CVS Flashcards

1
Q

What is acute limb ischemia

A

blockage of peripheral artery

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2
Q

Pathophy of acute limb ischemia

A

blockage reduced perfusion causing ischemia

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3
Q

5 RF of acute limb ischemia

A
  • Smoking
  • Diabetes mellitus
  • Obesity
  • Hypertension
  • Hypercholesterolaemia
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4
Q

The 6p’s (acute limb ischemia signs and symptoms)

A

Pulseless

Paraesthesia

Pain

Paralysis

Pallor

Perishing cold

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5
Q

Investigations for acute limb ischemia

A

clinical diagnosis

You can roughly localise the blockage by locating thebifurcation distal to the last palpable pulse.

doppler to confirm absence of pulse

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6
Q

Mangement of acute limb ischemia

A

EMERGENCY

Thrombolytic agent

angioplasty

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7
Q

2 complications of acute limb ischemia

A

amputation

death

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8
Q

What is acute pericarditis

A

Inflammation of the pericardium

90% idiopathic or due to viral infections

Associated with systemic autoimmune disorders too

Acute vs chronic: 4-6 weeks vs >3 months

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9
Q

SS of acute pericarditis

A

Pleuritic central chest pain, worse on lying down, better sitting forward, intermittent fevers

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10
Q

Investigations for acute pericarditis

A

Examination: pericardial friction rub, tachycardia

ECG shows global upwardly concave ST-segment (J-point) elevations with PR segment depressions in most leads with J-point depression and PR elevation in leads aVR and V1

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11
Q

Mangement of acute pericarditis

A

Management: NSAIDs, can add colchicine.

  • Corticosteroids
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12
Q

What is acute rheumatic fever

A

Rare but common in developing countries (major cause of death and heart disease)

Improvement in developed countries due to penicillin and improved social conditions and reduction in virulence of the GpA BHS

Autoimmune disease following a group A streptococcal infection.

Can affect joints, heart, brain, skin

Effects on heart can lead to permanent illness: chronic changes to heart valves referred to as chronic rheumatic disease

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13
Q

SS of acute rheumatic fever

A

Symptoms appear 1-5 weeks after sore throat

  • Arthritis and toxicity with mild carditis (chest pain, SOB if severe), fever
  • Palpitations, heart murmur, signs of heart failure
  • Subcutaneous nodules/ erythema nodosum (swollen fat under skin causing red bumps and patches), chorea (jerky involuntary movements)
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14
Q

Investigation for acute rheumatic fever

A

Diagnosis based on Jones 2015 criteria

  • Throat swabs, ESR, CRP, FBC. ECHO
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15
Q

Management for acute rhematic fever

A

Management: eradicate streptococcal infection, suppress inflammation, provide supportive treatment especially if complications such as HF

  • Penicillin, aspirin, HF treatment if necessary cardiac surgery if treatment fails), diazepam if chorea present
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16
Q

what is angina

A

Pain/constricting discomfort in the chest

Radiating to the neck/shoulders/jaw/arms

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17
Q

Difference between stable and unstable angina presentation

A

Stable:
Occurs predictably
Lasting less than 15 mins, relieved by rest
with physical exertion or emotional stress
relieved within minutes of rest or GTN
unstable:
New onset or abrupt
often occurring at rest
lasts longer than 15 minutes

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18
Q

RF of angina

A
  • smoking
  • hyperlipidaemia
  • age
  • common in men but increases for women after menopause
  • hypertension
  • diabetes
  • obesity
  • exercise
  • ethnicity
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19
Q

Pathophysiology of angina

A

Caused by an insufficient blood supply to myocardium

Atherosclerotic plaque inadequate oxygen to myocardium at times when oxygen demand increases (exercise)

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20
Q

SS of angina

A

chest pain

pain radiating to jaw neck and left arm

SOB

Dizziness

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21
Q

Investigation for angina

A

clinical history

Physical examination

blood test- rule out anaemia

ECG

Q-RISK

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22
Q

Management for angina (first line)

A

First line- Beta blocker or CCB, if both contraindicated or not tolerated then monotherapy with one of the following: nitrate, ivabradine, nicorandil, ranolazine

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23
Q

Management for angina (2 line)

A

Second line: if on B-blocker then add CCB. if on CCB then add b-blocker

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24
Q

Other management for angina

A

Aspirin
GTN
lifestyle advice
Primary prevention -> statins
secondary prevention-aspirin/clopidogrel, acei, statin, anti HTN

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25
Q

Complications of angina

A

Stroke

MI

Unstable angina

sudden cardiac death

anxiety

depression

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26
Q

draw the diagram outlining MI/NSTEMI/UNDTABLE ANGINGA

A

chest pain……. Non -cardiac
:
:
ACS ……….. STEMI (ST elevation)
:
:
Unstable angina/NSTEMI (ecg shows no st elevation)
:
:
if normal troponin levels, then = unstable angina
if raised troponin levels then NSTEMI

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27
Q

What is the initial 2 medication offered to NSTEMI and unstable patients (early management)

A

Antiplatelet - 300mg aspirin
Anti-thrombin - fondaparinux

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28
Q

STEMI early management

A

offer 300 mg of aspirin
assess eligibility for reperfusion therapy:
if yes offer PCI or fibrinolysis
if no proceed with medical management, offer ticagrelor with aspirin

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29
Q

5 post MI medications

A

ACEi
Clopidogrel
B-blocker
statin
rivaroxaban

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30
Q

2 things to do post MI

A

cardiac rehab and secondary prevention

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31
Q

What is angina pectoris: prinzmetal’s /variant

A

Coronary artery spasm

Common in patients with underlying heart disease but can occur in healthy people as well

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32
Q

Pathophysiology of angina pectoris: prinzmetal’s/ variant

A
  • Not fully clear but is thought to be linked with low nitric oxide (secondary to reduced acetylcholine release), increased adrenergic activities, vasoconstrictor mediators (thromboxane, serotonin etc)
  • Acetylcholine normally results in the release of nitric oxide and also act directly as a vasodilator at rest
  • Thromboxane/serotonin are involved in platelet activation/recruitment. There is more of these mediators in prinzmetal
  • Increased adrenergic activities can cause an increase in heart rate and peripheral vasoconstriction
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33
Q

RF for angina pectoris: prinzmetal’s/ variant

A
  • Heart disease
  • Stress
  • Drugs such as cocaine, sympathomimetics such as epinephrine
  • Alcohol
  • Smoking
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34
Q

