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Phase 2a Lecture Notes > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Thrombosis

A

is blood coagulation inside a vessel

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2
Q

Where can thrombosis occur

A

arterial circulation: high pressure, platelet rich
venous circulation: low pressure, fibrin rich

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3
Q

Normal bleeding time

A

2-9 minutes, 9-15 platlet dysfunction, 15+ critical

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4
Q

How to measure bleeding time

A

The time from the beginning of incision until the termination of bleeding is considered as the BT. A standard filter paper should be used every 30 seconds to draw off it until the blood completely stops

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5
Q

Arterial thrombosis-anatomy + symptoms

A

Coronary circulation- angina
Cerebral circulation- stroke syptoms
Peripheral circulation- pain in leg
Other territories- SMA- bellyache

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6
Q

Arterial thrombosis-etiology

A

Atherosclerosis
Inflammatory
Infective
Trauma
Tumours
Unknown- Platelet driven

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7
Q

Arterial thrombosis-Presentations

A

Myocardial infarction
CVA- cerebral vascular accident or stroke
Peripheral vascular disease
Others

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8
Q

Arterial thrombosis: treatment- coronary

A

Aspirin + other antiplatelets
Anticoagulants
Thrombolytic therapy: streptokinase tissue plasminogen activator
Reperfusion – Catheter directed treatments and stents
TPA generates plasmin, degrades fibrin- dissolve clots

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9
Q

Anticoagulants example and action

A

LMWH (low molecular weight heparins) and UFH (unfractionated heparin)- enhances antithrombin ability to inactive thrombin (factor IIa), factor Xa and factor IXa
Fondaparinux- inhibits factor Xa directly

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10
Q

Aspirin- thrombosis treatment

A

inhibits platelet function

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11
Q

Why is Fondaparinux used instead of heparin?

A

Rate of serious bleeding with Fondaparinux was much lower than with heparin because Fondaparinux has a lower half life

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12
Q

Arterial thrombosis: treatment- cerebral

A

Aspirin, other anti-platelets
Thrombolysis- Catheter directed treatments
Reperfusion

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13
Q

Why is heparin not used for strokes?

A

Limited efficacy and an increased risk of bleeding complications

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14
Q

Venous thrombosis-anatomy

A

Peripheral –Ileofemoral, femoro-popliteal
Other sites – Cerebral, Visceral
Fibrin driven

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15
Q

Venous thrombosis-diagnosis

A

Signs and symptoms-very non specific (specific= calf pain and chest pain/breathlessness)
Blood tests –D-dimer –sensitive but not specific- not used often for in patients
Imaging-usually required- ultrasound, or CT/MRI

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16
Q

Vichow’s triad

A

increased risk of vascular thrombosis- Hypercoagulability of blood, statis of flow+ Vessel wall injury/ Endothelial damage

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17
Q

What are the three components of Virchows triad?

A

intravascular vessel wall damage, stasis of flow, and the presence of a hypercoagulable state

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18
Q

Venous thrombosis-aetiology- Virchows triad blood flow

A

Immobilisation:
Surgery
Long haul flights
Trauma
Injury – physical, chemical

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19
Q

Venous thrombosis-aetiology- Virchows triad blood constituent

A

Mainly genetic
others:
Malignancy
Oestogens

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20
Q

Venous thrombosis-treatment

A

Heparin or LMWH
Warfarin
DOAC- main treatment for DVT
Endo-vascular- for longer clots in younger patients- clot destroyed or removed using catheter
Surgical- very rare

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21
Q

DOAC

A

direct oral anticoagulants

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22
Q

Warfarin action

A

Inhibits enzyme responsible for activating vitamin K, depletes body of functional vitamin K and reduce synthesis of vitamin K dependent factors clotting factors (10, 9, 7, 2)

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23
Q

When would the treatment of DVT be more aggressive?

A

DVT is very large, blocks major veins, or produces severe pain and swelling of the limb

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24
Q

Venous thrombosis-prevention

A

Mechanical or chemical thromboprophylaxis after risk assessment upon entrance to hospital
Also early mobilisation and good hydration

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25
Q

Heparin (UFH)

A

Given IV- typically continually
Binds to antithrombin and increases its activity
Indirect thrombin inhibitor
Short half life- good if you need to stop quickly ie for surgery

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26
Q

Aim APTT for heparin

A

activated partial thromboplastin time- ratio 1.8-2.8

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27
Q

Low molecular weight heparin

A

Smaller molecule, less variation in dose and renally excreted
Once daily, weight-adjusted dose given subcutaneously
Used for treatment and prophylaxis

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28
Q

Is HIT more common after LMWH or UFH?

A

LMWH is less likely than UFH to cause antibody generation and thus patients do not develop clinical HIT (Heparin‐induced thrombocytopenia)

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29
Q

Warfarin

A

Orally active
Prevents synthesis of active factors II, VII, IX and X
Antagonist of vitamin K
Long half life (36 hours)
Prolongs the prothrombin time

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30
Q

Problems with warfarin

A

Difficult to use,
Individual variation in dose
Need to monitor using INR (international normalised ratio, derived from prothrombin time)

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31
Q

NOAC / DOAC

A

Orally active
Directly acting on factor II or X
No blood tests or monitoring
Shorter half lives so bd or od
Used for extended thromboprophylasis and treatment of AF and DVT/PE
Not used in pregnancy

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32
Q

Whay are DOAC/NOAC not used in metal heart valves?

A

Shown to cause increase stroke rate

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33
Q

Fondaparineux

A

example of a Pentasaccharide so indirect Xa inhibitor

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34
Q

Pulmonary Embolism- symptoms

A

breathlessness, pleuritic chest pain

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35
Q

QT interval

A

Total duration of de/repolarization, QT interval increases when HR increases, Should be 0.35-0.45s

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36
Q

Pulmonary Embolism- signs

A

tachycardia, tachypnoea, pleural rub

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37
Q

Pulmonary Embolism vs DVT

A

PE and DVT have similar symptoms, risk factors and signs

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38
Q

Pulmonary Embolism- Differential diagnosis

A

Musculoskeletal, Infection, Malignancy, Pneumothorax, Cardiac, GI causes

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39
Q

Treatment PE

A

Supportive treatment
LMW Heparin
Oral warfarin for 6 months
DOAC/NOAC
Treat underlying cause

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40
Q

Prevention of PE

A

Anticoagulation
IVC filters- catches clot to prevent embolism to the lung

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41
Q

Pulmonary Embolism -Massive

A

Haemodynamic instability
Hypotension, cyanosis, severe dyspnoea, right heart strain/ failure
Rare

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42
Q

Pulmonary Embolism -Massive- treatment

A

Surgery

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43
Q

What is the commonest cause of vascular disease?

A

atherosclerosis

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44
Q

Pathophysiology for strokes

A

Atherosclerosis
Inflammatory
Vasospastic
Compression
Traumatic
Pro-thrombotic conditions

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45
Q

What happens to the plaque when we get an acute clinical complication?

A

plaque ruptures, it causes can causes ulceration
Thrombosis leading to ischemia (can become chronic)/necrosis (aneurysm development)

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46
Q

Plaque ulceration

A

acute thrombosis with occlusion, dislodging and peripheral embolism

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47
Q

Risk factors in PAD (peripheral arterial disease)?

A

Modifiable- Smoking
Hypertension
Diabetes
Hypercholesterolaemia
Non-Modifiable- age/sex

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48
Q

Acute ischemia in lower limbs

A

6Ps
Acute-embolus (AF, MI)
Acute on chronic-thrombus

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49
Q

Chronic ischemia in lower limbs

A

IC- intermittent claudication decreased mobility
Rest pain- end stage, constant pain
Tissue loss
Burgers test

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50
Q

6Ps for limb ischemia

A

pallor (unhealthy pale apperance), pain, paresthesia (abnormal sensation), paralysis, pulselessness, and poikilothermia

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51
Q

poikilothermia

A

inability to maintain a constant core temperature independent of ambient temperature

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52
Q

Burgers test-

A

Have the patient lie supine and raise the leg above the level of the head. If the sole of the foot becomes pale then the test is positive

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53
Q

Positive burgers test

A

sole of foot goes pale when raised above level of head while lying supine, suggests more severe ischaemia with distal limb artery involvement

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54
Q

What is the name of the circle consisting the arterial supply to brain?

A

Circle of willis- anterior MCA, ACA+ anterior choroidal artery
-posterior- vertebral artery, basilar, PCA

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55
Q

Ischaemic vs haemorrhagic stroke

A

Ischaemic 60%
Haemorrhagic 30%
Carotid Disease ( results from a blockage or narrowing of the carotid arteries)-50% of ischaemic strokes

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56
Q

In TIA/stroke is embolization or thrombosis more common?

A

Thrombosis is more common

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57
Q

True Aneurysms

A

True- involves all three layers of the arterial blood vessel wall, Weakening of the arterial wall leading to dilatation leading to outpouring
Commonest location is the infra-renal aorta

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58
Q

False aneurysms

A

False- caused by bleeding with in the artery wall

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59
Q

Mycotic aneurysm

A

Mycotic- weakness in wall relating to infection

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60
Q

What is the definition of an aneurysm?

A

bulging, weakened area in the wall of a blood vessel resulting in an abnormal widening or ballooning greater than 50% of the vessel’s normal diameter (width)

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61
Q

What information does a duplex ultrasound give you?

A

duplex ultrasound can show how blood flows to different parts of the body. It can also tell the width of a blood vessel and reveal any blockages

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62
Q

Duplex ultrasound

A

using high frequency sound waves to look at the speed of blood flow, and structure of the leg veins

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63
Q

What are the advantages of MRA over CTA?

