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2A > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

where can thrombosis occur?

A
  • arterial circulation: high pressure: platelet rich
  • venous circulation: low pressure fibrin rich
  • Coronary circulation
  • Cerebral circularion
  • Peripheral circulation
  • Other territories
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2
Q

what causes Arterial thrombosis?

A

Atherosclerosis
Inflammation
Infection
Trauma
Tumours

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3
Q

what are Arterial thrombosis Presentations?

A

Myocardial infarction
CVA - stroke
Peripheral vascular disease
Others

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4
Q

what is Leriche Syndrome?

A

occlusion in the distal aorta or proximal common iliac artery
traid of:
Thigh/buttock claudication
Absent femoral pulses
Male impotence

claudation mean pain due to lack of oxygen

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5
Q

what is Buerger’s Test?

A

assesses for peripheral vascular disease
- legs lifted for 1-2 mins - pallor observed
- sitting with legs hanging - blue then dark red due to vasodilation
healthy response is remaining pink colour

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6
Q

what are Arterial coronary thrombosis treatments?

A
  • aspirin/antiplatelets
  • LMWH or Fondaparinux or UFH
  • Thrombolytic therapy: streptokinase tissue plasminogen activator
  • Reperfusion – Catheter directed treatments and stents
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7
Q

what is Prinzmetal’s angina?

A
  • transient episodes of coronary artery spasm
  • occurs at rest/sleep
  • calcium channel blockers
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8
Q

what are the treatments for Arterial cerebral thrombosis (stroke)?

A
  • Aspirin, other anti-platelets, Thrombolysis - eg for stroke
  • Catheter directed treatments (eg blasting thrombus), Reperfusion
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9
Q

what are treatments of thrombosis in other arterial sites of the body?

A
  • Antiplatelets
  • statins
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10
Q

what are venous thrombosis signs/symptoms?

A

non -specific
- can be calf pain, chest pain, breathlessness

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11
Q

what is a blood test for venous thrombosis?

A

D-dimer - not specific
- used to show theres no thrombus

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12
Q

how is a venous thrombus usually diagnosed?

A

imaging eg MRI

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13
Q

what is virchows triad?

A

factors that contribute to the development of thrombosis:
- blood flow - immobilisation - eg - long flights, surgury
- endothelium injury - trauma, infection
- blood constituents - genetic or conditions that lead to Hypercoagulability

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14
Q

what are the treatments for venous thrombosis?

A

Heparin or LMWH
Warfarin
DOAC - anticoagulants

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15
Q

what are preventions for venous thrombosis?

A
  • Mechanical or chemical thromboprophylaxsis - stockings
  • early mobilisation and good hydration
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16
Q

how is heparin given?

A

IV, continusly given, closely monitered

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17
Q

how is Low molecular weight heparin given?

A

Once daily, weight-adjusted dose given subcutaneously

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18
Q

what factors synthesis does warfarin prevent?

A

2, 7, 9, 10
(Antagonist of vitamin K)

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19
Q

what do New Oral Anticoagulant Drugs NOAC / DOAC act on?

A

factor 2 & 10

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20
Q

when is aspirin prescribed?

A

arterial thrombosis
- Inhibits thromboxane formation

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21
Q

how does clopidogrel act as an antiplatelet?

A

inhibits ADP induced platelet aggregation by irreversibly binding to the p2y12 receptors

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22
Q

what are signs/symptoms of DVT?

A

Symptoms: leg pain, swelling
Signs: tenderness, swelling, warmth, discolouration

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23
Q

what are signs/symptoms of pulmonary embolism and what can cause it?

A
  • symptoms - breathlessness, pleuritic chest pain, syncope
  • Signs: tachycardia, tachypnoea, pleural rub,
    Signs of DVT
  • complication of DVT
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24
Q

what is a complications of pulmonary embolism?

A

Chronic thromboembolic pulmonary hypertension (CTEPH
- from fibrous tissue blocking vasculature

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25
Q

what is Pulmonary Embolism Differential diagnosis?

A

acute coronary syndrome
pneumonia
HF
Pneumothorax
musculoskeletal
pericarditis

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26
Q

how is pulmonary embolism treated?

A
  • Supportive treatment - eg O2
  • Anticoagulants: LMW Heparin & Oral warfarin, DOAC/NOAC
  • Treat underlying cause
  • embolectomy if severe
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27
Q

what are outcomes of atherosclerosis?

A
  • ulceration
  • thrombosis - acute ischemia
  • growth - chronic ischemia
  • necrosis - aneurysm development
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28
Q

what is acute/chronic lower limb ischaemia?

A

acute - 6Ps - acute-embolus (normally in heart - clots moves to peripheral circulation)
- includes acute on chronic ishaemia

chronic - rest pain, tissue loss

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29
Q

investigations of peripheral vascular disease

A
  • physical examination - eg ulcers, hair loss, pallor
  • Ankle-brachial pressure index (ABPI)
  • Duplex ultrasound – shows the speed and volume of blood flow
  • Angiography (CT or MRI)
  • hand held doppler - weak pulse
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30
Q

management of limb ischaemia/caudation

A

caudation:
- lifestyle changes/exercise
- mediaction - Atorvastatin,Clopidogre
- bypass/stenting
ischaemia:
- Endovascular angioplasty and stenting
- Endarterectomy
- Endovascular thrombectomy/thrombolysis using catheter
- bypass surgery

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31
Q

what are 6Ps in limb ischaemia?

A

pain, pulselessness, pallor, poikilothermia, paresthesias, and paralysis

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32
Q

when is bypass surgery used in peripheral vascular disease?

