CARDIO Flashcards

(579 cards)

1
Q

ATHEROSCEROSIS
Define atherosclerosis

A

Build up of plaque in the intima of an artery

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2
Q

ATHEROSCLEROSIS
What can an atherosclerotic plaque cause?

A
  1. Heart attack
  2. Stroke
  3. Gangrene
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3
Q

ATHEROSCLEROSIS
what are the risk factors for atherosclerosis?

A
  1. Family history
  2. Increasing age
  3. Smoking
  4. High serum cholesterol (LDL)
  5. Obesity
  6. Diabetes
  7. Hypertension
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4
Q

ATHEROSCLEROSIS
What are the constituents of an atheromatous plaque?

A

Lipid core
Necrotic debris
Connective tissue surrounded by foam cells
Fibrous cap
Lymphocytes

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5
Q

ATHEROSCLEROSIS
In which arteries would you most likely find an atheromatous plaque?

A

Peripheral and coronary arteries - circumflex, LAD and RCA
Focal distribution along the length

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6
Q

ATHEROSCLEROSIS
What histological layer of the artery may be thinned by an atheromatous plaque?

A

Media

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7
Q

ATHEROSCLEROSIS
What is the precursor for atherosclerosis?

A

Fatty streaks

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8
Q

ATHEROSCLEROSIS
What can cause chemoattractant release?

A

Endothelial cell injury

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9
Q

ATHEROSCLEROSIS
What is the function of chemoattractants?

A

Signal leukocytes and produce a concentration gradient

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10
Q

ATHEROSCLEROSIS
What is the function of leukocytes?

A

Leukocytes accumulate and migrate into vessel walls and release cytokines leading to inflammation

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11
Q

ATHEROSCLEROSIS
What inflammatory cytokines are found in plaques?

A

IL-1
IL-6
IFN-gamma

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12
Q

ATHEROSCLEROSIS
Describe the process of leukocyte recruitment

A
  1. Capture
  2. Rolling
  3. Slow rolling
  4. Adhesion
  5. Transmigration
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13
Q

ATHEROSCLEROSIS
What types of molecules are present during leukocyte recruitment?

A
  1. Chemoattractants
  2. Selectins (1-3)
  3. Integrins (3-5)
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14
Q

ATHEROSCLEROSIS
Describe the 5 steps of progression of atherosclerosis

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaque/advanced lesions
  4. Plaque rupture
  5. Plaque erosion
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15
Q

ATHEROSCLEROSIS
At what age do fatty streaks begin to appear?

A

< 10 years old

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16
Q

ATHEROSCLEROSIS
What are the constituents of fatty streaks?

A

Foam cells and T lymphocytes within the intimal layer of the vessel wall

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17
Q

ATHEROSCLEROSIS
What are the constituents of intermediate lesions?

A

Foam cells
Smooth muscle cells
T lymphocytes
Platelet adhesion and aggregation
Extracellular lipid pools

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18
Q

ATHEROSCLEROSIS
What are the constituents of fibrous plaques?

A

Fibrous cap overlies lipid core and necrotic debris
Smooth muscle cells
Macrophages
Foam cells
T lymphocytes

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19
Q

ATHEROSCLEROSIS
What are fibrous plaques able to do?

A

Impede blood flow and they are prone to rupture

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20
Q

ATHEROSCLEROSIS
Why might a plaque rupture?

A

Fibrous plaques are constantly growing and receding
Fibrous cap has to be resorbed and redeposited in order to be maintained
If balance is shifted in favour of inflammatory condition, the cap becomes weak and the plaque ruptures
Thrombus formation and vessel occlusion

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21
Q

ATHEROSCLEROSIS
What the primary treatment for atherosclerosis?

A

Percutaneous Coronary Intervention (PCI)

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22
Q

ATHEROSCLEROSIS
What is the major limitation of PCI?

A

Restenosis

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23
Q

ATHEROSCLEROSIS
How can restenosis be avoided following PCI?

A

Drug eluting stents –> anti-proliferative and drugs that inhibit healing

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24
Q

ATHEROSCLEROSIS
What is the key principle behind pathogenesis of atherosclerosis?