A

MRA can be performed without a as harmful contrast agent and has no radiation, unlike CTA. Also, CTA relies on a working pumps (ie heart in good condition), where as MRA does not

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64
Q

Treatment for PAD- Risk factor modification

A

Antiplatelets
Statin
Stop smoking
Good control of BP
Good control of DM
ACE inhibitors?
exercise program

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65
Q

Invasive treatment for PAD –Lower Limbs

A

Endo-vascular:
Stenoses
Short occlusions
DEB- drug eluting balloon
DES- drug eluting stent
Bypass surgery using graft to bypass blockage: Better patency and limb salvage rates than DEB/DES, however higher morbidity and mortality

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66
Q

Intermittent claudication (IC)

A

lower extremity skeletal muscle pain that occurs during exercise due to insufficent O2 supply to meet demands of skeletal muscle

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67
Q

Should a patient with IC have exercise or angioplasty or surgery?

A

Exercise first as long as it not too severe

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68
Q

AAA Treatment- pros and cons

A

Endovascular: -ie stents
-Lower morbidity and mortality
-Life long surveillance
Open surgery: -Higher initial morbidity and mortality, chance of dying around surgery are higher, but lower long term morbidity and mortality after surgery

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69
Q

What is the current NICE recommendation for AAA repair open surgery or EVAR?

A

EVAR only for patients with hostile abdomens, medical comorbidities or anaesthetic risks that contra-indicate open surgery

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70
Q

Carotid Endarterectomy vs Endovascular stenting for AAA

A

Open surgery much more common than endovasuclar stenting

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71
Q

What prevents blood flowing distally?

A

Muscle contraction and valves

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72
Q

Pathophysiology of venous disease

A

Venous return
-Valves
-Muscle pump
Incompetence
Obstruction
Mixed

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73
Q

Where is the SFJ (sapheno-femoral junction) located?

A

4 patient fingerbreadths lateral and inferior to pubic tubercle on common side

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74
Q

Investigation for venous disease

A

Duplex- Gold standard
MRV- Pelvic
Venography- Pelvic

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75
Q

Treatment – Superficial Venous Disease

A

Lifestyle
Compression
Sclerotherapy
Endo-venous treatments
Surgical stripping

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76
Q

What is the current NICE recommendation for treatment of VVs (varicose veins)?

A

endothermal ablation- lasers

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77
Q

Treatment – Deep Venous Disease

A

Lifestyle
Compression
Stents
Valves

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78
Q

Greatest risk factor for coronary artery disease

A

age

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79
Q

Risk Factors For Atherosclerosis

A

Age
Tobacco Smoking
High Serum Cholesterol
Obesity
Diabetes
Hypertension
Family History- very strong predictor

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80
Q

Distribution of Atherosclerotic Plaques

A

Found within peripheral and coronary arteries
Focal distribution along the artery length

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81
Q

Atherosclerotic Plaques distribution governed by

A

haemodynamic factors- Changes in flow/turbulence (eg at bifurcations) cause the artery to alter endothelial cell function. Wall thickness is also changed leading to neointima. Altered gene expression in the key cell types is key.

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82
Q

Which of the following is not in artery walls
Tunica intima
Tunica media
Epithelial cells
Neutrophils

A

Epithelial cells- endothelial not epithelium

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83
Q

Atherosclerotic plaque structure

A

Lipid
Necrotic core
Connective tissue
Fibrous “cap”

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84
Q

Result of atherosclerotic plaque

A

Occlusion of the vessel lumen- resulting in a restriction of blood flow (angina)
“rupture”- thrombus formation – can be fatal

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85
Q

Response to Injury hypothesis of Atherosclerosis

A

-Initiated by an injury to the endothelial cells which leads to endothelial dysfunction.
-Signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.
-Inflammation ensues

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86
Q

Progression of Atherosclerosis

A

Fatty streaks
Intermediate Lesions
Fibrous Plaques/ Advanced Lesions
Plaque Rupture
Plaque erosion

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87
Q

Fatty streaks

A

Earliest lesion of atherosclerosis
Consist of aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall

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88
Q

Intermediate Lesions- layers

A

Lipid laden macrophages (foam cells)
Vascular smooth muscle cells
T lymphocytes
Adhesion and aggregation of platelets to vessel wall
Isolated pools of extracellular lipid

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89
Q

Fibrous Plaques or Advanced Lesions

A

Impedes blood flow
Prone to rupture
Fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes

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90
Q

Plaque Rupture

A

Fibrous cap has to be resorbed and redeposited in order to be maintained
If balance shifted eg in favour of inflammatory conditions (increased enzyme activity), the cap becomes weak and the plaque ruptures
Leads to thrombus (clot) formation and vessel occlusion

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91
Q

Plaque Erosion

A

Second most prevalent cause of coronary thrombosis
Small early lesions

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92
Q

plaque rupture vs plaque erosion

A

Ruptured plaque has a large lipid core with abundant inflammatory cells, red thrombus.
Eroded plaques have a small lipid core, disrupted endothelium, more fibrous tissue and a larger lumen, white thrombus.

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93
Q

Treatment of coronary artery disease

A

PCI - Percutaneous Coronary Intervention
More than 90% of patients require stent implantation
Restenosis was a major limitation, no longer though due to drug eluting stents

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94
Q

What are coronary stents used in patients today made of?

A

Plastic

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95
Q

Acute Coronary Syndromes

A

spectrum of acute cardiac conditions
from unstable angina to varying degrees of evolving
myocardial infarction (MI)

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96
Q

Rank degrees of MI from least to most severe

A

-Unstable angina- No ECG changes
-Non-Q wave MI
Non-ST-elevation M
-Q wave MI
ST elevation MI

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97
Q

Unstable angina

A

*Cardiac chest pain at rest
*Cardiac chest pain with crescendo pattern
*New onset or deterioration of previous angina

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98
Q

Diagnosis for unstable angina based on

A

history
ECG
troponin (no significant rise in
unstable angina)

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99
Q

treatment during an episode of stable anhinga

A

GTN spray

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100
Q

Stable angina

A

Chest pain caused by insufficient blood supply to myocardium and included by physical exertion or emotional stress

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101
Q

Prinzmetal angina

A

chest discomfort or pain at rest with ST segment elevation, seen on ECG

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102
Q

STEMI investigation

A

ST segment elevation, pathological Q waves after a few days, seen on ECG
Increased troponin levels

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103
Q

STEMI

A

complete occlusion of major CA, leads to full thickness damage of heart muscle

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104
Q

NSTEMI

A

partial occlusion of major CA or complete occlusion of minor CA, leads to partial thickness damage of the heart

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105
Q

NSTEMI investigation

A

ST depression +/ T wave inversion
Increased troponin levels

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106
Q

ST elevation on ECG

A

> 1mm of ST elevation (ST wave higher than PQ wave) in two contiguous leads on the 12 lead ECG

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107
Q

Non-Q wave vs Q MI

A

retrospectively, few days after MI
non-Q wave or Q-wave MI on the basis of whether new
pathological Q waves develop on the ECG

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108
Q

Non-Q wave MI on ECG

A

Poor R wave progression, ST elevation and biphasic

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109
Q

Q wave MI on ECG

A

Complete loss of R wave

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110
Q

Myocardial infarction- symptoms

A

Acute central chest pain, nausea, sweating, dyspnoea, SOB, palpitations, pallor

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111
Q

Dyspnoea

A

difficult or laboured breathing

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112
Q

Myocardial infarction- mortality

A
  • Early mortality - 30% outside hospital
  • 15% in hospital
  • Late mortality - 5% first year
  • 2-5% annually thereafte
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113
Q

Myocardial infarction- risk factors

A

higher age, DM, renal failure, ethnicity, smoking, HTN, obesity + sedentary lifestyle

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114
Q

MI differentials

A

Pericarditis, PE, myocarditis, GORD, aortic dissection

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115
Q

Myocardial infarction effect on cardiac muscles

A

Usually causes permanent heart muscle damage although
this may not be detectable in small MIs

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116
Q

Initial Management of STEMI

A

*Get in to hospital quickly – 999 call
*Paramedics – if ST elevation, contact primary PCI
centre for transfer for emergency coronary
angiography
*Take aspirin 300mg immediately
*Pain relief

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117
Q

MI treatment- MONA

A

Morphine, O2 (sats below 94%), Nitrates and Aspirin

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118
Q

Hospital management of STEMI after diagnosis

A

*Oxygen therapy only if hypoxic
*Pain relief – opiates/ nitrates
*Aspirin +/- platelet P2Y12 inhibitor
*Consider beta-blocker
*Consider other antianginal therapy
*Consider urgent coronary angiography e.g. if
troponin elevated or unstable angina refractory
to medical therapy

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119
Q

MI complications- Darth Vader

A

Death
Arrhythmia
Rupture
Tamponade
HF

Valve disease
Aneurysm
Dressler syndrome
Embolism
Recurrence regurgitation

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120
Q

ACS (acute coronary syndrome

A

Umbrella term that includes- STEMI, unstable angina + NSTEMI

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121
Q

Most common causes of ACS

A

MI due to atherothrombosis- type 1

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122
Q

Causes of type 2 MI

A
  • Myocardial oxygen demand/supply mismatch
  • coronary vasospasm without plaque rupture
    *drug abuse (amphetamines, cocaine)
    *dissection of the coronary artery related to defects of
    the vessel connective tissue- more common in middle aged women
    *thoracic aortic dissection
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123
Q

Causes of Myocardial oxygen demand/supply mismatch

A

sepsis, acute lung pathology, thyrotoxicosis,
pulmonary embolism, anaemia, haemorrhage or
other causes of hypotension/hypovolaemia –
underlying stable coronary artery disease may or
may not be a contributing factor

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124
Q

Tako-Tsubo cardiomyopathy (Stress-induced cardiomyopathy)

A

-May present as MI
-Often precipitated by acute stress such as extreme emotional distress in susceptible individuals

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125
Q

Tako-Tsubo cardiomyopathy (Stress-induced cardiomyopathy)- pathophysiology

A

Causes transient LV systolic dysfunction, typically ballooning of the left ventricular apex during systole that recovers over days or a few weeks with limited or no permanent damage

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126
Q

Troponin

A

Protein complex consisting of troponin C, troponin I and troponin T that regulates actin:myosin contraction

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127
Q

Troponin as markers of cardiac muscle injury

A

*Cardiac-specific isoforms of troponin T and troponin I are
highly sensitive markers for cardiac muscle injury

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128
Q

Diseases with positive troponin markers

A
  • Gram-negative sepsis
  • pulmonary embolism
  • myocarditis
  • heart failure
  • tachyarrhythmias
  • cytotoxic drugs
  • vigorous exercise
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129
Q

Effect of aspirin on platelet inhibition

A

Irreversible inactivation of COX-1 (responsible for thromboxane production)

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130
Q

P2Y12

A

Plays role in amplification of platelet activation- e.g clopidogrel, prasugrel, and ticagrelor

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131
Q

P2Y12 inhibitors

A

Work by inhibiting P2Y12 action, so no platelet activation
Can have irreversible or reversible effect on platelets
Increase risk of bleeding so need to exclude serious bleeding prior to administration

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132
Q

Which is a more effective antiplatelet Prasugrel or clopidogrel?