A

(graft of vein)
after stents fail
- better patency and limb salvage rates

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33
Q

what are the treatment options for aortic aneurysm?

A
  • endovascular - stents - require more follow ups etc.
  • open surgery - no further follow ups or treatments - prefered option for long-term outcomes
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34
Q

what are the symptoms of aortic aneurysm?

A

-normally asymptomatic until severe
- Pain in the chest, abdomen, or back
- Hoarseness or difficulty swallowing (TAA)
- Shortness of breath
- Pulsating sensation in the abdomen
- (pre)Syncope
- Signs of shock (in cases of a ruptured aneurysm)

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35
Q

what is the most common aortic aneurysm?

A

abdominal
thoracic

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36
Q

what are treatments for venous disease

A
  • lifestyle
  • compression
  • sclerotherapy- injection causing vein to shrink
  • endo-venous
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37
Q

what is Cor pulmonale?

A
  • pulmonary heart disease
  • right side of the heart becomes enlarged/strained due to pulmonary hypertension
  • eg due to pulmonary embolism/fibrosis, COPD, Interstitial lung diseases, sleep apnea
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38
Q

What are pulmonary embolism investigations?

A
  • PE Wells score over 4=likely
  • D-dimer - +ve - measure blood clots
  • CT Pulmonary Angiography (CTPA) - gold
  • echo/ecg
  • xray - rules out pneumonia etc.
  • blood gases - t1 resp failure, decreased o2 and co2
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39
Q

what are risk factors for Pulmonary embolism?

A
  • DVT.
  • Recent surgery.
  • Significant immobility.
  • Active cancer.
  • pregnancy/postpartum
  • recent MI
  • increasing age
  • smoking, obesity, contraceptives
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40
Q

what is massive pulmonary embolism?

A

haemodynamic instability
- HYPOTENSION, cyanosis, severe dyspnoea, right heart strain/ failure
- rare
- clot is bigger and more severe symptoms

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41
Q

what can atherosclerosis cause?

A

heart attack, stroke etc.
- due to plaque rupture leading to thrombus formation, partial/complete arterial blockage leading to a heart attack

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42
Q

where are atherosclerotic plaques mainly found?

A

within peripheral and coronary arteries

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43
Q

what do atherosclerotic plaques consist of?

A

Lipid/ fatty streak
Necrotic core
Connective tissue
Fibrous “cap”

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44
Q

what is the first step in atherosclerosis progression?

A

fatty streaks
- aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall

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45
Q

what is the second step in atherosclerosis progression?

A

intermediate lesions:
layers of:
- foam cells
-Vascular smooth muscle cells
- T lymphocytes
- Adhesion and aggregation of platelets to vessel wall
- Isolated pools of extracellular lipid

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46
Q

what is the third step in atherosclerosis progression?

A

fibrous plaques/advanced lesions
- impede blood flow, may rupture
- covered by dense fibrous cap

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47
Q

what is the fourth step in atherosclerosis progression?

A

plaque rupture
- due to Fibrous cap not being resorbed and redeposited - eg due to inflammation cap weakens
- thrombus/clot formation and vessel occlusion

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48
Q

what is the fifth step in atherosclerosis progression?

A

plaque erosion
- can cause coronary thrombosis

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49
Q

what is the difference between plaque ruption and plaque erosion?

A

ruptured - large lipid core and inflammatory cells
erosion - small lipid core, disrupted endothelium, more fibrous tissue and a larger lumen

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50
Q

what is the treatment for coronary heart disease?

A
  • Percutaneous Coronary Intervention PCI
    (widens blocked arteries)
    (especially in STEMI)
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51
Q

What is the difference between STEMI and NSTEMI?

A

STEMI - complete blockage of coronary artery, more urgent
NSTEMI - partial blockage (ST-depression, T-wave inversion)

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52
Q

what is aspirin an irreversible inhibitor of?

A

platelet cyclo-oxygenase

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53
Q

what do statins inhibit?

A

HMG CoA reductase - reducing cholesterol synthesis

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54
Q

what kind of drugs can be used if statins are ineffective or not tolerated?

A

drugs that target PCSK9

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55
Q

what are acute coronary syndromes?

A

spectrum of conditions which include myocardial infarction with or without ST-segment-elevation, and unstable angina.

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56
Q

what is unstable angina an how is it diagnosed?

A

Clinical classification includes:
*Cardiac chest pain at rest
*Cardiac chest pain with crescendo pattern
*New onset angina
Diagnosis: history
ECG
troponin

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57
Q

what is the difference in symptoms between unstable/stable angina?

A

unstable - at rest, longer, more frequent
stable - with exercise/exertion, shorter, predictable

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58
Q

why is unstable angina more serious then stable angina?

A

unstable - ruptured/ unstable coronary artery plaques, can lead to heart attack
stable - narrowed but stable coronary artery plaques, usually no blockage

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59
Q

what other way may MI be classified?

A

Q-wave or non Q wave

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60
Q

what are risk factors of MI?

A

age
diabetes
renal failure
left ventricular systolic dysfunction

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61
Q

what signs/symptoms show MI?

A

cardiac chest pain - unremitting, severe but may be mild, occurs at rest
associated with sweating, breathlessness, nausea and vomiting

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62
Q

what is initial management of MI?

A
  • aspirin 300mg immediately
  • pain relief - opiates/nitrates
  • o2 if hypoxic
  • aspirin +/- platelet P2Y12 inhibitor
  • consider beta-blockers
  • Consider urgent coronary angiography e.g. if
    troponin elevated or unstable angina refractory
    to medical therapy
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63
Q

what is type 1 myocardial infarction?

