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Emily Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is atherosclerosis?

A
  • principal cause of heart attack, stroke and gangrene
  • plaque rupture leading to thrombus formation, partial/complete arterial blockage leading to a heart attack
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2
Q

Risk factors for atherosclerosis?

A
  • Age
  • smoking
  • obesity
  • high serum cholesterol
  • diabetes
  • hypertension
  • family history (don’t understand it)
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3
Q

Where are atherosclerotic plaques found?

A

Peripheral and coronary arteries

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4
Q

What affects distribution of atherosclerotic plaques?

A
  • haemodynamic factors
  • changes in flow/turbulence
  • cause artery to alter endothelial cell function
  • wall thickness changes -> neointima
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5
Q

What is the structure of a atherosclerotic plaque?

A
  • lipid
  • necrotic core
  • connective tissue
  • fibrous ‘cap
    (tunica media thins)
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6
Q

What is the response to injury hypothesis?

A
  1. injury to endothelial cells
  2. lead to endothelial dysfunction
    (LDL enters through vessel walls making them sticky)
  3. signals sent to circulating leukocytes
  4. leukocytes accumulate and migrate into vessel wall
  5. inflammation ensues
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7
Q

How are leukocytes recruited to vessel wall and what chemicals is it governed by?

A
  1. Wall is sticky so captured
  2. roll along wall slower and slower (selectins)
  3. firm adhesion (interns and chemoattractants)
  4. transmigration through vessel wall
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8
Q

What is the progression of atherosclerosis?

A
  1. Fatty streaks
    - Consist of aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall
  2. Intermediate lesions
    - Lipid laden macrophages (foam cells)
    - Vascular smooth muscle cells
    - T lymphocytes
    - Adhesion and aggregation of platelets to vessel wall
    - Isolated pools of extracellular lipid
  3. Fibrous plaques or advanced lesions
    - impedes blood flow
    - prone ot rupture
    - covered by dense fibrous cap made of ECM (collagen + elastin)
  4. Plaque rupture
    - fibrous cap has to be resorbed and redeposited in order to be maintained
    - if balance shifts in favour of inflammatory conditions, cap becomes weak + plaque ruptures
    - thrombus formation

OR
5. Plaque erosion
- hard to tell the difference, not as severe
- clot usually lies above erosion

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9
Q

What is the treatment for coronary artery disease?

A
  1. Percutaneous Coronary Intervention (PCI)
    - stent (steel) with drugs (sirolimus) that prevent restenosis
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10
Q

What is the role of aspirin?

A
  • NSAID
  • Antiplatelet
  • irreversible inhibitor of platelet cycle-oxygenase
  • blocking formation of thromboxane A2
  • producing an inhibitory effect on platelet aggregation
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11
Q

What is the role of Clopidogrel/ticagrelor?

A

Antiplatelet = stops platelets sticking together and forming a clot

inhibitors of the P2Y12 ADP receptor on platelets and other drugs with antiplatelet actions

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12
Q

What is the action of statins?

A

inhibit HMG CoA reductase, reducing cholesterol synthesis

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13
Q

What is the action of PCSK9 inhibitors?

A

monoclonal antibodies that inhibit PCSK9 protein in the liver which leads to improved clearance of cholesterol from the blood

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14
Q

What do anticoagulants do? Give some examples

A

Anticoagulants work by preventing the formation of blood clots. They do this by *Inhibiting thrombin in the body that are involved in the clotting process
Eg Warfarin, Heparin

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15
Q

What are the clinical classifications for unstable angina?

A
  • cardiac chest pain at rest
  • cardiac chest pain with crescendo pattern
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16
Q

What are the clinical symptoms classification of myocardial infarction?

A
  • cardiac chest pain
  • unremitting
  • occurs at rest
  • sweating, breathlessness, nausea and/ or vomiting
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17
Q

What is the management for chest pain?

A
  • Paramedics -> of ST elevation contact primary PCI centre for transfer
  • take aspirin 300mg immediately
  • pain relief
  • oxygen therapy if hypoxic
  • aspirin +/- platelet P@y12 inhibitor
  • consider beta blocker
  • consider other antianginal therapy
  • coronary angiography (if troponin elevated)
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18
Q

What is the main cause of Acute Coronary Syndrome?

A

Plaque rupture

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19
Q

What is troponin?

A
  • protein complex regulates actin:myosin contraction
  • highly sensitive marker for cardiac muscle injury
  • positive in pulmonary embolism, myocarditis, heart failure, arrhythmias, cytotoxic drugs
    (not specific for ACS - goes up in exercise too!)
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20
Q

How do you treat NSTEMi and STEMi differently?

A

STEMI - urgently put a stent in as it implies continued damage to blood vessels

NSTEMI - not as urgent, so can do coronary angiography

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21
Q

What factors affect response to clopidogrel?

A
  • dose
  • age
  • weight
  • disease states such diabetes mellitus
  • drug interactions
  • genetic variants: CYP2C19
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22
Q

What would a STEMI look like on an ECG in the first few hours after symptoms present?

A

ST elevation
Tall t-waves

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23
Q

What would a STEMI look like on an ECG a few days after symptoms started?

A

Inversion of T-waves and presence of pathological q waves

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24
Q

What would a NSTEMI look like on an ECG?

A

ST depression; this indicates a worse prognosis
○ Transient ST elevation
○ T-wave changes.
(Be aware that the ECG may be normal in more than 30% of patients.)

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25
Q

How would you diagnose an NSTEMI with a normal ECG?

A

Perform a blood test. Troponin above the 99th percentile. Recommended to do 2 tests 2 hours apart and measure the difference

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26
Q

What leads of an ECG represent the septal view of the heart?

A

V1 and V2

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27
Q

What leads of an ECG represent the anterior view of the heart?

A

V3: anterior view of the heart
V4: anterior view of the heart

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28
Q

What leads represent the inferior view of the heart?

A

V5: lateral view of the heart
V6: lateral view of the heart
Lead I: lateral view
aVR: lateral view
aVL: lateral view

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29
Q

What leads represent the inferior view of the heart?

A

Lead II
Lead III
aVF

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30
Q

What are the two types of cardiac myocytes?

A
  1. Atrioventricular conductions system (slightly faster conduction)
  2. General cardiac myocyte
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31
Q

What is the result of left and right sided cardiac failure?

A

Right = venous hypertension and congestion
Left = pulmonary congestion and then overload of right side

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32
Q

What is the effect of patent foramen oval?

A
  • defect in central septum
  • eventually produces cardiac arrhythmias, pulmonary hypertension, right ventricular hypertrophy and cardiac failure
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33
Q

What are the complications of patent ductus arteriosus (PDA)?

A
  • unusual after birth, breathing closes it
  • left right side shunting overloads lung circulation with pulmonary hypertension
    and right side cardiac failure
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34
Q

What is tetralogy of fallot and its complications?

A

4 main features
1. pulmonary stenosis (narrowing of valve to lungs)
2. ventricular septal defect
3. extraposition/overriding ventricular septal defect/aorta (aorta above VSD so more deoxygenated blood enters circulation)
4. right ventricle hypertrophy

right ventricle blood is shunted into the left heart producing cyanosis (blue lips) from birth

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35
Q

What is a ‘fallot spell’?

A

When a baby with tetralogy fallot starts feeding,
RV deoxygenated blood is shunted to LV
Deoxygenated blood is then pumped around the body
Causes baby to look blue

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36
Q

What is the treatment of tetralogy of fallot? And complications?