A

Prasugrel is a more efficient prodrug than clopidogrel as some people do not metabolise clopidogrel into its active form due genetic changes

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133
Q

Prodrug

A

compound with little or no pharmacological activity that metabolizes inside the body and converts into a pharmacologically active drug compound

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134
Q

Common adverse effects of P2Y12 inhibitors

A

*Bleeding e.g. epistaxis, GI bleeds, haematuria
*Rash
*GI disturbance

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135
Q

Idiosyncratic adverse effects of ticagrelor (P2Y12 inhibitors)

A

*Dyspnoea requires switching to
prasugrel or clopidogrel
*Ventricular pauses: may resolve

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136
Q

GPIIb/IIIa antagonists

A

Only IV
Used in combination with aspirin and P2Y12 inhibitors for PCI
*Increase risk of major bleeding so used selectively
*Reducing use globally due to more effective oral
antiplatelet therapy

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137
Q

Percutaneous Coronary Intervention (PCI)

A

non-surgical procedure that uses a catheter to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque build up

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138
Q

Anticoagulants

A
  • Target formation and/or activity of thrombin
    *Inhibit both fibrin formation and platelet activation
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139
Q

Anti-anginal therapy for ACS

A

beta blocker, nitrates, calcium antagonist

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140
Q

Secondary prevention for ACS

A

statins, ACEI, beta blocker, other antihypertensive
therapy

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141
Q

When would you consider glycoprotein IIb/IIIa antagonists for STEMI

A

patient undergoing primary PCI

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142
Q

Heart failure patients-pharmacological
therapy

A

diuretic, ACEI, beta blocker, aldosterone antagonist
(spironolactone, epleronone)

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143
Q

Gold standard pharmacological
therapy in ACS

A

Aspirin and P2Y12 inhibitor combination (assuming no contraindications
and confirmed diagnosis)

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144
Q

ACS management- diagnosis

A

history, ECG, troponin +/- coronary angiography;
consider other diagnoses if uncertain
Check no active or recent life-threatening bleeding/severe anaemia

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145
Q

ACS management- ST elevation

A

arrange primary PCI (PPCI)

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146
Q

ACS management- initial antithrombotic therapy

A

dual antiplatelet therapy (DAPT) +
anticoagulant; may use GPIIb/IIIa antagonist for PPCI

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147
Q

Two types of cardiac myocytes

A

Atrio-ventricular conduction system – slightly faster conduction
General cardiac myocyte

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148
Q

Normal systolic ejection fraction

A

60-65%

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149
Q

Cardiac failure

A

Failure to transport blood out of hear

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150
Q

Cardiogenic shock

A

severe cardiac failure

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151
Q

Left sided cardiac failure

A

pulmonary congestion and then overload of right side

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152
Q

Right sided cardiac failure

A

venous hypertension and congestion

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153
Q

Diastolic cardiac failure (HFpEF)

A

Stiffer heart

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154
Q

Embryogenesis of the heart- origin

A

mesoderm

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155
Q

Paradoxical Embolism (PDE)

A

venous thrombus crosses an intracardiac defect (ie unclosed foramen ovale) from right to left into the arterial circulation, should have been logged in the heart or lungs

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156
Q

4 main features of Tetralogy of Fallot

A
  • Pulmonary stenosis
  • Ventricular septal defect
  • Aorta overrides Ventricular septal defect
  • Right ventricle hypertrophy
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157
Q

Tetralogy of Fallot- pulmonary stenosis

A

right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction- performed in first 2 years of life, progressive cardiac debility and risk of cerebral thrombosis increases with age

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158
Q

When is troponin releases?

A

After damage to myocytes

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159
Q

Why do you repeat troponin test?

A

comparing your levels over time can help determine the extent of the heart damage and prognosis

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160
Q

Pericarditis- Dressler syndrome

A

Delayed pericarditic reaction following infarction (2-10 weeks)

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161
Q

Common angina exacerbating factors- supply

A

Anaemia, hypoxemia

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162
Q

Common angina exacerbating factors- demand

A

Hypertension
Tachyarrhythmia
Valvular heart disease

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163
Q

Common angina exacerbating factors- environmental

A

cold weather, heavy meals, emotional stress

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164
Q

Myocardial ischemia - physiology

A

imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:
1. Impairment of blood flow by proximal arterial stenosis
2. Increased distal resistance (left ventricular) hypertrophy
3. Reduced oxygen-carrying capacity of blood (anemia)

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165
Q

Common Non IHD causes of angina

A

Prinzmetal’s angina (coronary spasm)
Microvascular angina (Syndrome X)
Unstable angina (Crescendo angina)- gets worse, often mistake for heart attack

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166
Q

History: IHD

A

Personal details (demographics, identifiers)
Presenting complaint
History of PC + risk factors
Past medical history
Drug history, allergies
Family (1st degree mainly)/Social history
Systematic enquiry

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167
Q

Main Cardiac symptoms

A

Chest pain (tightness/ discomfort)
Breathlessness (at rest, have to sperate pulmonary from cardiac problems)

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168
Q

Factors pointing towards ischemic cardiac pain

A

Pain when exercise, elephant sitting on chest, front of chest

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169
Q

Chest pain: Differential diagnoses

A

Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Dissection of the aorta
Gastro-oesophageal (reflux, spasm, ulceration)
Musculo-skeletal (unlikely to be angina if after long period of exercise)
Psychological

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170
Q

Investigations of angina

A

Exercise testing, myoview scan, CT coronary angiography (best test but invasive), stress echo, perfusion MRI

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171
Q

Myoview scan

A

radioactive substance and x-ray used to create images which show blood flow to the heart muscle after stress and rest

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172
Q

Angina: drugs

A

Beta-blockers, Nitrate (dliates CA and vein), statin, aspirin, Ca channel blocker (reduce action of SMC, less O2 demand and cause vasodilation)

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173
Q

Beta blockers

A

Reduce HR and contracrility resulting lower CO so lower O2 demand on heart

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174
Q

β blockers: side-effects

A

Tiredness, nightmares, bradycardia, erectile dysfunction, cold hands and feet

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175
Q

β blockers: contra-indications

A

ASTHMATICS- Don’t give patients with asthma beta blockers

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176
Q

What class of drugs are Nitrates

A

Venodilators

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177
Q

Ca channel blockers

A

reduce action of SMC, less O2 demand and cause vasodilation

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178
Q

Main aspirin side effect

A

gastric ulceration

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179
Q

Statins

A

HMG CoA Reductase (enzyme involved in cholesterol synthesis) inhibitors, inhibits synthesis of cholesterol

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180
Q

Angina: treatment- first action drugs

A

Some combination of Aspirin, GTN, β Blocker, Statin

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181
Q

Angina: treatment- second action drugs

A

ACE inhibitor, long acting nitrate

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182
Q

Angina: treatment- invasive treatment

A

Revascularisation: PCI (percutaneous coronary intervention)/ CABG (open surgery)

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183
Q

Angina: treatment- last line drugs

A

Ca++ channel blocker
Potassium channel opener
Ivabradine

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184
Q

Pros of PCI (percutaneous coronary intervention)

A

Less invasive
Convenient
Repeatable
Acceptable

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185
Q

Cons of CABG (Coronary artery bypass graft)

A

Invasive
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay
Time for recovery

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186
Q

ECG

A

elctrocardiogram is a representation of the electrical events of the cardic cycle

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187
Q

Do electrical impulses that travel towards the electrode produce an upright or downwards deflection?

A

Towards=upright (positive) deflection

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188
Q

12 ECG leads

A

3 standard limb leads
3 augmented limb leads
6 precordial leads

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189
Q

Stannard Limb leads

A

I- RA to LA 0 degrees
II- RA to LL +60 degrees
III- LA to LL +120 degrees

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190
Q

Augmented limb leads

A

aVL- -30 degrees
aVR- -150 degrees
aVF- +90 degrees

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191
Q

Precordial leads measure

A

V1+V2= septal= RA+RV
V3+V4=anterior= anterior LV
V5+V6=lateral= lateral portion of LV

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192
Q

Stannard leads measure

A

I- lateral
II- inferior
III-Inferior

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193
Q

Augmented leads measure

A

aVR- none
aVL- lateral
aVF- inferior

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194
Q

P wave

A

Atrium depolarizing

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195
Q

Why is the a gap between P wave and QRS complex on normal ecg?