A

Myocardial infarction due to atherothrombosis

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64
Q

what causes most acute cardiac syndromes

A

Rupture of an atherosclerotic plaque and
consequent arterial thrombosis

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65
Q

what are some causes of type 2 MI?

A
  • drug abuse
  • pulmonary embolism
  • anaemia
  • haemorrhage
  • thyrotoxicosis
  • sepsis - causing o2 mismatch
    (imbalance between supply and demand other than coronary artery disease)
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66
Q

what is Tako-Tsubo/stress-induced cardiomyopathy?

A
  • due to extreme emotional distress
  • cause left ventricular systolic
    dysfunction    , typically ballooning of the left
    ventricular apex during systole
  • reversible within couple weeks
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67
Q

what does troponin show?

A

markers for cardiac muscle injury

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68
Q

what are the 3 P2y12 inhibitors?

A

thienopyridines - clopidogrel & prasugrel (better prodrug) - irreversible
ticagrelor - reversible - more rapid offset

used in antiplatelet therapy and in ACS

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69
Q

what are Adverse effects of P2Y12 inhibitors?

A

Bleeding e.g. epistaxis, GI bleeds, haematuria
Rash
GI disturbance
ticagrelor - Dyspnoea (shortness of breath), Ventricular pauses

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70
Q

what are features of GPIIb/IIIa antagonists?

A
  • used in combination, only IV
  • increase risk of major bleeding
  • reduced use due to better antiplatelet therapy
  • used in patients with delayed absorption of oral P2Y12 inhibitors
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71
Q

what do anticoagulants target?

A

formation/activity of thrombin
- Inhibit both fibrin formation and platelet activation

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72
Q

what are the main anticoagulants?

A

fondaparinux or heparin

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73
Q

what acute coronary syndrome is revascularisation used for?

A

NSTE
high risk unstable angina

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74
Q

what are some predisposing factors for ischaemic heart disease?

A
  • age
  • smoking
  • family history
  • diabetes
  • high BP, high lipids
  • kidney disease
  • obesity
  • physical inactivity
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75
Q

what are symptoms of ischaemic heart disease?

A
  • chest pain
  • breathlessness
  • fluid retention
  • palpitations
  • Syncope or pre-syncope - fainting
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76
Q

what are some differential diagnosis of ischaemic heart disease?

A

Pericarditis/ myocarditis - inflammation
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Dissection of the aorta
Gastro-oesophageal (reflux, spasm, ulceration)
Musculo-skeletal
Psychological

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77
Q

how is ischaemic heart disease treated?

A

lifestyle changes
asparin, Beta blockers, statins

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78
Q

what are the side effects of beta blockers?

A

tiredness, nightmares
erectile dysfunction
cold hands and feet

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79
Q

how do nitrates affect the heart?

A

vasodilation
- lower BP and afterload, in turn lowering venous return and preload
- reduce oxygen demand of the heart

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80
Q

how do Ca channel blockers affect the heart?

A
  • lower BP, lower O2 demand
  • Suppression of Abnormal Rhythms
  • increase blood flow
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81
Q

what is an antiplatelet agents (aspirin) side effect?

A

gastric ulceration

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82
Q

how do ACE inhibitors (ramipril) effect the cardiovascular system?

A
  • inhibit angiotensin 2 synthesis that cause vasoconstriction
  • LOWER BP
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83
Q

what are chronic coronary syndromes?

A

chronic mismatch between supply and demand in myocardial oxygen conspumtion

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84
Q

what medication is given for chronic coronary syndromes?

A

aspirin
b blockers
nitrates

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85
Q

what psychosocial factors can effect coronary heart diease?

A
  • anxiety/depression
  • lack of social support
  • work/family life - stress
  • ## anger/hostility
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86
Q

how are pscychosocial factors related to CHD assesed and what is done about it?

A
  • assessed by clinical interview or standardized questionnaires
  • in cases with increased risk multimodal, behavioural intervention, integrating counselling
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87
Q

what is Coronary Prone Behaviour Pattern?

A

‘type A’ behaviour
- eg highly competitive, ambitious, aggressive

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88
Q

what happens to a muscle during depolarisation?

A

contraction

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89
Q

what is the standard calibration of an ECG?

A

25mm/s
0.1 mV/mm

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90
Q

what does the p wave in an ECG show?

A

atrial depolarisation

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91
Q

what does the QRS wave show in an ECG?

A

ventricular depolarisation

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92
Q

what does the T wave show in an ECG?

A

ventricular repolarisation

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93
Q

what does the PR interval show in and ECG?

A
  • represents the time for electrical activity to move between the atria and the ventricles
  • time between atria depolarisation and ventricular depolarisation

(between P and Q point)

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94
Q

what are the 12 leads in an ECG?

A

3 standard limb leads
3 augmented limb leads
6 precordial leads

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95
Q

what is a normal PR interval range?

A

120 to 300 ms
(3 to 5 little squares)

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96
Q

what should the width of a QRS complex be?

A

less than 110 ms ( 3 little squares)

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97
Q

what leads is the QRS complex are upright?

A

lead 1 and 2

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98
Q

the QRS and what wave tend to have the same general direction in the limb leads?

A

T wave

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99
Q

in lead aVR, what are all the waves?

A

negative

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100
Q

where does the R and S wave increase in size?

A

R wave - V1 to at least V4
S wave - V1 to at least V3, disappear in V6

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101
Q

what part of a normal ECG may a ST segment be elevated?

A

V1 and V2
starts isoelectric

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102
Q

where is the P wave upright in a normal ECG?

A

1, 2, V2 to V6

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103
Q

what part of the ECG is there no Q wave (or less than 0.04s)?