A

surgical repair of ventricular septal defect
- can leave scar tissue on right ventricle causing problems later down the line (ventricular tachycardia)
- pulmonary valve regurgitation (often replaced)

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37
Q

What is happening in ventricular septal defect?

A
  • most common of congenital heart problems
  • abnormal connection between 2 ventricles
  • High pressure LV
  • low pressure RV
  • Blood flows from high pressure to low pressure chamber
  • so NOT BLUE
  • increased blood flow through lungs
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38
Q

What are the complications of large VSD?

A
  • increased respiratory rate
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39
Q

What is the eisenmengers syndrome?

A
  • high pressure pulmonary blood flow from VSD
  • damages to delicate pulmonary vasculature
  • resistance to blood flow through the lungs increases
  • RV pressure increases
  • shunt direction reverse
  • patient becomes BLUE
  • permanent high blood pressure
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40
Q

What is the most common type of atrial septum defect?

A
  • secondum (middle of atrial septum - 90%)
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41
Q

What is the physiology of an atrial septal defect?

A
  • higher pressure in LA than RA
  • shunt is left to right
  • increased flow into right heart and lungs
    (if large hole causes RH dilation)
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42
Q

What are the clinical signs of atrial septal defect?

A
  • pulmonary flow murmur
  • fixed split second heart sound
  • big pulmonary arteries on CXR
  • big heart on CXR
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43
Q

What is the physiology of an atrio-ventricular septal defect?

A
  • involves the ventricular septum, atrial septum, mitral and tricuspid valves
  • one big AV valve instead of two
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44
Q

What is the physiology of the patent ductus arteriosus?

A
  • shunted flow from pulmonary artery to aorta
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45
Q

What is complete transposition of the great arteries (TGA)?

A
  • aorta coming off the right ventricle and the pulmonary trunk off the left ventricle
  • male and diabetes
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46
Q

What is coarctation of the aorta?

A
  • secondary to an excessive obliterating process that normally closes ductus arteriosus (when baby takes first breath)
  • result is a narrowing of the aorta just after the arch
  • excessive blood flow being diverted through the carotid and subclavian vessels to supply rest of body
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47
Q

What are clinical signs of coarctation of the aorta?

A
  • can stop blood flow to left arm so left arm might have high blood pressure but right arm is normal
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48
Q

What is bicuspid aortic valve?

A
  • either only have 2 flaps instead of 3 OR 2 of them have fused together
  • degenerate quicker
  • aorta more prone to aneurysm (>55m operate)
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49
Q

What is the Fontan procedure?

A
  • for heart with only one usable ventricle
  • replum heart to form a passive venous circuit
  • passive connection of great veins to the pulmonary artery
  • uncertain long term
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50
Q

What is endocardial fibroelastosis?

A

secondary = a frequent complication of congenital aortic stenosis and coarctation
- lots of dense collagen and elastic tissue deposited on left ventricle -> increased stiffening of the heart

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51
Q

What is dextrocardia?

A
  • heart positioned more on right side of body
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52
Q

What is an aneurysm?

A

Dilation of part of the myocardial wall
- dilation of the walled sac allows blood stasis and thrombosis

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53
Q

What is cor pulmonale?

A

Right ventricular hypertrophy and dilatation due to pulmonary hypertension

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54
Q

How does acute rheumatic fever affect the heart?

A
  • development of immunity against the Group A beta-haemolytic Strep infection produces antibodies that cross react with cardiac myocytes producing localised inflammation and subsequent scarring
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55
Q

What is mitral valve disease?

A

calcification of the mitral valve
- usually asymptomatic
- unless had previous valvular disease or inflammation

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56
Q

What is mitral valve prolapse?

A
  • degeneration of the mitral valves
  • inner fibrous layer becomes loose and fragmented
  • valve doesn’t close properly
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57
Q

What are the causes of myocarditis?

A
  1. viruses
  2. rickettsia
  3. bacteria
  4. fungi
  5. metazoa
  6. hypersensitivity
  7. radiation
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58
Q

What is giant cell myocarditis?

A
  • aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells
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59
Q

What are cardiomyopathies?

A

Primary heart diseases mainly caused by genetics
- inherited

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60
Q

What are the different types of cardiomyopathy?

A
  1. Dilated cardiomyopathy (DCM) - dilated heart
    - Secondary dilated cardiomyopathy -> drugs, pregnancy
  2. Hypertrophic cardiomyopathy (HCM) - asymmetric hypertrophy with distortion of a papillary architecture
  3. Arrhythmogenic right ventricular cardiomyopathy (ARVC) - progressive dilation of right ventricle with fibrosis
  4. Restrictive cardiomyopathy - poor dilation of heart, reduces blood flow to body
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61
Q

What is hypertrophic cardiomyopathy caused by?

A

Sarcomeric protein gene mutations
- causing myofibril disarray/disorganisation

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62
Q

What is dilated cardiomyopathy caused by and its consequences?

A

Cytoskeletal gene mutations

Presents with heart failure symptoms
(in young people who you wouldn’t expect to have heart failure)

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63
Q

What causes arrhythmogenic cardiomyopathy?

A

Desmosome gene mutations
- programmed replacement of heart muscle (destroys muscle)
- cause arrhythmia

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64
Q

What are channelopathies?

A

Diseases in channel gating currents for Na, K or Ca
- long QT syndrome
- affect heart contractions
- normal structure of heart

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65
Q

What are some types of channelopathies?

A
  1. Long QT syndrome
  2. Short QT syndrome
  3. Brugrada syndrome
  4. CPVT - Catecholaminergic polymorphic ventricular tachycardia
  5. Wolff Progressive Syndrome
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66
Q

What is a very likely cause of a heart attack in healthy young people?

A

Inherited heart conditions

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67
Q

What is Marfan’s disease and how can it cause heart problems?

A
  • Genetic disease affecting connective tissue
  • can cause dilation of aorta
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68
Q

What is familial hypercholesterolaemia and how does it cause heart problems?

A
  • problem with LDL receptor
  • not affected by diet, purely genetic
  • features of cholesterol deposits on hands and eyes
  • increase massively atherosclerosis + CHD
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69
Q

What is cardiac myxoma?

A
  • most common cardiac tumour
  • bias towards atria
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70
Q

What is cardiac tamponade?

A

Compression of the heart leading to acute cardiac failure following bleeding into the pericardial space

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71
Q

What is haemopericardium?

A

Direct bleeding from vasculature wall through the ventricular wall following MI

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72
Q

What is vasculitis?

A

An inflammatory and variably necrotic process centred on the blood vessels that may involve arteries, veins or capillaries

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73
Q

What is polyarteritis nodosa (PAN)?

A
  • more in males
  • patchy necrotising inflammation of medium muscular arteries
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74
Q

What is hypersensitivity angitis?

A
  • presents with palpable purpura on legs (red/purple spots)
  • caused by bacterial or viral infections
  • resulting in inflammation of the smallest arteries and arterioles
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75
Q

What is churg-strauss syndrome?

A
  • granulomatous inflammation of blood vessels with intense eosinophilic infiltrates
  • strong association with asthma
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76
Q

What is giant cell arteritis?

A
  • commonest type of vasculitis of large vessels
  • or temporal arteritis
  • inflammation of blood vessels mainly in temporal arteries
    (can result in blindness if not treated)
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77
Q

What are different types of aneurysms?

A
  1. abdominal aortic aneurysm
  2. berry aneurysm
  3. dissecting aneurysm (splits arterial wall)
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78
Q

What are different types of vascular tumours?