SS for angina pectoris: prinzmetal’s/ variant

A
  • Rest chest pain common at midnight/morning and lasting between 5-30 minutes
  • Headache
  • Patient may have a history of coronary heart disease
  • Deranged vital signs such as tachycardia, tachypnoea, high BP
  • There might not be any focal cardiac examination finding unless patient has underlying heart disease
  • Raynaud phenomenon if severe
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35
Q

Ix for ngina pectoris: prinzmetal’s/ variant

A

Bloods

  • Most important blood test is Troponin to rule out ACS.
  • FBC, renal function, electrolytes, fasting blood glucose and lipid levels

X-ray/Imaging

  • CXR to rule out alternative causes

ECG

  • STAT ECG might show transient STE. 24 hour ECG tape can be used if symptoms have resolved

Special Tests

  • Coronary angiography is the investigation of choice. Other options include stress echocardiography
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36
Q

Management for angina pectoris: prinzmetal’s/ variant

A
  • Lifestyle management
  • Manage co-existing disease
  • GTN/Calcium channel blockers are mainstay of medical treatment (avoid beta blockers as may aggravate symptoms)
  • Revascularization
  • coronary artery stenting
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37
Q

Complication for angina pectoris: prinzmetal’s/ variant

A
  • Arrhythmias
  • MI
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38
Q

What is aortic coarctation

A

congenital narrowing of the aorta

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39
Q

RF for aortic coarctation

A
  • Men > Women
  • Turner’s syndrome
  • Aortic valve is bicuspid in 80% of cases
  • Patent ductus arteriosus
  • Ventricular septal defect
  • Mitral stenosis/regurgitation
  • Circle of Willis aneurysms
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40
Q

SS of aortic coarctation

A

asymptomatic

headaches and nose bleed to due to HTN

Claudication and cold legs

HTN in upper limbs

Week delayed pulse in legs

radio femoral delay

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41
Q

Ix for aortic coarctation

A

CXR
ECG
LVH
aortagraphy
CT/MRI

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42
Q

Management for aortic coarctation

A

Surgery

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43
Q

What is aortic stenosis

A
  • Narrowing of the aortic valve
  • Progressive disease
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44
Q

Pathophysiology of aortic stenosis

A
  • Calcification of the valve is most common cause.
  • Congenital, history of rheumatic heart disease
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45
Q

SS of aortic stenosis

A
  • Can be asymptomatic for many years
  • Shortness of breath with exertion, angina, syncope
  • Systolic murmur, mid-to-late peaking with a crescendo-decrescendo pattern, radiates to carotids
  • Can cause left ventricular hypertrophy, heart failure. Can lead to sudden cardiac death. Damaged valve prone to endocarditis
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46
Q

Ix for aortic stenosis

A

ECHO

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47
Q

Management of aortic stenosis

A

avoid heavy exertion, surgical intervention

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48
Q

What is aortic regurgitation

A
  • Diastolic leakage of blood from the aorta into the left ventricle
    • Acute :caused by endocarditis or aortic dissection
    • Chronic: asymptomatic for years until symptoms of heart failure develop
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49
Q

Pathophysiology of aortic regurgitation

A

Caused by disease of the aortic valve (bicuspid aortic valve, rheumatic fever, infective endocarditis, collagen vascular disease, degenerative aortic valve disease) or aortic root

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50
Q

Acute SS of aortic regurg

A

Acute presents with sudden onset pulmonary oedema and hypotension/cardiogenic shock. May also present as myocardial ischaemia or aortic root dissection

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51
Q

chronic SS for aortic regurg

A

Chronic: initial symptoms can include palpitations and uncomfortable awareness of pounding heart when lying on left side

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52
Q

Management for aortic regurg

A
  • Acute severe AR – urgent surgical intervention
  • Chronic severe AR – goals of treatment to prevent death, diminish symptoms, to prevent development of hear failure and avoid aortic root complications
    • Valve replacement
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53
Q

What is aortic aneurysm

A

Aneurysm is a bulge in the aorta

it can be abdominal (common) or thoracic

dissection is a tear

Aortic dissection can either be Type A (Ascending aorta) or Type 2 (Descending aorta)

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54
Q

Pathophys of aortic aneurysm

A
  • Arteries are made up of three layers from proximal to distal namely tunica intima, tunica media and tunica adventitia
  • Aortic aneurysm occurs when there is an irreversible degradation of the elastic lamellae (outermost part of the tunica intima) and associated smooth muscle loss
  • Aortic dissection occurs when there is a damage to the tunica intima and blood pulls inside the tunica media
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55
Q

RF for aortic aneurysm

A
  • Advanced age
  • Hypertension
  • Marfan syndrome
  • Smoking
  • Trauma
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56
Q

SS for aortic aneurysm

A
  • Sudden ripping/tearing chest pain radiating to the back
  • Shortness of breath
  • Abdominal/back pain
  • Asymmetric pulse
  • Abdominal pain/distension
  • Unequal blood pressure in both arms
  • Abdominal bruit
  • Flank haemorrhage
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57
Q

Ix for aortic aneurysm

A

Bloods

  • FBC (Anaemia-although not immediately)
  • Cross match
  • LFT/RFT (to look for end organ ischaemic damage)

Orifice Test

  • PR test when indicated

X-ray/Imaging

  • CXR (can initially show widened mediastinum if thoracic aneurysm/dissection)
  • CT-aortogram (widely used) or MRI angiography for confirmation

ECG

  • Might show ischaemic changes like STE/STD depending where the dissection occurs

Special Tests

  • If aneurysm/dissection in the context of trauma, A FAST scan can be done
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58
Q

Management for aortic aneurysm

A
  • Lifestyle/risk factor management (stop smoking etc)
  • Statin/Aspirin when indicated
  • Further Medical management depends on the size of the aneurysm (Refer to secondary care)
  • If between 3-4.4cm (Annual ultrasound), If 4.5-5.4 (3 monthly ultrasound), if >5.5cm (Immediate referral for surgery and 3 monthly ultrasound)
  • There is a one off screening program for over 65s in england which can rule out aneurysm for life if negative
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59
Q

Complication for aortic aneurysm

A
  • Cardiac tamponade
  • Cardiogenic shock
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60
Q

What are arrythmias

A

Arrhythmias are abnormalities of the heart rate or rhythm caused by disorders of impulse generation or conduction.