A

It is an inflammatory process

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25
ATHEROSCLEROSIS Define atherogenesis
The development of an atherosclerotic plaque
26
ANGINA Define angina
Type of ischaemic heart disease It is a symptom of O2 supply/demand mismatch to the heart
27
ANGINA What is the most common cause of angina?
Narrowing of the coronary arteries due to atherosclerosis
28
ANGINA Give 5 possible causes of angina
- atheroma/stenosis of coronary arteries - valvular disease - aortic stenosis - arrhythmia - anaemia
29
ANGINA How reduced does the diameter of an artery need to be before symptoms occur?
Diameter has to fall below 70%
30
ANGINA Name 3 types of angina
- Stable angina - Unstable angina - Prinzmetal's angina
31
ANGINA Name 3 non-modifiable risk factors for angina
1. Increasing age 2. Family history 3. Gender - Male 4. ethnicity - south Asian
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ANGINA Give 5 modifiable risk factors for angina
1. Smoking 2. Diabetes 3. Hypertension 4. Hypercholesterolaemia 5. Sedentary lifestyle/obesity 6. Stress 7. alcohol
33
ANGINA Name 3 exacerbating factors for angina that effect the supply of O2
1. Anaemia 2. Hypoxaemia 3. Polycythaemia 4. Hypothermia 5. Hyper/hypovolaemia
34
ANGINA Name 3 exacerbating factors for angina that effect the demand of O2
1. Hypertension 2. Tachyarrhythmia 3. Valvular heart disease 4. Hyperthyroidism 5. Cold weather 6. Heavy meals 7. Emotional stress
35
ANGINA Briefly describe the pathophysiology of angina that results from atherosclerosis
On exertion there is increase O2 demand Coronary blood flow is obstructed by an atherosclerotic plaque --> myocardial ischaemia --> angina
36
ANGINA Briefly describe the pathophysiology of angina the results from anaemia
On exertion there is increased O2 demand In someone with anaemia there is reduced O2 transport --> myocardial ischaemia --> angina
37
ANGINA Briefly describe the pathophysiology of Prinzmetal's angina
Occurs due to coronary artery spasm
38
ANGINA Name 3 differential diagnoses for angina
1. Pericarditis/myocarditis 2. PE 3. Chest infection 4. Dissection of aorta 5. GORD
39
ANGINA How would you describe the chest pain in angina?
Crushing central chest pain that is heavy and tight - angina pectoris
40
ANGINA What 3 things are used to assess whether it is typical angina, atypical pain or non-anginal pain?
1. Have central, tight, radiation to arms, jaw and neck 2. Precipitated by exertion 3. Relieved by rest or GTN spray 3/3 = Typical angina 2/3 = Atypical pain 1/3 = Non-anginal pain
41
ANGINA Give the clinical presentation of angina
1. Crushing central chest pain 2. Pain is relieved with rest or GTM spray 3. Pain is provoked by physical exertion 4. Pain may radiate to arms, neck or jaw 5. Dyspnoea 6. Nausea
42
ANGINA What investigations might you do in someone you suspect to have angina?
1. ECG - usually normal, sometimes ST depression, flat or inverted T waves 2. Echocardiography 3. CT angiography - high NPV and good at excluding disease (gold standard) 4. Exercise tolerance test - induces ischaemia 5. Invasive angiogram - tells you FFR (pressure gradient across stenosis) 6. SPECT - radio labelled tracer taken up by metabolising tissues
43
ANGINA How can angina be reversed?
Resting - reducing myocardial demand
44
ANGINA Describe the primary prevention for angina
1. Modify risk factors 2. Treat underlying causes 3. Low dose aspirin
45
ANGINA Describe the secondary prevention of angina
1. Modify risk facotrs 2. Pharmacological therapies for symptom relief and to reduce the risk of CV events 3. Interventional therapies (e.g. PCI)
46
ANGINA what is the management?
SYMPTOM RELIEF - GTN spray (if pain persists after 5 mins repeat dose, if pain remains after anther 5 mins call ambulance) ANTIANGINAL MEDICATION - 1st line = beta blocker or CCB - 2nd line = combination of BB + CCB (nifedipine) - long acting nitrate e.g. ivabradine
47
ANGINA Name 2 complications of angina
1. Acute coronary syndromes 2. Congestive cardiac failure 3. Conduction disease 4. Arrhythmia
48
PHARMACOLOGY Describe the action of beta blockers
Beta 1 specific Antagonise sympathetic activation and so are negatively chronotropic and inotropic Myocardial work is reduced and so is myocardial demand = symptom relief
49
PHARMACOLOGY Give 3 side effects of beta blockers
1. Bradycardia 2. Tiredness 3. Erectile dysfunction 4. Cold peripheries 5. nightmares
50
PHARMACOLOGY When might beta blockers be contraindicated?
DO NOT GIVE in asthma, heart failure/heart block, hypotension and bradyarrhythmia
51
PHARMACOLOGY Describe the action of nitrates
Venodilators Reduce venous return --> reduced preload --> reduced myocardial work and myocardial demand
52
PHARMACOLOGY Describe the action of Calcium channel blockers
Arterodilators Reduce BP --> Reduce afterload --> reduced myocardial demand
53
PHARMACOLOGY What drugs that might be use in someone with angina or in someone at risk of angina to improve prognosis?
1. Aspirin 2. Clopidogrel - antiplatelet 3. Atovostatin - Statin 4. ACEi - ramipril
54
PHARMACOLOGY How does aspirin work?
Antiplatelet Irreversibly inhibits COX --> reduced thromboxane 2 synthesis --> platelet aggregation reduced
55
PHARMACOLOGY What is a caution when prescribing aspirin?
Gastric ulceration
56
PHARMACOLOGY How does clopidogrel work?
Antiplatelet P2Y12 inhibitor --> prevents platelet activation
57
PHARMACOLOGY What are statins used for?
To reduce the amount of LDL in the blood
58
PHARMACOLOGY What is the function of P2Y12?
It amplifies platelet activation
59
PHARMACOLOGY Give 2 potential side effect of P2Y12 inhibitors
1. Bleeding 2. Rash 3. GI disturbances - ulceration
60
REVASCULARISATION What is revascularisation?
Used to restore coronary artery and increase blood flow
61
REVASCULARISATION Name 2 types of revascularisation
1. Percutaneous coronary intervention (PCI) 2. Coronary artery bypass graft (CABG)
62
REVASCULARISATION Give the pros and cons of PCI
ADVANTAGES 1. Less invasive 2. Convenient and acceptable 3. short recovery and repeatable DISADVANTAGES 1. High risk of restenosis 2. not good for complex disease 3. risk of stent thrombosis
63
REVASCULARISATION what are the pros and cons of CABG?
ADVANTAGES 1. Good prognosis after surgery 2. deals with complex disease DISADVANTAGES 1. Very invasive 2. Long recovery time 3. risk of stroke or bleeding
64
ACS What are acute coronary syndromes?
Encompasses a spectrum of acute cardiac conditions from unstable angina, NSTEMI and STEMI
65
ACS What is the common cause of ACS?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis
66
ACS What are uncommon causes of ACS?
1. Coronary vasospasm 2. Drug abuse 3. Coronary artery dissection 4. Thoracic aortic dissection
67
ACS Briefly describe the pathophysiology of ACS
- Rupture/erosion of fibrous cap on plaque leading to platelet aggregation and thrombus formation - In unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in partial occlusion - In MI the plaque has a necrotic centre and the thrombus results in total occlusion
68
ACS Describe type 1 MI
Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection
69
ACS Describe type 2 MI
MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension
70
ACS What is troponin a marker for?
Cardiac muscle injury
71
ACS Why do you see increased serum troponin in NSTEMI and STEMI?
The occluding thrombus causes necrosis of cells and so myocardial damage causing troponin to be raised
72
ACS Give 3 signs of unstable angina
1. Cardiac chest pain at rest 2. Cardiac chest pain with crescendo pattern 3. No significant rise in troponin
73
ACS Give 4 symptoms of MI
1. Unremitting and usually severe central cardiac chest pain 2. Pain occurs at rest 3. Sweating, pale, grey 4. Breathlessness 5. Nausea and vomiting
74
ACS Give 3 signs of MI
1. Hypo/hypertension 2. 3rd/4th heart sound 3. Signs of congestive heart failure 4. Ejection systolic murmur
75
ACS Name 3 possible differential diagnoses of MI
1. Pericarditis 2. Stable angina 3. Aortic dissection 4. GORD 5. Pneumothorax
76
ACS What investigations would you do on someone you suspect to have ACS?
1. ECG (within 10 mins) 2. Blood tests - troponin levels and rule out anaemia 3. Coronary angiography 4. Cardiac monitoring for arrhythmias 5. Chest x-ray
77
ACS what other biomarkers can be tested for in MI?
creatine-kinase-MB (CK-MB) myoglobin
78
ACS What might the ECG of someone with unstable angina show?
May be normal, or might show T wave inversion and ST depression
79
ACS What might the ECG of someone with NSTEMI show?
May be normal or might show T wave inversions and ST depression Might also be R wave regression, ST elevation and biphasic T wave in lead V3
80
ACS What might the ECG of someone with STEMI show?
ST elevation in the anterolateral leads After a few hours, T waves inlet and deep, broad, pathological Q waves develop
81
ACS What would the serum troponin level be like in someone with unstable angina?
Normal
82
ACS What would the serum troponin level be like in someone with NSTEMI/STEMI?
Significantly raised - troponin I and T
83
ACS A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?
1. Gram negative sepsis 2. PE 3. Myocarditis 4. Heart failure 5. Arrhythmias
84
ACS Describe the initial management of ACS
- Analgesia - morphine + sublingual GTN - Oxygen (if SpO2 > 94%) - dual antiplatelets - ALL patients = aspirin 300mg - if PCI = prasugrel or clopidogrel - if fibrinolysis = ticagrelor or clopidogrel MONA
85
ACS What is the overall treatment for STEMI?
PCI - if symptom onset within 12 hours and access to PCI within 120 minutes Thrombolysis e.g. alteplase or tenecteplase - If ineligible for PCI
86
ACS what is the management of an NSTEMI?
- anticoagulation = fondaparinux to most patients, unfractionated heparin if renal failure - use GRACE score to work out if patient requires PCI
87
ACS what is the grace score?
it is used to risk-stratify patients with unstable angina and NSTEMIs it estimates admission to 6 month mortality
88
ACS Describe the secondary prevention therapy for people after having a STEMI
- lifestyle changes - manage CVD risks - 12 months aspirin 75mg + ticagrelor if ACS was medically managed - lifelong aspirin + 12 months ticagrelor/prasugrel if ACS treated with PCI - ACEi
89
ACS Give 5 early complications of MI
- Post MI pericarditis (few days post MI) - cardiac arrest (due to VF) - heart block - cardiogenic shock - VSD - mitral regurgitation - left ventricular wall rupture
90
ACS Give 5 late complications of MI
- dresslers syndrome (2-6 weeks post MI) - heart failure - left ventricular aneurysm
91
DVT What is a DVT?
Blood clot within a blood vessel of the lower limb
92
DVT Give 5 risk factors for DVT
- AGE <40 - IMMOBILITY - surgery, hospitalisation, long-haul travel, bed-bound - TRAUMA - THROMBOPHILIA - MALIGNANCY - SMOKING - PREGNANCY - DRUGS - COCP, HRT, tamoxifen
93
DVT What are the clinical features of DVT?
- unilateral calf pain, redness and swelling - oedema distention of superficial veins rarely phlegmasia cerula dolens (blue and painful leg from both venous and arterial obstruction)
94
DVT What are the causes of DVT?
HYPERCOAGULABILITY - hereditary e.g. facter V leiden, antiphospholipid syndrome - acquired e.g. malignancy, chemo, COCP/HRT, pregnancy, obesity VENOUS STASIS - immobility e.g. surgery, flights - polycythaemia ENDOTHELIAL DAMAGE - surgery - catheter (PICC lines) - trauma - smoking
95
DVT What investigations might be done in order to diagnose a DVT?
1. WELLS score if WELLS >2 DVT likely - duplex ultrasound of leg within 4 hours (if not within 4 hrs, offer anticoagulation) - d-dimer if WELLS <1 DVT unlikely - D-dimer with results within 4 hrs (if not within 4hrs offer anticoagulation) - if D-dimer is raised = duplex USS - if D-dimer normal = no further Ix bloods - FBC, U&Es, LFTs, PT + APTT
96
DVT what is WELLS score?
calculates the risk of DVT and determines how a patient is investigated and treated
97
DVT what are the components of the WELLS score?
- active cancer - bedridden or recent major surgery - calf swelling >3cm compared to other leg - superficial veins present (non-varicose) - entire leg swollen - tenderness along veins - pitting oedema of affected leg - immobility of affected leg - previous DVT - alternative diagnosis likely (-2) all score +1
98
DVT how do you interpret the results of the WELLS score?
>2 = high risk of DVT/likely <1 = low risk of DVT/unlikely
99
DVT What is the treatment for DVT?
- no renal impairment = apixaban/rivaroxaban - renal impairment (CrCl<15ml/min) = LMWH or UFH + warfarin for 5 days, then warfarin alone - active cancer = consider DOAC or warfarin
100
DVT how long should you offer anticoagulation for?
at least 3 months
101
DVT Name the types of DVT
1. Spontaneous 2. Provoked - incidence of recurrence is low if you remove the stimulus
102
DVT How can DVTs and PEs be prevented?
1. Hydration 2. Early mobilisation 3. Compression sticking/pumps 4. Low dose LMW heparin
103
DVT What is low risk thromboprophylaxis treatment?
< 40 years Surgery < 30 mins Early mobilisation and hydration No chemical TED if surgical
104
DVT What is high risk thromboprophylaxis?
Hip, knee, pelvis, malignancy, risk factors, prolonged immobility All immobile medical, many surgical - Dalteparin s/c od
105
DVT what are the complications of a DVT?
Pulmonary embolism Post thrombotic syndrome Increased risk of bleeding Phlegmasia cerula dolens (venous and arterial obstruction resulting in blue painful leg)
106
PE what are the clinical features of PE?
MOST COMMON FEATURES - tachypnoea - crackles - tachycardia - fever SYMPTOMS 1. Breathlessness 2. Pleuritic chest pain 3. signs/symptoms of DVT 4. Cough/haemoptysis SIGNS 1. Tachycardia 2. Tachypnoea 3. pleural rub 4. hypoxia
107
PE What investigations might be done to diagnose a patient with PE?
- CXR (typically normal) - ECG (sinus tachy, S1Q3T3, RBBB + R axis deviation - if WELLS >4 = CTPA (V/Q scan as alternative in severe renal impairment) - if WELLS<4 = D-dimer
108
