis present?

A

Syncope

Angina

Dyspnoea

Sudden death

233
Q

What physical signs would you hear on aortic stenosis?

A

Slow rising carotid pulse (pulsus tardus)
& decreased pulse amplitude (pulsus parvus)

Heart sounds- soft or absent second heart sound, S4 gallop due to LVH.

Ejection systolic murmur- crescendo-decrescendo character.

234
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

235
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

236
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.

237
Q

What are the aetiologies of chronic mitral valve regurgitation?

A

Myxomatous degeneration (MVP)

Ischemic MR

Rheumatic heart disease

Infective Endocarditis.

238
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

239
Q

What are the symptoms of mitral valve regurgitation?

A

Exertion dyspnoea –exercise intolerance

Palpitations

Fatigue

240
Q

What are the signs of mitral valve regurgitation?

A

Pansystolic murmur at apex radiating to axilla

Soft S1

Displaced hyperdynamic apex

241
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

242
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

243
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.

244
Q

WHAT IS AORTIC VALVE REGURGITATION?

A

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

245
Q

What is the cause of AR?

A

Bicuspid aortic valve

Rheumatic

Infective endocarditis.

246
Q

What is the pathophysiology of AR?

A

Combined pressure AND volume overload

Compensatory Mechanisms: LV dilation, LVH

Progressive dilation leads to heart failure

247
Q

What are the symptoms of aortic valve regurgitation?

A

Exertional dyspnoea

Orthopnoea

Paroxysmal nocturnal dyspnoea

248
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)

249
Q

What would cardiac tests show you for AR?

A

CXR
Cardiomegaly

ECHO
LV dilation and hypertrophy

250
Q

What is the management for AR?

A

Vasdilators
ACEi only if symptomatic or HTN

Surgical
Replace valve before LV dysfunction

251
Q

WHAT IS MITRAL VALVE STENOSIS?

A

Obstruction of LV inflow that prevents proper filling during diastole

252
Q

What is the aetiology of mitral valve stenosis?

A

Rheumatic heart disease

Infective endocarditis

Mitral annular calcification.

253
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

254
Q

What are the symptoms of MS?

A

Dyspnoea

Fatigue

Palpitations

Chest pain…

255
Q

What are the signs in MS?

A

Malar flush on cheeks

Low volume pulse

Tapping, non displaced apex beat

Rumbling mid-diastolic murmur

Loud opening S1

256
Q

What tests can you do on MS 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

257
Q

How would you manage a patient with MS?

A

If in AF, rate control

Anticoagulatewith warfarin

Diuretics

Percutaneous mitral balloon valvotomy

258
Q

WHAT IS INFECTIVE ENDOCARDITIS?

A

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc). It’s like a really bad infection, but with the added extras of showering infectious crap all around your bloodstream, and/or eating holes in your heart valves.

259
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.

260
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

261
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.

262
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

263
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.

264
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)

265
Q

What are some peripheral stigmata of infective endocarditis?

A

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

266
Q

How can you diagnose infective endocarditis?

A

Cultures may remain negative in 2% to 5% of patients with IE. Certain organisms: cell media; special media or microbiological methods, or may require long incubtion 7-21/7. The most common cause for negative blood cultures in patients with IE is prior antimicrobial therapy. WBC is rarely helpful. Raised CRP is almost always present.

267
Q

How can you treat infective endocarditis?

A

Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc Surgery.

268
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

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