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61
Q

What is atrial fibrillation

A

A supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction.

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62
Q

What is ECG finding of AFib

A
  • Irregularly irregular R-R intervals(when atrioventricular conduction is not impaired)
  • Absence of distinct repeating P waves
  • Irregular atrial activations.
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63
Q

3 different classifications of Afib

A

Paroxysmal AF – episodes lasting longer than 30 seconds but less than 7 days (often less than 48 hours), that are self-terminating and recurrent

Persistent AF – episodes lasting longer than 7 days (spontaneous termination of the arrhythmia is unlikely to occur after this time) or less than seven days but requiring pharmacological or electrical cardioversion

Permanent AF – AF that fails to terminate using cardioversion, AF that is terminated but relapses within 24 hours, or longstanding AF (usually longer than 1 year) in which cardioversion has not been indicated or attempted

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64
Q

What is atrial flutter and its ECG characteristics

A

Flutter wave (instead of P waves) organize atrial depolarisations of a rate around 300bpm producing a saw-tooth pattern in typical counterclockwise flutter.

Narrow QRS complex

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65
Q

ECG finding for ventricular tachyarrhythmia

A

Irregular R-R interval

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66
Q

Risk factors for arrythmia

A

Middle aged - older adults

Europe and North America

Comorbidities

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67
Q

RF for Afib

A

age

comorbidities - HTN, diabetes, HF, CHD ,CKD

Obesity

Obstructive sleep apnoea

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68
Q

Pathophysiology of arrythmia

A

ischemic

degeneration

mitral stenosis

metabolic

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69
Q

Pathophysiology of Afib

A

Left atrial arrhythmia

often in the form of rapidly firing ectopic foci located inside one or more pulmonary veins, and an abnormal atrial tissue substrate capable of maintaining the arrhythmia.

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70
Q

SS of arrythmias

A

Breathlessness

Palpitations

Syncope/dizziness

Chest discomfort

Reduced exercise tolerance

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71
Q

Ix for arrythmias

A

Patient Hx

ECG recording

Ambulatory ECG monitoring

External loop recorders

Implantable Loop Recorders (ILR)

Signal average ECG

Structural heart imaging – Chest x-ray/Echo/MRI

Electrophysiology study

‘Personal smart-tech’

Blood count, electrolyte levels, drug levels, thyroid study

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72
Q

Afib investigation

A

The diagnosis of AF requires rhythm documentation with an electrocardiogram (ECG) tracing showing AF. By convention, an episode lasting at least 30 seconds is diagnostic for clinical AF.

if pulse is irregular then 12 lead ECG , Ambulatory ECG monitoring

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73
Q

Management for afib and atrial flutter

A

Urgent referral
-If the onset of atrial fibrillation (AF) was within the last 48 hours urgently and haemodynamic instability/loss of consciousness/severe dizziness or syncope/ongoing chest pain/increasing breathlessness.

Comorbidities and lifestyle
-assess for signs and symptoms and do test to confirm or rule out underlying causes of AF

Rate control
-beta blocker
-rate limiting calcium channel blocker
-digoxin

Stroke risk
Asses CHA2DS2VASC and HAS-BLED score
anticoagulant option-
DOACS
Rhythm control
-Pharmacological - anti arrhythmic drugs
- Intervention- PVI ablatio, pharmacological cardioversion and DCCV

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74
Q

Ventricular tachyarrhythmia management

A

Emergency – 999

Urgent – transfer ASAP to A&E monitored by a defibrillator and all monitoring/IV line if possible.

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75
Q

Complications for arrythmias

A

stroke
TIA
HF

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76
Q

What is arterial embolism/thrombosis

A

occlusion of arteries

  • Most commonly affected arteries include those in the heart, brain, kidneys & lower limbs.
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77
Q

Pathophysiology of arterial embolism/thrombosis

A
  • A thrombus is a local formation of clot while an emboli is a clot that has broken off to lodge in another area of the body
  • Embolism/thrombosis occurs due to risk factors like lipidemia, cigarettes etc. These risk factors damage the vascular endothelium and consequently lead to arterial occlusion manifesting as ischaemia.
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78
Q

RF for arterial embolism/thrombosis

A
  • Smoking
  • Lipidemia
  • Sedentary lifestyle
  • Recent surgery
  • Hypertension
  • Obesity
  • Atrial fibrillation
  • Hypercoagulability states e.g thrombocytosis
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79
Q

SS for arterial embolism/thrombosis

A
  • Pain
  • Numbness/Tingling
  • Muscle spasm/weakness
  • Change in colour
  • Skin coldness
  • Checking CRT, pulse, sensation. All of which would be absent or delayed in peripheral vascular disease
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80
Q

Ix for arterial embolism/thrombosis

A

Bloods

  • Lipids. ESR. HBA1c. Renal/Liver function tests. Creatine kinase, Troponin, FBC

X-ray/Imaging

  • CT/MRI angiography. Arterial doppler. Echocardiogram

ECG

  • Can show ischaemic picture if heart involved

Special Tests

  • Ankle brachial pressure index
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81
Q

Management for arterial embolism/thrombosis

A
  • Urgent admission and anticoagulation should be started immediately.
  • Surgical embolectomy or intra-arterial thrombolysis if occlusion is from embolus
  • Angioplasty or bypass surgery or thrombolysis
  • Managing risk factors/comorbidities e.g smoking, lipidemia
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82
Q

Complication for arterial embolism/thrombosis

A
  • Necrosis/Gangrene
  • Chronic pain syndrome
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83
Q

What is atrial septal defect

A

Communication between the left and right side of the heart

hole in the septum that divides the atrial wall chambers

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84
Q

SS for atrial septal defect

A

Asymptomatic in infants and children

Subtle SOBOE/palpitations in second decade of life

Adults with large defect → fatigue, exercise intolerance, palpitations, syncope, SOB, peripheral oedema, thromboembolic manifestations, and cyanosis

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85
Q

Ix for atrial septal defect

A

Widely split second heart sound. Soft systolic ejection murmur

ECHO

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86
Q

Management for atrial septal defect

A

Diuretics for those that develop heart failure. Surgical closure

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87
Q

What is AV block and what are 4 subtypes called

A

Atrioventricular (AV) block (often referred to as “heart block”) involves the partial or completeinterruption of impulse transmission from theatria to theventricles

sub-types of AV blockincluding:

  • First-degree AV block
  • Second-degree AV block (type 1)
  • Second-degree AV block (type 2)
  • Third-degree (complete) AV block
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88
Q

ECG finding for first degree heart block

A
  • Rhythm: regular
  • P wave: every P wave is present and followed by a QRS complex
  • PR interval: prolonged >0.2 seconds (5 small squares)
  • QRS complex: normal morphology and duration (<0.12 seconds)
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89
Q

ECG finding for second degree type 1 heart block

A

Second-degree AV block (type 1) is also known asMobitz type 1 AV block orWenckebach phenomenon

ECG:

  • Rhythm: irregular
  • P wave: every P wave is present, but not all are followed by a QRS complex
  • PR interval: progressively lengthens before a QRS complex is dropped
  • QRS complex: normal morphology and duration (<0.12 seconds), but are occasionally dropped
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90
Q

ECG finding for second degree type 2 heart block

A

Second-degree AV block (type 2) is also known asMobitz type 2 AV block

ECG:

  • Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)
  • P wave: present but there are more P waves than QRS complexes
  • PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes
  • QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)
  • The QRS complex will be broad if the conduction failure is located distal to the bundle of His
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91
Q

ECG finding on a third-degree heart block

A

there isno electrical communication between the atria and ventricles due to acomplete failure of conduction

ECG:

  • Rhythm: variable
  • P wave: present but not associated with QRS complexes
  • PR interval: absent (as there is atrioventricular dissociation)
  • QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm (see introduction)
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92
Q

RF for 1 degree HB

A

often in athletes

post MI

Lyme disease

Congenital

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93
Q

RF for 2 degree t1 HB

A
  • Increased vagal tone: often seen in athletes (non-pathological)
  • Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
  • Inferior myocardial infarction
  • Myocarditis
  • Cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
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94
Q

RF doe 2 degree T2 HB

A
  • Myocardial infarction
  • Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease)
  • Cardiac surgery (especially surgery occurring close to the septum such as mitral valve repair)
  • Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)
  • Autoimmune (SLE, systemic sclerosis)
  • Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
  • Hyperkalaemia
  • Drugs (e.g. beta-blockers, calcium channel blockers, digoxin, amiodarone)
  • Thyroid dysfunction
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95
Q

RF 3 degree HB

A
  • Congenital: structural heart disease (e.g transposition of the great vessels), autoimmune (e.g maternal SLE)
  • Idiopathic fibrosis: Lev’s disease (fibrosis of the distal His-Purkinje system in the elderly) and Lenegre’s disease (fibrosis of the proximal His-Purkinje system in younger individuals)
  • Ischaemic heart disease: myocardial infarction, ischaemic cardiomyopathy
  • Non-ischaemic heart disease: calcific aortic stenosis, idiopathic dilated cardiomyopathy, infiltrative disease (e.g. sarcoidosis, amyloidosis)
  • Iatrogenic: post-ablative therapies and pacemaker implantation, post-cardiac surgery
  • Drug-related: digoxin, beta-blockers, calcium channel blockers, amiodarone
  • Infections: endocarditis, Lyme disease, Chagas disease
  • Autoimmune conditions: SLE, rheumatoid arthritis
  • Thyroid dysfunction
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96
Q

SS for 1 degree H block

A

asymptomatic

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97
Q

SS for 2 degree t1 H block

A

often asympto but can develop bradycardia and syncope, irregular pulse

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98
Q

SS for 2 degree t2 H block

A

Palpitations, Pre-syncope, Syncope, regular irregular pulse

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99
Q

SS for 3 degree H block

A
  • Palpitations
  • Pre-syncope/syncope
  • Confusion
  • Shortness of breath (due to heart failure)
  • Chest pain
  • Sudden cardiac death
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100
Q

Ix for AV block

A

ECG

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101
Q

Management for AV block

A

Stop any AV blocking drugs

if symptomatic then pacemaker

from second t2 onwards place on cardiac monitor as a result of risk of complete AV block

third degree: cardiac monitor, transcutaneous pacing/temporary pacing wire
orisoprenaline infusion, pacemaker

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102
Q

Complication for the different AV block subtype

A

First deg→ afib

Second deg T1 → haemodynamically compromised

second T2- complete AV block

third→ sudden cardiac death

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103
Q

What is bbb

A

A bundle branch block is a condition in which there is a delay or blockage along the pathway that electrical impulses travel to make a heartbeat.

The delay or blockage can occur on the pathway that sends electrical impulses either to the left or the right side of the bottom chambers (ventricles) of your heart.

Bifascicular → involves both right bundle branch block as well as blockade of one of the fascicles of the left bundle branch.

Trifasicular → is present when 3rd degree heart block exists along bifasicular block

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104
Q

Pathophysiology of BBB

A

A bundle branch block is a condition in which there is a delay or blockage along the pathway that electrical impulses travel to make a heartbeat.

The delay or blockage can occur on the pathway that sends electrical impulses either to the left or the right side of the bottom chambers (ventricles) of your heart.

Bifascicular → involves both right bundle branch block as well as blockade of one of the fascicles of the left bundle branch.

Trifasicular → is present when 3rd degree heart block exists along bifasicular block

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105
Q

RF FOR lbbb

A

Dilated Cardiomyopathy (the main cause of LBBB) Left ventricular hypertrophic cardiomyopathy (LBBB) HTN
MI myocarditis

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106
Q

RF for RBBB

A

RBBB Thin tall young people
MI myocarditis

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107
Q

SS for BBB

A

asymptomatic

underlying cause symptoms like MI with chest pain or SOB

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108
Q

ECG criteria for RBBB

A
  • MarRoW
  • QRS > 120 ms (3 small squares)
  • RSR’ pattern in V1-V3
  • Wide, slurred S wave in lateral leads – I, aVL, V5-V6
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109
Q

ECG criteria for LBBB

A
  • WiLliaM
  • QRS duration > 120ms (3 small squares)
  • Dominant S wave in V1
  • Broad, monophasic R wave in lateral leads – I, aVL, V5-V6
  • Absence of Q waves in lateral leads
  • Prolonged R wave > 60ms in leads V5-V6
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110
Q

Management for BBB

A

Patient based

treat any underlying cause

if hx of syncope due to it then pacemaker

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111
Q

Complication for BBB

A
  • Complete heart block
  • Ventricular tachycardia
  • Ventricular fibrillation
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112
Q

What is cardiac tamponade

A

Accumulation of blood, fluid, pus, clots, or gas in pericardial space

Results in reduced ventricular filling and reducing cardiac output and subsequent haemodynamic compromise

Often: pericardial effusion cardiac tamponade

  • Iatrogenic (cardiac surgery/intervention), trauma, malignancy, idiopathic effusion, viral, radiation, uraemia
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113
Q

SS of cardiac tamponade

A

Dyspnoea, tachycardia and tachypnoea cold and clammy extremities

Distended neck veins, hypotension tachycardia, tachypnoea and hepatomegaly

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114
Q

Mangement for cardiac tamponade

A

Medical emergency!

emergency. Managed in ITU. Pericardiocentesis is definitive treatment

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115
Q

What is cardiomyopathy

A

Myocardial disorder

Heart muscle is structurally and functionally abnormal

Without CAD, HTN, Valvular or congenital heart diseases.