PE when would a V/Q scan be used over CTPA?
- patients allergic to contrast - severe renal impairment - pregnancy
109
PE what is the WELLS two-level score?
used to determine the probability of PE >4 = high probability <4 = low probability
110
PE what are the components of the WELLs two level score?
- clinical signs + symptoms of DVT (+3) - PE is no.1 diagnosis (+3) - tachycardia <100 (+1.5) - immobilisation for >3 days - previous PE/DVT (+1.5) - haemoptysis (+1) - malignancy with treatment in last 6 months (+1)
111
What is the treatment for a PE?
massive PE = thrombolysis e.g. alteplase non-massive PE = - no renal impairment = apixaban/rivaroxaban - renal impairment (CrCl<15ml/min) = LMWH or UFH + warfarin for 5 days, then warfarin alone - active cancer = consider DOAC or warfarin
112
PE how long would you offer anticoagulation for?
- provoked = 3 months - unprovoked = 6 months
113
PE If a patient can not be placed on anticoagulation following a PE, what alternative treatment should be considered?
IVC filter - prevents more clot travelling from the leg to the lungs surgical embolectomy
114
PE what are the complications?
- cor pulmonale - pulmonary infarction - heparin-associated thrombocytopaenia
115
THROMBUS Define thrombosis
Blood coagulation inside a vessel
116
THROMBUS How would you describe an arterial thrombus?
Platelet rich (a 'white thrombosis')
117
THROMBUS How would you describe a venous thrombosis?
Fibrin rich (a 'red thrombosis')
118
THROMBUS What are the potential consequences of an arterial thrombosis?
1. Coronary circulation = MI 2. Cerebral circulation = Stroke 3. Peripheral circulation = Peripheral vascular disease (e.g. gangrene)
119
THROMBUS What investigations would you do to diagnose an arterial thrombosis?
MI = history, ECG, cardiac enzymes Stoke = History and examination, CT/MRI scan PVD = History and examination, ultrasound, angiogram
120
THROMBUS What is the treatment for arterial thrombosis?
1. Aspirin 2. LMW heparin 3. Thrombolytic therapy: streptokinase tissue plasminogen factor 4. Treat risk factors
121
PHARMACOLOGY How does heparin work?
Inhibits thrombin and factor Xa Indirect thrombin inhibitor - binds to antithrombin and increased its activity
122
PHARMACOLOGY How do you monitor heparin?
Activated partial thromboplastin time Aim ratio: 1.8-2.8
123
PHARMACOLOGY Why is LMW heparin often used instead of normal heparin?
Smaller molecule, less variation in dose and renally excreted
124
PHARMACOLOGY How does warfarin work?
Inhibits production of vitamin K dependent clotting factors (2, 7, 9, 10) Prolongs the prothrombin time
125
PHARMACOLOGY What is warfarin an antagonist of?
Vitamin K
126
PHARMACOLOGY Why is warfarin difficult to use?
Lots of interactions Needs almost constant monitoring Teratogenic
127
PHARMACOLOGY How is warfarin measured?
Using International Noramlised Ratio (derived from prothrombin time) Usual target = 2-3 Higher range = 3-4.5
128
PHARMACOLOGY How does Direct Acting Oral Anticoagulant (DOAC) work?
Directly acts on factor 2 (thrombin) or 10 No blood test or monitoring needed just given od or bd
129
PERICARDITIS How much serous fluid is there between the visceral and parietal pericardium?
50 ml
130
PERICARDITIS What is the function of the serious fluid between the visceral and parietal pericardium?
Lubricant and so allows smooth movement of the heart inside the pericardium
131
PERICARDITIS What is the function of the pericardium?
Restrains the filling volume of the heart
132
PERICARDITIS what is the innervation of the pericardium?
phrenic nerve
133
PERICARDITIS what is the pathophysiology of pericarditis?
- Pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes - A fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop
134
PERICARDITIS Describe the aetiology of pericarditis
IDIOPATHIC VIRUSES (most common = coxsackie), mumps, EBV, CMV, varicella, HIV less common - autoimmune - TB - trauma - uraemia secondary to kidney disease - post-MI syndrome - dressler syndrome - connective tissue disorders - malignancy - hypothyroidism
135
PERICARDITIS Define acute pericarditis
Acute inflammation of the pericardium with or without effusion
136
PERICARDITIS Give 5 symptoms of pericarditis
1. CHEST PAIN - severe, sharp and pleuritic (worse on inspiration/lying flat - relieved by sitting forward) 2. Dyspnoea 3. Cough 4. Hiccups 5. Skin rash 6. Fever and myalgia 7. peripheral oedema
137
PERICARDITIS Describe the chest pain in acute pericarditis
Severe, sharp, pleuritic, rapid onset, can radiate to arm (trapezius ridge) Relieved by sitting up/leaning forward exacerbated by lying flat may last from hours to days
138
PERICARDITIS Why might someone with pericarditis have hiccups?
Due to irritation to the phrenic nerve
139
PERICARDITIS What is the major differential diagnosis of acute pericarditis?
Myocardial infarction
140
PERICARDITIS Name 3 differential diagnoses for acute pericarditis
1. MI 2. Angina 3. Pneumonia 4. Pleurisy 5. PE 6. GORD 7. pneumothorax
141
PERICARDITIS What investigations might you do on someone who you suspect to have pericarditis?
1. ECG - diagnostic 2. CXR 3. Bloods - FBC, ESR and CRP, Troponin 4. Echocardiogram - usually normal, rule out silent pericardial effusion
142
PERICARDITIS What might the ECG look like in someone with acute pericarditis?
1. Saddle shaped ST elevation 2. PR depression
143
PERICARDITIS What does a raised troponin in acute pericarditis suggest?
Myopericarditis
144
PERICARDITIS How can acute pericarditis be clinically diagnosed?
Patient has to have at least 2 of the following: 1. Chest pain 2. Friction rub 3. ECG changes 4. Pericardial effusion
145
PERICARDITIS where is the pericardial rub heard?
left sternal edge as patient leans forward
146
PERICARDITIS What is the treatment for pericarditis?
idiopathic/viral - 1st line = NSAIDs + colchicine - 2nd line = NSAIDs, colchicine + low-dose prednisolone bacterial - IV antibiotics + pericardiocentesis with washout, cultures
147
PERICARDITIS what are the complications?
- pericardial effusion - cardiac tamponade - myocarditis - constrictive pericarditis
148
PERICARDITIS What is the treatment for chronic constrictive pericarditis?
Surgical excision of thickened pericardium
149
PERICARDITIS What is haemopericaridum?
Direct bleeding from vasculature through the ventricular wall following MI
150
PERICARDIAL EFFUSION What is pericardial effusion?
Abnormal accumulation of fluid in the pericardial cavity It commonly accompanies an episode of acute pericarditis
151
PERICARDIAL EFFUSION What is a complication of pericardial effusion?
Cardiac tamponade
152
PERICARDIAL EFFUSION Why does chronic pericardial effusion rarely cause tamponade?
Parietal pericardium is able to adapt when effusion accumulate slowly and so tamponade is prevented
153
CARDIAC TAMPONADE what is cardiac tamponade?
Cardiac tamponade occurs when a large amount of pericardial fluid restricts diastolic ventricular filling and causes marked reduction in cardiac output
154
CARDIAC TAMPONADE Briefly explain the pathophysiology of cardiac tamponade
Accumulation of pericardial fluid --> increase in intra-pericardial pressure --> poor ventricular filling --> decrease in CO
155
CARDIAC TAMPONADE what are the causes?
idiopathic pericarditis iatrogenic (cardiothoracic surgery) malignancy aortic dissection rheumatological - SLE, RA, scleroderma
156
CARDIAC TAMPONADE What are the signs of Cardiac tamponade?
Beck's triad: 1. low BP but high HR 2. Increased JVP 3. Quiet S1 and S2 - Pulsus paradoxus = pulses fade on inspiration - Kussmaul's sign = rise in jugular venous pressure with inspiration
157
CARDIAC TAMPONADE what are the symptoms?
- shortness of breath - chest discomfort - peripheral oedema - confusion
158
CARDIAC TAMPONADE what are the investigations for cardiac tamponade?
- ECG – tachycardia + electrical alternans - trans-thoracic echo (TTE) is diagnostic – echo-free space around heart - CXR - enlarged heart - bloods - inflammatory markers, troponin
159
CARDIAC TAMPONADE What is the treatment of cardiac tamponade?
Pericardiocentesis (drainage)
160
What is chronic constrictive pericarditis?
Calcification thickens the pericardium and affects cardiac effusion
161
MYOCARDITIS What can cause myocarditis?
most common = coxsackie B others Viral infection - coxsackie B, adenovirus, herpes lyme disease toxoplasmosis autoimmune - SLE, dermatomyositis, sarcoidosis drug-induced - antipsychotics, immunotherapies hypersensitivity reactions
162
MYOCARDITIS what are the risk factors?
peri-partum and post-natal periods Younger age Exposure to certain drugs or allergens Background of autoimmune conditions
163
MYOCARDITIS what are the clinical features?
SIGNS tachycardia fever displaced apex beat S3 gallop peripheral oedema SYMPTOMS chest pain - worse lying flat, improved by sitting forward shortness of breath fatigue syncope palpitations
164
MYOCARDITIS what are the investigations?
- ECG (sinus tachy, T wave inversions) - serum troponin/CK MB - CRP/ESR (may be elevated) - echo
165
MYOCARDITIS what is the management?
- supportive care (bed rest, fluid balance, oxygen) - immunosuppressive therapy if autoimmune - heart failure therapies (ACEi, BB, diuretics)
166
PVD what is the epidemiology of peripheral vascular disease?
Men > women Usually affects the aorta-iliac and infra-inguinal arteries
167
PVD what is the pathophysiology of peripheral vascular disease?
Commonly atherosclerosis leading to claudication of vessels Other (rarer) causes of claudication: - aortic coarctation, - temporal arteritis, - Buerger’s disease. End stage PVD= Critical Limb Ischaemia (6 P’s)
168
PVD Give 5 risk factors for peripheral vascular disease
Smoking Diabetes HTN Sedentary lifestyle Hyperlipidaemia History of CAD Age (>40)
169
PVD what is the clinical presentation of peripheral vascular disease?
- Pain in lower limbs on exercise, relieved on rest- intermittent claudication - Severe unremitting pain in foot (esp at night- hangs foot out of bed) - Leg may be pale, cold, loss of hair, skin changes
170
PVD what are the investigations for peripheral vascular disease?
1st line = ankle brachial pressure index (ABPI), duplex ultrasound < 0.3 = critical ischaemia ECG Bloods - FBX, U&E, random glucose/HbA1c, serum cholesterol, lipid profile
171
PVD what classification is used?
fontaine classification for different stages of PVD
172
PVD what are the different stages of PVD?
1 = asymptomatic 2 = intermittent claudication 3 = critical limb ischaemia 4 = tissue loss (ulceration/gangrene)
173
PVD what is the site of the disease when the claudication is at the following sites? 1. unilateral buttock 2. unilateral thigh 3. unilateral calf
buttock = common iliac thigh = common femoral calf = superficial femoral
174
PVD what are the treatments for peripheral vascular disease?
- exercise control risk factors - stop smoking - diabetes control - HTN control - diet/weight management - statin (atorvastatin 80mg) - antiplatelet (clopidogrel 75mg) surgery - endovascular procedures - bypass surgery
175
CRITICAL LIMB ISCHAEMIA What is critical limb ischaemia?
Critical limb ischaemia is defined as rest or night pain for greater than 2 weeks , with or without tissue loss such as ulceration It is a form of chronic limb ischaemia
176
CRITICAL LIMB ISCHAEMIA what are the risk factors?
- increasing age - PVD - CVD co-morbidities (diabetes, HTN, hypercholesterolaemia, obesity) - family history of vascular disease - smoking - sedentary lifestyle
177
CRITICAL LIMB ISCHAEMIA what are the clinical features?
- nocturnal resting pain for >2 weeks - evidence of aortoiliac disease - cool peripheries SIGNS - non-healing ulcer - surrounded by shiny hairless skin - gangrene - absent/diminished pulses - reactive hyperemia
178
CRITICAL LIMB ISCHAEMIA how is the pain described?
aching pain at rest often nocturnal patients often hang their legs out of the bed to relieve the pain
179
CRITICAL LIMB ISCHAEMIA what is aortoiliac disease?
also known as Leriche syndrome triad of: - claudication of buttocks and thighs - absent or decreased femoral pulses - erectile dysfunction
180
CRITICAL LIMB ISCHAEMIA what are the investigations?
1st line = duplex USS. ABPI 0.5-0.9 = claudication <0.5 = critical limb ischaemia
181
CRITICAL LIMB ISCHAEMIA what is the treatment for critical limb ischaemia?
Revascularisation (e.g. stenting, angioplasty, bypassing) Amputation if unsuitable
182
ACUTE LIMB ISCHAEMIA what is it?
a sudden decrease in perfusion due to arterial occlusion, and can result in rapid ischaemia.
183
ACUTE LIMB ISCHAEMIA What can cause acute ischaemia?
Embolism/thrombosis - AF - MI - valvular vegetations
184
ACUTE LIMB ISCHAEMIA what is the most common site of embolisation?
femoral artery
185
ACUTE LIMB ISCHAEMIA when are different tissues affected by lack of blood?
nerves = after 6 hrs muscles = after 6-10 hrs skin = last to show
186
ACUTE LIMB ISCHAEMIA what are the risk factors?
modifiable - diabetes - smoking - HTN - sedentary lifestyle non-modifiable - family history of CVD - age >40
187
ACUTE LIMB ISCHAEMIA Give 6 symptoms of acute ischaemia
1. Pain 2. Pale 3. Paralysis 4. Paraesthesia 5. Perishing cold 6. Pulseless
188
ACUTE LIMB ISCHAEMIA how can you tell if the cause is embolic or thrombotic?
EMBOLIC - sudden onset - cardiac history - arrhythmia (AF) - cold mottled skin - clear demarkation THROMBOTIC - progressive onset - no cardiac history - peripheral artery disease - no arrhythmias - cool and cyanotic - no clear demarkation
189
ACUTE LIMB ISCHAEMIA what are the investigations?
1st line = duplex USS ABPI ECG contrast-enhanced CT angiogram
190
ACUTE LIMB ISCHAEMIA what is the classification?
rutherford classification 1 = viable 2= threatened 3 = irreversible
191
ACUTE LIMB ISCHAEMIA what is the management?
initially LMWH based on rutherford classification I (viable) = catheter-directed thrombolysis/thrombectomy (within 6-24hrs) IIa = catheter-directed thrombolysis or percutaneous thromboembolectomy IIb = percutaneous/open thromboembolectomy, bypass surgery III = amputation