A

Delay in AV node, normally 0.12-0.2s

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196
Q

QRS complex

A

Ventricular depolarisation

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197
Q

T wave

A

Ventricular repolarisation

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198
Q

U wave

A

afterdepolarizations which follow repolarization, small round symmetrical and positive (same direction as T wave) in lead II, more prominent at slower HR

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199
Q

QT interval

A

Total duration of de/repolarization, QT interval increases when HR increases, Should be 0.35-0.45s

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200
Q

ECG rule 1- PR interval

A

PR interval should be 120-200 ms or 3-5 squares

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201
Q

ECG rule 2- QRS complex length

A

QRS<110ms, less than 3 squares

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202
Q

ECG rule 3- QRS direction

A

QRS complex should be dominating upright in leads I and II

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203
Q

ECG rule 4- QRS and T wave

A

QRS and T waves tend to have the same general direction in the limb leads

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204
Q

ECG rule 5- aVR

A

All waves are negative in lead aVR

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205
Q

ECG rule 6- R+S wave V1-6

A

R wave must grow from V1 to at least V4
S wave must grow from V1 to at least V3 and disappear in V6

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206
Q

ECG rule 7- ST segment and V1+V2

A

ST segment should start isoelectric expect in V1 and V2 where it may elevate

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207
Q

ECG rule 8- P wave direction

A

P wave should be upright in I, II and V2 to V6

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208
Q

ECG rule 9- Q wave

A

No Q wave (or very small one less than 0.04s) in I, II, V2 to V6

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209
Q

ECG rule 10- T wave direction

A

T wave must be upright in I, II, V2 to V6

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210
Q

Determining the HR using ECG

A

n=number of big boxes between 2 QRS complexes
Divide 300 by n (1500 if small boxes)
OR count number of beats in 10s (number of seconds per page) and *6

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211
Q

Quadrant approach- ECG

A

QRS complex in leads I and aVF, determine if they are predominantly +ive or -ive, shows normal axis or left/right deviation

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212
Q

Quadrant approach-
Lead aVF=+ive
Lead I= +ive

A

Normal axis

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213
Q

Quadrant approach-
Lead aVF=+ive
Lead I= -ive

A

RAD (right axis deviation)

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214
Q

Quadrant approach-
Lead aVF=-ive
Lead I= +ive

A

LAD (left axis deviation)

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215
Q

R bundle branch block- ECG

A

V1- RSR1- M pattern, slowed appearance on ECG
V6- QRS, normal

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216
Q

L bundle branch block- ECG

A

V1- W appearance
V6- M appearance

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217
Q

What does right/left axis deviation suggest

A

In themselves are rarely significant- minor dedications occur in tall, thin individuals (R) or short, fat individuals (L).
However, should alert you to look for other signs of R/L hypertrophy. Right axis deviation may suggest a pulmonary embolus. Left axis deviation can suggest a conduction defect.

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218
Q

Cardiomyopathy

A

primary heart muscle disease – often genetic

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219
Q

Hypertrophic cardiomyopathy (HCM)

A

caused by sarcomere protein gene mutations, ECG is abnormal, v large deflections and pronounced t waves as a result of thick wall

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220
Q

HCM symptoms

A

angina, dyspnoea, palpitations, dizzy spells or syncope

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221
Q

Dilated cardiomyopathy (DCM)

A

LV/RV or 4 chamber dilatation and dysfunction, often caused by cytoskeletal gene mutations

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222
Q

DCM symptoms

A

Similar to heart failure

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223
Q

Arrhythmogenic cardiomyopathy (ARVC/ALVC)

A

characterised by progressive fibrofatty replacement of the myocardium caused by desmosome gene mutations

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224
Q

Arrhythmogenic cardiomyopathy (ARVC/ALVC) main feature

A

Arrhythmia

225
Q

True or false , not all cardiomyopathies carry an arrhythmic risk

A

False, All cardiomyopathies carry an arrhythmic risk

226
Q

Inherited arrhythmia (channelopathy)

A

defects in ion (K+, NA+, Ca2+) channels caused by ion channel protein gene mutations

227
Q

Channelopathies examples

A

long QT, short QT, Brugada and Catecholaminergic polymorphic ventricular tachycardia (CPVT)

228
Q

Channelopathies impact on heart structure

A

Channelopathies have a structurally normal heart

229
Q

Long QT syndrome

A

abnormal feature of the heart’s electrical system that can lead to a potentially life-threatening arrhythmia

230
Q

Most likely cause of sudden cardiac death in young people

A

due to an inherited condition, likely a cardiomyopathy or ion channelopathy

231
Q

Familial hypercholesterolaemia (FH)

A

Inherited abnormality of cholesterol metabolism, leads to serious premature coronary and other vascular disease

232
Q

Mechanisms of BP control- Targets for therapy

A

CO + peripheral resistance
Systems to target- RAAS, SNS (noradrenaline), local vasoconstrictor/dilators mediators

233
Q

Mechanisms of BP control- ACE inhibitors

A

Inhibits ACE, so inhibits conversion of angiotensin i > angiotensin ii

234
Q

Angiotensin ii action

A

Increases action of SNS so increase peripheral resistance + CO, increase salt retention and vascular growth

235
Q

ACE inhibitors- clinical indications

A

Hypertension, heart failure, diabetic

236
Q

Most widely used ACE inhibitors

A

Ramipril, perindopril, enalapril, trandopril

237
Q

ACE inhibitors- adverse effects

A

Relate to reduced angiotensin ii formation
Related to increased kinins- ACE also causes breakdown of bradykinin

238
Q

ACEi Contraindications

A

History of angio-oedema (heredity, recurrent or from previous ACEi exposure)
Pregnant/ Breastfeeding women
Not as effective in patients of black African or Caribbean origin

239
Q

Angiotensin II Receptor Blockers (ARB)- main clinical indications

A

Hypertension
Diabetic nephropathy
Heart failure (when ACE-I contraindicated)

240
Q

Angiotensin II Receptor Blockers (ARB)- examples

A

Known as the -sartans, irbesartan, valsartan, losartan and candesartan

241
Q

Angiotensin II Receptor Blockers (ARB)- adverse effects

A

Symptomatic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema

242
Q

ACE inhibitors- adverse effects- angiotensin ii formation

A

hypotension, acute renal failure- angiotensin ii constricts efferent arteriole, hyperkalaemia, teratogenic effects in pregnancy

243
Q

ACE inhibitors- adverse effects- increased kinins

A

Cough, rash, anaphylactoid reactions

244
Q

Calcium Channel Blockers (CCB)

A

Vasodilators, not Ca2+ antagonists

245
Q

Calcium Channel Blockers (CCB)- Main clinical indications

A

Hypertension
Ischaemic heart disease (IHD) – angina
Arrhythmia (tachycardia

246
Q

Most common type of CCB

A

AMLODIPINE

247
Q

CCB- Dihydropyridines

A

drug ending in -dipine, Peripheral arterial vasodilators, Preferentially affect vascular SMC

248
Q

CCB- Phenylalkylamines

A

Verapamil, main effects on heart- ive chronotopic+ -ive inotropic

249
Q

CCB- Benzothiazepines

A

diltiazem, Intermediate heart/peripheral vascular effects

250
Q

CCB causes of adverse effects

A

Due to peripheral vasodilatation (mainly dihydropyridines),
Due to negatively chronotropic effects (mainly verapamil/diltiazem),
Due to negatively inotropic effects (mainly verapamil)

251
Q

CCB adverse effects- peripheral vasodilation

A

Dihydropyridines
Flushing, headache, oedema, palpitations

252
Q

CCB adverse effects- negatively chronotropic effects

A

verapamil/diltiazem
Bradycardia
Atrioventricular block

253
Q

CCB adverse effects- -ive chronotropic effects

A

Verapamil
Worsening of cardiac failure

254
Q

What non CV side effect is common with verapmil vs other CCB

A

Constipation

255
Q

Beta-adrenoceptor blockers (BB)- main clinical indications

A

Ischaemic heart disease (IHD) – angina
Heart failure
Arrhythmia
Hypertension

256
Q

Cardioselective

A

used to imply β-1 selectivity however this is a misnomer given since up to 40% of cardiac β-adrenoceptors are β-2

257
Q

Beta-adrenoceptor blockers (BB) adverse effects

A

Fatigue, headache, sleep disturbance/nightmares- as BB can cross Blood-brain barrier
Bradycardia, hypotension, cold peripheries
Erectile dysfunction-
Worsens Asthma (may be severe) or COPD
PVD – Claudication or Raynaud’s

258
Q

Giving BB for heart failure

A

Heart failure – if given in standard dose or acutely- must be give in low dose and titrated

259
Q

Diuretics classes and action on kidney

A

Thiazides and related drugs (distal tubule)
Loop diuretics (loop of Henle)
Potassium-sparing diuretics
Aldosterone antagonists

260
Q

Diuretics main clinical indications

A

Hypertensin, heart failure

261
Q

Main adverse effects of diuretics

A

Hypovolaemia+ Hypotension (mainly loop diuretics)
Low serum potassium (hypokalaemia)
Low serum sodium (hyponatraemia)
Low serum magnesium (hypomagnesaemia)
Low serum calcium (hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Impaired glucose tolerance/Erectile dysfunction (mainly thiazides)

262
Q

Anti-hypertensin drug for pregnant women

A

METHYLDOPA- Centrally acting

263
Q

1st step anti-hypertensive for diabetics +/ <55

A

ACE-inhibitor or Angiotensin II receptor Blocker

264
Q

1st step anti-hypertensive for >55 +/ Afro-Caribbean

A

CBB

265
Q

Step 2 antihypertensive

A

ACE-I / ARB + CCB OR Thiazide like diuretic

266
Q

Step 3 antihypertensive

A

ACE-I / ARB + CCB and Thiazide like diuretic

267
Q

Step 4 antihypertensive

A

Resistant hypertension consider BB+ others

268
Q

Types of heart failure

A

Heart failure due to left ventricular systolic dysfunction - LVSD
Heart failure with preserved ejection fraction (diastolic failure- issue with filling of heart) – HFPEF
Acute heart failure / Chronic heart failure

269
Q

Acute vs Chronic heart failure

A

Acute- sudden heart attack
Chronic- develops slowly over weeks/months treated with pharmacology

270
Q

Heart failure

A

complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired, caused by structural or functional abnormalities of the heart

271
Q

Most common causes of heart failure

A

Coronary artery disease

272
Q

Treatment concept for chronic heart failure

A

Main benefit from vasodilator therapy via neurohumoral blockade (RAAS - SNS) and not from LV stimulants