A
  1. haemngioma = benign proliferation of blood vessel tissue
  2. glomus tumour = a benign neoplasm under nails or on foot
  3. haemangioendothelioma = tumours of endothelial cells
  4. angiosarcoma = neoplasm of endothelial cells
  5. kapsosi sarcoma = HIV/AIDs
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79
Q

What is an embolism?

A

The passage of material through the venous or arterial circulations

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80
Q

What are different types of embolisms?

A
  • air embolism
  • acute decompression sickness
  • amniotic fluid embolism
  • fat embolism
  • bone marrow embolism
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81
Q

What are the risk factors of IHD?

A
  • age
  • smoking
  • family history
  • diabetes mellitus
  • male
  • hyperlipidemia
  • kidney disease
  • obesity
  • physical inactivity
  • stress
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82
Q

What are the exacerbating factors for supply and demand for angina?

A

Angina is the mismatch of oxygen supply and demand

Supply:
- anemia
- hypoxemia

Demand:
- hypertension
- tachyarrhythmia
- valvular heart disease

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83
Q

What environmental factors cause IHD?

A
  • exercise
  • cold
  • heavy meals (blood diverted to the gut)
  • emotional stress
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84
Q

Other than limitation of supply what else causes angina?

A
  1. Impairment of blood flow by proximal arterial stenosis
  2. Increased distal resistance eg left ventricular hypertrophy
  3. Reduced oxygen-carrying capacity of blood eg anemia
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85
Q

What are the different types of angina?

A
  1. crescendo angina - increases gradually over months
  2. unstable angina -
  3. prinzmetal’s angina - coronary spasm (v. rare)
  4. microvascular angina - angina with apparently normal coronary arteries
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86
Q

How are IHD symptoms different to heart failure?

A

Both: chest pain and breathlessness

Heart failure: no fluid retention, palpitation, syncope

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87
Q

What are different diagnoses for chest pain?

A

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

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88
Q

What investigations can you do for stable angina?

A
  • CT coronary angiography
  • exercise testing and watch ECG
  • movies scan
  • stress scan (see which regions of heart doesn’t function properly)
  • coronary angiography (cameras in coronary arteries)
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89
Q

What are the drugs for stable angina?

A
  • beta blockers
  • nitrates = GTN (reduce pain)
  • statin (lower blood cholesterol)
  • aspirin (anti platelet - with a stent)
  • calcium channel blockers
  • ACE inhibitors (reduce BP, relaxation of blood vessels)
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90
Q

What are the side effects of beta blockers?

A
  • tiredness, nightmares
  • don’t give to asthma (blocks receptor in the lungs)
  • erectile dysfunction
  • cold hands and feet
  • bradycardia
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91
Q

What is the function of nitrates?

A

Venodilators
- venous capacitance dilate
(give headache at first)

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92
Q

What are the pros and cons of PCI and CABG (bypass)?

A

PCI:
pros
- less invasive, convenient, repeatable, acceptable
Cons:
- risk stent thrombosis + restenosis

CABG
pros: prognosis, deals with complex disease
Cons: invasive, risk of stroke, bleeding, can’t do if frail, length of stay, time for recovery

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93
Q

What causes elevation and depression in an ECG?

A

depolarisation moves towards an electrode = positive elevation

depolarisation moves away = negative depression

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94
Q

When does the atrium repolarise on a ECG?

A

During QRS complex but cannot be seen as ventricle depolarisation is greater

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95
Q

What do all the parts of the ECG signify?

A

P wave = atrial depolarisation
PR interval = Electrical impulse held at AV node
QRS complex = ventricle depolarisation
ST = depolarisation complete
T wave = ventricle repolarisation

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96
Q

What does a short PR interval represent?

A
  • early activation of the ventricle
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97
Q

What does a long PR interval represent?

A

First degree heart block

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98
Q

How do you determine the heart rate on an ECG?

A

Rule of 300/1500 = 10s rule
Count number of big boxes between 2 QRS completes and divide 300 by that number
(if not regular count number of complexes and multiply by 6)

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99
Q

What are the causes of pericarditis?

A
  1. viral (common) - enteroviruses
  2. bacterial
  3. autoimmune (common)
  4. neoplastic (secondary metazoic tumours)
  5. metabolic (uraemia)
  6. traumatic and iatrogenic (e.g. pacemaker lead insertion)
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100
Q

What 3 things control blood pressure?

A
  1. Cardiac output + peripheral resistance
  2. interplay between RAAS and SNS (sympathetic)
  3. Local vascular vasoconstrictor and vasodilator mediators
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101
Q

How does RAAS and SNS affect blood pressure?

A

Both increase peripheral resistance

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102
Q

How can we interfere with RAAS and SNS systems to reduce blood pressure?

A
  1. ACE inhibitor - stops angiotensin II being formed
  2. Calcium channel blockers - vasodilators, reducing perisperhal resistance
  3. Beta blocker - slow heart beat affecting cardiac output
  4. alpha blockers - reduce peripheral resistance
  5. Renin inhibitor
  6. Aldosterone antagonist
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103
Q

When are ACE inhibitors used? Example?

A
  • hypertension
  • heart failure
  • diabetic nephropathy
    end in ‘pril’ e.g. ramipril
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104
Q

What are the adverse effects of ACE inhibitors?

A
  1. Related to reduced angiotensin II formation
    - hypotension (over do it)
    - acute renal failure (used in kidneys)
    - hyperkalaemia (link to aldosterone –> cause potassium excretion)
    - teratogenic effects in pregnancy (important in fetal development)
  2. Related to increased Kinin production (ACE also breaks down bradykinin -> cause these symptoms)
    - cough
    - rash
    - anaphylactoid reactions
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105
Q

What is angiotensin II receptor blockers used for?

A
  • hypertension
  • diabetic neprhopathy
  • heart failure (when ACE-i contraindicated)
    end in ‘sartan’
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106
Q

What are the adverse effect of angiotensin II receptor blockers?

A
  • symptomatic hypotension (especially volume depleted patients - as angiotensin regulated there volume)
  • hyperkalaemia
  • potential for renal dysfunction
  • rash
  • angio-oedema
  • don’t give to pregnant women

generally very well tolerated

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107
Q

When are calcium channel blockers used? Example?

A
  • hypertension
  • ischaemic heart disease (angina)
  • arrhythmia

mostly end in ‘pine’ e.g. amlodipine

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108
Q

What are the 3 main types of calcium channel blockers?

A
  1. Dihydropyridines e.g. amlodipine
    - target peripheral resistance
  2. Phenylalkylamines - verapamil
    - target heart mainly, slows HR, reduce contraction force
  3. Benzothiazepines - diltiazem
    - intermediate heart/peripehral vascular effects
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109
Q

What are the adverse effects of calcium channel blockers?

A
  1. DUe to peripheral vasodilation
    - flushing, headache, oedema, palpitations (body increases CO to increase blood pressure)
  2. Due to negatively chronotropic effects
    - bradycardia (slow HR)
    - atrioventricular block
  3. Due to negatively inotropic effects
    - worsening of cardiac failure
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110
Q

When are beta adrenoceptor blockers used ?

A
  • ischaemic heart disease (angina)
  • heart failure
  • arrhythmia
  • hypertension
    end in ‘Prolol’ e.g. bisoprolol
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111
Q

Are beta blockers selective?

A

Some are more selective then others

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112
Q

How do beta blockers affect asthma patients?

A

Affect beta 2 receptors in the lungs
- can cause asthmatic attack

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113
Q

What are the adverse effects of beta blockers?