A

1, 2, V2 to V6

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104
Q

what part of a normal ECG must a T wave be upright?

A

1, 2, V2 to V6

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105
Q

what should a P wave look like in an ECG?

A

+ve in lead 1 and 2
-ve in lead aVR
<3 squares in duration, <2.5 squares in amplitude
commonly biphasic in lead V1
best seen in lead 2

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106
Q

in an ECG, what shows right atria enlargement?

A

pointed P wave, over 2.5mm
- P pulmonale

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107
Q

in an ECG, what shows left atrial enlargement?

A

M shaped/bifid P wave
- P mitrale

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108
Q

what shows WPW, wolff-parkinson-white syndrome in an ECG?

A

short PR interval
(and tachycardia)

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109
Q

what does a long PR interval show?

A

1st degree heart block

110
Q

what is second degree heart block type 1 know as?

A

Mobitz type 1 AV block or Wenckebach phenomenon.

111
Q

ecg finding on 2nd degree heart block type 1?

A
  • increasing prolongation of PR interval
  • occasional QRS dropped
112
Q

what causes 2nd degree heart block type 1?

A

Increased vagal tone: often seen in athletes
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
Inferior myocardial infarction
Myocarditis
Cardiac surgery

113
Q

what causes first degree heart block?

A

Enhanced vagal tone: often seen in athletes (non-pathological)
Post myocardial infarction
Lyme disease
Systemic lupus erythematosus
Congenital
Myocarditis
Electrolyte derangements
thyroid
drugs

114
Q

what is management of first degree heart block?

A
  • AV blocking drugs should be stopped
  • normally asymptomatic so no intervention
  • pacemaker is symptomatic
115
Q

what symptoms in 2nd degree heart block type 1?

A
  • Irregular pulse
  • Bradycardia
  • pre/syncope
116
Q

ecg findings in Mobitz type 2 AV block

A
  • regular normal PR
  • intermittently dropped QRS complexes
117
Q

treatment of 2nd degree heart block type 2

A
  • underlying cause treated - pacemaker if untreatable
  • cardiac monitoring - risk of progression to complete AV block
  • Temporary pacing or isoprenaline if haemodynamically compromised due to bradycardia
118
Q

what are features of 3rd degree heart block?

A
  • complete failure of conduction
  • P wave and QRS present but no association - working independantly
119
Q

symptoms/signs of 3rd degree heart block

A

Palpitations
Pre-syncope/syncope
Confusion
Shortness of breath (due to heart failure)
Chest pain
Sudden cardiac death
bradycardia
irregular pulse

120
Q

ecg of bundle branch block

A
  • broad QRS
  • RSR’ pattern in V1-V3
  • Wide, slurred S wave in lateral leads: I, aVL, V5-V6
121
Q

cause of AV/heart block

A

idiopathic - fibrosis and sclerosis of the conduction system

122
Q

what are Narrow complex tachycardia?

A

narrow QRS
- atrial fib/flutter
- sinus Supraventricular tachycardia
- Supraventricular tachycardia

123
Q

what are Broad Complex Tachycardia?

A

broad QRS
- atrial fib/flutter with bundle branch block
- ventricular tachycardia
- Polymorphic ventricular tachycardia eg torsades de pointes

124
Q

how is torsades de pointes treated?

A

IV magnesium

125
Q

what is the outcome of Torsades de pointes?

A
  • return to sinus rhytham
  • ventricular tachycardia - can lead to cardiac arrest
126
Q

what causes prolonged QT interval?

A
  • Long QT syndrome (an inherited condition)
  • Medications eg antipsychotics, amiodarone
  • Electrolyte imbalances - hypokalaemia, hypomagnesaemia and hypocalcaemia
127
Q

what should the S wave be in a QRS complex?

A

depth shouldnt exceed 30 mm

128
Q

what shows an abnormal T wave?

A

symetrical, tall, peaked, biphasic or inverted

129
Q

in what lead is the QT interval measured?

A

lead aVl

130
Q

how does QT interval change with heart rate?

A

heart rate increases = QT decreases

131
Q

what should a QT interval be?

A

0.35-0.45s

132
Q

how is the heart rate calculated using an ECG?

A
  • counting number of big boxes between QRS complexes, then divide into 300
  • count number of beats per page and times by 6 (one page of ECG shows 10 seconds of rhythm)
133
Q

what can abnormalities in the QRS axis show?

A

ventricuar enlargement
conduction blocks
- normal is from-30 to +90

134
Q

what is the difference between RBBB and LBBB?

A

RBBB - affects RV electrical conduction - terminal force of QRS is higher than baseline
LBBB - affects LV electrical conduction - terminal force of QRS is below baseline

135
Q

what is acute pericarditis?

A

an inflammatory pericardial syndrome with or without effusion

136
Q

where does pericardial effusion occur and what does the fluid consist of?

A
  • pericardial sac
  • Transudates (low protein content)
    Exudates (associated with inflammation)
    Blood
    Pus
    Gas - bacterial
137
Q

what is Pericardial tamponade?

A

severe pericardial effusion - lots of fluid causing increased intra-pericardial pressure and lower CO

138
Q

what causes transudative pericardial effusion

A

Increased venous pressure can reduce drainage from the pericardial cavity eg due to:
Congestive heart failure
Pulmonary hypertension

139
Q

what causes exudative pericardial effusion

A

Inflammatory:
Infection eg tb
Autoimmune and inflammatory conditions SLE, RA
Injury to the pericardium (e.g., after myocardial infarction, surgery or trauma)
Uraemia (raised urea) secondary to renal impairment
Cancer
Medications

140
Q

what are symptoms/signs of pericardial effusion

A

Chest pain
Shortness of breath
A feeling of fullness in the chest
Orthopnoea (shortness of breath on lying flat)
(hiccups, dysphagia, horse voice)
Hypotension
Raised JVP

141
Q

how is pericardial effusion diagnosed?