192
HEART FAILURE Define heart failure
cardiac output struggles to meet the metabolic demands of the body
193
HEART FAILURE what are the different categories of heart failure?
HF with reduced ejection fraction (systolic dysfunction) HF with preserved ejection fraction (diastolic dysfunction) Left sided HF Right sided HF
194
HEART FAILURE what are the causes of HF with reduced ejection fraction (systolic dysfunction)?
damage to myocytes e.g. ischaemic heart disease
195
HEART FAILURE what are the causes of HF with preserved ejection fraction (diastolic dysfunction)?
increased ventricular stiffness e.g. HTN reduced relaxation e.g. constrictive pericarditis
196
HEART FAILURE what are the causes of left sided HF?
increased LV afterload e.g. HTN increased LV preload e.g. aortic regurgitation
197
HEART FAILURE what are the causes of right sided HF?
increased RV afterload e.g. pulmonary HTN increased RV preload e.g. tricuspid regurgitation
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HEART FAILURE what are the risk factors for heart failure?
1. >65 y/o 2. African descent 3. Men 4. Obesity 5. Previous MI - previous MI - HTN - valvular disease - arrhythmias - cor pulmonale - T2DM - renal failure
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HEART FAILURE Why are men more commonly effected by heart failure than women?
Women have 'protective hormones' meaning they are less at risk of developing HF
200
HEART FAILURE Describe the pathophysiology of heart failure
When the heart fails, compensatory mechanisms attempt to maintain CO As HF progresses, these mechanism are exhausted and become pathophysiological
201
HEART FAILURE What are the compensatory mechanisms in heart failure?
1. Sympathetic system 2. RAAS 3. Natriuretic peptides 4. Ventricular dilation 5. Ventricular hypertrophy
202
HEART FAILURE What are the 3 cardinal symptoms of heart failure?
1. SOB 2. Fatigue 3. Peripheral oedema
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HEART FAILURE what are the clinical signs of left heart failure?
1. Pulmonary crackles 2. S3 and S4 and murmurs 3. Displaced apex beat 4. Tachycardia 5. fatigue
204
HEART FAILURE what are the clinical features of right HF?
1. Raised JVP 2. Ascites 3. peripheral oedema
205
HEART FAILURE what are the clinical features of heart failure?
SOFA PC - shortness of breath - orthopnea - fatigue - ankle swelling - pulmonary oedema (due to backflow from decreased CO; produced cough with pink frothy sputum) - cold peripheries Raised JVP End respiratory crackles
206
HEART FAILURE what is the classification system for heart failure?
New York heart association (NYHA)
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HEART FAILURE What investigations might you do initially do in someone who you suspect has HF?
1. ECG 2. CXR 3. BNP - brain natriuretic peptide 4. Trans-thoracic echo (TTE)
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HEART FAILURE What 4 signs might you see on a CXR taken from someone with HF?
ABCDE A - alveolar oedema (bat wing shadowing) B - Kerley B lines C - cardiomegaly D - dilated upper lobe vessels E - effusions (pleural)
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HEART FAILURE what is the management for chronic HF?
1st line = BB + ACEi (started one at a time) If ACEi not tolerated, try ARB or hydralazine with nitrate 2nd line = aldosterone antagonist (SPIRONOLACTONE) 3rd line = cardiac resynchronisation therapy (CRT) or ICD insertion, digoxin (particularly in AF) or ivabradine other options: - fluid restriction - loop diuretics (for symptom management) - annual flu + pneumococcal vaccine
210
Give an example of an ACEi that is commonly used in HF
Ramipril
211
What is cor pulmonale?
Right sided heart failure caused by chronic pulmonary arterial hypertension
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Name 3 BB that are used in treatment of HF
1. Propranolol 2. Bisoprolol 3. Atenolol 4. Carvedilol
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HEART FAILURE what is the treatment for acute HF?
- treat any underlying causes - oxygen if SpO2<94% - fluid restriction <1.5L - IV diuretic (furosemide) - inotropes/vasopressors (dobutamine)
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What might you give to someone with hypertension if they are ACE inhibitor intolerant?
Angiotensin receptor blocker (ARB) - losartan, valsartan, candesartan
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HEART FAILURE How can chronic HF be prevented?
Stop smoking Eat more healthy Exercise Avoid large meals Vaccinations Treat underlying cause - dysarrhythmias or valve disease
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HTN What is the clinical definition of hypertension?
BP > 140/90 mmHg
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HTN Name 4 conditions that hypertension is a major risk factor for
1. Stroke 2. MI 3. HF 4. Chronic renal failure 5. Cognitive decline 6. Premature death
218
HTN What are the blood pressure readings for someone to be diagnosed with Stage 1 hypertension?
Clinic BP = 140/90 ABPM = 135/85
219
HTN What are the blood pressure readings for someone to be diagnosed with Stage 2 hypertension?
Clinic BP = 160/100 ABPM = 150/95
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HTN What are the blood pressure readings for someone to be diagnosed with severe hypertension?
Systolic BP = >180 Diastolic BP = >110
221
HTN Name the 2 types of hypertension
1. Essential (primary) hypertension 2. Secondary hypertension
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HTN What causes essential hypertension?
Unknown cause - multifactorial involving: - genetic susceptibility - Excessive sympathetic nervous system activity - Abnormalities of Na+/K+ membrane transport - High salt intake - Abnormalities in renin-angiotensin-aldosterone system
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HTN Give 5 causes of secondary hypertension
ROPE R - renal disease O - obesity P - pregnancy E - endocrine (Conn's, Cushing's, pheochromocytoma) most common = primary hyperaldosteronism - Conn's syndrome
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HTN Name 3 endocrine disease that can cause secondary hypertension
1. Conn's syndrome - hyperaldosteronism 2. Cushing's syndrome - excess cortisol --> increase BP 3. Phaemochromocytoma - adrenal gland tumour, excess catecholamines --> high BP 4. hyperthyroidism 5. acromegaly
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HTN Name 5 risk factor for hypertension
Modifiable: - alcohol intake - sedentary lifestyle - diabetes mellitus - sleep apnoea - smoking Non-modifiable: - Increasing age - family history - ethnicity - afro-Caribbean
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HTN What is the clinical presentation of hypertension?
Usually asymptomatic Found on screening headaches - occipital, worse in morning
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HTN what is the clinical presentation of malignant hypertension?
hypertensive retinopathy visual disturbance cardiac symptoms e.g. chest pain oliguria or polyuria
228
HTN Why might you examine the eyes of someone with hypertension?
Very high BP can cause immediate damage to small vessels --> seen in the eyes --> retinopathy
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HTN What investigations might you do in someone with hypertension?
1. 24 hour ambulatory blood pressure monitoring --> confirm diagnosis 2. ECG and Bloods --> identify secondary causes - urinalysis - protein, albumin:creatine ratio, haematuria - blood tests - serum creatinine, eGFR, glucose - fundoscopy - retinal haemorrhage, papillodema - ECG - left ventricular hypertrophy
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HTN What is the treatment target for hypertension for the following: a) People aged <80? b) People aged >80?
a) < 140/90 mmHg b) < 150/90 mmHg
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HTN What are the 2 main types of treatment for hypertension?
1. Lifestyle modifications - reduce salt, loss weight, reduce alcohol 2. Drug therapy = ACD
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HTN Describe the pharmacological intervention for someone with hypertension
IF <55 OR T2DM 1. ACEi/ARB 2. ACEi/ARB + CCB or ACEi/ARB + thiazide-like diuretic (indapamide) 3. ACEi/ARB + CCB + thiazide-like diuretic 4. if K+<4.5 add spironolactone, if K+>4.5 add alpha/beta-blocker IF >55 + NO T2DM OR BLACK 1. CCB 2. CCB + ACEi/ARB* or CCB + thiazide like diuretic 3. CCB + ACEi/ARB* + thiazide-like diuretic 4. if K+<4.5 add spironolactone, if K+>4.5 add alpha/beta-blocker *note ARB is preferred in african-caribbean/black ethnicities
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HTN what is the first line for patients <55 or T2DM?
ACEi if afro-caribbean + T2DM, ARB more preferable
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HTN what is the first line therapy for >55 or afro-caribbean (any age)
CCB
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HTN What other pharmacological interventions might you give to someone with hypertension (except ACD)?
Beta blockers - bisoprolol statins - simvastatin
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HTN Will anti-hypertensives make someone feel better?
No, usually treating hypertension doesn't relive symptoms except headache
237
HTN Write an equation for BP
BP = CO x TPR
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PHARMACOLOGY Name 2 systems that are targeted pharmacologically in the treatment of hypertension
1. RAAS 2. Sympathetic nervous system
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PHARMACOLOGY Give 4 functions of angiontensin II
1. Potent vasoconstrictor 2. Activated sympathetic nervous system - increased NAd 3. Activates aldosterone - Na+ retention 4. Vascular growth, hyperplasia and hypertrophy
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PHARMACOLOGY Give 3 ways in which the Sympathetic nervous system (NAd) leads to increased BP
1. Noradrenaline is a vasoconstrictor = increase TPR 2. NAd has positive chronotropic and inotropic effects 3. It can cause increase renin release
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PHARMACOLOGY In what diseases are ACE inhibitors clinically indicated?
1. Hypertension 2. Heart failure 3. Diabetic nephropathy
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PHARMACOLOGY Name 3 ACE inhibitors
1. Ramipril 2. Enalapril 3. Perindopril 4. Trandolapril 5. Lisinopril
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PHARMACOLOGY what are the side effects of ACE inhibitors?
1. Hypotension 2. Hyperkalaemia 3. Acute renal failure 4. Teratogenic 5. cough - from build up of kinin
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PHARMACOLOGY You see a patient who is taking ramipril. They say that since starting the medication they have had a dry and persistent cough. What might have caused this?
ACE inhibitors lead to a build up of kinin One of the side effects of this is a dry and chronic cough
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PHARMACOLOGY What are ARBs?
Angiotensin II receptor blockers
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PHARMACOLOGY At which receptor do ARB's work?
AT-1 receptor - prevent angiotensin II binding
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PHARMACOLOGY In what diseases are ARBs clinically indicated?
1. Hypertension 2. Heart failure 3. Diabetic nephropathy
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PHARMACOLOGY Name 3 ARBs
1. Candesartan 2. Valsartan 3. Losartan
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HTN A patient with hypertension has come to see you about their medication. You see in their notes that ACE inhibitors are contraindicated. What might you prescribe them instead?
An ARB e.g. candesartan
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PHARMACOLOGY Give 4 potential side effect of ARBs
1. Hypotension 2. Hyperkalaemia 3. Renal dysfunction 4. Rash Contraindicated in pregnancy
251
PHARMACOLOGY In what diseases are calcium channel blockers clinically indicated?
1. Hypertension 2. IHD 3. Arrhythmia
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PHARMACOLOGY Name 2 calcium channel blockers
1. Amlopipine 2. Felodipine 3. Diltiazem 4. Verapamil
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PHARMACOLOGY Name 2 dihydropyridines and briefly explain how they work
Class of CCBs Amlodipine and felodipine Arterial vasodilators
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PHARMACOLOGY Name a calcium channel blocker that acts primarily on the heart
Verapamil Negatively chronotropic and inotropic (reduce HR and force of contraction)
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PHARMACOLOGY Name a CCB that acts on the heart and on blood vessels
Diltiazem
256
PHARMACOLOGY On what channels do CCB work?
L type Ca2+ channels
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PHARMACOLOGY Give 3 potential side effects that are due to the vasodilatory ability of CCBs
1. Flushing 2. Headache 3. Oedema 4. Palpitations
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PHARMACOLOGY Give 2 potential side effects that are due to the negatively chronotropic ability of CCBs
1. Bradycardia 2. Atrioventricular block 3. Postural hypotension
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PHARMACOLOGY Give a potential side effect that is due to the negatively inotropic ability of CCBs
Worsening cardiac failure
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PHARMACOLOGY Give 4 potential side effects of verapamil
1. Worsening of cardiac failure (-ve inotrope) 2. Bradycardia (-ve chronotrope) 3. Atrioventricular block (-ve chronotrope) 4. Constipation
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PHARMACOLOGY A patient comes to see you who has recently started taking calcium channel blockers for their hypertension. They complain of constipation. What calcium channel blocker might they be taking?
Verapamil