A
  • fatigue (from reduced adrenaline)
  • headache
  • sleep disturbance/nightmares
  • bradycardia (slow HR)
  • hypotension (from slow HR)
  • cold peripheries
  • erectile dysfunction (

worsening of: asthma, COPD (allowed to have it unlike asthmatics), PVD, heart failure (need to give dose slowly)

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114
Q

What are the benefits of water soluble diuretics?

A
  • less likely to enter the brain > less sleep disturbances + nightmares
  • excreted by kidney
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115
Q

When are diuretic used?

A

Act on kidneys to increase excretion of water and sodium (has affect on ion channels and heart)

  • hypertension
  • heart failure
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116
Q

What are the 4 classes of diuretics? Examples?

A
  1. thiazides and related drugs (distal tubule) e.g. bendroflumethiazide
  2. Loop diuretics (loop of Henle) e.g. furosemide
  3. potassium sparing diuretics e.g. spironolactone
  4. Aldosterone antagonists
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117
Q

What are the adverse effects of diuretics?

A
  • hypovolaemia + hypotension (reduced volume in blood)
  • low serum K, Na, Mg, Ca
  • raised uric acid (gout)
  • erectile dysfunction (mainly thiazides)
  • impaired glucose tolerance
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118
Q

What are the treatment steps for hypertension of someone under 55 yrs?

A
  1. ACE-i or angiotensin II receptor blocker
  2. ACE-i or ARB + CCB
  3. AND thiazide like diuretics
  4. resistant hypertension = spironolactone, high dose TLD, alpha blocker, beta blocker
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119
Q

What are the treatment steps for hypertension of an over 55 year old or afro Caribbean any age?

A

Afro-caribean = low renin

  1. calcium channel blocker
  2. ACE-i or ARB + CCB
  3. Add thiazide like diuretics
  4. resistant hypertension = spironolactone, high dose TLD, alpha blocker, beta blocker
120
Q

What are the main 2 types of heart failure?

A
  1. heart failure due to left ventricular systolic dysfunction LVSD
  2. heart failure with preserved ejection fraction (diastolic failure) HFPEF
121
Q

What is heart failure?

A

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired.
- functional or structural
- MC is Coronary artery disease

122
Q

What do you want drugs to target in heart failure?

A

treatment directed at the response to the heart failure
- drugs target the overreaction of RAAS and SNS

123
Q

What are the steps in heart failure management?

A
  1. symptomatic treatment of congestion (complain of oedema = diuretics, but heart not treated)
  2. disease influencing therapy (neurohumoral blockade)
    - inhibition of RAAS and SNS
  3. medications
    a) first line = ACE-i and beta blockers (low slow dose increase)
    b) aldosterone antagonists (stop sodium + water retention)
    c) Consider aldosterone receptor antagonist and Neprilysin inhibitor (ARNI)
    d) consider SGLT 2 inhibitor

ACE-i intolerant = use angiotensin receptor blocker
+ ARB intolerant = hydralazine/ nitrate combination

124
Q

What are natriuretic peptides?

A

Heart secretes them when the heart walls are stretched

125
Q

What do SGLT2 inhibitors do?

A

Diabetic drug = used to lower blood glucose

Also useful in heart failure
- add on to other drugs, help improve outcomes

126
Q

How do nitrates work?

A
  • arterial and venous dilators
  • reduction of preload and after load
  • lower BP
127
Q

When are nitrates used? Example?

A
  • ischaemic heart disease
  • heart failure

e.g. GTN spray

128
Q

What is the drug treatment for chronic stable angina?

A
  1. antiplatelet therapy e.g. aspirin
  2. lipid-lowering therapy e.g. statins
  3. short acting nitrate - GTN spray for acute attack, chest pain
    4.a) first line = beta blocker or calcium channel blocker
    b) intolerant = switch
    c) not controlled = combine
    d) intolerant/uncontrolled = long acting nitrate etc.
129
Q

What is the treatment steps for Acute coronary syndrome (NSTEMI + STEMI)?

A
  1. pain relief = opiates (diamorphine = pure heroine) and GTN spray
  2. dual antiplatelet therapy = aspirin + clopidogrel
  3. antithrombin therapy = fondaparinux
  4. consider glycoprotein IIb IIa inhibitor
  5. background angina therapy = beta blocker, long acting nitrate, CCB
  6. lipid lowering = statins
  7. assess cardiac function (has heart attack caused damage) = therapy for LVSD/ heart failure - ACE-i, BB
130
Q

What is the role of digoxin?

A

(comes from foxglove plant)

  • cardiac glycoside
  • inhibit Na/K pump
  • reduce heart rate, increase force of contraction (doesn’t impair heart function any further as same CO)

critical the right dosage is given

used in AF (block AV node) and severe heart failure

131
Q

What is sinus tachycardia?

A

Under normal circumstances at rest, our heart should be in sinus rhythm with an accompanying rate of 60-100 bpm. If the defining features of normal sinus rhythm are met but the heart rate is fast (> 100 bpm), we call it sinus tachycardia.

ECG: one P wave per QRS, constant PR interval

132
Q

What is supraventricular tachycardia?

A

is caused by the electrical signal re-entering the atria from the ventricles.
- self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12).

133
Q

What is the main cause of hypertension?

A

Nothing, idiopathic

134
Q

Should you investigate someone with hypertension?

A

No, only investigate if they have other symptoms.

  • early onset <30yrs
  • phaechromotoma
135
Q

How do you recognise malignant hypertension?

A

hypertension
- affects kidneys, urine test
- eyes (retinal haemorrhages)

136
Q

At what blood pressures do you start treatment?

A
  • at low CVD risk 160/100 mmHG
  • at high CVD risk 140/90 mmHg
137
Q

Should hypertension medication make the patient feel better?

A

It is a symptomless disease
- so depends on the person but might feel no change

138
Q

What are blood pressure targets?

A

Target
- routine <140/90 mmHg
- previous stroke <130/80 mmHg
- heavy proteinuria <130/80 mmHg
- CKD and diabetes <130/80 mmHg
- Older patients <150/90 mmHg (too low will make them fall over)

139
Q

What types of illness will hypertension cause?

A
  • Stroke (MC link)
  • IHD
  • Chronic Kidney Disease
  • Dementia
  • heart failure
  • Peripheral vascular disease
  • Myocardial infarction
140
Q

How many years of your life would you lose with hypertension?

A

5 years on average
(going on medication restores this completely)

141
Q

What lifestyle changes will lower blood pressure?

A
  • weight loss
  • high salt intake
  • alcohol
  • exercise
    (smoking isn’t a risk factor but it increases the damage of hypertension)
142
Q

How do diuretics work?

A

Reduce circulating sodium
- so won’t make you pee more as your body will rebalance itself by reducing sodium levels

143
Q

Which drugs increase blood pressure?

A
  • NSAIDs
  • SNRIs e.g. venlafaxine
  • corticosteroids
  • oestrogen containing oral contraceptives
  • stimulants e.g. methylphenidate
  • anti-anxiety drugs e.g. Gabapentin
  • Anti-TNFs
144
Q

When can you stop taking hypertension medication?

A

It is a lifelong treatment
- as soon as you stop the blood pressure will rise again

145
Q

What might be causing the hypertensive medication to not work?

A
  • not taking tablets
  • change in lifestyle = weight gain or new drugs
146
Q

Are there any circumstances when hypertension treatment needs to be stopped?

A
  • surgery = general anaesthesia hypotension can be a problem and antihypertensive block attempts to increase BP therefore ACE inhibitors need to be stopped
147
Q

What are the 3 types of aortic stenosis?

