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Cardiovascular > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

Basic features of the heart

A
  • Normal weight 280-340 g male, 230-280 g female
  • Two sides, right thinner than left
  • Two stage electrical generated contraction
  • Sarcomere proteins
  • Contraction initiated by depolarisation and changes to calcium concentration
  • Protein conformational change – contraction
  • Removal of calcium (energy dependent) for relaxation to occur
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2
Q

What are the 2 types of cardiac myocytes?

A
  • Atrio-ventricular conduction system – slightly faster conduction
  • General cardiac myocyte
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3
Q

What can all cells do in the heart?

A

Act as a pacemaker
Normal cardiac conduction
Normal coronary circulation
Blood flow through myocardium from aortic root is diastolic

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4
Q

Key features of myocardial hypertrophy and heart failure

A
  • Normal systolic ejection fraction 60-65%
  • Failure to transport blood out of heart = cardiac failure
  • Cardiogenic shock = severe failure
  • Frank–Starling mechanism and pericardial sac limitations
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5
Q

What also increases as venous return increases?

A

Cardiac volume

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6
Q

What happens if you exceed stretch capability of sarcomeres?

A

cardiac contraction force diminishes

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7
Q

What is a hypertrophic response triggered by?

A

angiotensin 2
ET-1
insulin-like growth factor 1
TGF-β

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8
Q

What is left sided cardiac failure?

A

pulmonary congestion and then overload of right side.

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9
Q

What is right sided cardiac failure?

A

venous hypertension and congestion.Right-sided

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10
Q

Congenital heart disease

A

> results from faulty embryonic development
may complicate up to 1% of all live births.
misplaced structures or arrest of the progression of normal structure development.

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11
Q

What happens when there is an initial left to right shunt in congenital heart disease?

A
  • VSD, ASD, PDA, truncus arteriosus, anonymous pulmonary venous drainage, hypoplastic left heart syndrome
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12
Q

What happens when there is right to left shunt in congenital heart disease?

A
  • Tetralogy of Fallot, tricuspid atresia
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13
Q

What happens if there is no shunt in congenital heart disease?

A
  • Complete transposition of great vessels
  • Coarctation
  • Pulmonary stenosis
  • Aortic stenosis
  • Coronary artery origin from pulmonary artery
  • Ebstein malformation
  • Endocaradial fibroelastosis
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14
Q

Anatomy of the pericardium

A

A fibro-serous fluid filled sac
Separates the heart and roots of the great vessels from other mediastinal structures
fibrous and serous
Serous divided into outer parietal and internal visceral (= epicardium)
Fist into balloon = 2 layers and pericardial reflections
Great vessels found here

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15
Q

What is the pericardial cavity?

A

potential space between outer parietal and visceral

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16
Q

What is a cardiac tamponade?

A

rapid collection of pericardial fluid – heart is restricted and impairs filling – when you have more fluid than usual in this area – blood after trauma – that means there isn’t much space in the heart to contract – aware of this space

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17
Q

What is pericarditis?

A

inflammation of pericardium
Chest pain, can cause acute cardiac tamponade due to accumulation of fluid in pericardial cavity
Pleura pericardium peritoneum – all have visceral and parietal – visceral inner parietal outer

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18
Q

Where is the left atrium found?

A

Mainly outside the pericardial space

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19
Q

Pericardium physiology

A

Mechanical function restrains the filling volume of the heart
Similar properties to rubber initially stretchy but becomes stiff at higher tension
Thus pericardial sac has a small reserve volume

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20
Q

Tamponade physiology

A

If this volume is exceeded of the pericardial sac the pressure is translated to the cardiac chambers
Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount

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21
Q

Acute tamponade

A

quickly resolved by smallest volume reduction in pericardial space

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22
Q

Chronic pericardial effusion

A

Chronic accumulation allows adaptation of the parietal pericardium
This compliance reduces the effect on diastolic filling of the chambers
As a result very slowly accumulating effusions rarely cause tamponade

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23
Q

What is acute pericarditis?