A
  • echo
  • fluid analysis
142
Q

how is pericardial effusion treated?

A
  • drainage - surgical/Needle pericardiocentesis
  • treatment of underlying cause eg NSAIDS, aspirin
143
Q

what 2 of 4 criterias need to be made for a diagnosis of pericarditis?

A
  • chest pain
  • pericardial rubs
  • ecg changes
  • pericardial effusion
144
Q

what causes pericarditis?

A
  • infections - viral (enterovirus etc.) or bacterial (Mycobacterium tuberculosis)
  • autoimmune - sjogren syndrome, rheumatoid arthritis, scleroderma
  • neoplastic - lung/breast cancer
  • metabolic - uraemia, myxoedema
  • trauma - direct/indirect injury
145
Q

what are the symptoms/signs of pericarditis?

A
  • chest pain: serve, sharp, rapid onset, left anterior chest or epigastrium, worse with inspiration and lying down
  • low grade fever
  • pericardial rub
146
Q

what are the differential diagnosis for pericarditis?

A
  • myocardial ischaemia/infarction
  • pneumonia
  • pulmonary embolus
  • Gastro-oesophageal reflux
  • shingles
  • pancreatitis
147
Q

what investigations are done for pericarditis?

A
  • clinical examinations - pericaridal rub, tachycardia, fever, signs of effusion
  • ECG Saddle-shaped ST-elevation, PR depression
  • Bloods - inflammatory markers
  • Echocardiogram
148
Q

how is an ECG different in pericarditis?

A
  • Saddle shaped st elevation
  • PR depression
149
Q

how is pericarditis managed?

A
  • treat underlying condition eg viral/autoimmune
  • Sedentary activity until resolution of symptoms and ECG/CRP
  • NSAIDs: ibuprofen aspirin
  • colchicine
  • corticoseroids if contraindications for above
  • pain-relief, antibiotics?
150
Q

what do blood tests for pericarditis show?

A
  • FBC - Modest increase in WCC, mild lympocytosis
  • Troponin - Elevations suggest myopericarditis
  • ESR & CRP
151
Q

what is the most common cause of pericarditis?

A

viral pericarditis

152
Q

what is Hypertrophic cardiomyopathy?

A
  • autosomal genetic condition
  • caused by sarcomere protein mutation
  • LV wall thickenss
153
Q

what signs/symptoms can HCM cause?

A

angina,
dyspnoea, palpitations,
dizzy spells
syncope

154
Q

what is dilated cardiomyopathy

A

disease of heart muscle characterized by dilation and enlargement of of one or both ventricles, with impaired contractibility
- cytoskeleton gene mutation

155
Q

what kind of symptoms does DCM present with?

A

heart failure symptoms

156
Q

what is Arrhythmogenic cardiomyopathy?

A
  • desmosome gene mutation condition
  • heart muscle replaced with scar/fatty cells
  • mostly affects RV
157
Q

what are the main cardiac channelopathies?

A

long QT
short QT
Brugada
CPVT- Catecholaminergic polymorphic ventricular tachycardia
(can only be identified by ECG - no symptoms until an event occurs)

158
Q

what is sudden arythmic death syndrome - SADS?

A

when a patient dies due to abnormal heart/arrhythmia but otherwise healthy

159
Q

what is Familial hypercholesterolaemia ?

A

an inherited abnormality of cholesterol metabolism
- leads to serious premature coronary and other vascular disease

160
Q

what is important to consider when precribing to a patient with long QT syndrome?

A

QT prolonging drugs - can kill patient
eg some antidepressants etc.
(and recreational drugs)

161
Q

what are some examples of Aortovascular syndromes?

A

Marfan - fibrillin mutation
Loeys-Dietz
vascular Ehler Danlos (EDS)

162
Q

what system do BP drugs target?

A

RAAS
sympathetic nervous system - noradrenaline
both increase/maintain BP

163
Q

what groups of drugs decrease BP?

A

ACE inhibitors
ARB - angiotensin receptor blocker
calcium channel blockers
beta blockers
aldesterone antagonists
alpha blockers
renin inhibitors - rarely used
centrally acting drugs

164
Q

what is the most common ACE inhibitor?

A

Ramipril

165
Q

what are side effects of ACE inhibitor?

A
  1. related to angiotensin 2
    - hypotension
    - acute renal failure
    - hyperkalaemia
    - teratogenic effects - baby
  2. related to kinins
    - cough
    - rash
    - anaphylactoid reactions
166
Q

what are the types of calcium channel blocker?

A
  1. dihydropyridines - eg amlodipine
    - affects peripheral arterial vasodilators
  2. verapamil - main effects on heart
  3. diltiazem - cardiac and peripheral effects
167
Q

what are adverse effects of CCB?

A
  • Due to peripheral vasodilatation (mainly dihydropyridines)
    Flushing
    Headache
    Oedema
    Palpitations
  • Due to negatively chronotropic effects (mainly verapamil/diltiazem)
    Bradycardia
    Atrioventricular block
  • Due to negatively inotropic effects (mainly verapamil)
    Worsening of cardiac failure
  • Verapamil causes constipation
168
Q

what are side effects of Beta blockers

A

Fatigue
Headache
Sleep disturbance/nightmares

Bradycardia
Hypotension
Cold peripheries

Erectile dysfunction

Worsening of: Asthma (may be severe) or COPD
PVD – Claudication or Raynaud’s
Heart failure – if given in standard dose or acutely

169
Q

what are the classes of diuretics?