A
  1. supravalvular
  2. subvalvular
  3. valvular
148
Q

What is the main aetiology of aortic stenosis?

A

Degenerative calcification

149
Q

What is the pathophysiology of aortic stenosis?

A
  1. a pressure gradient develops between the left ventricle and the aorta
  2. LV function initially maintained by compensatory pressure hypertrophy
  3. when compensatory mechanisms exhausted, LV function declines
150
Q

What are the physical signs of aortic stenosis?

A
  • slow rising carotid pulse
  • soft or absent 2nd heart sound
  • ejection systolic murmur
    (volume does not tell you anything about severity)
151
Q

What is the prognosis for aortic stenosis?

A

Angina + AS: 50% survive for 5 years.
Syncope + AS: 50% survive for 3 years,
HF + AS mean survival is <2 years.
Risk of SCD in asymptomatic or minimally symptomatic patients is rare (<2%).

152
Q

What 2 measurements are obtained in ECHO for aortic stenosis?

A

Two measurements obtained are:
1. Left ventricular size and function: LVH, Dilation, and EF
2. Doppler derived gradient and valve area (AVA) = shows velocity of blood across the valve

153
Q

What is the grading of severity for aortic stenosis?

A

Mild >1.5cm2
moderate 1-1.5cm2
severe <1cm2

154
Q

What is the management for aortic stenosis?

A

General:
Fastidious dental hygiene / care (reduce risk of infection)
Consider IE prophylaxis in dental procedures

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

Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation

155
Q

What is chronic mitral regurgitation?

A

Backflow of blood from LV to the LA during systole

156
Q

What is the pathophysiology of mitral stenosis?

A
  1. Pure Volume Overload
  2. Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
    - Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
    - Progressive left ventricular volume overload leads to dilatation and progressive heart failure.
157
Q

What are the physical signs of mitral stenosis?

A
  • pan systolic murmur (murmur stays the same sound throughout systole)
  • exertion dyspnoea
  • heart failure
158
Q

Are medications necessary for mitral stenosis? and should you give prophylaxis medication?

A

Have effects on secondary effects of mitral stenosis like AF

  • no indication for prophylactic vasodilators such as ACE-i, hydralazine
159
Q

What is the aetiology of chronic aortic regurgitation?

A
  • bicuspid aortic valve
  • rheumatic
  • infective endocarditis
160
Q

What is the pathophysiology of aortic regurgitation?

A
  • combined pressure AND volume overload
  • compensatory mechanism: LV dilation, LVH. Progressive dilation leads to heart failure
161
Q

What are the physical signs of aortic regurgitation?

A
  • wide pulse pressure e.g. 180/60 (big difference between systolic and diastolic pressures
  • diastolic blowing murmur
  • Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
  • Systolic ejection murmur: due to increased flow across the aortic valve
162
Q

Should vasodilators be given for aortic regurgitation?

A

vasodilators = ACEis potentially improve stroke volume and reduce regurgitation but indicated only in CCF or hypertension

163
Q

Define aortic regurgitation?

A

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

164
Q

What are indications for surgery in aortic regurgitation?

A

ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole

165
Q

Define mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole

166
Q

What is the predominant cause of mitral stenosis and how does this effect prevalence?

A

Rheumatic carditis
- decreasing due to a reduction of rheumatic heart disease.

167
Q

What is the pathophysiology of mitral stenosis?

A
  • Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying)
    worse with exercise, fever, tachycardia, and pregnancy
  • Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation.
  • Right heart failure symptoms: due to Pulmonary venous HTN
  • Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure
168
Q

Why does mitral stenosis cause mortality?

A

Due to progressive pulmonary congestion, infection, and thromboembolism

169
Q

What are the signs of mitral stenosis?

A
  • low pitched dsiatolic murmur (movement of blood from LA to LV in diastole)
  • mitral facies = CO low > vasoconstriction > pink patches on cheek
  • prominent ‘a’ wave in jugular venous pulsation (pulmonary htn + RVH)
170
Q

What is the management for mitral stenosis?

A

Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly

Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
- Duiretics for fluid overload

Surgery = mitral balloon valvotomy or replacement

IE prophylaxis = patients with prosthetic valves or a Hx of IE for dental procedures

171
Q

Define infective endocarditis.

A

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc).

172
Q

What are the types of infective endocarditis?

A
  1. left sided native IE (mitral or aortic)
  2. left sided prosthetic IE
  3. Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
  4. Device related IE (pacemakers, defibrillators, with or without valve IE)
  5. Prosthetic = can be early (within year) or late (after a year) post op
173
Q

How to catch infective endocarditis?

A
  • abnormal valve = regurgitant or prosthetic valves
  • introduce infectious material into the blood stream or directly onto the heart during surgery
  • have had IE previously
174
Q

what is the epidemiology of endocarditis?

A
  1. elderly
  2. young IV drug abusers
  3. young with congenital heart disease
  4. anyone with prosthetic heart valves
175
Q

What is the modified DUKEs criteria for diagnosis of IE?

A

Definite IE = 2 major, 1 major+3minor, 5 minor
Possible IE = 1 major, 1 major +3minor, 5 minor

Major
-Pathogen grown from blood cultures
- evidence of endocarditis on echo, or new valve leak

Minor:
Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures

176
Q

What are peripheral signs of IE?

A
  • splinter haemorrhages
  • Osler’s nodes = small, TENDER, purple, erythematous subcutaneous nodules are usually found on the pulp of digits
  • Janeway lesions = macular, NONTENDER, on fingers plasma or sole
  • Roth spots on fundoscopy = red spots on retina

JOSH R

177
Q

When should you operate with IE?

A
  1. infection cannot be cured with antibiotics
  2. complications (aortic roots abscess, severe valve damage)
  3. remove infected devices
  4. replace valve after infection cured
  5. remove large vegetation before they embolise
178
Q

Can we prevent IE?

A
  • For years, patients with valve disease were given antibiotic prophylaxis during interventions (esp dental)
  • NICE guidance in 2008 recommended not to give prophylaxis to anyone
  • ESC guidance is to consider prophylaxis in high risk patients (prosthetic valves, previous IE, cyanotic heart disease)
179
Q

What is a normal QRS axis in an ECG?

A

-30 to +90 degrees

180
Q

What does left axis deviation on a ECG show?

A

Left anterior fascicular block
Left bundle branch block
Left ventricular hypertrophy

181
Q

What does right axis deviation show on a ECG?

A

Left posterior fascicular block
Right heart hypertrophy/strain

182
Q

What do different P wave abnormalities show?

A

Low amplitude
Atrial fibrosis, obesity, hyperkalaemia

High amplitude ‘Tall’
Right atrial enlargement

Broad notched ‘Bifid’
Left atrial enlargement

Alternative pacemaker foci
Focal atrial tacycardias
‘wandering pacemaker’

183
Q

What affects the PR interval?

A

Prolonged in disorders of AV node and specialised conducting tissue

Shorter in younger patients or in pre-excitation (Wolf-Parkinson-White)

184
Q

What abnormalities can occur with the QRS complex and what does this signify?

A

Broad QRS
Ventricular conduction delay / bundle branch block

Small QRS complexes
Obese patient
Pericardial effusion
Infiltrative cardiac disease

Tall QRS complexes
Left ventricular hypertrophy
(S wave in V1 and R wave in V5/V6 >35mm)
Thin patient

185
Q

What can changes in the T wave signify?

A
  • myocardial infarction
  • ischaemia
186
Q

What are the different types of tachycardias?

A
  • atrial fibrillation
  • atrial flutter
  • Supraventricular tachycardia
  • Focal atrial tachycardia
  • Ventricular tachycardia
  • Ventricular fibrillation
187
Q

What can cause bradycardia?