273
Q

Heart Failure- basic pharmacology

A

Symptomatic treatment of congestion- Diuretics
Disease influencing therapy-neurohumoral blockade
Inhibition of RAAS + SNS

274
Q

Heart failure pharmacology- first line- triple therapy

A

Diuretic, ACE inhibitors and beta blocker therapy- Low dose and slow up titration

275
Q

Sacubitril/Valsartan (Entresto) in Heart Failure

A

Sacubitril – neprilysin inhibitor (increases levels of natriuretic peptides, increases vasodilation)
Valsartan –angiotensin II blocker

276
Q

SGLT2 Inhibitors + heart failure

A

1st used for DM, work by lower plasma glucose levels by blocking reabsorption of filtered glucose, which falls as plasma levels fall
Also found useful heart failure treatment

277
Q

Nitrates

A

Arterial and venous dilators
Reduction of preload and afterload
Lower BP
Comes in tablet, spray (for angina pain) and IV (for emergency)

278
Q

Nitrates main uses

A

Ischaemic heart disease (angina)
Heart failure

279
Q

CAD- Chronic stable angina symptoms

A

Anginal chest pain
Predictable
Exertional
Infrequent
Stable

280
Q

CAD- Unstable angina / acute coronary syndrome (NSTEMI) symptoms

A

Unpredictable
May be at rest
Frequent
Unstable

281
Q

CAD- ST elevation Myocardial Infarction (STEMI) symptoms

A

Unpredictable
Rest pain
Persistent
Unstable

282
Q

Chronic stable angina- pharmacology treatment

A

Antiplatelet therapy, Lipid-lowering therapy (statins), GTN spray for acute attack,
1st line treatment BB or CCB (switch then combined),
last line- long acting nitrate

283
Q

Acute coronary syndromes (NSTEMI and STEMI)- pharmacology treatment

A

Pain relief: GTN spray, Opiates – diamorphine
Dual antiplatelet therapy
Antithrombin therapy
Consider Glycoprotein IIb IIIa inhibitor (high risk cases)
Background angina therapy: BB, long acting nitrate, CCB
Lipid lowering therapy: Statins
Therapy for LVSD/heart failure as required

284
Q

Antiarrhythmic drugs- Vaughan Williams classification

A

Class I: Sodium channel blockers
Class II: BB
Class III: Prolong the action potential
Class IV: CCB, that act on heart

285
Q

Antiarrhythmic drugs- digoxin

A

Cardiac glycoside- toxin so narrow therapeutic range
Inhibit Na/K pump
Enhances vagal tone
Increased ectopic activity
Increased force of contraction- due to increase Ca2+ in muscle from Na+/K+ pump failing

286
Q

Antiarrhythmic drugs- digoxin uses

A

Used in atrial fibrillation (AF) to reduce ventricular rate response
Use in severe heart failure as positively inotropic

287
Q

Antiarrhythmic drugs- Amiodarone

A

treats ventricular arrhythmias and atrial fibrillation

288
Q

Anatomy of the Pericardium

A

2 continuous layer
Visceral single cell layer adherent to epicardium
Parietal layer- Fibrous
50 ml of serous fluid

289
Q

What lies outside of the pericardium

A

Left atrium is mainly outside the pericardium
Great vessels and LV+RA+RV lie within

290
Q

Cardiac tamponade

A

excessive fluid accumulates in the pericardium, in turn compressing the heart and restricting the filling of the cardiac chambers

291
Q

Physiology of the pericardium

A

Mechanical function restrains the filling volume of the heart, initially stretchy but stiff at higher tension, so the pericardial sac has a small reserve volume

292
Q

What happens when the small reserve volume of the pericardium is exceeded

A

If this volume is exceeded the pressure is translated to the cardiac chambers

293
Q

Acute pericarditis

A

inflammatory pericardial syndrome with or without effusion

294
Q

Pericardial fusion

A

a build-up of fluid between the layers of pericardium

295
Q

Acute pericarditis- Aetiology Infectious

A

Viral (common)
Bacterial: Mycobacterium tuberculosis
other bacteria rare- very sick high mortality

296
Q

Acute pericarditis- Aetiology Non- Infectious

A

Autoimmune (common):
Sjögren syndrome, rheumatoid arthritis, scleroderma,
systemic vasculitides
Neoplastic:
Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).
Metabolic:
Uraemia, myxoedema
Trauma- direct/indirect injury- often as a result of cardiac procedures

297
Q

Acute pericarditis- Clinical presentation

A

Chest pain (sharp and pleuritic, doesn’t have heavy tight description like IHD)
Dyspnoea
Cough
Hiccups (phrenic)

298
Q

Acute pericarditis- past medical history

A

Cancer, Rheumatological Dx, Pneumonia, Cardiac procedure (PCI, ablation), MI

299
Q

Pericarditis- Clinical examination

A

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

300
Q

Pericardial friction rub

A

Grating, to-and-fro sound produced by friction of the heart against the pericardium. This sounds similar to sandpaper rubbed on wood

301
Q

ECG - Pericarditis

A

Saddle shape ST wave
PR depression
No reciprocal changes

302
Q

ECG- pericarditis vs STEMI

A

pericarditis differ from STEMI such as in pericarditis, ST elevations are concave in shape and T-wave inversions do not occur in the presence of ST elevations

303
Q

Signs of taponade

A

Low blood pressure (hypotension). Bulging neck veins. Heartbeats that sound distant or muffled

304
Q

Pericarditis- management

A

Sedentary activity until resolution of symptoms- only for athletes
NSAIDs and aspirin at very high doses
Colchicine (causes nausea and diarrhoea) reduces recurrence

305
Q

Acute pericarditis recurrence

A

15-30% recurrence, Colchicine reduced recurrence rate by 50%

306
Q

Most common types of valvular heart disease

A

Aortic Stenosis
Mitral regurgitation
Aortic Regurgitation
Mitral Stenosis

307
Q

Normal Aortic Valve Area

A

3-4 cm2

308
Q

Aortic Stenosis

A

Symptoms occur when valve area is 1/4th of normal

309
Q

Aortic Stenosis- types

A

Valvular- commonest type- degenterative, rheumatic
Supravalvular
Subvalvular

310
Q

Congenital cause of aortic stenosis

A

Bicuspid aortic valve- BAV, 0.5-2% of pop, 1st degree relative’s need screening

311
Q

Pathophysiology of Aortic Stenosis

A

A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines

312
Q

Presentation of Aortic Stenosis

A

Triad- scope, angina, dyspnoea
Syncope (exertional)- 15%
Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
Dyspnoea (shortness of breath): on exertion due to heart failure (systolic and diastolic)-50%, occurs when servere
Sudden death <2%

313
Q

Aortic stenosis- physical signs

A

Small vol, slow rising pulse- heart is struggling to eject blood
Heart sounds- soft or absent second heart sound- aortic valve not closing properly or at all
Ejection systolic murmur- crescendo-decrescendo- large gradient between LV and aorta

314
Q

Natural history MR (mitral regulation)

A

The onset of symptoms is an indication of poor prognosis if left untreated

315
Q

Investigation of aortic stenosis

A

Echocardiogram- LV size and function, gradient between aorta and LV (using Doppler probe) and aortic valve area (how much is it opening/closing)

316
Q

Management of AS- general

A

Fastidious dental hygiene/ care- high risk of infection causing infective endocarditis
Consider IE prophylaxis in dental procedures- when high risk

317
Q

Management of AS- medical

A

Limited role as mechanical problem, vasodilators are relatively contraindicated in severe AS

318
Q

Management of AS- replacement

A

Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation

319
Q

TAVI (Transcatheter Aortic Valve Implantation)

A

Blow up balloon using catheter to crack open damaged aortic valve, damage aortic valve is withdrawn, new aortic valve is left behind

320
Q

Indications for AS intervention

A

Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing ejection fraction
Any patient undergoing CABG with moderate or severe AS
Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS

321
Q

Mitral Regurgitation

A

Backflow of blood from the LV to the LA during systole due to incompetent valve- mild MR seen in 80% of pop

322
Q

MR- volume or pressure problem?

A

Volume overload problem

323
Q

Primary vs Secondary MR

A

Primary MR- disease of leaflets
Secondary- normal valve architecture but impaired colures due to abnormal LV/LA geometry

324
Q

Primary MR causes

A

Myxomatous degeneration (MVP)
Rheumatic heart disease
Infective Endocarditis

325
Q

Secondary MR causes

A

dilated cardiomyopathy- too much tissue

326
Q

Pathophysiology of MR

A

Pure Volume Overload
Compensatory Mechanisms: LA enlargement, LV hypertrophy 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

327
Q

Physical signs and symptoms of MR

A

Auscultation: pansystolic murmur at the apex radiating to the axilla- intensity of murmur correlates with severity
Exertion Dyspnoea
HF

328
Q

Natural History of MR

A

Once symptomatic, mortality sharply rises

329
Q

Investigations in MR

A

ECG: LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment

330
Q

Management of MR- medications

A

Rate control for atrial fibrillation with beta-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates / Diuretics in acute MR
Chronic HF Rx if chronic MR with CCF (congestive cardiac failure/ heart failure)
No indication for ‘prophylactic’ vasodilators such as ACEI, hydralazine

331
Q

Management of MR- genral

A

Serial echocardiography
IE prophylaxis during dental procedure

332
Q

Management of MR- surgery

A

Surgical replacement/repair, TEER- transcatheter edge to edge repair

333
Q

Indications for surgery in severe MR

A

ANY Symptoms at rest or exercise (repair if feasible)
Asymptomatic:
If EF <60%, LVESD >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg

334
Q

Aortic Regurgitation

A

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

335
Q

Aetiology of Chronic AR

A

Bicuspid aortic valve, Rheumatic- usually with AS
Infective endocarditis

336
Q

Pathophysiology of AR

A

Combined pressure AND volume overload
Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

337
Q

Physical Exam findings of AR

A

Wide pulse pressure due to high systolic pressure (due to increased pressure) and low diastolic pressure (leaking back into LV)
Auscultation- Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve

338
Q

Natural History of AR

A

Asymptomatic until 4th or 5th decade
Rate of Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnoea: exertional, orthopnoea (when lying flat), and paroxysmal nocturnal dyspnoea (when sleeping)
Palpitations: due to increased force of contraction and ectopics

339
Q

The Evaluation of AR

A

CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function

340
Q

Management of AR- general

A

IE prophylaxis
Serial Echocardiograms

341
Q

Management of AR- medical

A

Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN

342
Q

Management of AR- surgical

A

Definitive Treatment- aortic valve replacement/repair
(TAVI in exceptional cases only if unsuitable for SAVR- surgical aortic valve replacement)

343
Q

AR- Indications for Surgery

A

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

344
Q

Mitral Stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole

345
Q

normal MV area

A

4-6cm2

346
Q

MS- MV area

A

Transmitral gradients and symptoms begin at areas less than 2 cm2

347
Q

MS predominant cause

A

Rheumatic carditis

348
Q

MS Pathophysiology

A

Progressive Dyspnea (SOB) (70%): LA dilation > pulmonary congestion
Increased Transmitral Pressures: Leads to LA enlargement and AF.
RHF symptoms: due to Pulmonary venous HTN
Haemoptysis (coughing up blood): due to rupture of bronchial vessels due to elevated pulmonary pressure

349
Q

Physical Signs of MS

A

prominent “a” wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Mitral facies
Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex

350
Q

Management of MS

A

Identify patient early who might benefit from percutaneous mitral balloon valvotomy

351
Q

Causes of hypertension

A

Often unspecific underlying cause
Screening limited to early onset (<30) with no RFs, hypertension resistant to 3 drugs or malignant hypertension

352
Q

Significance of hypokalaemia with hypertension

A

Suggests hyperaldosteronism

353
Q

Primary investigation with extreme high BP

A

Look at eyes for evidence of blood vessel damage- leakage of blood from vessels, swelling

354
Q

Average BP response to one hypertensive with moderate hypertension

A

Systolic decrease by 8-10 mmHg
Diastolic decrease by 4-6 mmHg

355
Q

White coat hypertension

A

Hypertension when you only see doctors, 1/4 of pop

356
Q

Investigations for BP

A

Clinical measure
Unattended BP measure (Dr leaves room)
Home self measurement
Ambulatory BP measurement (over a 24 period)

357
Q

Threshold for treatment

A

Low risk for CVD- 160/100mmHg
High risk for CVD- 140/90 mmHg
CVD risk calc using Qrisk3

358
Q

Hypertension vs age

A

Hypertension strongly correlates with age, more common in male pre-menopause age, more common in females post-menopause

359
Q

Hypertension symptom relief

A

Usually asymptomatic
Only symptomatic relief with treatment is headaches

360
Q

Who needs hypertension treatment

A

Routine- <140/90 mmHg
Previous stroke/ heavy proteinuria/ CKD AND diabetes- <130/80 mmHg
Older patients- <150/90 mmHg- increased due to increased risk of falls due to lower BP when standing, need to measure older person BP when standing

361
Q

No of drugs to control hypertension

A

1 drug- 39%
2 drug- 40%
3 drug- 16%
4 drug- 4%
4+ drugs- 1%

362
Q

Main illness that HBP contributes to

A

Stroke, HF, dementia, PVD, renal failure, MI

363
Q

Untreated HBP impact on life expectancy

A

Average 50 male with HBP- 5 years loss of life, 7 years loss of disease free life

364
Q

Average benefit of HBP treatment

A

Gain 5 years of life expectancy
30% decrease in stroke risk
40% decrease in MI risk

365
Q

Smoking effect on BP

A

On average smokers have lower BP as on average they are thinner

366
Q

Lifestyle factors that influence BP

A

Weight, salt intake, exercise, alcohol intake

367
Q

Main type of BP lowering medicine (action of drug)

A

BB (reduce renin release/cardic contractility), CCB, ACE inhibitors (block formation of angiotensin 2), diuretics (reduce circulating Na+)

368
Q

Drug causes of increased BP

A

NSAIDs, SNRIs, corticosteroids, oestrogen containing oral contraceptives, stimulants, anti-anxiety drugs, anti-TNFs

369
Q

Length of time for BP treatment

A

Treatment needed lifelong, treatment withdrawal leads to rebound in BP

370
Q

Circumstances when BP lowering tablets should be stopped

A

During general anaesthesia, as it causes hypotension

371
Q

Genetic transmission of congenital heart defects

A

Foetal recurrence
Background population- 1%
Father with Congen HD- 2.2%
Mother with Congen HD- 5.7%

372
Q

Tetralogy of Fallot

A

Ventricular septal defect- shifts forward, obstructs pulmonary outflow track leads to pulmonary stenosis, hypertrophy of RV, overriding aorta

373
Q

Tetralogy of Fallot - physiology

A

The stenosis of the RV outflow leads to the RV being at higher pressure than the left
Therefore blue blood passes from the RV to the LV
The patients are BLUE- wont survive an episode untreated

374
Q

Tetralogy of Fallot – surgical repair

A

Mostly repaired before the age of 2, most do well, often get pulmonary valve regurgitation in adult life and require redo surgery and arrhythmias can occur

375
Q

Ventricular septal defect (VSD)

A

Hole between high pressure LV and low pressure RV, common, treatment dependent on size of hole

376
Q

Ventricular septal defect (VSD) - Physiology

A

High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber
Therefore NOT blue
Increased blood flow through the lungs can lead to Eisenmenger’s syndrome (if large hole)

377
Q

Eisenmengers syndrome

A

High pressure pulmonary blood flow

378
Q

Eisenmengers syndrome- pathophysiology

A

High pressure pulmonary blood flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
The patient becomes BLUE

379
Q

Small Ventricular septal defect (VSD)

A

Can live normal lives without treatment
loud systolic murmur
higher risk of infection due to high velocity stripping lining of heart

380
Q

Atrial septum defects (ASD)

A

Abnormal connection between atria, common, often presents in adulthood (if moderate/smaller)

381
Q

Atrial septum defects (ASD) - Physiology

A

Slightly higher pressure in the LA than the RA
Shunt is left to right
Therefore NOT blue
Increased flow into right heart and lungs

382
Q

Atrial septum defects (ASD) – clinical signs

A

Pulmonary flow murmur
Fixed split second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X ray

383
Q

Closing Atrial septum defects (ASDs) techniques

A

Surgical
Percutaneous (key hole technique)
Earlier in life the better

384
Q

Atrio-Ventricular Septal Defects- AVSD

A

Hole in centre of heart, Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves, often associated with downs syndrome

385
Q

AVSD - physiology- complete defect

A

Breathless as neonate
Poor weight gain
Poor feeding
Torrential pulmonary blood flow
Needs repair or PA band in infancy
Repair is surgically challenging

386
Q

AVSD - physiology- partial defect

A

Can present in late adulthood
Presents like a small VSD / ASD
May be left alone if there is no right heart dilatation

387
Q

Patent Ductus Arteriosus

A

Failure of ductus to close, leading to link between aorta and pulmonary artery, so increased blood flow in pulmonary vasculature

388
Q

Patent Ductus Arteriosus- clinical signs

A

Continuous ‘machinery’ murmur
If large, big heart, breathless
Eisenmenger’s syndrome

389
Q

Coarctation (narrowing) of the aorta

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

390
Q

Coarctation of the aorta - physiology- severe

A

Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair

391
Q

Coarctation of the aorta - physiology- mild

A

Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term

392
Q

Coarctation repair

A

Surgical vs percutaneous repair
Subclavian flap repair, End to end repair, Coarctation angioplasty

393
Q

Do congenital heart defects treatment end after childhood

A

No, should have regular check up throughout childhood

394
Q

Bicuspid AV

A

Bicuspid not tricuspid AVs, common 1-2% of pop, more common in males

395
Q

BAV aortopathy

A

BAV is usually associated with coarctation of aorta and ascending aortic dilation, some need protective surgery

396
Q

Pulmonary Stenosis

A

Narrowing of the outflow of the right ventricle

397
Q

Pulmonary stenosis physiology- severe

A

Right ventricular failure as neonate
Collapse
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation

398
Q

Pulmonary stenosis physiology- moderate/mild

A

Well tolerated for many years
RV hypertrophy

399
Q

Pulmonary stenosis treatment

A

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

400
Q

Fontan circulation

A

Only one useable ventricle, SVC to pulmonary artery as baby, IVC to pulmonary circulation, lead to passive venous return system

401
Q

infective endocarditis (IE)

A

Infection of heart valve/s or other endocardial lined structures within the heart

402
Q

infective endocarditis- Structures that can be infected

A

Septal defects, pacemaker leads, surgical patches ect

403
Q

Treatment of infective endocarditis

A

Antibiotics/ antimicrobials- based on blood cultures, often don’t penetrate heart very well
May require cardiac surgery to remove the infectious material and/or repair the damage
Treatment of other complications (emboli, arrythmia, heart failure, etc)

404
Q

Types of infective endocarditis

A

-Left sided native IE (mitral or aortic)
-Left sided prosthetic IE
-Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
-Device related IE (pacemakers, defibrillators, with or without valve IE
-Prosthetic; Early (within year) or Late (after a year) post op

405
Q

Infective endocarditis- risk factors

A

Abnormal valve; regurgitant or prosthetic valves are most likely to get infected.
Infectious material in the blood stream or directly onto the heart during surgery
Have had IE previously

406
Q

Rheumatic heart disease

A

condition in which the heart valves have been permanently damaged by rheumatic fever- uncommon as rheumatic fever is more uncommon

407
Q

Rheumatic fever

A

Very rare complication that can develop after a bacterial throat infection. It can cause painful joints and heart problems. Most people make a full recovery, but it can come back

408
Q

The epidemiology of endocarditis

A

Historically- a disease of the young affected by rheumatic heart disease
Now- elderly
-iv drug users
-young with congenital HD
-anyone with prosthetic heart valves

409
Q

IE Incidence

A

Rare, more common in males, PVE in the 1st post op year is 1-4%, after 1st year is 1%/year

410
Q

Endocarditis presentation

A

New regurgitant heart murmur, embolic event s of unknown origin, sepsis of unknown origin, fever, many symptoms!!