Degree of dysfunction ranges from lifelong symptomless forms to major health problems, such as progressive heart failure, arrhythmia, thromboembolism and sudden cardiac death.

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116
Q

What are the 4 major types of cardiomyopathies

A
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC)
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117
Q

Primary vs secondary cardiomyopathy

A

Primary: Idiopathic. No specific cause.

Secondary: chronic kidney disease, cirrhosis, obesity, sarcoidosis, amyloidosis, SLE, diabetes, thyroid disease, thiamine deficiency, etc

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118
Q

Management for cardiomyopathy

A
  • Symptomatic management
  • Mainly directed towards treatment of heart failure and prevention of VTE and sudden death
  • Implantable cardioverter defibrillators in high risk patients to prevent sudden death
  • Surgical myectomy/ alcohol septal ablation
  • Heart transplant
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119
Q

What is coronary artery disease

A
  • Narrowing of the coronary arteries which leads to heart problem
    • Narrowing can occur as a result of blood clot or atherosclerosis
    • complete blockage leads to heart muscles dying leading to MI
  • Coronary flow occurs during diastole
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120
Q

RF for CHD

A
  • smoking
  • unhealthy diet (hyperlipidaemia)
  • age
  • common in men but increases for women after menopause
  • hypertension
  • diabetes
  • obesity
  • exercise
  • ethnicity
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121
Q

Pathophysiology of CHD

A

atherosclerosis

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122
Q

SS for CHD

A

angina

cold sweats

dizziness

neck pain

shortness of breath

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123
Q

Ix for CHD

A

ECG

Echocardiogram

stress test

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124
Q

Management for CHD

A

Immediate management - ABCDE
atorvastatin
Warfarin
beta blocker
ACEi
ARB

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125
Q

What does MONARCH stand for in CHD Management

A

Morphine

Oxygen

Nitrates

Aspirin 300mg

Reperfusion PCI

Clopidogrel/Ticagrelor

Heparin or LMWH

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126
Q

Complication for CHD

A

angina

MI

HF

Stroke

anxiety

reduced qualy

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127
Q

Pathophysiology of DVT

A

A clot develops at a site of damage to a vessel wall (e.g. an atherosclerotic plaque, or perhaps a site of trauma). This can impair venous drainage of the leg.

128
Q

RF for DVT

A
  • Stasis/immobility – e.g. hospital bed, long flight
  • Dehydration
  • Oestrogen (pregnancy, and to a lesser extent, theCOCpill)
  • Genetic clotting defect (e.g. lack of protein C)
  • Obesity (atherosclerosis)
  • Age (old)
  • Varicose veins
  • Surgery
  • Previous DVT/embolism
  • Trauma
  • Infection
  • Malignancy

Virchow’s triadof risk factors:

  • Stasis
  • Hypercoagulability
  • Vessel wall injury
129
Q

SS for DVT

A
  • Red, swollen leg (particularly calf)
  • Tenderness
  • Pitting oedema
  • Fever
130
Q

IX for DVT

A

WELLS score
- Venography
- D-dimer - negative test rules out dvt
- Leg measurement

131
Q

WELLS score

A
  • Score >3 –Treat as DVT –and also perform a compression USS to confirm
  • Score 1-2 –Treat as DVT– and perform compression USS to confirm
  • Score 0 –do a D-dimer test. If negative, then unlikely to be DVT. If positive,Treat as DVT,and perform compression USS.
132
Q

Management for DVT

A

LMWH

Warfarin

Thrombolysis

133
Q

Complication for DVT

A

PE
ODEMA

134
Q

What is endocarditis

A

inflammation of the inner layer of the heart known as the endocardium

135
Q

Difference between acute and subacute endocarditis

A

ACUTE
- Present as a rapidly progressive disease with high fevers, rigors, and sepsis
- Usually, staphylococcus aureus
- Mostly happens in healthy hearts

SUBACUTE
- Delayed and presents as non-specific symptoms such as weight loss, fatigue, low-grade fever dyspnoea over several weeks to months
- Usually, streptococcus viridans
- Mostly occurs in pre-existing heart disease

136
Q

RF for endocarditis

A
  • bacteria in other parts
  • gum disease
  • STI
  • Damaged heart valves
137
Q

SS for endocarditis

A

Murmurs

join aches

fever

SOB

Osler nodes

138
Q

Ix for endocarditis

A

blood test

CT

MRI

X-ray

ECG

139
Q

Management for endocarditis

A

ADMIT

Antibiotics

140
Q

Complication for endocarditis

A

septic emboli

stroke

seizures

141
Q

What are giant cell arteries

A

a type of chronic vasculitis characterized by granulomatous inflammation in the walls of medium and large arteries

142
Q

RF for giant cell arteries

A
  • It usually affects people over 50 years of age.
  • European background
  • Females
143
Q

SS for giant cell arteries

A

Fever

Fatigue

anorexia

Weight loss

Depression

scalp tenderness

jaw claudication

visual disturbance

144
Q

Investigation for Giant cell arteries

A

refer

temporal artery biopsy

ESR

CRP

FBC

LFT

145
Q

What is HF

A

ability of the heart to maintain the circulation of blood is impaired as a result of structural or functional impairment of ventricular filling or ejection.

146
Q

What is ejection fraction

A
  • Heart failure with preserved ejection fraction (HF-PEF)
  • heart failure with reduced ejection fraction
  • LVEF less than or equal to 35-40%
147
Q

symptomatic severity class types of heart failure

A

Class I — no limitation of physical activity. Ordinary physical activity does not cause undue fatigue, breathlessness, or palpitations.