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PHARMACOLOGY In what diseases are beta blockers clinically indicated?
1. IHD 2. Heart failure 3. Arrhythmia 4. Hypertension
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PHARMACOLOGY Name 3 beta blockers
1. Bisoprolol (beta 1 elective) 2. Atenolol 3. Propranolol (beta 1/2 nonselective)
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PHARMACOLOGY Give 5 potential side effects of beta blockers
1. Fatigue 2. Headache 3. Sleep disturbances/nightmares 4. Bradycardia 5. Hypotension 6. Cold peripheries 7. Erectile dysfunction 8. Bronchospasm
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PHARMACOLOGY Give 3 conditions in which Beta blockers can worsen them
1. Asthma or COPD 2. PVD 3. Heart failure
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PHARMACOLOGY In what diseases are diuretics clinically indicated?
1. Heart failure 2. Hypertension
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PHARMACOLOGY Name 4 classes of diuretics
1. Thiazides 2. Loop 3. Potassium sparing 4. Aldosterone antagonists
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PHARMACOLOGY Where in the kidney do thiazide diuretics work?
The distal tubule
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PHARMACOLOGY Name a thiazide
Bendroflumethethiazide
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PHARMACOLOGY Name a loop diuretic
Furosemide Bumetanide
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PHARMACOLOGY Name a potassium sparing diuretic
Spironolactone Eplerenone
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PHARMACOLOGY Why are potassium sparing diuretics especially effective?
They have anti-aldosterone effects too
273
PHARMACOLOGY Give 5 potential side effects of diuretics
1. Hypovolaemia 2. Hypotension 3. Reduced serum Na+, K+, Mg+, Ca2+ 4. Increased uric acid --> gout 5. Erectile dysfunciton 6. Impaired glucose tolerance
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HTN You see a 45 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?
ACE inhibitors e.g. ramapril or ARB e.g. candesartan
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HTN You see a 65 y/o patient who has recently been diagnosed with hypertension. What is the first line treatment?
Calcium channel blockers (as this patient is over 55) e.g. amlodipine
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HTN You see a 45 y/o patient who has recently started taking ACE inhibitors for their hypertension. Unfortunately their hypertension still isn't controlled. What would you do next for this patient?
You would combine ACE inhibitors or ARB with calcium channel blockers
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HTN You see a 45 y/o patient who has been taking ACE inhibitors and calcium channel blockers for their hypertension. Following several tests you notice that their blood pressure is still high. What would you do next for this patient?
You would combine the ACEi/ARB and calcium channel blockers with a thiazide-like diuretic e.g. indapamide
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PHARMACOLOGY What is the counter regulatory system to RAAS?
Atrial Natriuretic Peptide/BNP (ventricular natriuretic peptide) hormones
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PHARMACOLOGY Where are ANP and BNP produced?
The heart
280
PHARMACOLOGY What metabolises ANP and BNP?
Neprilysin (NEP)
281
PHARMACOLOGY What are the functions of ANP and BNP?
1. Increased renal excretion of Na+ and water 2. Vasodilators 3. Inhibit aldosterone release
282
PHARMACOLOGY Why can Neprilysin (NEP) inhibitors work for heart failure treatment?
NEP metabolises ANP and BNP NEP inhibitors therefore increase levels of ANP and BNP in the serum
283
PHARMACOLOGY In what diseases are nitrates clinically indicated?
1. IHD 2. Heart failure
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PHARMACOLOGY Name 2 nitrates that are used pharmacologically
1. GTN spray (short acting) 2. Isosorbide mononitrate (long acting)
285
PHARMACOLOGY How do nitrates work in the treatment of heart failure?
They are venodilators so reduce preload and therefore BP
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PHARMACOLOGY Give 2 potential side effects of nitrates
1. Headache 2. GTN syncope 3. Tolerance
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PHARMACOLOGY How do anti-arrhythmic drugs work?
Interfere with the action potential of the heart in different phases
288
PHARMACOLOGY What classification is used to group anti-arrhythmic drugs?
Vaughan Williams classification
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PHARMACOLOGY Name two class 1 drugs of the Vaughan Williams classification
Class 1 are Na+ channel blockers 1a = disopyramide, quinidine 1b = lidocaine 1c = flecainide (tachycardias)
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PHARMACOLOGY Name three class 2 drugs of the Vaughan Williams classification
Class 2 are Beta blockers Propranolol Atenolol Bisoprolol
291
PHARMACOLOGY Name a class 3 drug of the Vaughan Williams classification
Class 3 rugs prolong the action potential Amiodarone Side effects are likely with these
292
PHARMACOLOGY Name two class 4 drugs of the Vaughan Williams classification
Class 4 drugs are calcium channel blockers (but NOT dihydropyridines as they don't effect the heart) Verapamil Dilitiazem
293
PHARMACOLOGY How does digoxin work?
Inhibits the Na+/K+ pump therefore making the action potential more positive and ACh is released from parasympathetic nerves
294
PHARMACOLOGY What are the main effect of digoxin?
1. Bradycardia 2. Reduced atrioventricular conduction 3. Increased force of contraction (positive inotrope)
295
PHARMACOLOGY Give 3 potential side effects of digoxin
1. Nausea 2. Vomiting 3. Diarrhoea 4. Confusion Also has a narrow therapeutic range
296
PHARMACOLOGY In what disease is digoxin clinically indicated?
1. Atrial fibrillation 2. Severe heart failure
297
PHARMACOLOGY What does furosemide block?
The Na+/K+/2Cl- transporter
298
PHARMACOLOGY Why are beta blockers good in chronic heart failure?
They block reflex sympathetic responses which stress the failing heart
299
PHARMACOLOGY How does amiodarone work?
Prolongs action potential by delaying depolarisation
300
PHARMACOLOGY Name 4 potential effects of amiodarone
1. QT prolongation 2. Interstitial lung disease 3. Hypothyroidism 4. Abnormal liver enzymes
301
ABNORMAL ECGS What aspect of the heart is represented by leads II, III and aVF?
Inferior aspect
302
ABNORMAL ECGS What might ST elevation in leads II, II and aVF suggest?
RCA blockage Leads represent inferior aspect of heart, RCA supplies inferior aspect
303
ABNORMAL ECGS Give 3 effects hyperkalaemia on an ECG
GO - absent P wave GO TALL - tall T wave GO long - prolonged PR GO wide - wide QRS
304
ABNORMAL ECGS Give 2 effects of hypokalaemia on an ECG
1. Flat T waves 2. QT prolongation 3. ST depression 4. Prominent U waves
305
ABNORMAL ECGS Give an effect go hypocalcaemia on an ECG
1. QT prolongation 2. T wave flattening 3. Narrowed QRS 4. Prominent U waves
306
ABNORMAL ECGS Give an effect of hypercalcaemia on an ECG
1. QT shortening 2. Tall T wave 3. No P waves
307
ARRHYTHMIAS What controls the sinus node discharge rate?
Autonomic nervous system
308
ARRHYTHMIAS Define sinus rhythm
A P wave precedes each QRS complex
309
ARRHYTHMIAS Define cardiac arrhythmia
Abnormality of cardiac rhythm
310
ARRHYTHMIAS Give 3 potential consequences of arrhythmia
1. Sudden death 2. Syncope 3. Heart failure 4. Chest pain 5. Palpitations May also be asymptomatic
311
ARRHYTHMIAS Define bradycardia
< 60 bpm
312
TACHYCARDIA Define tachycardia
> 100 bpm
313
BRADYCARDIA Give 2 causes of bradycardia
1. Conduction tissue fibrosis 2. Ischaemia 3. Inflammation/infiltrative disease 4. Drugs
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BRADYCARDIA what are the adverse clinical features for bradycardia?
- shock (hypotension, pallor, sweating, cold, clammy, confusion or impaired consciousness) - syncope - MI - HF
315
BARDYCARDIA what is the emergency management?
LIFE-THREATENING FEATURES - 1st line = atropine 500 micrograms IV - if response unsatisfactory repeat 500 micrograms atropine (up to max 3mg), or adrenaline 2-10 micrograms IV, - arrange transvenous pacing NO LIFE-THREATENING FEATURES - if risk of asystole treat as above - if not at risk of asystole, observe
316
BRADYCARDIA what are the risk factors for asystole in bradycardia?
- complete heart block with broad QRS - recent asystole - Mobitz type II AV block - ventricular pause > 3 seconds
317
TACHYCARDIA Give 2 broad categories of tachycardia
1. Supraventricular tachycardias 2. Ventricular tachycardias
318
TACHYCARDIA What are the signs of unstable tachycardia?
- shock (hypotension, pallor, sweating, cold, confusion) - syncope - MI - heart failure
319
TACHYCARDIA what is the emergency management?
ADVERSE SIGNS PRESENT - 1st line = synchronised DC cardioversion (up to 3 shocks) treat according to whether SVT or VT
320
SVT what is it?
any tachyarrhythmia arising above the Bundle of His AVNRT is the most common type
321
SVT what are the different types?
ATRIAL + REGULAR - sinus tachycardia - atrial tachycardia - atrial flutter ATRIAL + IRREGULAR - AF AV NODE - AVRT (including Wolff-Parkinson-White syndrome) - AVNRT - junctional tachycardia
322
SVT are the QRS complexes broad or narrow in SVT?
narrow (<0.12s)
323
SVT what are the risk factors?
- increasing age - female - hyperthyroidism - smoking - excessive caffeine or alcohol - stress - medication (salbutamol, atropine, decongestants) - recreational drug use (cocaine, methamphetamines)
324
SVT what are the clinical features?
SYMPTOMS - may be asymptomatic - palpitations - SOB - dizziness - life-threatening (chest pain, syncope, confusion, sweating) SIGNS - tachycardia - tachypnoea - life threatening (hypotension, pallor, cold + clammy, pulmonary oedema, raised JVP)
325
SVT what are the life-threatening features?
shock (hypotension, pallor, sweating, cold extremities) syncope myocardial ischaemia (chest pain) heart failure (pulmonary oedema, raised JVP)
326
SVT what are the investigations?
12 lead ECG = regular, narrow complex tachycardia, 151-250 bpm to consider - TFTs = hyperthyroidism - U&Es + metabolic panel
327
SVT what is the management?
UNSTABLE - synchronised DC shock (up to 3 attempts) - if unsuccessful, 300mg amiodarone IV + repeat shock STABLE - 1st line = vagal manoeuvres (Valsalva, carotid sinus massage) - 2nd line = adenosine 6mg, if unsuccessful give 12mg then 18mg - 3rd line = verapamil or BB - long term = catheter ablation
328
SVT what are the complications?
- syncope - congestive heart failure - life-threatening arrhythmias - sudden death
329
WPW what is Wolff-Parkinson-White syndrome?
a congenital pre-excitation syndrome that occurs due to presence of an accessory electrical pathway between atria and ventricles
330
WPW what are the clinical features of Wolff-Parkinson-White syndrome?
- often asymptomatic - palpitations - dizziness - syncope
331
WPW what are the investigations?
12 LEAD ECG - delta waves (slurred upstroke in QRS) - short PR interval (<120ms) - broadened QRS if a re-entrant circuit has developed, there will be narrow complex tachycardia BLOODS - TFTs IMAGING - echocardiogram - cardiac catheterisation
332
WPW what is the management?
CONSERVATIVE - if asymptomatic, may be monitored MEDICAL - amiodarone - sotalol INTERVENTIONAL AND SURGICAL - radiofrequency ablation EMERGENCY TREATMENT - if unstable = synchronised DC cardioversion - stable + narrow QRS, 1st line = vagal manoeuvres, 2nd line = adenosine - stable + broad QRS 1st line = procainamide or flecainide, 2nd line = DC cardioversion
333
WPW which drugs are contraindicated in WPW syndrome?
any drugs that block AVN activity could cause dangerous arrhythmias - digoxin - adenosine - non-dihydropyridine CCBs (verapamil and diltiazem)
334
ATRIAL FIBRILLATION Define atrial fibrillation
Chaotic irregular atrial rhythm at 300-600 bpm AV node responds intermittently – irregular ventricular rate
335
ATRIAL FIBRILLATION what are the risk factors?
- increasing age - DM - hyperthyroidism - HTN - congestive heart failure - valvular heart disease - coronary artery disease - dietary + lifestyle (excessive caffeine, alcohol, smoking, medication use (thyroxine or beta-agonists))
336
ATRIAL FIBRILLATION what are the different types?
- first episode - paroxysmal ( recurrent episodes that stop on their own in <7 days) - persistent (recurrent episodes last >7days) - permanent (continuous AF that is refractory to treatment)
337
ATRIAL FIBRILLATION what is the clinical presentation of atrial fibrillation?
SYMPTOMS - palpitations - dyspnoea - chest pain (red flag) - syncope (red flag) SIGNS - irregularly irregular pulse - hypotension (red flag) - evidence of HF (red flag)
338
ATRIAL FIBRILLATION what are the causes of atrial fibrillation?
PIRATES Pulmonary - PE, COPD Ischaemic heart disease Rheumatic heart disease Anaemia, Alcohol, Advancing age Thyroid disease (hyperthyroid) Electrolyte disturbance (hypo/hyperkalaemia) Sepsis, Sleep apnoea
339
ATRIAL FIBRILLATION Briefly describe the pathophysiology of atrial fibrillation
continuous rapid activation of the atria with no organised mechanical action at 300-600bpm
340
ATRIAL FIBRILLATION what are the investigations?
- ECG (irregular QRS complexes, absent P waves + chaotic baseline) - serum electrolytes including magnesium, calcium + phosphate - TFTs to consider - troponin - CXR - transthoracic echo
341
ATRIAL FIBRILLATION Describe 2 characterics of an ECG taken from someone with atrial fibrillation
1. Absent P waves 2. Irregular and rapid QRS complexes 3. Fine oscillation of the baseline 'Irregularly irregular'
342
ATRIAL FIBRILLATION What score can be used to calculate the risk of stroke in someone with atrial fibrillation?
CHA2D2 VAS
343
ATRIAL FIBRILLATION What does the CHA2DS2 VASc score take into account
CHD HTN Age (>75) = 2 points DM Stroke (previous) = 2 points Vascular disease Age 65-74 Sex (female) Score >1 = anticoagulation