411
Q

IE Clinical presentation

A

Depends on site, organism, etc
Signs of systemic infection (fever, sweats, etc)
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction
Valve dysfunction; heart failure, arrythmia

412
Q

IE Diagnosis: Modified Dukes Criteria

A

2 major criteria, 5 minor criteria
Definite IE- 2 major, 1 major+3 minor, 5 minor
Possible IE- 1 major, 1 major+1 minor, 3 minor

413
Q

IE Diagnosis: Modified Dukes Criteria- major

A

Pathogen grown from blood cultures
Evidence of endocarditis on echo, or new valve leak

414
Q

IE Diagnosis: Modified Dukes Criteria- minor

A

Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures

415
Q

Echocardiography- Transthoracic echo (TTE)

A

Safe, non-invasive, no discomfort, often poor images so lower sensitivity

416
Q

Echocardiography- Transoesophageal (TOE/TEE)

A

Excellent pictures but more invasive. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration.

417
Q

IE- Peripheral stigmata

A

Petechiae 10 to 15%
Splinter haemorrhages
Osler’s nodes
Janeway lesions
Roth spots on fundoscopy

418
Q

Petechiae

A

Macular petechial and embolic skin lesions

419
Q

Splinter haemorrhages

A

Splinter haemorrhages found below finger nails

420
Q

Osler nodes

A

Tender nodules in the digits of a patient with infective endocarditis

421
Q

Janeway Lesions

A

Haemorrhages and nodules in the fingers of the patient with infective endocarditis.

422
Q

Diagnosis of IE

A

Blood cultures (not always shown due to previous anti microbial therapy), raised CRP, ECG (ischemia or infarction, new appearance of heart block), TTE/TOE (detect vegetation)

423
Q

C reactive protein

A

Protein that your liver makes, raised when there is inflammation on the body

424
Q

IE treatment- When to operate

A

Antibiotics not working, complications to valve that needs replacing, need to remove infected devices

425
Q

IE prevention

A

consider prophylaxis in high risk patients during dental procedures (prosthetic valves, previous IE, cyanotic heart disease)
Talk to the patient and the dentist!

426
Q

ECG- Basic principles

A

Amplitude of deflection is related to mass of myocardium
* Width of deflection reflects speed of conduction
* Positive deflection is towards the lead/vector

427
Q

ECG- Abnormalities of P wave- Low amplitude

A

-Atrial fibrosis, obesity, hyperkalaemia

428
Q

ECG- Abnormalities of P wave- Alternative pacemaker foci

A

-Focal atrial tachycardias
-‘wandering pacemaker’

429
Q

ECG- Abnormalities of P wave- High amplitude ‘Tall’

A

-Right atrial enlargement

430
Q

ECG- Abnormalities of P wave- Broad notched ‘Bifid’

A

Left atrial enlargement

431
Q

ECG- abnormalities of PR interval

A

Prolonged in disorders of AV node and specialised conducting tissue

432
Q

ECG- QRS abnormalities- Broad QRS

A

-Ventricular conduction delay / BBB
Tall QRS complexes

433
Q

ECG- QRS abnormalities- Tall QRS complexes

A

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

433
Q

ECG- QRS abnormalities- Small QRS complexes

A

-Obese patient
-Pericardial effusion
-Infiltrative cardiac disease

434
Q

ECG- QRS normal

A

normally<120ms, Predominantly negative in V1, transitioning to postive by V6

435
Q

ECG- PR interval normal

A

120-200ms

436
Q

ECG- P wave normal

A

Normally <120 ms wide
Positive inferior leads
Positive in lead I
Negative in aVR
Biphasic in V1

437
Q

ECG- QT interval normal

A

Corrected for heart rate (380 – 450ms)

438
Q

ECG- QT interval abnormalities

A

Excessively rapid or slow repolarisation can be arrhythmogenic
“Long QT” or “Short QT” syndromes
Congenital, drugs, electrolyte disturbances

439
Q

ECG- ST segment abnormalities

A

Normally isoelectric, Can be elevated in early repolarisation, myocardial infarction, pericarditis/myocarditis

440
Q

ECG- T wave abnormalities

A

Direction of deflection usually similar to QRS (in limb leads), but in opposite direction in bundle branch block

441
Q

Common tachycardias

A

Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Focal atrial tachycardia
Ventricular tachycardia
Ventricular fibrillation

442
Q

ECG- irregularly, irregular QRS complexes

A

AF- ECG

443
Q

ECG- organised, saw shaped

A

Atrial flutter- ECG

444
Q

Atrial fibrillation vs atrial flutter

A

In atrial fibrillation, the atria beat irregularly.
In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles

445
Q

Atrial fibrillation vs atrial flutter- ECG appearance

A

In atrial flutter, there is a “sawtooth” pattern on an ECG
In atrial fibrillation, the ECG test shows an irregular ventricular rate

446
Q

Bradycardia causes

A

Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs

447
Q

AV conduction problems

A

1st degree AV block, second degree AV block (2 p wave :1 QRS), Third degree AV block

448
Q

1st degree AV block

A

Abnormally slow conduction through the AV node, ECG- PR interval> 0.2s, without disruption of atrial to ventricular conduction

449
Q

2nd degree heart block- Mobitz Type 1

A

PR interval gradually increases until AV node falls completely and no QRS wave is seen, then repeats

450
Q

2nd degree heart block- Mobitz Type 2

A

Sudden unpredictable loss of AV conduction and loss of QRS with constant PR interval

451
Q

3rd degree AV heart block

A

no electrical connection, V independent of A

452
Q

ECG appearance- LBBB

A

WiLLiaM- V1= complex resembles W- deep downward deflection (dominant S wave)
-V6= complex resembles M- broad, notched or ‘M’ shaped R wave

453
Q

Normal appearance of V1

A

QRS predominantly- -ive

454
Q

Normal appearance of V6

A

QRS predominantly- +ive

455
Q

Ischaemia ECG

A

T wave flattening inversion, ST segment depression

456
Q

Infarction ECG

A

ST segment elevation, T wave normal

457
Q

ECG- anterior wall affected

A

Leads- V2-4
Artery- LAD

458
Q

ECG- Anteroseptal wall affected

A

Leads- V1-4
Arterty- LAD

459
Q

ECG- anterolateral wall affected

A

Leads- I, aVL, V3-6
Artery- LAD, circumflex

460
Q

ECG- inferior wall affected

A

Leads- II, III, aVF
Artery- RCA

461
Q

ECG- lateral wall affected

A

Leads- I, aVL, V5-6
Artery- circumflex

462
Q

ECG- Hyperkalaemia

A

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

463
Q

ECG- Hypokalaemia

A

Flattening of T wave, QT prolongation

464
Q

ECG- Hypercalcaemia`

A

QT shortening

465
Q

ECG- hypocalcaemia

A

QT prolongation

466
Q

ECG- saddle ST segment, depression of PR segment

A

Pericarditis

467
Q

ECG- ST elevation in leads V2-V5 and aVL

A

Anterolateral MI

468
Q

Ectopic heart beats

A

Extra beat out of sinus rhythm arising from ectopic regions of atria or ventricles

469
Q

Complications of ectopic beats

A

High burden VE can cause heart failure
High burden AE can progress to AF

470
Q

Ectopic beats symptomatic relief treatment

A

from reassurance/ BB

471
Q

Ectopic beats- referral

A

-High burden ectopy (>5% of Heat beats, though risk prob not increased till >20% of Heart beats)
– Refractory to BB
– Structural heart disease
– Syncope

472
Q

Atrial Fibrillation

A

Commonest sustained arrhythmia
Irregularly irregular pulse
Paroxysmal (self terminating) OR Persistent
Rapid firing- loss of A mechanical contraction
-irregular, often rapid, V response

473
Q

AF treatment

A

Treat underlying cause
Rate control- BB (don’t use for asthmatics), CCB, digoxin
Acute sinus rhythm restoration- electrical/ pharmacological cardioversion
Maintain sinus rhythm- (Flecainide, Dronedarone, Sotalol, Amiodarone)
Permeant fix- pulmonary vein isolation, Catheter based AF therapy

474
Q

AF complications

A

High stroke risk (use CHA2DS2-VASc), mitigate risk with anticoagulation (warfarin/ DOAC using ORBIT score) and balance bleeding risk

475
Q

ECG- absent P waves, narrow QRS, tachycardia

A

Supraventricular tachycardia- SVT

476
Q

SVT management

A

Advice on Valsalva manoeuvres
Can try beta blocker/CCB
Permeant cure- Catheter ablation AVNRT- invasive

477
Q

ECG- no clear PR interval, slurred appearance (delta wave) of QRS

A

Accessory pathways- Congenital remnant muscle strands between atrium and ventricle

478
Q

Wolff Parkinson white syndrome

A

Episodes of abnormally fast HR.
Caused by an extra electrical connection in the heart.
Congenital, although symptoms may not develop until later in life, episodes can be fatal

479
Q

ECG-wolff parkinson white syndrome

A

short PR interval (<120 ms), prolonged QRS complex (>120 ms), and a QRS morphology consisting of a slurred delta wave

480
Q

ECG- wide QRS complex- beyond 120 milliseconds — originating in the ventricles, tachycardia

A

ventricular tachycardia

481
Q

Ventricular tachycardia causes

A

Diseased ventricles
-Myocardial infarction
-Cardiomyopathy

482
Q

Electrical storm

A

3 or more sustained episodes of VT or VF, or appropriate ICD shocks during a 24-hour period
High risk/ poor prognosis

483
Q

Electrical storm treatment

A

Correct underlying cause (electrolyte imbalance, ischaemia, infection, HF)
-BB, sedation
-amiodarone +/- lignocaine
-override pacing
-general anaesthesia/ Neuraxial blockade
– Catheter ablation

484
Q

ECG- Tachycardias- narrow complex

A

SVT, AF/flutter

485
Q

ECG- Tachycardias- broad complex

A

VT
SVT with BBB/preexcitation

486
Q

Who is a higher risk of “silent MI”

A

Diabetics are at greater risk of having MI without chest pain, likely as a result of cardiac autonomic dysfunction

487
Q

ECG- sinus tachycardia, RV strain (in V1,2,3), S1Q3T3

A

PE

488
Q

S1Q3T3

A

presence of S wave in lead I and Q wave and inverted T wave in lead III, PE (not always shown, but characteristic)

489
Q

Heart failure (HF)

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

490
Q

Causes of HF

A

-myocardial dysfunction
-Hypertension,
-alcohol excess,
-cardiomyopathy,
-valvular,
-endocardial,
-pericardial causes.