A

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion

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24
Q

How can we make a clinical diagnosis of acute pericarditis?

A

Clinical diagnosis made with 2 of 4 from:
Chest Pain (85-90%)
Friction rub (33%)
ECG changes (60%)
Pericardial effusion (up to 60% usually mild)

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25
Q

Infectious causes of acute pericarditis

A

Viral (common): Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis).

Bacterial: Mycobacterium tuberculosis (other bacteria rare).

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26
Q

Autoimmune conditions that can cause pericarditis?

A

Sjögren syndrome, rheumatoid arthritis, scleroderma,
systemic vasculitides

27
Q

Neoplastic conditions that cause acute pericarditis?

A

Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).

28
Q

Metabolic causes of pericarditis?

A

Uraemia, myxoedema,

29
Q

Traumatic and Iatrogenic reasons for pericarditis?

A

Early onset (rare):
Direct injury (penetrating thoracic injury, oesophageal perforation).
Indirect injury (non-penetrating thoracic injury, radiation injury).

Delayed onset: Pericardial injury syndromes (common) iatrogenic trauma (e.g.coronary percutaneous intervention, pacemaker lead insertion and radiofrequency ablation).

30
Q

What percentage of pericarditis diagnoses are idiopathic?

A

Seasonal with viral trends
Higher in young, previously healthy patients

31
Q

Clinical presentations of pericarditis

A

Chest pain:
Severe
Sharp and pleuritic
Rapid onset
Left anterior chest or epigastrium

Other symptoms:
Dyspnoea
Cough
Hiccups (phrenic)
Systemic disturbance
Cancer, Rheumatological Dx, Pneumonia, Cardiac procedure (PCI, ablation), MI

32
Q

What are the differential diagnosis for acute pericarditis?

A

Pneumonia
Pleurisy
Pulmonary Embolus
Chostocondritis
Gastro-oesophageal reflux
Myocardial ischaemia/infarction
Aortic dissection
Pneumothorax

33
Q

What are the investigations for pericarditis?

A

Clinical examination
-Pericardial rub – pathognomonic, crunching snow
-Sinus tachycardia
-Fever
-Signs of effusion (pulsus paradoxus, Kussmauls sign)

ECG
Bloods
CXR
Echocardiogram

34
Q

What is pulsus paradoxus?

A

Normally fall of less than 10mmHg in Bp with inspiration

35
Q

What does the ECG for acute STEMI look like?

A

Segments look like saddle
No PR depression ‘
There is inferior ST depression

36
Q

What is the ECG for pericarditis?

A

Diffuse ST segment elevation
Concave ST segment – may resemble acute injury pattern of STEMI
No reciprocal ST depression
Saddle shaped
PR depression
Mechanism is epicardial inflammation as adjacent to pericardium ( parietal is inert)

37
Q

What would blood tests show for pericarditis?

A

FBC
-Modest increase in White cell count, mild lympocytosis

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

Troponin
-Elevations suggest myopericarditis

CXR
-Often normal in idiopathic
-Pneumonia common with bacterial
-Modest enlargement of cardiac silhouette rule out effusion (>300ml to be detectable!)

38
Q

Management for pericarditis

A

Sedentary activity until resolution of symptoms and ECG/CRP
Probably only applies to athletes - 3 months
NSAID (Ibuprofen 600mg TDS PO 2/52) or Aspirin (750-1000mg BD PO 2/52)
Colchicine (0.5mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence

39
Q

What is the prognosis for acute pericarditis?

A

Most have good long term prognosis
Cardiac tamponade rarely occurs
Constrictive pericarditis may occur in 1% of patients with acute idiopathic pericarditis
15 – 30% of patients with acute pericarditis will develop recurrence
Colchicine reduced recurrence rate by 50%

40
Q

What are the major complications in prognosis for acute pericarditis?

A

Fever >38°C
Subacute onset
Large pericardial effusion
Cardiac tamponade
Lack of response to aspirin or NSAIDs after at least 1 week of therapy

41
Q

What are the minor complications in prognosis for acute pericarditis?