A

Thiazides and related drugs (distal tubule)

Loop diuretics (loop of Henle)

Potassium-sparing diuretics

Aldosterone antagonists

170
Q

what are the adverse effects of diuretics?

A

hypovolaemia
hypotension
low serum potassium, sodium, magnesium,calcium
raised uric acid
impaired glucose tolerance
erectile dysfunction

171
Q

what drugs are best used in pregnancy for hypertension?

A

methyldopa - centrally acting

172
Q

what population has CCB most commonly prescribed for hypertension?

A

over 55
or afro-caribean any age

173
Q

what groups of people are best prescribed ACE inhibitors/ARB?

A

diabetics
under 55

174
Q

what are the types of heart failure?

A

Heart Failure with Reduced Ejection Fraction HFrEF - (systolic) (LVSD)

Heart failure with preserved ejection fraction HFPEF - (diastolic failure)

Acute heart failure / Chronic heart failure
(left sided most common)

175
Q

what is the first line treatment for heart failure?

A

ACE inhibitors
beta blockers

176
Q

when is Sacubitril – neprilysin inhibitor used?

A

in heart failue in addition to other treatment eg beta-blockers

177
Q

what are the effects of nitrates on the cardiovacsular system?

A

Arterial and venous dilators
Reduction of preload and afterload
Lower BP
- eg for ischaemic heart disease
- eg GTN spray

178
Q

what is the first line treatment for chronic stable angina?

A

beta blockers
calcum channel blockers

179
Q

what medication is used for acute coronary syndrome?

A

diamorphine for pain
anti-platelets
antithrombin
aspirin
beta bloackers
statins
therapy for treatment eg ACE inhibitors

180
Q

what is the Vaughan Williams classification
for antiarrhythmic drugs?

A

Class I: Sodium channel blockers -
Ia - disopyramide, quinidine, procainamide
Ib - lidocaine, mexilitene
Ic - flecainide, propafenone

Class II: Beta adrenceptor antagonists - propranolol, nadolol, carvedilol (non-selective)
bisoprolol, metoprolol (β1-selective)

Class III: Prolong the action potential - amiodarone, sotalol

Class IV: Calcium channel blockers - verapamil, diltiazem

181
Q

what are features of digoxin?

A
  • Cardiac glycoside, antiarrhythmic drug
  • Inhibit Na/K pump
  • causes bradycardia and slows down conduction
  • narrow theraputic range
182
Q

what are the uses and side effects of amiodarone?

A

antiarrhythmic medication
side effects:
- QT prolongation
- liver dysfunction
- hypo/hyperthyroidism
- sun sensitivity
- corneal microdeposits
- optic neuropathy
- multiple drug interactions - eg warfarin
- very large volume of distribution

183
Q

what are the types of aortic stenosis?

A
  • supravalvular
  • subvalvular
  • valvular
184
Q

when do symptoms of aortic stenosis occur?

A

when valve area is 1/4 of normal area (normal is 3-4cm2)

185
Q

what are the causes of aortic stenosis?

A
  • congenital: congenital aortic stenosis/bicuspid valve
  • acquired: calcification, rheumatic heart disease
186
Q

what are the 3 presentations of aortic stenosis?

A

syncope - fainting/loss of conciousness
angina
dyspnoea - difficulty breathing

187
Q

what are the physical signs of aortic stenosis?

A
  • Slow rising carotid pulse & decreased pulse amplitude
  • Heart sounds- soft or absent second heart sound, S4 gallop due to LVH
  • Ejection systolic murmur- crescendo-decrescendo character.
188
Q

what investigations are done to diagnose aortic stenosis?

A

echocardiogram
- Left ventricular size and function: LVH, Dilation, and EF
- Doppler derived gradient and valve area (AVA) - under 1cm2 is severe

189
Q

what is the management of aortic stenosis?

A
  • Aortic Valve Replacement (if symptomatic):
    Surgical
    TAVI – Transcatheter Aortic Valve Implantation
  • if asymptomatic then surveillance
  • NO vasodilators in servere AS
  • consider prophylaxis in dentals due to infection risk
190
Q

what is mitral regurgitation?

A

backflow of blood from the LV to the LA during systole
(mildly seen in 80% of pop)

191
Q

what are the causes of mitral regurgitation?

A
  • Myxomatous degeneration (MVP)
  • Ischemic MR
  • Rheumatic heart disease
  • Infective Endocarditis
192
Q

what is the Compensatory Mechanism for mitral regurgitation?

A

Left atrial enlargement, LVH and increased contractility
- Progressive LV volume overload leads to dilatation and progressive HF

193
Q

what are the signs/symptoms of mitral regurgitation?

A
  • pansystolic murmur at the apex radiating to the axilla, In chronic MR, the intensity of the murmur does correlate with the severity
  • Exertion Dyspnoea: ( exercise intolerance)
  • heart failure
194
Q

what are the investigations for mital regurgitation?

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
195
Q

what is the management for mitral regurgitation?

A
  • medications - b-blockers, anticoagulation, nitrate/diuretics for acute MR
  • serial echo
  • IE prophylaxis - for prosthetic valves/dental procedures
  • surgery IF any symptoms at rest or exercise, or EF below 65% etc.
196
Q

what is aortic regurgitation?

A

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

197
Q

what causes aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic
Infective endocarditis

198
Q

what is the Compensatory Mechanisms for aortic regurgitation?

A

LV dilation, LVH. Progressive dilation leads to heart failure

199
Q

what are the ausculations of aortic regurgitation?