344
ATRIIAL FIBRILLATION what features would suggest the need for synchronised DC cardioversion?
- shock (HTN, pallor, sweating, col, clammy extremities, confusion or LOC) - syncope - MI - Heart failure (pulmonary oedema +/- raised JVP)
345
ATRIAL FIBRILLATION Describe the treatment for atrial fibrillation
HAEMODYNAMICALLY UNSTABLE - 1st line = synchronised DV cardioversion STABLE onset <48hrs - 1st line = rate control (BB or CCB)* - 2nd line = rhythm control (flecanide or amiodarone) onset >48hrs - 1st line = rate control (BB or CCB)* + anticoagulation for at least 3 weeks, then offer rhythm control if appropriate *consider digoxin 1st line in patients with AF + HF, those who do no exercise or other drugs excluded avoid CCB in HF avoid non-selective BB (e.g. propranolol) in asthma
346
ATRIAL FIBRILLATION which medications are used for rate control?
1st line = beta-blocker (bisoprolol) or CCB (diltiazem/verapamil) consider digoxin 1st line when AF + HF 2nd line = combination therapy with any two - beta-blocker (bisoprolol) - diltiazem - digoxin
347
ATRIAL FIBRILLATION what medications are used for rhythm control?
if no structural/ischaemic heart disease = flecainide or amiodarone if structural/ischaemic heart disease = amiodarone
348
ATRIAL FIBRILLATION What is the long term treatment for atrial fibrillation?
Catheter ablation
349
ATRIAL FIBRILLATION if a patient undergoes ablation, do you stop anticoagulation?
do not stop anticoagulation even if AF is no longer detectable only stop after consulting CHADSVASC and HASBLED
350
ATRIAL FIBRILLATION what are the complications of atrial fibrillation?
- increased risk of stroke - due to static blood in the atria - the blood pools and it remains still, causing it to clot and embolise
351
ATRIAL FLUTTER What is atrial flutter?
Fast but organised waves in the atrium Atrial rate 250-350 bpm it is a type of AV re-entry tachycardia (AVRT)
352
ATRIAL FLUTTER Describe the ECG pattern taken from someone with atrial flutter
1. Narrow QRS 2. Saw tooth flutter (F) waves
353
ATRIAL FLUTTER Describe the pathophysiology of atrial flutter
the P wave produces a sawtooth pattern with regular conduction to the ventricles - Wave of contraction around the atria causing the repolarisation of the AV node
354
ATRIAL FLUTTER what are the risk factors for atrial flutter?
- atrial fibrillation
355
ATRIAL FLUTTER what are the causes of atrial flutter?
more likely to occur with pulmonary disease: - COPD - obstructive sleep apnoea - PE - pulmonary hypertension other causes: - ischaemic heart disease - sepsis - alcohol - cardiomyopathy - thyrotoxicosis
356
ATRIAL FLUTTER what is the clinical presentation of atrial flutter?
Palpitations Breathlessness chest pain Dizziness Syncope fatigue
357
ATRIAL FLUTTER what is the management for atrial flutter?
- Cardioversion - Give a LMWH - Shock with defibrillator - Catheter ablation = definitive treatment – creates a conduction block - IV Amiodarone – restore sinus rhythm
358
VENTRICULAR TACHYCARDIA what is it?
a broad-complex tachycardia originating from ventricles has potential to precipitate ventricular fibrillation (VF) so requires urgent treatment
359
VENTRICULAR TACHYCARDIA what are the risk factors?
- electrolyte abnormalities (hypokalaemia, hypomagnesaemia) - structural heart disease (previous MI, cardiomyopathies) - drugs causing QT prolongation (clarithromycin, erythromycin) - inherited channelopathies
360
VENTRICULAR TACHYCARDIA what are the different types?
- monomorphic VT (commonly caused by MI) - polymorphic VT (commonly caused by prolonged QT, example = torsade de pointes)
361
VENTRICULAR TACHYCARDIA what is the management of pulsed VT?
IF ADVERSE FEATURES PRESENT (HF, MI, shock syncope) - 1st line = synchronised DC cardioversion (up to 3 attempts) - 2nd line = amiodarone 300mg IV over 10-20 mins IF NO ADVERSE FEATURES PRESENT - 1st line = amiodarone 300mg IV - 2nd line = synchronised DC cardioversion if drug therapy fails - ICD implanted
362
TORSADES DE POINTES what is it?
a form of polymorphic VT associated with prolonged QT
363
TORSADES DE POINTES what are the causes?
- congenital - antiarrhythmics (amiodarone, sotalol) - tricyclic antidepressants - antipsychotics - chloroquine - erythromycin - electrolyte abnormalities (hypocalcaemia, hypokalaemia, hypomagnesaemia) - myocarditis - hypothermia - subarachnoid haemorrhage
364
TORSADES DE POINTES what is the management?
IV magnesium sulphate
365
ARRHYTHMIAS What are ectopic beats?
Non sustained beats arising from ectopic regions of atria or ventricles Very common, generally benign arrhythmias caused by premature discharge
366
LONG QT SYNDROME what are the causes of long QT syndrome?
1. Congenital 2. hypokalaemia, 3. hypocalcaemia 4. Drugs - amiodarone, tricyclic antidepressants 5. bradycardia 6. Acute MI 7. diabetes
367
LONG QT SYNDROME what is the clinical presentation of long QT syndrome?
SYMPTOMS - syncope - dizziness - palpitations - dyspnoea - collapse or sudden cardiac death SIGNS - sensorineural deafness (congenital)
368
LONG QT SYNDROME which abnormal heart rhythm are people with long QT syndrome at risk of developing?
torsades de pointes
369
LONG QT SYNDROME what is the management?
conservative - avoid precipitating factors beta-blocker (propranolol) to prevent ventricular arrhythmia ICD may be considered
370
HEART BLOCK Where can heart blocks occur?
1. Block in either AVN or bundle of His = AV block 2. Block lower in conduction system = Bundle Branch Block
371
HEART BLOCK Describe a first degree heart block
Fixed prolongation of the PR interval due to delayed conduction to the ventricles - PR interval >0.22s - asymptomatic
372
HEART BLOCK Describe a second degree heart block
There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles
373
HEART BLOCK Describe a Mobitz type 1 second degree heart block
PR interval gradually increases until AV node fails and no QRS is seen PR interval returns to normal and the cycle repeats
374
HEART BLOCK Describe a Mobitz type 2 second degree heart block
Sudden unpredictable loss of AV conduction and so loss of QRS PR interval is constant but every nth QRS is missing wide QRS
375
HEART BLOCK Describe a third degree heart block
Atrial activity fails to conduct to the ventricles P waves and QRS complexes occur independently ventricular contractions are maintained by spontaneous escape rhythm originating below the block
376
HEART BLOCK What are the treatments for heart blocks?
1st = asymptomatic, watch and wait --> atropine Mobitz 1 = no pacemaker if asymptomatic, pacemaker if symptomatic Mobitz 2 = pacemaker even if asymptomatic 3rd = transcutaneous pacing followed by permanent pacemaker
377
HEART BLOCK what are the causes of heart block?
Athletes Sick sinus syndrome IHD – esp MI Acute myocarditis Drugs Congenital Aortic valve calcification Cardiac surgery/trauma
378
BUNDLE BRANCH BLOCK What kind of heart block is associated with wide QRS complexes with an abnormal pattern?
Right bundle branch block (RBBB) and Left bundle branch block (LBBB)
379
BUNDLE BRANCH BLOCK Explain the pathophysiology of a BBB
Lack of simultaneous ventricular contractions LBBB = R before L RBBB = L before R
380
BUNDLE BRANCH BLOCK What changes would you see on an ECG from someone with a LBBB?
WiLLiaM slurred S wave in V1 (resembles W) R wave in V6 (resembles M) wide QRS with notched top in V6
381
BUNDLE BRANCH BLOCK What changes would you see on an ECG from someone with a RBBB?
MaRRoW R wave in V1 (resembles M) slurred S wave in V6 (resembles W) wide QRS RSR pattern in V1
382
ARRHYTHMIAS Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?
DC cardioversion
383
VALVE DISEASE Name 4 valvular heart diseases
1. Aortic stenosis 2. Mitral regurgitation 3. Mitral stenosis 4. Aortic regurgitation
384
VALVE DISEASE Why does medical intervention have a limited role in aortic and mitral stenosis treatment?
Aortic and mitral stenosis are mechanical problems
385
AORTIC STENOSIS what is it?
Narrowing of the aortic valve resulting in obstruction to left ventricular stroke volume
386
AORTIC STENOSIS Name the 3 types of aortic stenosis
1. Surpavalvular 2. Subvalvular 3. Valvular = most common
387
AORTIC STENOSIS What are the causes of aortic stenosis?
- Calcification and fibrosis of normal trileaflet aortic valve = 80% of cases - congenital bicuspid valve - rheumatic fever (rare, seen in developing countries)
388
AORTIC STENOSIS what are the risk factors?
- advancing age - congenital bicuspid valve (turners syndrome + coarctation of aorta) - rheumatic fever - chronic kidney disease - HTN - Smoking - mediastinal radiotherapy
389
AORTIC STENOSIS Describe the pathophysiology of aortic stenosis
Obstruction to left ventricular emptying results in left ventricular hypertrophy Increased myocardial oxygen demand, relative ischaemia of the myocardium and consequent angina and arrhythmias Left ventricular systolic function typically conserved
390
AORTIC STENOSIS what are the symptoms of aortic stenosis?
Occur when valve area is 1/4 of normal (normal - 3-4 cm2) - exertional dyspnea (SOB) - chest pain (angina-like) - exertional syncope - fatigue
391
AORTIC STENOSIS what are the signs of aortic stenosis?
MURMUR - ejection systolic murmur over aortic area - radiating to carotids and apex - crescendo-decrescendo - thrill if severe - left ventricular heave ASSOCIATED FEATURES - diminished S2 - slow rising pulse - narrow pulse pressure - S4 heart sound FEATURES OF HF - crackles - raised JVP - peripheral oedema
392
AORTIC STENOSIS What investigation might you do in someone who you suspect to have aortic stenosis?
ECG - L axis deviation - ST depression - increased R wave amplitude and S wave depth TTE (trans-thoracic echo) - aortic valve are reduced BLOODs - BNP raised if HF CXR - rule out respiratory pathology
393
AORTIC STENOSIS what murmur is heard with aortic stenosis?
- ejection systolic murmur over aortic area - radiating to carotids and apex - crescendo-decrescendo - thrill if severe - left ventricular heave
394
AORTIC STENOSIS Describe the management for someone with aortic stenosis
valve replacement via open heart surgery (SAVR) or transcatheter (TAVI) can have balloon valvuloplasty to stretch valve
395
AORTIC STENOSIS what factors affect treatment choice?
SAVR (open-surgery) - young - few comorbidities - need additional procedures e.g. CABG TAVI (trans-catheter) - older - multi-morbid - high operative risk
396
AORTIC STENOSIS what factors affect valve choice (bioprosthetic or mechanical)?
MECHANICAL - younger (mechanical valves are more durable) - suitable for anticoagulation BIOPROSTHETIC - older patients (>65) - anticoagulation contraindicated
397
AORTIC STENOSIS What are the indications for valve replacement
- severe aortic stenosis and symptomatic - severe aortic stenosis and asymptomatic but have one of the following - heart failure - symptoms on exercise testing
398
AORTIC STENOSIS what are the complications?
- heart failure - complications from surgery - endocarditis - valve thrombus - haemolysis - aortic regurgitation
399
MITRAL REGURGITATION What is mitral regurgitation?
Backflow of blood from the LV to the LA during systole LV volume overload
400
MITRAL REGURGITATION What can cause mitral regurgitation?
1. Myxomatous degeneration (mitral valve prolapse) - most common cause 2. Ischaemic mitral valve 3. Rheumatic heart disease 4. IE 5. dilating left ventricle
401
MITRAL REGURGITATION Describe the pathophysiology of mitral regurgitation
Circulatory changes depend on speed on onset and severity Long standing MR produces little increase in left atrial pressure – accommodated by large LV In acute MR an increased in LA pressure increases pulmonary venous pressure and pulmonary oedema Left ventricle dilates but more so in chronic MR
402
MITRAL REGURGITATION what are the risk factors?
- history of cardiac infection e.g. rheumatic fever, endocarditis - cardiac trauma - history of ischaemic heart disease e.g. MI - congenital heart disease - cardiomyopathy - HTN - structural heart disease - dopaminergic drugs e.g. cabergoline, pergolide
403
MITRAL REGURGITATION what are the symptoms of mitral regurgitation?
- Exertional dyspnoea - Reduced exercise tolerance - Fatigue - Paroxysmal nocturnal dyspnoea - Palpitations
404
MITRAL REGURGITATION what are the signs of mitral regurgitation?
MURMUR - Pan-systolic murmur - Radiates to left axilla - blowing at apex - S3 heart sound - Quiet S1 - displaced apex towards axilla
405
MITRAL REGURGITATION what is the murmur?
- Pan-systolic murmur - Radiates to left axilla - blowing at apex
406
MITRAL REGURGITATION What investigations might you do in someone who you suspect to have mitral regurgitation?
1. ECG 2. CXR 3. Echo 4. doppler and colour flow doppler to measure severity
407
MITRAL REGURGITATION What is the management of mitral regurgitation?
ACUTE SEVERE 1st line = emergency surgery to repair/replace CHRONIC SEVERE, SYMPTOMATIC - if LVEF <60% or LV end-systolic diameter >40mm = surgery to repair/replace - if LVEF >60% or LV end-systolic <40mm = watchful waiting CHRONIC SEVERE, ASYMPTOMATIC - if suitable for surgery = surgical repair/replace - if unsuitable for surgery = Transcatheter replacement, optimise HF meds, consider cardiac resynchronisation therapy
408
MITRAL REGURGITATION what are the complications?
- AF - pulmonary hypertension - LV dysfunction and HF - post-op endocarditis - prosthesis failure
409
AORTIC REGURGITATION What is aortic regurgitation?
Leakage of blood into LV from aorta during diastole due to ineffective coaptation of aortic cusps
410
AORTIC REGURGITATION What causes aortic regurgitation?
acute - infective endocarditis - rheumatic fever - aortic dissection chronic - rheumatic disease - bicuspid aortic valve - aortic endocarditis
411
AORTIC REGURGITATION what is the pathophysiology of aortic regurgitation?