Class II — slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue, or palpitations.

Class III — marked limitation of physical activity. Comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue, or palpitations.

Class IV — unable to carry out any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased

148
Q

Pathophysiology of heart failure

A

factors that can increase myocardial work may aggravate existing HF or initiate

cardiac damage → decreases CO → neuroendocrine activation → increased peripheral resistance

Fluid retention can also decrease CO

149
Q

RF for HF

A

CHD
AGE
Diabetes.
High blood pressure.
Obesity.
Other Conditions Related to Heart Disease.
Valvular Heart Disease.

150
Q

Right sided HF symptoms

A

Fatigue
increased peripheral venous pressure
ascites
enlarge liver and spleen
distended jugular vein
anorexia or GI distress
weight gain
oedema

151
Q

Left sided heart failure symptoms

A

Restlessness
confusion
orthopnoea
tachycardia
exertional dyspnoea
fatigue
cyanosis
PND
Pulmonary congestion

152
Q

Ix for HF (what is sued to suspect HF)

A

BNP

153
Q

What is the gold standard to confirm HF

A

ECHO

154
Q

NICE guideline for Ix for HF pathway

A

measure NT-proBNP (can also perform ecg, CXR blood test urinalysis peak flow or spirometry at this point)
if bnp levels more than 2000 ng/l then refer urgently to be seen within 2 weeks
if bnp between 400-2000 then refer urgently to be seen within 6 weeks
if bnp below 400 then hf not confirmed and consider other causes

155
Q

Management for HF

A

offer diuretics for fluid retention like furosemide
if HF with pr EF then manage comorbidities and cardiac rehab
if HF with red EF then offer aceI, BB and an MRA like spironolactone

156
Q

Complication for HF

A
  • depression
  • cardiac arrhythmias
  • chronic kidney disease
  • sexual dysfunction
  • sudden cardiac death
157
Q

RF for HTN

A
  • Age -increased risk with age
  • sex-More common in male than female
  • ethnicity
  • genetic factor
  • social deprivation
  • lifestyle
  • stress and anxiety
  • Other things that can raise BPCocaine and other substance of abusecombine oral contraceptivecorticosteroidsNSAIDLiquoricesymptathomemtic
158
Q

stage HTN reading

A

14/90 to 159/99

159
Q

Stage 2 HTN reading

A

160/100 or higher but lower than 180/120

160
Q

Stage 3 or severe HTN reading

A

higher than 180/120

161
Q

diagnosis for HTN

A

see notes

162
Q

nice guideline for HTN for treatment (diagram)

A

see notes

163
Q

example of conditions that cause secondary HTN

A
  • Renal artery stenosis
  • Pheochromocytoma
  • Aortic coarctation
  • Cushing disease
  • Conn’s syndrome
  • Hyperparathyroidism
164
Q

complications for HTN

A

increase risk of:
heart disease
stroke
chronic kidney disease
peripheral artery disease

165
Q

What is isolated systolic HTN and what is caused by and what can increase the risk of

A

sys rises but diastolic remains in the normal range

diastolic less than 80 but systolic is 130 or higher

common in people older than 65

166
Q

what is isolated systolic
HTN caused by

A

Caused by :

  • Artery stiffness
  • An overactive thyroid (hyperthyroidism)
  • Diabetes
  • Heart valve disease
  • Obesity
167
Q

Whts does isolated systolic HTN increase your risk of

A

increase your risk of strokes, heart disease or ckf

168
Q

iatrogenic causes of HTN examples

A

HTN caused by a medication

sympathomimetics (amphetamine)

NSAIDS and COX inhibitor (ibuprofen)

Corticosteroids (prednisone)

CNS stimulants (caffeine)

Oestrogen and Progesterone (contraceptives and ERT)

Immunosuppressants (cyclosporine)

169
Q

what is hypercholesterolaemia

A
  • Hypercholesterolemia, an elevation of total cholesterol (TC) and/or low-density lipoprotein (LDL)-cholesterol or non-HDL-cholesterol in the blood(dyslipidaemia).
  • increase in both cholesterol and triglycerides
  • primary e.g. genetic
  • secondary e.g. underactive thyroid
170
Q

RF for hypercholesterolaemia

A
  • Family history
  • Diet- food high in saturated fats
  • lack of physical activity
  • obesity
171
Q

Pathophysiology of hypercholesterolaemia

A
  • Plaques of atheroma within inside lining of arteries
  • Many constituents: white blood cells, lipids (cholesterol and fatty acids), calcium, fibrous connective tissue
  • Over time gets larger and thicker → arterial narrowing → poor blood flow
  • Sometimes atheroma develops a tiny crack (rupture) → blood clot
172
Q

SS hypercholesterolaemia

A
  • Hypercholesterolemia does not cause any symptoms but may eventually lead to heart attack, peripheral artery disease, or stroke due to atherosclerosis.
  • Familial hypercholesterolemia is associated with:
    • Xanthelasma palpebrarum (yellowish patches underneath the skin around the eyelids)
    • Arcus senilis (white or gray discoloration of the peripheral cornea)
    • Xanthomata (deposition of yellowish cholesterol-rich material) of the tendons
173
Q

Ix hypercholesterolaemia

A

Health check programme
- Incidental finding on bloods
- Symptoms (angina/claudication)
- Risk factors
- Comorbidities
- QRISK

174
Q

Management hypercholesterolaemia

A

Statins
lipid lowering therapies e.g ezetimibe

175
Q

complications for hypercholesterolaemia

A
  • atherosclerosis
  • heart attack
  • stroke
  • any cvd
176
Q

When to suspect FH hypercholesterolaemia

A

total cholesterol level greater than 7.4mmol/l and or

family history of premature CHD

177
Q

Pathophysiology of hypertensive HF

A
  • Cardiac failure is a clinical syndrome where due to ventricular dysfunction, the heart has an impaired ability to cope with the metabolic requirements of the body and can lead to fluid retention, fatigue and breathlessness. This is due to the heart being unable to provide the tissue with adequate perfusion, leading to elevated pulmonary or systemic venous pressure which could lead to organ congestion.
  • Abnormalities can be with systolic or diastolic function, or both.
  • In systolic failure there is left ventricle dysfunction, leading to an increased diastolic volume and pressure and decreased ejection fraction (<40%).
  • In diastolic failure, there is a filling defect of the left ventricle, leading to an increased end-diastolic pressure and normal volume and a normal ejection fraction (>50%).
  • In right ventricular failure systemic venous pressure increases which can lead to fluid extravasation and congestion in the peripheries leading to oedema in the ankles and feet, and congestion in the abdominal viscera leading to hepatic dysfunction, and malabsorption.
178
Q