A
  • AV conduction problems
  • sinus bradycardia
  • junctional rhythm
188
Q

What are the different AV conduction problems?

A

1st degree = prolonged PR interval
2nd degree = 2:1 ventricle will miss every other electrical impulse
3rd degree = ventricles will miss impulses even more

189
Q

What are the 2 subtypes of 1st degree AV conduction block?

A

Mobitz Type 1 = PR interval gradually increases until AV node fails completely and no QRS wave is seen
(then starts all over again)

Mobitz Type 2 = sudden unpredictable loss of AV conduction and loss of QRS . Due to loss of conduction in bundle of His, purkinje fibres

190
Q

What is ECG shape of a left bundle branch block?

A

V1 = ‘W’ shape
V6 = ‘M’ shape
wiLLiam

191
Q

What is the ECG of a right bundle branch block?

A

maRRow
V1 = M
V6 = W

192
Q

What is atrial, ventricular ectopic palpitations?

A
  • normal sinus beat, then an ‘ectopic’ beat that comes too early
    (can feel the beat after the ectopic beat as heart has filled up more so a bigger push out of blood)
193
Q

What is treatment and management for ectopic beats?

A

-Very Common
Non sustained beats arising from ectopic regions of atria or ventricles
Generally benign
High burden VE can cause heart failure
High burden AE can progress to AF

Most patients will gain symptomatic relief from reassurance/betablockers

Who to refer
High burden ectopy (>5%, though risk prob not increased till >20%)
Refractory to BB
Structural heart disease
Syncope

194
Q

What is the pathway for treating AF?

A
  1. treat underlying cause = alcohol, thyroid, obesity
  2. Rate control = BB, CCb
  3. restore sinus rhythm acutely = electrical cardio version
  4. maintain sinus rhythm = amiodarone
195
Q

What does a narrow QRS complex and no p waves signify the condition is?

A

Supraventricular tachycardia
(p waves hidden by quick QRS complexes)

196
Q

What are accessory pathways?

A
  • Congenital remnant muscle strands between atrium and ventricle
  • Delta wave = No pause at AV node, so no gap between P wave and QRS complex, slurred together
197
Q

What is orthodromic AVRT?

A

Atrioventricular Re-entry tachycardia
Orthodromic = when the electrical impulse travels in the same direction as normal physiologic conduction,
- propagate through His-purkinje system, depolarise ventricles and circulate back to atria via accessory pathway causing a premature atrial beat
- normal QRS complex <0.12s (impulse still travels through His-purkinje network)
- Regular ventricular rate
- P wave retrograde after QRS

198
Q

What is an antidromic AVRT?

A

Re-entry impulse travels in retrograde direction through the AV node.
- premature atrial impulse travels from the atria to ventricles via the accessory pathway and then back to the atria via the AV node

ECG:
- wide QRS complex
- regular ventricular rate
- P wave not visible (if it is, it is retrograde and occurs before QRS)
- Delta waves

199
Q

What is pre-excitation tachycardia?

A
  • impulse not held at the AV node but goes straight from SAN through accessory pathway to ventricles

ECG:
- short PR interval
- Delta wave (depolarisation of ventricular myocardium will start where the accessory pathway inserts into the ventricle and the impulse will spread slowly because it will propagate outside of the conduction system - slow start to QRS)
- wider QRS complex (delta wave included in it)

200
Q

What is Wolff-Parkinson-White syndrome?

A

Evidence of pre-excitation with tachyarrhythmias

201
Q

How can you tell on an ECG that it is ventricular tachycardia?

A

P wave is occurring completely independently to ventricle activity

202
Q

What is an electrical storm?

A

3 or more sustained episodes of VT or VF, or appropriate ICD shocks during a 24-hour period
- high risk
- manage on CCU/ITU

203
Q

What is the treatment for an electrical storm?

A
  1. Correct any provoking factors e.g. electrolyte (K/Mg), ischaemia, infection, heart failure
  2. Beta blockers, sedation
  3. Amiodarone +/- lignocaine
  4. Overdrive pacing
  5. General anaesthesia / Neuraxial blockade
  6. Catheter ablation
204
Q

What is the difference between a narrow and broad complex tachycardia?

A

Narrow =
- supravenctricular tachycardia
- AF/flutter

Broad:
- Ventricular tachycardia
- SVT with BBB/preexcitation

205
Q

What is heart failure?

A

An inability of the heart to deliver blood (and O2) at a rate commensurate with the
requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.
(not enough blood to fill heart but heart is pumping correctly)

206
Q

What are the main causes of heart failure?

A

MC = myocardial dysfunction from IHD

others:
- hypertension
- alcohol excess
- cardiomyopathy
- valvular
- endocardial
- pericardial causes

207
Q

What are the signs of HF?

A
  • tachycardia
  • displaced apex beat
  • raised JVP
  • added heart sounds and murmurs
  • hepatomegaly (pulsatile and tender)
  • peripheral and sacral oedema
  • ascites
208
Q

What are the different classes of heart failure?

A

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

209
Q

What are the main phenotypes of HF?

A

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

In addition, there are other phenotypes dependent on the dominant feature, including:
HF due to severe valvular heart disease (HF-VHD)
HF with pulmonary hypertension (HF-PH)
HF due to right ventricular systolic dysfunction (HF- RVSD)

210
Q

What is the treatment for heart failure?

A
  • Diuretics
  • ACE-i
  • BB
211
Q

What is the ECG for pericarditis?

A
  • ST elevation
  • PR depression

Then returns to baseline and diffuse T wave inversions

212
Q

What is the difference between atrial fibrillation and flutter?

A

Atrial Fib = receive disorganised electrical signals, rapid irregularly irregular heart beat

Atrial Flutter = atria receive organised electrical signals that are faster, atria beats more frequently than ventricles so only every other beat gets to ventricles

213
Q

What genetic factors increase likelihood of having a venous thrombosis?

A

Factor V Leiden (5%)
PT20210A (3%)
Antithrombin deficiency
Protein C deficiency
Protein S deficiency

214
Q

What are ways venous thrombosis can be acquired?

A
  1. Anti-phospholipid syndrome (antibodies attack tissues causing blood clots to form)
    - Lupus anticoagulant
  2. Hyperhomocysteinaemia = high homocysteine level in your blood increasing risk of blood clots
215
Q

What is heparin?

A
  • glycosaminoglycan
  • binds to antithrombin and increases its activity
  • indirect thrombin inhibitor
216
Q

How is low molecular weight heparin different?

A
  • smaller molecule, less variation in dose and renal excreted

(used for treatment and prophylaxis)

217
Q

What is prophylaxis?

A

treatment given or action taken to prevent disease.

218
Q

What is warfarin?

A
  • prevents synthesis of active factors II, VII, IX and X
  • antagonist of Vit K
    -anticoagulant
  • prolongs the prothrombin time
  • difficult to use, need to monitor very regularly
    (measure INR = international normalised ratio, derived from prothrombin time)
219
Q

What is prothrombin time?

A

The prothrombin time is the time it takes plasma to clot after addition of tissue factor.

This measures the quality of the extrinsic pathway (as well as the common pathway) of coagulation

220
Q

What is INR?

A

The international normalised ratio ( INR)
- is a laboratory measurement of how long it takes blood to form a clot.
- It is used to determine the effects of oral anticoagulants on the clotting system

Usual target range 2-3

221
Q

What are New Oral Anticoagulant Drugs (NOAC/DOAC)?