- Chronic regurgitation volume loads the left ventricle and results in hypertrophy and dilation - SV increases so increased pulse pressure and myriad of clinical symptoms - Contraction of ventricle deteriorates – LV failure - Adaptations to the volume load entering the LV do not occur in acute AR and patients present with pulmonary oedema and reduced SV
412
AORTIC REGURGITATION what are the risk factors?
- male sex - advancing age - congenital heart disease - bicuspid valve - previous rheumatic heart disease - previous endocarditis - aortic root disorders (marfan, ankylosing spondylitis)
413
AORTIC REGURGITATION Give 3 symptoms of aortic regurgitation
- exertional dyspnoea - fatigue - palpitations - orthopnoea - paroxysmal nocturnal dyspnoea
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AORTIC REGURGITATION what are the signs of aortic regurgitation?
MURMUR - early diastolic murmur - decrescendo - soft, high-pitched - collapsing (waterhammer) pulse - wide pulse pressure - displaced apex OTHER SIGNS - austin flint murmur = rumbling mid-diastolic murmur, loudest at apex, suggests severe disease - corrigans sign = visible distension + collapse of carotid arteries - millers sign = visible pulsation of uvula - Quinckes sign = visible pulsations in nail bed when compressed - De Mussets sign = heartbeat associated with head bobbing - Traubes sign = pistol shot sound over femoral arteries - Duroziezs sign = audible systolic + diastolic murmur on compression of femoral artery
415
AORTIC REGURGITATION what is the murmur?
- early diastolic murmur - decrescendo - soft, high-pitched - collapsing (waterhammer) pulse - wide pulse pressure - displaced apex
416
AORTIC REGURGITATION What investigations might you do in someone who you suspect to have aortic regurgitation?
CXR - cardiomegaly, aortic root enlargement ECHO - assess severity ECG - left ventricular hypertrophy cardiac catheterisation
417
AORTIC REGURGITATION Describe the management for someone with aortic regurgitation
MILD - MODERATE - lifestyle modifications - ACEi (ramipril) - Beta-blockers (bisoprolol) SEVERE DISEASE - loop diuretic (furosemide) - aortic valve repair/replacement
418
AORTIC REGURGITATION what are the complications?
- LV dysfunction + HF - AF - sudden cardiac death - recurrence of endocarditis
419
MITRAL STENOSIS What is mitral stenosis?
Obstruction of LV inflow that prevents proper filling during diastole
420
MITRAL STENOSIS Name 3 causes of mitral stenosis
1. Rheumatic heart disease 2. IE 3. Mitral annular calcification - rarer
421
MITRAL STENOSIS Describe the pathophysiology of mitral stenosis
Thickening and immobility of the valve leads to obstruction of blood flow from left atrium to left ventricle Left atrial pressure increases – left atrium dilation and hypertrophy Pulmonary venous, arterial and right heart pressure increases
422
MITRAL STENOSIS what are the symptoms of mitral stenosis?
1. progressive dyspnoea 2. Haemoptysis (coughing up blood) 3. palpitations (AF) 4. chest pain
423
MITRAL STENOSIS what are the signs of mitral stenosis?
rumbling mid-diastolic murmur with opening snap - decrescendo-presystolic crescendo 1. malar flush 2. AF 3. tapping apex beat 4. low volume pulse 5. loud snapping S1
424
MITRAL STENOSIS what is the murmur?
rumbling mid-diastolic murmur with opening snap - decrescendo-presystolic crescendo
425
MITRAL STENOSIS What investigations might you do in someone who you suspect to have mitral stenosis?
1. ECG - AF, left atrial hypertrophy causes bifid P wave 2. CXR - large L atrium, pulmonary oedema 3. Echo - gold standard for diagnosis
426
MITRAL STENOSIS Describe the management for mitral stenosis
lifestyle optimise HF meds valve repair/replacement percutaneous balloon dilation
427
VALVE DISEASE In what type of valvular heart disease would you hear a mid-diastolic murmur and a 1st heart sound snap?
Mitral stenosis
428
VALVE DISEASE In what type of valvular heart disease would you hear a pan systolic murmur?
Mitral regurgitation
429
VALVE DISEASE In what type of valvular heart disease would you hear an ejection systolic murmur?
Aortic stenosis
430
VALVE DISEASE In what type of valvular heart disease would you see a wide pulse pressure and hear an early diastolic blowing murmur and systolic ejection murmur?
Aortic regurgitation
431
INFECTIVE ENDOCARDITIS What is infective endocarditis?
an infection of the endocardium or vascular endothelium of the heart
432
INFECTIVE ENDOCARDITIS what are the different types of infective endocarditis
acute - develop over days to weeks (s.aureus) subacute - develops over weeks to months (s.viridans) non-bacterial thrombotic - associated with malignancy or SLE
433
INFECTIVE ENDOCARDITIS Which type of infective endocarditis is more likely to spread systemically?
Left sided IE - more likely to cause thrombo-emboli (Right sided IE could spread to the lungs)
434
INFECTIVE ENDOCARDITIS what are the risk factors for infective endocarditis?
- IV drug use - poor dental hygiene - skin and soft tissue infections - dental treatment - IV cannula - cardiac surgery - pacemaker - immunocompromised
435
INFECTIVE ENDOCARDITIS Which bacteria are most likely to cause infective endocarditis?
1. Staphylococcus aureus = MOST COMMON 2. Streptococcus viridian's (alpha haemolytic) 3. Staphlococcus epidermidi (coagulase negative staph)
436
INFECTIVE ENDOCARDITIS which bacteria is associated with IV drug use?
staph aureus
437
INFECTIVE ENDOCARDITIS which bacteria are associated with prosthetic valves?
s. aureus s. epidermidis
438
INFECTIVE ENDOCARDITIS which bacteria are associated with colon cancer?
strep bovis
439
INFECTIVE ENDOCARDITIS which bacteria is associated with infection of native valves?
strep viridans
440
INFECTIVE ENDOCARDITIS which bacteria is associated with poor dental hygiene and infection following dental procedures?
strep viridans
441
INFECTIVE ENDOCARDITIS which bacteria is most commonly associated with pregnancy?
group B strep
442
INFECTIVE ENDOCARDITIS Give 3 groups of people who are at risk of infective endocarditis
more common in developing countries males > females 1. Elderly 2. IV drug users 3. Those would prosthetic valves 4. Those with rheumatic fever 5. Young with congenital heart disease
443
INFECTIVE ENDOCARDITIS Describe the pathophysiology of infective endocarditis
- Usually the consequence of the presence of organisms in the blood and abnormal cardiac endothelium that facilitates adherence and growth - A mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valve - Virulent organisms destroy the valve, producing regurgitation and worsening heart failure
444
INFECTIVE ENDOCARDITIS What is the hallmark of infective endocarditis?
Vegetation - lumps of fibrin hanging of heart valves
445
INFECTIVE ENDOCARDITIS Name 2 sites where vegetation is likely in infective endocarditis
1. Atrial surface of AV valves 2. Ventricular surface of SL valves
446
INFECTIVE ENDOCARDITIS what are the symptoms of infective endocarditis?
Fever Headache Rigors Night sweats Malaise Weight loss
447
INFECTIVE ENDOCARDITIS what are the signs of infective endocarditis
1. Splinter haemorrhages - on nails 2. Osler's nodes - on hands 3. Janeway lesions - on hands 4. Roth spots - in eyes 5. embolic skin lesions - skin 6. petechiae - skin 7. Heart murmurs anaemia splenomegaly clubbing valve disease
448
INFECTIVE ENDOCARDITIS Name the criteria that is used in the diagnosis of infective endocarditis
Duke's criteria
449
INFECTIVE ENDOCARDITIS Give the 2 major points in the Duke's criteria that if presence can confirm a diagnosis of infective endocarditis
1. Two positive blood cultures 2. Positive echo showing endocardial involvement
450
INFECTIVE ENDOCARDITIS what is the minor criteria for Modified Dukes criteria?
- predisposing heart condition or IVDU - fever >38 - immunological phenomenon (glomerulonephritis, osler nodes, roths spots, rheumatoid factor) - microbiological evidence not meeting major criteria - vascular abnormalities
451
What investigations might you do in someone who you suspect to have infective endocarditis?
BLOODS - raised WCC, neutrophilia, raised CRP + ESR BLOOD CULTURES - 3 sets, 1 hour apart, ideally before initiating abx ECHO - to confirm dx CXR - rule out other causes ECG URINALYSIS
452
INFECTIVE ENDOCARDITIS what are the pros and cons of a trans-thoracic echo (TTE)?
Advantages: 1. Safe 2. Non-invasive, no discomfort Disadvantage: 1. Poor images
453
INFECTIVE ENDOCARDITIS what are the pros and cons of a trans-oesophageal echo (TOE)?
Advantage: 1. Excellent images Disadvantage: 1. Discomfort 2. Small risk of perforation or aspiration
454
INFECTIVE ENDOCARDITIS Describe the treatment for infective endocarditis
BLIND THERAPY (when organism not known) - native valve = amoxicillin (+/- gentamicin) - pen allergy/MRSA = vancomycin (+/- gentamicin) - prosthetic valve (vancomycin + rifampicin + gentamicin) NATIVE VALVE S.AUREUS - 1st line = flucloxacillin - 2nd line = vancomycin + rifampicin PROSTHETIC VALVE S.AUREUS - 1st line = flucloxacillin + rifampicin + gentamicin STREP VIRIDANS - 1st line = benzylpenicillin - 2nd line = vancomycin + gentamicin HACEK - 1st line = ceftriaxone
455
INFECTIVE ENDOCARDITIS Give 4 indications for surgery in IE
1. Antibiotics not working 2. Complications 3. To remove infected devices 4. To replace valve after infection cured 5. To remove large vegetations before they embolism
456
INFECTIVE ENDOCARDITIS Why is it important to remove large vegetations?
To prevent them embolising and causing a stroke, MI etc
457
INFECTIVE ENDOCARDITIS Why might blood cultures be negative in a person with IE?
They may have previously received antibiotics
458
PHARMACOLOGY What additional property makes propranolol the most useful beta blocker to help control the arrhythmias which occur immediately following a heart attack?
It can also block sodium channels
459
PULMONARY STENOSIS What is pulmonary stenosis?
Narrowing of the RV outflow tract
460
PULMONARY STENOSIS How does a patient present with pulmonary stenosis?
Right ventricular failure Collapse Poor pulmonary blood flow right ventricular hypertrophy Tricuspid regurgitation
461
PULMONARY STENOSIS How is pulmonary stenosis treated?
Ballon valvuloplasty Open valvotomy Open trans-annular patch Shunt (to bypass blockage)
462
VALVE DISEASE What are 3 problems with a bicuspid aortic valve?
1. Degenerate quicker than normal valves 2. Become regurgitant earlier than normal valves 3. Associated with coarctation and dilation of ascending aorta
463
MITRAL STENOSIS Why does mitral stenosis cause AF?
Increased LA pressure Stretches myocytes in the atria and irritates pacemaker cells --> AF
464
PERICARDITIS What is Dressler's syndrome?
Myocardial injury stimulates formation of autoantibodies against the heart Cardiac tamponade may occur Dressler's is a secondary form of pericarditis
465
PERICARDITIS Give 3 symptoms of Dressler's syndrome
1. Fever 2. Chest pain 3. Pericardial rub Occurs 2-10 weeks after MI
466
EQUATIONS Write an equation for mAP
mAP = DP + 1/3PP
467
EQUATIONS Give the equation for stroke volume
SV = EDV - ESV
468
CHRONIC ISCHAEMIA What is a consequence of peripheral arterial occlusion?
Gangrene
469
CHRONIC ISCHAEMIA Give 2 diseases that result from stress induced ischaemia
1. Exercise induced angina 2. Intermittent claudication
470
CHRONIC ISCHAEMIA Give 2 disease that result from ischaemia due to structural/functional breakdown
1. Critical limb ischaemia 2. Vascular dementia
471
CHRONIC ISCHAEMIAGive an example of infarction
Gangrene
472
CHRONIC ISCHAEMIA What is intermittent claudication?
A symptom describing muscle pain that is caused by moderate ischaemia Intermittent claudication occurs when exercising (stress induced) and is relieved with rest
473
CHRONIC ISCHAEMIA What can intermittent claudication lead on to if left untreated?
Critical ischaemia
474
CHRONIC ISCHAEMIA Intermittent claudication: is O2 supply normal or low at rest and when you begin exercise?
Normal Intermittent claudication is stress induced so at rest and when you begin exercise O2 supply is able to meet demand
475
CHRONIC ISCHAEMIA Intermittent claudication: is O2 supply normal or low when you do moderate/hard exercise?
Low O2 supply is unable to meet demand --> anaerobic respiration --> lactic acid
476
CHRONIC ISCHAEMIA Intermittent claudication: is O2 supply normal or low after a short rest?
Low It takes longer to recover as you're getting rid of the lactic acid After a long rest = normal
477
CHRONIC ISCHAEMIA Give a symptom of intermittent caludication
Muscle cramps
478
CHRONIC ISCHAEMIA Name 2 diseases that are due to moderate ischaemia
1. Angina 2. Intermittent claudication
479
ANEURYSM Name 3 causes of an aneurysm
1. Atherosclerotic (most common) 2. Ateriomegaly 3. Collagen disease - Marfans, vascular Ehlers Danlos 4. tobacco smoking
480
ANEURYSM Name 2 types of aortic aneurysm
1. Abdominal aortic aneurysm (AAA) 2. Thoracic abdominal aneurysm (TAA)
481
ANEURYSM What classifies as an Abdominal aortic aneurysm?
> 3 cm Dilation affects all 3 layers of the vascular tunic
482
ACS what are the risk factors for acute coronary syndromes?
age male family history smoking hypertension diabetes mellitus obesity and sedentary lifestyle
483
HEART FAILURE what does the level of brain natriuretic peptide (BNP) tell you?
- levels are directly correlated to ventricular wall stress and the severity of heart failure - the levels are increased in those with heart failure
484
HEART FAILURE what additional investigations should be undertaken for acute heart failure?
- serum troponin - D-dimer
485
COR PULMONALE what are the causes of cor pulmonale?
- chronic lung disease - pulmonary vascular disorders - neuromuscular and skeletal diseases
486
COR PULMONALE what are the signs of cor pulmonale?
- cyanosis - tachycardia - raised JVP - RV heave - pan-systolic murmur due to tricuspid regurgitation - hepatomegaly - oedema
487
COR PULMONALE what are the symptoms of cor pulmonale?
- dyspnoea - fatigue - syncope
488
COR PULMONALE what investigations should be undertaken for cor pulmonale?
arterial blood gas - hypoxia - sometimes shows hypercapnia
489