RF for Hypertensive heart failure

A
  • Hypertension
  • Advanced age
  • Female gender
  • Obesity
  • Diabetes
  • Chronic kidney disease
  • Coronary artery disease
179
Q

SS for hypertensive heart failure

A
  • Fatigue
  • Shortness of breath at rest
  • Peripheral oedema (feet and ankles)
  • Persistent cough or wheeze
  • Reduced exercise tolerance
  • Peripheral oedema in feet and ankles – deep visible palpable imprint on digital pressure.
  • Enlarged liver - on palpation can be detected below right costal margin, may be able to illicit hepatojugular reflux.
  • Abdominal distention, can have ascites
  • Visibly raised JVP – large alpha or V waves may be seen, even at rest.
  • Pulmonary crackles on auscultation
  • S3 may be heard on auscultation
180
Q

Ix for hypertensive heart failure

A
  • Chest X-ray – enlarged cardiac silhouette, pleural effusion, fluid in major fissures, kerley B lines, upper lobe pulmonary venous congestion. ECG – may show previous MI, LVH, LBBB or any arrhythmia, such as AF, may indicate towards of cardiac failure Echocardiogram - to evaluate any structural abnormalities.
  • Systolic heart failure: dilated left/right ventricle and low EF, left ventricular hypertrophy, abnormal diastolic filling patterns
  • Diastolic: left ventricular diastolic dysfunction, left ventricle filling defect, normal EF. Cardiac MRI – can be used to further determine aetiology such as amyloidosis, sarcoidosis and myocarditis
181
Q

Management for Hypertensive heart failure

A

Conservative

  • Dietary and lifestyle changing advice. Dietary sodium intake reduction, daily weights, regular exercise.

Medical

  • BP control (see management algorithm in hypertension)
  • ACE inhibitors, beta blockers, ARBs can be used for long term management.
  • Diuretics, nitrates and digoxin for any symptomatic relief.
  • Implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy (CRT) devices can be considered in some patients. ICDs should be considered in patients with good expected clinical outcomes with symptomatic SVT or VF. CRTs can be considered in patients with an EF <35%, on ECG widened QRS (>0.15s) and LBBB. A CRT can also have an ICD incorporated.
  • In some patients (severe cardiorenal syndrome) venovenous filtration can be considered in an intensive care setting.

Surgical

  • CABG can be considered in patients who have multivessel coronary artery disease
  • Valvular replacement can be considered in patients, especially those with primary mitral regurgitation.
182
Q

Complications for hypertensive heart failure

A
  • Chronic renal insufficiency
  • Pleural effusion
  • Anaemia
  • Acute decompensation of chronic heart failure
  • Acute renal insufficiency
  • Sudden cardiac death
183
Q

What is innocent heart murmur

A

Young children have small, slim chests so heart is near to stethoscope

Blood travelling through heart and blood vessel can make a murmur like noise

184
Q

RF for innocent heart murmur

A

Common in babies and young children

Heart is usually working fine

185
Q

Ix for innocent heart murmur

A

Sometimes fevers can bring on heart murmurs in children. Get them back in in 1-2 weeks time for review

186
Q

Management for innocent heart murmur

A

Obviously if symptomatic or other symptoms discuss with paediatrician / cardiology

187
Q

What is mitral stenosis

A

Narrowing of the mitral valve

188
Q

Pathophysiology of mitral stenosis

A

rheumatic fever. Degenerative calcification, congenital mitral
stenosis, infective endocarditis, etc.

189
Q

SS of mitral stenosis

A

Progressive breathlessness is main symptom. Shortness of breath on
exertion, orthopnoea, paroxysmal nocturnal dyspnoea

Palpitations due to AF

Malar flush, raised JVP, laterally places apex beat, right ventricular heave, loud first heart-sound with an opening snap in early diastole

Mid-late diastolic murmur, best heard with the patient in the left lateral position, with the bell of the stethoscope

190
Q

Ix for mitral stenosis

A

CXR: left atrial enlargement and interstitial oedema. Mitral valve calcification

ECG- AF, left atrial enlargement and right ventricular hypertrophy

ECHO

191
Q

Management for mitral stenosis

A

Diuretics

long acting nitrates

beta blocker

percutaneous mitral commissurotomy

Valve replacement

192
Q

What is mitral valve prolapse

A

Bulging of one or both of the mitral valve leaflets into the left atrium

During ventricular systole

193
Q

Pathophysiology of mitral valve prolapse

A

Genetic?

Myxomatous Degenenration

194
Q

Ix for mitral valve prolapse

A

Usually incidental finding on clinical examination or ECHO

195
Q

Management for mitral valve prolapse

A

Low risk vs high risk

No treatment/ beta-blockers/surgical repair or replacement

196
Q

What is mitral regurgitation

A

Mitral valve not closing properly, causing abnormal leaking from left ventricle through the mitral valve and back into the left atrium with the left ventricle contracts

197
Q

Pathophysiology of mitral regurgitation

A

Causes: traumatic, mechanical, infectious, degenerative, congenital or metabolic

Acute caused by: infective endocarditis, ischaemic papillary muscle dysfunction or rupture

198
Q

investigation for Mitral regurgitation

A

cxr, ECG,ECHO

199
Q

what is patent ductus arteriosus

A

Should be closed after birth but remains open

  • No umbilical cord: Increased oxygen levels and decreased prostaglandin from placenta help close PDA
  • So poor oxygenation (born prematurely) or increased prostaglandins in foetal circulation or increased sensitivity to prostaglandins keep it open
  • Rubella infection also keeps it open
200
Q

SS for patent ductus arteriosus

A

Small PDA – asymptomatic

Large PDA – LRTI, feeding difficulties, poor growth, failure to thrive

Tachycardia, tachypnoea, wide pulse pressure, bounding peripheral pulses

201
Q

Ix for patent ductus arteriosus

A

Continuous murmur. Described as machinery murmur or Gibsons’ murmur

  • Accentuated in systole
  • Best heard in left infraclavicular area
202
Q

Management for patent Ductus arteriosus

A
  • Diuretics in those with features of HF
  • Non surgical or surgical closure
  • In asymptomatic well infants: wait until 1 year of age with regular ECHO to check for spontaneous closure. If still open by 1 year of age  close with surgery
203
Q