A
  • orally active - like aspirin + warfarin
  • directly act on factor II or X
  • no blood tests or monitoring
  • Shorter half lives so bd or od
  • used for extended thromboprophylaxis and treatment of AF and DVT/PE
222
Q

How does clopidogrel work?

A

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

223
Q

What is haemopytsis?

A

Coughing up blood

224
Q

What is the difference in murmur sounds between mitral stenosis and aortic regurgitation?

A

MS = MID-diastolic murmur

AR = early in diastole
- collapsing pulse and Quincke’s sign (nailbed pulsation).

225
Q

In some heart defects is the ejection systolic murmur louder on inspiration or expiration?

A

Inspiration
- pulmonary stenosis
(right sided murmurs)

Expiration
- left sided murmurs,
- aorta is on the left

226
Q

What is BNP and its function?

A

brain natriuretic peptide
- secreted by the ventricular myocardium that acts to compensate for the symptoms of heart failure by promoting diuresis, natriuresis, vasodilatation and suppression of sympathetic tone and renin-angiotensin-aldosterone activity.

227
Q

What causes the irregularly irregular heart rhythm in atrial fibrillation?

A

Aberrant electrical activity from myocytes surrounding the pulmonary veins overwhelms the sino-atrial node, causing re-entry circuits.
- This propagates irregular electrical activity of the atria, causing AF.

228
Q

What is torsades de pointes?

A
  • collapse due to prolonged QT interval
  • characterised by rapid, irregular QRS complexes, which appear to be ‘twisting’ around the baseline shown on the ECG.

(can be caused by medication e.g. clarinthromycin)

229
Q

How long should the PR interval normally be?

A

0.12 - 0.2s

230
Q

What is the most likely bacteria to cause rheumatic fever?

A

Streptococcus pyogenes

231
Q

What is cor pulmonale?

A

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.

232
Q

How do you differentiate between heart failure and COPD?

A

Heart failure presents with orthopnoea (shortness of breath when lying down)

233
Q

Why does mitral stenosis cause difficulty to swallow?

A
  • left atria enlargement can compress the oesophagus
    (gives rise to double heart border)
234
Q

What is the difference between arterial and venous ulcers?

A

Arterial
- pale, painful and punched out
- pain sitting down = critical ischaemia

Venous
- red and oozing with irregular margins (varicose veins)

235
Q

What is the difference between liquefactive and coagulative necrosis?

A

Coagulative = type of accidental cell death typically caused by ischaemia or infarction
- develop semi-solid debris
- chronic

liquefactive = acute necrosis that results in a transformation of tissue into a liquid viscous mass

236
Q

If lead I is positive and aVF is positive what is the axis deviation?

A

Normal = 0 to +90 degrees

237
Q

If lead I is positive and aVF is negative what is the axis deviation?

A

Possible LAD
Is lead II positive?
Yes -> Normal (0 to -30 degrees)
No -> LAD (-30 to -90 degrees)

238
Q

If lead I is negative and aVF is positive what is the axis deviation?

A

RAD (+90 to 180 degrees)

239
Q

If lead I is negative and aVF is negative what is the axis deviation?

A

Extreme Axis Deviation (-90 to 180 degrees)

240
Q

What is the way to remember the acute management of an MI?

A

MONA
morphine
oxygen <94%
nitrates
aspirin

241
Q

What would you find in an X-ray for heart failure?

A

ABCDE
* A – alveolar oedema
* B – Kerley B lines
* C – cardiomegaly
* D – dilation of UPPER lobe vessels
* E – effusions

242
Q

In heart failure what causes upper lobe venous dilation?

A

increase in left atrial pressure

243
Q

What is Prinzmetal angina?

A

(variant angina)
- it develops when a coronary artery supplying blood and oxygen to your heart goes into spasm and narrows suddenly
- don’t experience angina during exercise
- can cause ST elevation

244
Q

What is the difference in BNP and ANP?

A

BNP = released from ventricles in response to stretch, a marker for heart failure

ANP = released from ATRIA in response to stress

245
Q

What is the valsalva manoeuvre?

A

Hold the nose and mouth closed during forceful expiration to stimulate vagus nerve to return the heart into sinus rhythm
- used for supraventricular tachycardia in young people

246
Q

What are HAS-BLED and CHA2-DS2-VASc used for?

A

CHAD = stroke risk in patients with AF

HAS-BLED = estimates risk of bleeding in patients on anticoagulation medication

247
Q

What drugs are used to treat a venous thrombosis?

A

Heparin and warfarin
- as both target the clotting factors

248
Q

What drugs are used to treat a arterial thrombosis?

A

Aspirin + clopidrogrel
- as both target platelets

249
Q

Explain the method of action of heparin.

A
  • Bind to antithrombin and increases it activity
    (antithrombin inactivates several enzymes of the coagulation system)
  • indirect thrombin inhibitor
250
Q

Explain the method of action of warfarin.

A

Antagonist of vitamin K
- interferes with hepatic synthesis of vitamin K dependent clotting factors = II, VII, IX, X (1972)
- prolongs the prothrombin time

251
Q

What is the D-dimer test used for?

A

Confirm a diagnosis of a DVT
- fibrin degradation product released during fibrinolysis
- high = DVT, DIC or inflammation

(used with Well’s score)

252
Q

What is the presentation for Acute Limb Ischaemia?

A

6P’s - pallor, perishingly cold, pain, parenthesis, paralysis, pulseless

253
Q

What is Dressler’s syndrome?

A

Delayed pericarditis as a result of a previous MI. Usually occurs between 1-4 weeks after. But can occur years later

(thought that myocardial injury stimulates the formation of antibodies against the heart
muscle.)

254
Q

What would an ECG show of someone with pericarditis?

A

Saddle shaped ST elevation with PR depression

255
Q

What is the benefit of giving colchicine?

A

Prevents the recurrence of pericarditis

256
Q

What is Beck’s triad which is indicative of cardiac tamponade?

A

Hypotension
Muffled heart sounds
Raised JVP (jugular venous pressure)

3 D’s: Distant heart sounds
Distended jugular veins
Decreased arterial pressure

257
Q

What is the most common cause of IE in non-IV drug users?

A

Viridians Streptococci can be a result of poor oral hygiene

258
Q

What is the most common cause of IE in IV drug users?

A

S.Aureus

259
Q

Describe how rheumatic fever can lead to mitral stenosis?

A

There is a sharing of antigens between strep A and ones found on the heart.
This leads to an immune response causing the wall of the valve to thicken
This first leads to regurgitation which develops into stenosis

260
Q

First line investigation for AS?

A

ECG-

L- LBBB due to calcification
L- left axis deviation
L- LVH
P- poor R wave progression

261
Q

What are some key presentations for secondary hypertension?

A

Papilledema, flame shaped haemorrhage and cotton wool spots on eyes
Also cardiac and renal symptoms e.g., chest pain

262
Q

What can cause systolic vs diastolic heart failure?

A

systolic = IHD, MI, Hypertension, Cardiomyopathies

Diastolic = Cardiac tamponade, Constrictive pericarditis, Hypertension

263
Q

What is congestive heart failure?

A

Failure of both the right and left ventricles

264
Q

Describe how the heart compensates for heart failure?

A

HF causes a drop in MAP that initially stimulates baroreceptors

This decreases vagal tone increases sympathetic tone leading to increase an increase in heart rate and contractility

The sympathetic system also stimulates the contraction of arteries and veins and the release of adrenaline

The renin-angiotensin-system is also stimulated in heart failure due to reduced kidney perfusion.