A

Myopericarditis
Immunosuppression
Trauma
Oral anticoagulant therapy

42
Q

Viral causes of pericarditis

A

Commonest cause in developed world
Viral serology futile as self limiting illness

43
Q

Purulent bacterial pericarditis and effusion causes of pericarditis

A

Staph, strep and pneumococci (Pneumonia, empyema)
Rare <1%
Very sick, high mortality

44
Q

Tuberculous effusion TB pericarditis

A

90% HIV +ve in developed countries
17-40% Constrictive pericarditis - high mortality
Pericardectomy (~50% 5 yr survival)

45
Q

Dressler’s syndrome (Post cardiac injury syndromes

A

Late post MI 1-2 weeks post MI

46
Q

What is VTE?

A

Venous thromboemobilism

common and potentially fatal condition.
It involves blood clots (thrombi) developing in the circulation. T
his usually occurs secondary to stagnation of blood and hyper-coagulable states

47
Q

What happens in a DVT?

A

When a thrombus develops in the venous circulation, it is called a deep vein thrombosis (DVT).

48
Q

What is a pulmonary embolism?

A

Once a thrombus has developed can travel (embolise) from the deep veins
Through the right side of the heart and into the lungs,
Becomes lodged in the pulmonary arteries. This blocks blood flow to areas of the lungs

49
Q

What is an atrial septal defect and what can it cause?

A

If the patient has a hole in their heart
the blood clot can pass through to the left side of the heart and into the systemic circulation. If it travels to the brain, it can cause a large stroke.

50
Q

Risk factors of DVT/PE?

A

Immobility
Recent surgery
Long haul travel
Pregnancy
Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
Malignancy
Polycythaemia
Systemic lupus erythematosus
Thrombophilia

51
Q

What do we give to patients to prevent VTE?

A

prophylactic treatment

52
Q

What are thrombophilias?

A

Thrombophilias are conditions that predispose patients to develop blood clots. There are a large number of these:

53
Q

Egs of Thrombophilias?

A

Antiphospholipid syndrome
Factor V Leiden
Antithrombin deficiency
Protein C or S deficiency
Hyperhomocysteinaemia
Prothombin gene variant
Activated protein C resistance

54
Q

What are people with increased risk of VTE given?

A

prophylaxis unless contraindicated. Prophylaxis is usually with low molecular weight heparin, such as enoxaparin.

SE: bleeding or existing anticoagulation with warfarin or a DOAC.

55
Q

Presentation of DVT?

A

Unilateral (BILATERAL very rare)
Calf or leg swelling
Dilated superficial veins
Tenderness to the calf (particularly over the site of the deep veins)
Oedema
Colour changes to the leg

56
Q

Blood test for VTE?

A

D-dimer
It is almost always raised if there is a DVT

57
Q

What is required for a diagnosis of DVE?

A

Doppler ultrasound of the leg

58
Q

What are used to diagnose PEs?

A

CT pulmonary angiogram (CTPA)
ventilation-perfusion (VQ) scan

59
Q

Initial Management of DVT/PE?

A

Anticoagulation
apixaban or rivaroxaban
Started immediately after suspected DVT or PE

60
Q

Long term coagulation options:

A

DOAC
Warfarin
LMWH

61
Q

DOAC

A

oral anticoagulants that do not require monitoring
apixaban, rivaroxaban, edoxaban and dabigatran.

62
Q

Warfarin

A

vitamin K antagonist. The target INR for warfarin is between 2 and 3 when treating DVTs and PEs. It is the first-line in patients with antiphospholipid syndrome

63
Q

Low molecular weight heparin (LMWH)

A

first-line anticoagulant in pregnancy.

64
Q

What is Budd-Chiari syndrome?

A

lood clot (thrombosis) develops in the hepatic vein, blocking the outflow of blood. It is associated with hyper-coagulable states. It causes acute hepatitis.

Cardiovascular (14 decks)

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