COR PULMONALE what is the management for cor pulmonale?
- treat the underlying cause - oxygen - diuretics - venesection if haematocrit >55 - heart-lung transplant in young patients
490
HTN what is malignant hypertension?
markedly raised diastolic BP usually over 120mmHg and progressive renal disease usually evidence of acute haemorrhage and papilledema
491
HTN what are the consequences of malignant hypertension?
- cardiac failure (LVH) - blurred vision (papilledema) - haematuria - due to fibrinoid necrosis of glomeruli - severe headache and cerebral haemorrhage
492
ACS what are the risk factors of MI?
Age, male, history of CVD, FHx Premature menopause DM, smoking, hypertension, hyperlipidaemia, obesity, sedentary lifestyle
493
AORTIC DISSECTION what is the epidemiology of aortic dissection?
- men>female - 40-60yrs - 65% occur in ascending aorta
494
AORTIC DISSECTION what is an aortic dissection?
- there is a tear in the tunica intima , and blood then splits the vessel wall and dissects through the tunica media . - a false lumen is created as the blood in the media layer propagates both proximally and distally. Abnormal flow through this false lumen can occlude flow through the branches of the aorta.
495
AORTIC DISSECTION Describe the pathophysiology of an aortic dissection
Tear in intimal lining of aorta --> column of blood under pressure enters aortic wall forming haematoma --> separates intima from adventitia --> false lumen False lumen extends --> intimal tears
496
AORTIC DISSECTION what are the risk factors of aortic dissection?
Hypertension- most common risk factor Trauma Vasculitis Cocaine use Connective tissue disorders- Turners + noonans
497
AORTIC DISSECTION what are the clinical features of aortic dissection?
-Sudden and severe tearing pain in chest radiating to back -Hypotension -Asymmetrical blood pressure -Syncope - Aortic regurgitation, coronary ischaemia, cardiac tamponade - Peripheral pulses may be absent
498
AORTIC DISSECTION what is the classification system for aortic dissections?
Stanford - type A - ascending aorta +/- aortic arch - type B - descending aorta only
499
AORTIC DISSECTION what are the investigations of aortic dissection?
-ECG/cardiac enzymes - rule out MI -Chest x-ray - widening mediastinum -CT scanning- definitive imaging - echo - TTE/TOE - bloods - FBC, U&Es, group and save, crossmatch - gold standard = CT angiography
500
AORTIC DISSECTION what is the management of aortic dissection?
TYPE A - blood transfusion - IV labetalol - urgent surgical repair TYPE B - conservative management (bed rest + analgesia) - IV labetalol - thoracic endovascular aortic repair (TEVAR)
501
BUNDLE BRANCH BLOCK what are the causes of RBBB?
- normal variant (more common with increasing age) - right ventricular hypertrophy - PE - MI - Atrial septal defect - cardiomyopathy or myocarditis
502
BUNDLE BRANCH BLOCK what is the pathophysiology of RBBB?
Right bundle doesn’t conduct Impulse spreads from left ventricle to right Late activation of RV
503
BUNDLE BRANCH BLOCK what is the clinical presentation of RBBB?
Asymptomatic syncope/presyncope
504
BUNDLE BRANCH BLOCK what is the treatment for RBBB?
Pacemaker CRT – cardiac resynchronisation therapy Reduce blood pressure
505
BUNDLE BRANCH BLOCK what is the clinical presentation of LBBB?
Asymptomatic syncope/presyncope
506
BUNDLE BRANCH BLOCK what is the pathophysiology of LBBB?
Left bundle doesn’t conduct Impulse spreads from right ventricle to left Late activation of LV
507
BUNDLE BRANCH BLOCK what is the treatment for LBBB?
Pacemaker CRT – cardiac resynchronisation therapy Reduce blood pressure
508
BUNDLE BRANCH BLOCK what are the causes of LBBB?
A new LBBB is always pathological IHD Aortic valve disease
509
HEART BLOCK what are the investigations for heart block?
ECG
510
HEART BLOCK what is the treatment for heart block?
Cardioversion - Give a LMWH - Shock with defibrillator Catheter ablation – creates a conduction block IV Amiodarone – restore sinus rhythm
511
HEART BLOCK what is the presentation of first degree heart block?
asymptomatic
512
HEART BLOCK what is the clinical presentation of Mobitz type 1 second degree heart block?
light-headedness dizziness syncope
513
HEART BLOCK what is the clinical presentation of Mobitz type 2 second degree heart block?
SOB postural hypotension chest pain
514
HEART BLOCK what is the clinical presentation of third degree heart block?
dizziness blackouts
515
AORTIC ANEURYSM what is the epidemiology abdominal aortic aneurysm?
- incidence increases with age - men > females - most commonly occur below renal arteries
516
AORTIC ANEURYSM what are the risk factors for abdominal aortic aneurysm?
- Smoking- MAJOR - Family history - Connective tissue disorders- Marfan’s, Ehlers-Danlos - Age - Atherosclerosis - Male
517
AORTIC ANEURYSM what is the clinical presentation of an unruptured abdominal aortic aneurysm?
- often asymptomatic - causes symptoms if expanding rapidly - pain in abdomen, loin or groin - pulsatile abdominal swelling - bruit on ascultation
518
AORTIC ANEURYSM what is the clinical presentation of a ruptured abdominal aortic aneurysm?
- intermittent/continuous abdominal pain - radiates to back, iliac fossa or groin - painful pulsatile mass - hypovolaemic shock - syncope - nausea, vomiting - profound anaemia - sudden death
519
AORTIC ANEURYSM what are the investigations for abdominal aortic aneurysm?
- Abdominal ultrasound – can assess aorta to degree of 3mm - CT or MRI angiography scans
520
AORTIC ANEURYSM what is the management for abdominal aortic aneurysm?
- ruptured = urgent repair (do not wait for imaging) - symptomatic = repair indicated regardless of diameter - asymptomatic AAA = surveillance until high risk of rupture - 5.5cm in men and 5.0cm in women
521
AORTIC ANEURYSM what are the complications of abdominal aortic aneurysm?
- rupture of AAA - thromboembolisms - fistula formation
522
ENDOCARDITIS what antibiotics are used for endocarditis?
INITIAL BLIND THERAPY - native valve = amoxicillin (consider gentamicin) - pen allergy = vancomycin + gentamicin NATIVE S.AUREUS - flucloxacillin - pen allergy = vancomycin + rifampicin PROSTHETIC VALVE S.AUREUS - flucloxacillin + rifampicin + gentamicin - pen allergy = vancomycin + rifampicin + gentamicin FULLY SENSITIVE STREP (S.VIRIDANS) - benzylpenicillin - pen allergy = vancomycin + gentamicin LESS SENSITIVE STREP - benzylpenicillin + gentamicin - pen allergy = vancomycin + gentamicin
523
ENDOCARDITIS how can endocarditis be prevented?
- good oral health - no IV drug use - educate surgery patients on symptoms
524
MI ECG ECG changes in which regions indicates a lateral MI?
lead I aVL V5 V6
525
MI ECG ECG changes in which regions indicates an inferior MI?
lead II lead III aVF
526
MI ECG ECG changes in which regions indicates a septal MI?
V1 V2
527
MI ECG ECG changes in which regions indicates an anterior MI?
V3 V4
528
MI ECG ECG changes in lateral regions are caused by which artery in an MI?
lateral = circumflex
529
MI ECG ECG changes in inferior regions are caused by which artery in an MI?
inferior = RCA
530
MI ECG ECG changes in anterior regions are caused by which artery in an MI?
anterior = LAD
531
MI ECG A blockage in the LAD will cause ECG changes in which regions?
anterior - V3, V4 septal - V1, V2
532
MI ECG A blockage in the RCA will cause ECG changes in which regions?
inferior - leads II, III, aVF
533
MI ECG A blockage in the circumflex artery will cause ECG changes in which regions?
lateral - lead I, aVL, V5, V6
534
RISK SCORE which tool is used to estimate the risk of developing a heart attack or stroke in the next 10 years?
QRISK3
535
PHARMACOLOGY what is the mechanism of action for apixaban?
DOAC - inhibits factor Xa
536
HYPERTROPHIC CARDIOMYOPATHY what is hypertrophic cardiomyopathy?
genetic disorder characterised by left ventricular hypertrophy -> causes diastolic ventricular malfunction
537
HYPERTROPHIC CARDIOMYOPATHY what is the pathophysiology of hypertrophic cardiomyopathy?
thickened septum below aortic valve causes outflow tract obstruction -> causes left ventricular hypertrophy
538
HYPERTROPHIC CARDIOMYOPATHY what are the clinical features?
most = asymptomatic - SOB - fatigue - dizziness - syncope - chest pain - palpitations
539
HYPERTROPHIC CARDIOMYOPATHY what are the examination findings?
- ejection systolic murmur at lower left sternal border - 4th heart sound - thrill at lower left sternal border
540
HYPERTROPHIC CARDIOMYOPATHY what are the investigations?
- ECG - LV hypertrophy - CXR - usually normal, can show pulmonary oedema - echo - genetic testing
541
HYPERTROPHIC CARDIOMYOPATHY what is the management?
- beta blockers - surgical myectomy - ICD - heart transplant
542
CARDIOMYOPATHY what are the different types?
- hypertrophic - dilated - restrictive - arrythmogenic right ventricular
543
HTN what is the most common cause of secondary hypertension?
primary hyperaldosteronism - Conn's syndrome
544
PERCARDITIS What are the side effects of colchicine?
Diarrhoea and nausea
545
ARTERIAL ULCER what are the features?
- symmetrical shape - well-defined borders - punched out appearance - loss of hair surrounding (shiny) - pale, dry, gangrenous with cool surrounding skin - minimal bleeding when knocked/touched - painful, particularly at night
546
ARTERIAL ULCER what are the common locations?
lower legs tops of feet or toes
547
ARTERIAL ULCERS what are the investigations?
- doppler USS - ABPI
548
ARTERIAL ULCER what is the management?
- analgesia - wound management (maintain moist environment) no compression bandages
549
VENOUS ULCERS where are they most commonly found?
around medial and lateral malleolus
550
VENOUS ULCERS what is the appearance?
- shallow - irregular borders - oedema, erythema + brown pigment - warm skin surrounding
551
VENOUS ULCER what are the investigations?
- doppler USS - venous duplex USS - venous pressure assessment
552
VENOUS ULCERS what is the management?
- lifestyle modifications - leg elevation - compression bandages - emollient use
553
CARDIAC ARREST what is it?
sudden loss of heart function
554
CARDIAC ARREST what are the 4 arrest rhythms?
- pulseless electrical activity (PEA) - asystole - ventricular fibrillation - pulseless ventricular fibrillation
555
CARDIAC ARREST which of the arrest rhythms are shockable rhythms?
ventricular fibrillation pulseless ventricular fibrillation
556
CARDIAC ARREST which of the arrest rhythms are non-shockable?
pulseless electrical activity asystole
557
CARDIAC ARREST what are the reversible causes of cardiac arrest?
4Hs + 4Ts - hypoxia - hypovolaemia - hypo/hyperkalaemia - hypothermia - thrombosis - toxins - tension pneumothorax - tamponade (cardiac)
558
CARDIAC ARREST what are the signs?
- unresponsive - absence of pulse - fixed, dilated pupils - absent breath sounds - pallor/cyanosis
559
CARDIAC ARREST what are the symptoms that commonly precede cardiac arrest?
chest pain SOB nausea
560
CARDIAC ARREST what are the investigations?
- pulse check - attach manual/automatic defib - ABG
561
CARDIAC ARREST what are the investigations post-ROSC?
- echo - blood tests
562
CARDIAC ARREST what is the management for all cardiac arrests?
- call for assistance - commence CPR 30:2 ratio - defib assessment - rhythm check every 2 mins - treat reversible causes - manage airway
563
CARDIAC ARREST what is the management for shockable rhythms?
- shock ASAP then resume CPR - rhythm check - give 1mg adrenaline after 3rd shock + after alternating shocks - give 300mg amiodarone after 3rd shock + 150mg after 5th shock
564
CARDIAC ARREST what is the management for non-shockable rhythms?
- no shocks given - rhythm check - adrenaline 1mg ASAP and after alternating cycles of CPR
565
CARDIAC ARREST what is the management post-ROSC?
- intensive care support - induced hypothermia - manage underlying cause
566
CARDIAC ARREST what are the complications?
brain damage kidney failure heart failure death
567
VARICOSE VEINS what is it?
superficial veins dilated and tortuous are visible and palpable are an indicator of superficial lower extremity venous insufficiency
568
VARICOSE VEINS what is the pathophysiology?
leaky valves cause retrograde blood flow, resulting in increased pressure on distal valves superficial veins are thin-walled so cannot withstand increased pressure. This results in dilatation and tortuosity.
569
VARICOSE VEINS what are the risk factors?
genetics/family history increasing age female obesity pregnancy history of DVT prolonged sitting or standing
570
VARICOSE VEINS what are the clinical features?
SYMPTOMS - discomfort (dull ache, worse after prolonged standing) - itching - night cramps - restless legs SIGNS - visible + palpable dilated veins - oedema - signs of chronic venous insufficiency (ulceration, venous eczema, telangiectasia)
571
VARICOSE VEINS what are the investigations?
primary - duplex USS - ABPI
572
VARICOSE VEINS what is the management?
1st line = endothermal ablation 2nd line = foam sclerotherapy 3rd line = surgery conservative - compression hoisery - lifestyle (wt loss, exercise, leg elevation when resting)
573
MI COMPLICATIONS what is the most common cause of death following MI?
ventricular fibrillation (cardiac arrest)
574
MI COMPLICATIONS what type of MI most commonly causes acute mitral regurgitation?
infero-posterior MI
575
MI COMPLICATIONS what is the pathophysiology of acute mitral regurgitation following MI?
ischaemia or rupture of papillary muscle
576
MI COMPLICATIONS how does acute mitral regurgitation after MI present?
- acute hypotension - pulmonary oedema - early-to-mid systolic murmur
577
MI COMPLICATIONS how does a ventricular septal defect following MI present?
usually occurs in first week following MI - pansystolic murmur - acute heart failure
578
MI COMPLICATIONS how does a left ventricular free wall rupture present?
occurs 1-2 weeks after - acute HF - cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
579
MI COMPLICATIONS which MI region most commonly causes atrioventricular blocks and bradyarrhythmia?
inferior MI