Therefore, Angiotensin II is secreted ,which causes vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys. These mechanisms are beneficial initially as they increase blood volume, maintaining a high CO

265
Q

What are 3 differential diagnosis of DVT’s?

A

Cellulitis
Ruptured baker’s cyst
Calf muscle haematoma

266
Q

What is the gold standard test for diagnosing PE?

A

CPTA- computed tomographic pulmonary angiography

267
Q

What are the 2 shockable rhythms for a cardiac arrest?

A

Ventricular tachycardia
Ventricular fibrillation

268
Q

What are the two non-shockable rhythms?

A

Asystole- when there is no electrical activity
Pulseless electrical activity

269
Q

What are the different types of supraventricular tachycardia?

A

A sinus tachycardia

Focal atrial tachycardia

Atrioventricular re-entry tachycardia

AV nodal re-entry tachycardia

270
Q

What is sinus tachycardia?

A

Conduction happens correctly in the SAN but the impulses are initiated at too high a frequency.

This can be due to infection, pain, exercise, anxiety, dehydration, bleed, sepsis, drugs, anaemia

271
Q

What is focal atria tachycardia?

A

A group of cells in the atria act as the pacemaker going quicker than the SAN node often seen in patients with chronic lung disease. Normal P wave

272
Q

What is a junctional tachycardia?

A

Where cells within the AVN become the pacemaker

273
Q

What causes Torsades de Pointes?

A

A prolonged QT interval means that there is a longer peroid before ventriuclar repolarisation

274
Q

How would you treat Torsades de Pointes?

A

Correct the disturbance
Magnesium sulphate
cardioversion if the problem does not resolve

275
Q

What is ventricular bigeminy?

A

When ventricular ectopics are occurring so frequently that they happen after every sinus beat

276
Q

What is type A Wolf -Parkinson- White syndrome?

A

Type A (left-sided): positive delta wave in the precordial leads (I, II, III, aVL, aVR, aVF), R>S in V1

277
Q

What is type B Wolf -Parkinson- White syndrome?

A

Type B (right-sided): negative delta wave in leads I and II

(accessory pathway is down right side of heart)

278
Q

What are the two Stanford classifications of aortic dissection and which is more common?

A

Type A: is when the dissection involves the ascending aorta. Accounts for 60-70% of cases

Type B: involves only the descending aorta (distal to subclavian) accounts for 30-40% of cases

279
Q

How would you manage a type A aortic dissection?

A

ABCDE

Give a beta-blocker/CCB and then perform endovascular repair

280
Q

How would you manage type B aortic repair?

A

Give beta-blocker or CCB (labetalol, verapamil)

Consider surgery if serious if not monitor.

281
Q

What is Buerger’s test?

A

The first part involves the patient lying on their back (supine). Lift the patient’s legs to an angle of 45 degrees at the hip. Hold them there for 1-2 minutes, looking for pallor. Pallor indicates the arterial supply is not adequate to overcome gravity, suggesting peripheral arterial disease. Buerger’s angle refers to the angle at which the leg is pale due to inadequate blood supply. For example, a Buerger’s angle of 30 degrees means that the legs go pale when lifted to 30 degrees.

The second part involves sitting the patient up with their legs hanging over the side of the bed. Blood will flow back into the legs assisted by gravity. In a healthy patient, the legs will remain a normal pink colour. In a patient with peripheral arterial disease, they will go:

Blue initially, as the ischaemic tissue deoxygenates the blood
Dark red after a short time, due to vasodilation in response to the waste products of anaerobic respiration

282
Q

Describe the epidemiology of shock?

A

Septic shock is the most common form of shock in ICU. The annual incidence of septic shock is 0.3 to 0.7 per 1000.

Cardiogenic occurs in 7-9% of MI.

Hypovolaemic is the most common in children worldwide due to diarrhoea and trauma.

283
Q

What is shock?

A

Shock is a life-threatening, generalised form of acute circulatory failure with inadequate oxygen delivery to, and consequently oxygen utilisation by, the cells

284
Q

What are the different causes of shock?

A

Septic- infection with any organism it causes acute vasodilation from inflammatory cytokines

Anaphylactic- IgE mediated histamine release which causes vasodilation and results in hypotension and no airway

Neurogenic- spinal cord injury, epidural or spinal anaesthesia results in hypotension and bradycardia

Hypovolaemic- loss of >20% of the body’s fluid or blood supply makes it impossible for the heart to pump sufficient amounts of blood around the body. Non-haemorrhagic causes include burns and diabetic ketoacidosis.

Cardiogenic (pump dysfunction): most commonly occurs after myocardial infarction but other causes include tachyarrhythmias (e.g., atrial fibrillation or ventricular tachycardia), bradyarrhythmia’s, toxic substances

285
Q

Describe what happens when patient goes into shock?

A

Hypoperfusion is a lack of adequate oxygen delivery at a cellular level.
This triggers a systemic stress response, including tachycardia and peripheral vasoconstriction.
Once these mechanisms are overwhelmed it leads to organ dysfunction and failure and death.

In septic shock vasodilation results in the lack of perfusion, Results in cardiac impairment .

In cardiogenic, tissue hypoperfusion from loss of cardiac output induces tissue inflammation

286
Q

What are the key presentations of shock?

A

Hypotension
Tachycardia
Skin changes
Oliguria
Fever
Chest pain
Dyspnoea
Hypoxaemia

287
Q

What are the signs of septic shock?

A

Fever
Tachycardia
High respiratory rate
Increased white cell count

288
Q

What are the signs of hypovolaemic shock?

A

inadequate tissue perfusion, clammy cold skin, tachycardia, sweating, tachycardia, then falling to hypotension and bradycardia

289
Q

What are the symptoms of septic shock?

A

pyrexia, nausea and vomiting, vasodilation and bounding pulse

290
Q

What investigations would you perform for a patient in shock?

A

Lactate levels (sepsis). Venous blood gas, full blood count, glucose, ECG, C-reactive protein

291
Q

How would you manage septic shock?

A

Sepsis
Give fluids for BP
Antibiotics
Community-acquired pneumonia – ceftriaxone
MRSA – vancomycin
Pseudomonas – cefepime + metronidazole

292
Q

How would you treat cardiogenic shock?

A

give IV fluids, loop diuretic, vasodilator

293
Q

What is the prognosis for shock?

A

Shock has a high mortality but this is dependent on cause. Septic shock has case-fatality rates of 40% to 50%, reaching up to 80%.

The odds of dying from a myocardial infarction increase by over 20-fold when it is complicated by shock. Hospital mortality of cardiogenic shock reaches around 60%.

Of these deaths, 70% to 80% occur in the first 30 to 60 days after onset of cardiogenic shock.

294
Q

Describe each of the different murmurs

A

The two most common murmurs:
aortic stenosis → ejection-systolic murmur
mitral regurgitation → pansystolic murmur

The two less common murmurs:
aortic regurgitation → early diastolic murmur
mitral stenosis → mid-diastolic murmur

295
Q

What is essential and secondary hypertension?

A

Essential = occurs independent of any identifiable cause
Secondary = occurs as a result of an identifiable cause e.g. CKD, hyper/hypothyroidism, primary hyperaldosteronism, stress, aortic coarctation, pheochromocytoma etc.

296
Q

What is the mechanism of action of spironolactone?

A

inhibition of aldosterone receptor in distal tubules

297
Q

What does a high or low INR indicate?

A

international normalised ratio (INR) blood test tells you how long it takes for your blood to clot.

high INR = haemorrhage (H-H)
low INR = clotting (lo-lot)

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