491
Q

Commonest cause of HF

A

Myocardial dysfunction, typically as a result of IHD

492
Q

Is HF usually curable?

A

No, typically it can only be treated, however if there is a modifiable cause (ie alcohol) it can be cured

493
Q

The main phenotypes of HF

A

HF with reduced ejection fraction (HFrEF)- LV weak
HF with preserved ejection fraction (HFpEF)- LV stiff

494
Q

Ejection fraction

A

% of blood that ejected from LV, women- 60-65%
men- 55-60%

495
Q

Other phenotypes of HF

A

HF due to severe valvular heart disease (HF-VHD)
HF with pulmonary hypertension (HF-PH)
HF due to right ventricular systolic dysfunction (HF-RVSD)

496
Q

HF- symptoms

A

Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight

497
Q

HF- clinical signs

A

Tachycardia
Displaced apex beat
Raised JVP (Juglar venous pluse)
Added heart sounds and murmurs, 3rd H sound
Hepatomegaly, especially if pulsatile and tender
Peripheral and sacral oedema
Ascites

498
Q

NYHA- class system

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)

499
Q

Causes of acute decompensation of chronic heart failure

A

AMI
Uncorrected HBP
Obesity
Superimp. infection
AF & arrhythmias
Excess alcohol
Endocrine
-ve inotropes (Ca/beta)
NSAIDS
Treatment and Na+ noncompliance.
Lack of information given to patient about diet, medications, etc.

500
Q

Treatment of HF

A

Diuretics, ACEI (not 1st line, not as effective in black people), aldosterone antagonists, BB (doesn’t have to be cardiac selective)

501
Q

AF- ECG

A

ECG- irregularly, irregular QRS complexes

502
Q

Atrial flutter- ECG

A

ECG- organised, saw shaped

503
Q

Abnormally slow conduction through the AV node, ECG- PR interval> 0.2s, without disruption of atrial to ventricular conduction

A

1st degree AV block

504
Q

PR interval gradually increases until AV node falls completely and no QRS wave is seen, then repeats

A

2nd degree heart block- Mobitz Type 1

505
Q

Sudden unpredictable loss of AV conduction and loss of QRS with constant PR interval

A

2nd degree heart block- Mobitz Type 2

506
Q

no electrical connection, V independent of A

A

3rd degree AV heart block

507
Q

WiLLiaM- V1= complex resembles W- deep downward deflection (dominant S wave)
-V6= complex resembles M- broad, notched or ‘M’ shaped R wave

A

ECG appearance- LBBB

508
Q

Leads- V2-4
Artery- LAD

A

ECG- anterior wall affected

509
Q

Leads- V1-4
Arterty- LAD

A

ECG- Anteroseptal wall affected

510
Q

Leads- I, aVL, V3-6
Artery- LAD, circumflex

A

ECG- anterolateral wall affected

511
Q

Leads- II, III, aVF
Artery- RCA

A

ECG- inferior wall affected

512
Q

Leads- I, aVL, V5-6
Artery- circumflex

A

ECG- lateral wall affected

513
Q

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

A

ECG- Hyperkalaemia

514
Q

Flattening of T wave, QT prolongation

A

ECG- Hypokalaemia

515
Q

QT shortening

A

ECG- Hypercalcaemia`

516
Q

QT prolongation

A

ECG- hypocalcaemia

517
Q

Pericarditis

A

ECG- saddle ST segment, depression of PR segment

518
Q

Anterolateral MI

A

ECG- ST elevation in leads V2-V5 and aVL

519
Q

CHA2DS2-VASc

A

AF Stroke risk score

520
Q

ORBIT

A

Bleeding Risk Score for Atrial Fibrillation predicts bleeding risk in patients on anticoagulation for afib

521
Q

Supraventricular tachycardia- SVT

A

ECG- absent P waves, narrow QRS, tachycardia

522
Q

short PR interval (<120 ms), prolonged QRS complex (>120 ms), and a QRS morphology consisting of a slurred delta wave

A

ECG-wolff parkinson white syndrome

523
Q

Most common causes of heart failure

A

coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension

524
Q

Cor pulmonale

A

alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system resulting in pulmonary hypertension- type of RHF

525
Q

Hypertension and heart failure

A

Prolonged hypertension promotes left ventricular hypertrophy which will eventually lead to heart failure

526
Q

Restrictive Cardiomyopathy

A

Muscles of ventricles stiffen and can’t fill with blood
may be asymptomatic or present with symptoms of cardiac failure
Rarest type of Cardiomyopathy

527
Q

Arrhythmogenic right ventricular cardiomyopathy/dysplasia

A

rare familial disorder that may cause ventricular tachycardia and sudden cardiac death in young, apparently healthy individuals
male predominance; first presentation often in adolescence

528
Q

ECG- RBBB

A

QRS duration > 120ms
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)

529
Q

Right bundle branch block (RBBB) cause

A

normal variant, pulmonary embolism, cor pulmonale

530
Q

Left bundle branch block (LBBB) cause

A

IHD, hypertension, cardiomyopathy, idiopathic fibrosis

530
Q

ECG RBBB- MaRRoW=RBBB

A

broad QRS
‘M’- M pattern on V1
‘W’- sloped s wave in V5 (w)

531
Q

ECG LBBB- WiLLiaM=LBBB

A

broad QRS
‘W’- W pattern in V1
‘M’- W pattern in V6

532
Q

Prolonged QT syndrome

A

Seen on ECG
Causes by a congenital or acquired (certain medications, health conditions- hypothermia/ calcemia/ magensemia/ kalemia/ thyrodism)

533
Q

Prolonged QT syndrome- compliactions

A

Torsades de pointes, VF, sudden death

534
Q

Torsades de pointes

A

twisting of the points- Ventricles beat chaotically, causing ECG to appear twisted, heart pumps out less blood
If episode does not correct its self- VF can occur

535
Q

Types of shock

A

Cardiogenic shock (due to heart problems)
Hypovolemic shock (caused by too little blood volume)
Anaphylactic shock (caused by allergic reaction)
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Obstructive shock (caused by something outside of the heart which prevents the heart from pumping enough blood)

536
Q

Shock

A

Life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly

537
Q

Atrioventricular nodal reentrant tachycardia (AVNRT)

A

Type of paroxysmal supraventricular tachycardia that results due to the presence of a re-entry circuit within or adjacent to the AV node

538
Q

ECG- Atrioventricular nodal reentrant tachycardia (AVNRT)

A

heart rate between 140 and 280 beats per minute (bpm), and in the absence of aberrant conduction, a QRS complex of fewer than 120 millisecond

539
Q

Murmurs of valvular disease- Systolic

A

Aortic stenosis, mitral regurgitation, mitral valve prolapse, tricuspid regurgitation

540
Q

Murmurs of valvular disease- Diastolic

A

Aortic regurgitation, mitral stenosis

541
Q

Murmurs of valvular disease- systolic ASMR

A

AS- Aortic stenosis
MR- Mitral regurgitation

542
Q

Murmurs of valvular disease- Diastolic ARMS

A

AR- Aortic regurgitation
MS- Mitral stenosis

543
Q

Rumbling mid-diastolic murmur with opening snap

A

Mitral stenosis

544
Q

Pansystolic murmur radiating to left axilla

A

Mitral regurgitation

545
Q

Ejection systolic murmur radiating to carotids and apex

A

Aortic Stenosis

546
Q

Early diastolic murmur

A

Aortic regurgitation

547
Q

Hypovolemic shock

A

Hypotension, tachycardia, weak thready pulse, cool, pale, moist skin- common after trauma
Decreased CO
Increased SVR

548
Q

Cardiogenic shock

A

Hypotension, tachycardia, weak thready pulse, cool, pale, moist skin
Decreased CO
Increased SVR

549
Q

Neurogenic shock

A

Hypotension, bradycardia, warm dry skin
Decreased CO, venous+ arterial vasodilation, loss sympathetic tone

550
Q

Anaphylactic shock

A

Hypotension, tachycardia, cough, dyspnoea, pruritis, urticaria, restlessness, decreased LOC
Decreased CO
Decreased SVR

551
Q

Septic shock

A

Hypotension, tachycardia, full bounding pulse, tachypnoea, decrease U/O, fever
Pink, warm, flushed skin
Decreased CO
Decreased SVR

552
Q

First line hypertensive for <55

A

ACEi (angiotensin-II receptor antagonist if ACEi intolerant)

553
Q

First line hypertensive for >55 or black

A

CCB or diuretic

554
Q

2nd line hypertensive treatment

A

ACEi + CCB or ACEi or diuretic

555
Q

3rd line hypertensive treatment

A

ACEi + CCB + diuretic

556
Q

Hypertensives in pregnancy

A

ACEi + ARD are NOT used as they can cause fetotoxicity

557
Q

ACEi contraindications

A

Absolute- Hypersensitivity reactions, pregnancy
Relative- Abnormal renal functions, aortic valve stenosis, hypovolemia

Phase 2a Lecture Notes (14 decks)

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