A
  • Diastolic blowing murmur at the left sternal border
  • Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
  • Systolic ejection murmur: due to increased flow across the aortic valve
200
Q

what are the signs/symptoms of aortic regurgitation?

A
  • Wide pulse pressure
  • Hyperdynamic and displaced apical impulse
  • syspnoea
  • palpitations
201
Q

what are investigations for aortic regurgitation?

A
  • chest xray - enlarged cardiac silhouette and aortic root enlargement
  • ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function
202
Q

what is the management of aortic regurgitation?

A
  • vasodilators
  • serial echos to monitor
  • surgical - TAVI in exceptional cases
203
Q

what is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole

204
Q

what are the causes of mitral stenosis?

A
  • Rheumatic carditis is the predominant cause
  • infective endocarditis
  • mitral annular calcification
205
Q

what are the signs/symptoms of mitral stenosis?

A
  • Progressive Dyspnea
  • Right heart failure symptoms
  • mitral facies (rosey cheeks) due to vasoconstriction due to low cardiac output
  • prominent “a” wave in jugular venous pulsations
206
Q

what are the heart sounds in mitral stenosis?

A
  • diastolic murmur
  • Loud Opening S1 snap
207
Q

how does mitral stenosis effect the heart?

A
  • pulmonary hypertension
  • RV hypertrophy
  • LA dilation
  • LA enlargement and fibrillation
208
Q

what are the investigations for mitral stenosis?

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
209
Q

what is the management of mitral stenosis?

A
  • serial echo
  • medication eg b-blockers, diuretics
  • percutaneous mitral balloon valvotomy.
  • IE prophylaxis
  • Mitral valve replacement - symptomatic with class3/4 symptoms
210
Q

what is stage 1 & 2 and severe hypertension?

A

stage 1 BP over 140/90 (HBPM over 135/85)
stage 2 BP over 160/100 (HBPM over 150/95)
severe BP over 180, or over 110

211
Q

when are antihypertensive drugs offered?

A
  • if under 80yrs stage 1 and target organ damage/CVD/renal disease/diabetes/CVD risk over 20%
  • or stage 2 any age
212
Q

what is ABPM?

A

ambulatory blood pressure monitoring over 24hours
- used to diagnose hypertension if clinical BP is 140/90

213
Q

what should BP targets be?

A

under 140/90 for under 80yrs
under 150/90 for over 80yrs

214
Q

what are some congenital heart defects?

A

Ventricular septal defect
Atrial septal defect
Atrio-ventricular septal defects
Patent ductus arteriosus
Coarctation of the Aorta
Bicuspid aortic valve and aortopathy
Pulmonary stenosis
Tetralogy of Fallot

215
Q

what are some clinical signs of a ventricular septal defect?

A
  • tachycardia
  • big heart on chest xray
  • increased Resp rate
  • small breahless skinny baby
216
Q

what syndrome can a ventricular septal defect cause?

A

Eisenmengers syndrome

217
Q

what are some clinical signs of an atrial septal heart defect?

A
  • pulmonary flow murmur
  • Fixed split second heart sound
  • big pulmonary arteries, big heart on chest xray
  • may have increased chest infections and right heart dilation
218
Q

what people may often have atrio-ventricular septal defects?

A

downs syndrome

219
Q

what are some clinical signs of AVSD?

A
  • breathless neonate
  • poor weight gain/feeding
  • Presents like a small VSD / ASD
220
Q

what are some clinical signs of Patent Ductus Arteriosus?

A
  • Continuous ‘machinery’ murmur
  • If large, big heart, breathless
  • Eisenmenger’s syndrome
221
Q

what are clinical signs of coarctation of aorta

A
  • Right arm hypertension
  • Bruits (buzzes) over the scapulae and back from collateral vessels
  • Murmur
222
Q

what is tertalogy of fallot?

A

congenital heart defect
- ventricular septal defect
- pulmonary stenosis
- hypertrophy of RV
- overriding aorta

223
Q

what is the most common congenital heart defect?

A

ventricular septal defect

224
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).

225
Q

who most commonly gets endocarditis?

A

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

226
Q

what is the 2 major criteria of infective endocarditis?

A
  • Pathogen grown from blood cultures
  • evidence of endocarditis on echo, or new valve leak, regurgitation
227
Q

what is the 5 minor criteria of infective endocarditis?

A
  • Predisposing factors
  • Fever over 38
  • embolism evidence - janeway lesions
  • Immune phenomena - oslers/roths
  • Equivocal blood cultures
228
Q

what is the modified dukes criteria to diagnose endocarditis?

A

One major plus three minor criteria
Five minor criteria

229
Q

what are the 4 peripheral signs of endocarditis?

A
  • roth spots - on eye fundoscopy
  • osler nodes - on digits
  • janeway lesions - on palms/soles
  • splinter hemorrhages - on nails
230
Q

investigations of endocarditis

A

blood culture - Staphylococcus aureus, strep/enterococcus
echo (TOE) - Vegetations seen

231
Q

what is the treatment of infective endocarditis?

A
  • antibiotics/antimicrobials
  • surgery to remove the infectious material and/or repair the damage
232
Q

on an ECG, what shows left/right atrial enlargement?

A

right - tall p wave
left - Broad notched ‘Bifid’ P wave

233
Q

when is the PR interval prolonged?

A

in disorders of AV node and specialised conducting tissue

234
Q

what is the most common reason for a broad QRS?

A

Ventricular conduction delay / bundle branch block
Pre-excitation
- eg damage from heart attack

235
Q

when is a QRS complex small?

A

Obese patient
Pericardial effusion
Infiltrative cardiac disease

236
Q

what is the QRS in Left ventricular hypertrophy?

A

tall

237
Q

what does QT interval represent?

A

ventricular depolarisation and repolarisation

238
Q

what part of the ECG is important to look at in ischaemia?

A

ST segment

239
Q

what are some reasons for T wave inversion?

A

Ischaemia/infarction
Myocardial strain (hypertrophy)
Myocardial disease (cardiomyopathy

240
Q

what does a LBBB look like in an ECG?

A

QRS looks like a W in V1 and M in V6
- WiLLiam

241
Q

what does a RBBB look like in and ECG?

A

QRS looks like M in V1 and W in V6
- MaRRow

242
Q

what shows Ischaemia & Infarction in an ECG?

A
  • T wave flattening inversion
  • ST segment depression
  • ST segment elevation
  • Q waves – old infarction
243
Q

what shows Hyperkalaemia in ECG?

A

Tall T waves, flattening of P waves, broadening of QRS… eventually ‘sine wave pattern’

244
Q

what shows Hypokalaemia in an ECG?

A

Flattening of T wave, QT prolongation

245
Q

what shows Hypercalcaemia in an ECG?

A

QT shortening

246
Q

what shows Hyporcalcaemia in an ECG?

A

QT prolongation

247
Q

what is the most common sustained arrhythmia?

A

AF

248
Q

what can no P wave suggest?

A

supraventricular tachycardia
or AF

249
Q

what is heart failure?

A

An inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures

250
Q

what most commonly causes heart failure?

A

myocardial dysfunction due to IHD, hypertension, excess alcohol

251
Q

what are the main phenotypes for heart failure?

A

HF with reduced ejection fraction (HFrEF)
HF with preserved ejection fraction (HFpEF)

252
Q

what are symptoms of right sided heart failure?

A
  • peripheral edema, ascites
  • hepatomegaly
  • jugular venous distension (JVD) and raided pressure
  • abdo discomfort
253
Q

what are symptoms of left sided heart failure?

A
  • dyspnea, orthopnea
  • fatigue
  • elevated JVP
  • coughing/wheezing
254
Q

what causes left sided heart failure?

A
  • high BP
  • alvular heart disease (aortic stenosis or mitral regurgitation)
  • coronary artery disease
  • MI
255
Q

what causes right sided heart failure?

A
  • often secondary to left sided
  • pulmonary hypertension
  • chronic lung diease eg COPD, pulmonary fibrosis
  • right-sided valvular heart disease
256
Q

what is definition for left vs right heart failure?

A

left - left ventricle fails to effectively pump oxygen-rich blood from the lungs to the rest of the body.
right - right ventricle fails to effectively pump blood to the lungs for oxygenation.

257
Q

what are the symptoms of heart failure?

A

Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight

258
Q

what are the signs of heart failure?

A
  • Tachycardia
  • Displaced apex beat (normally 5th intercostal space)
  • Raised JVP (Jugular venous pressure)
  • Added heart sounds and murmurs
  • Hepatomegaly, especially if pulsatile and tender
  • Peripheral and sacral oedema
  • Ascites
259
Q

what is the new york heart association cassification for heart failure?

A

Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)

260
Q

what causes acute decompensation (suddun worsening) of chronic heart failure?

A
  • AMI - acute myocardial infarction
  • Uncorrected BP
  • Obesity
  • Superimp. infection
  • AF & arrhythmias
  • Excess alcohol
  • Endocrine (DM/T4..)
    -ve inotropes (Ca/beta)
  • NSAIDS
  • Treatment and Na+ noncompliance.
  • Lack of information given to patient about diet, medications, etc
261
Q

what medications are used to treat heart failure?

A
  • first line - ACE inhibitors and beta-blockers lisenced for HF
    (angiotensin receptor blocker considered if ACE not tolerated)
  • aldosterone antagonists
  • mineralocorticoid receptor antagonist
  • diuretics - relieve breathlessness and oedema
  • loop diuretics
  • thiazide only in mild fluid retention
  • digoxin - for patients with sinus rhythm, for symptoms caused by acute exacerbations
  • ivabradine - Blocker of the If current in the SA node - slows HR and treats angina
  • NO Rate-limiting calcium-channel blockers for patients with reduced ejection fraction
262
Q

why is IV-iron prescribed in heart failure?

A
  • improves exercise tolerance
  • may reduce the propensity for hospitalization of patients with HFrEF
263
Q

should oxygen be given to patients with heart failure?

A

No
- only if sat below 90, or COPD

264
Q

what causes Aortic dissection?

A

tear in aorta that propagates
- high BP
- trauma
- Connective Tissue Disorders eg Marfan syndrome, Ehlers-Danlos syndrome

265
Q

symptoms of aortic dissection

A
  • Sudden, Severe Chest and abdo Pain
  • weakness, numbness, or paralysis in the limbs
  • diff in BP between arms
  • syncope
  • hypertension, Hypotension as the dissection progresses
266
Q

between what layers does aortic dissection happen?

A

intima and media

267
Q

what is the Stanford system classification of aortic dissection?

A

Type A – affects the ascending aorta, before the brachiocephalic artery
Type B – affects the descending aorta, after the left subclavian artery

268
Q

investigations for aortic dissection

A
  • ecg/xray to exclude other
  • CT angiogram (MRI more detail)
269
Q

treatment for aortic dissection

A
  • analgesia
  • BP/HR control - beta-blockers
  • surgery: A - open sugery, B - TEVAR catheter, grafts
270
Q

complications of aortic dissection

A
  • Myocardial infarction
  • Stroke
  • Paraplegia (motor or sensory impairment in the legs)
  • Cardiac tamponade
  • Aortic valve regurgitation
  • Death

2A (9 decks)

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