What is pericardial effusion

A

Collection of fluid in pericardial space

Many causes. Local vs systemic

  • Local e.g.: Acute/chronic pericarditis → effusion
  • Systemic e.g.: kidney failure → rise in urea →uremic pericarditis → effusion
204
Q

SS for pericardial effusion

A

Small to moderate formed over some time: asymptomatic

Quick forming → cardiac tamponade → symptoms

Chest pain similar to pericarditis, light headedness, palpitations

205
Q

Management for pericardial effusion

A

Large effusions →drained if >1month

  • Smaller effusions → followed up with regular ECHO clinical examination
  • Oxygen therapy, treat underlying condition, surgery (pericardiocentesis?)
206
Q

what is postural hypotension

A
207
Q

Pathophysiology of postural hypotension

A

stand up→ blood shifts from chest to diaphragm → reduces venous return → reduces filling of vernicles → decrease preload → reduced CO

This gravity induced drop BP is detected by baroreceptors →triggers baroreflex → vasoconstriction and compensatory tachycardia, also increase total peripheral resistance

HOWEVER, postural hypotension occurs when this mechanism to regulate BP are impaired.

It can occur due to:

  • Failure of baroreflexes (autonomic failure)
  • Volume depletion
  • End-organ dysfunction
208
Q

RF postural hypotension

A

Pregnancy

Drugs

Age

Addison’s disease

Diabetes

Parkinsons disease

209
Q

SS postural hypotension

A

Dizziness

weakness

confusion

Blurred vision

Nausea

Headache

syncope

210
Q

Ix postural hypotension

A

Diagnosis is made by doing a lying and standing blood pressure. The patient lies down for 15 minutes, and the blood pressure is taken. The patient is then asked to stand for 2 minutes, and the blood pressure is taken again. A drop of >20mmHg along with symptoms is postural hypotension.

210
Q

Management postural hypotension

A

Management mainly involvesavoiding exacerbating factors

  • Heat
  • Long periods of immobility
  • Large meals
  • Dehydration
  • Sitting with crossed legs

Fludrocortisone

Midodrine

Pyridostigmine

211
Q

complication of postural hypotension

A

increases falls

decrease ADL

212
Q

What is phlebitis/Thrombophelbitis

A

Superficial veins become inflamed and blood clot can occur

  • Phlebitisrefersto inflammation of a vein and it can be caused by any insult to the blood vessel wall, impaired venous flow, or coagulation abnormality
  • Thrombophlebitisrefers to the formation of a blood clot associated with phlebitis
213
Q

Pathophysiology of phlebitis/ thrombophlebitis

A

blood flow stasis

damage to the blood vessels walls

Hyper-coagulability of bloods

IV infusion, Obesity, Pregnancy, smoking, oral contraceptive

214
Q

Rf for phlebitis/ thrombophlebitis

A

thrombophilia disorder

hx of thrombophlebitis

215
Q

SS of phlebitis/ thrombophlebitis

A
  • Localized redness & swelling of the vein affected
  • Pain or burning along the length of the vein
  • Vein feeling hard and cord-like
216
Q

Ix of phlebitis/ thrombophlebitis

A

doppler ultrasonography

biopsy/screening

217
Q

Management for phlebitis/ thrombophlebitis

A

compression socks

keep legs elevated

NDAIDS

Hirudoid cream

Fondaparinux

218
Q

Complication for phlebitis/ thrombophlebitis

A

Suppurative thrombophlebitis (
a serious complication resulting in pus in the the vein, that can lead to the patient becoming septic)

219
Q

What is peripheral vascular disease

A

chronic condition due to atherosclerosis of arteries

220
Q

Pathophysiology of peripheral vascular disease

A
  • High cholesterol, smoking, diabetes can cause arterial narrowing through inflammatory mediators
  • Narrowing of the arteries cause tissue hypoperfusion/hypoxia to tissues downstream of infarct
  • Signs/symptoms due to hypoperfusion
221
Q

RF for peripheral vascular disease

A
  • Diabetes
  • Smoking
  • Hypertension
  • Lipidaemia
222
Q

SS for peripheral vascular disease

A

pain

hx of cvd

weak/absent pulses

bruit

223
Q

Ix for peripheral vascular disease

A

lipids

doppler

224
Q

Management for peripheral vascular disease

A

Lifestyle advice

  • e.g. smoking cessation, healthy diet, weight loss/exercise

Pharmacological treatment of identifiable cause

  • e.g. Treating hypertension, diabetes, lipidemia

Symptomatic treatment with antiplatelets (aspirin, clopidogrel) and vasodilators (cilostazol-only effective in intermittent claudication)

Surgical management (revascularisation) only used when lifestyle/pharmacological management has failed

Revascularization also recommended for those with critical limb ischaemia (restpain/ABPI <0.3)

225
Q

Complication for peripheral vascular disease

A

amputation

226
Q

what is premature beats

A

Extra heartbeats that begin in the atria or ventricles. These extra beats disrupt the regular heart rhythm, sometimes causing patients to describe a fluttering or skipped beat in their chest

227
Q

Pathophys of premature beats

A
  • Premature beats are abnormal contractions that begin in the ventricles or atria
  • These extra contractions usually beat sooner than the next expected regular heart beat and they often interrupt the normal order of pumping
  • Certain triggers, heart diseases, scarring or changes in the body can make cells in the ventricles electrically unstable and electrical impulses to be misrouted
228
Q

RF for premature beats

A
  • Caffeine, tobacco, alcohol and illicit drugs
  • Exercise - if you have certain types of PVCs
  • Hypertension
  • Anxiety
  • Heart disease including CHD, CAD, previous MI, HF or cardiomyopathy
229
Q

SS for premature beats

A

FHx

Palpitation

fluttering

Syncope

Fatigue

Atypical chest pain

230
Q

Ix for premature beats

A

Bloods

  • FBC, TFTs, Electrolytes, calcium, magnesium

ECG

  • An ECG will detect extra beats and identify the pattern and source
  • 24 hour ECG monitoring
231
Q

Management premature beats

A

Conservative

  • Lifestyle changes: Eliminating common triggers such as caffeine or tobacco

Medical

  • Beta blockers
  • Calcium channel blockers
  • Antiarrhythmic drugs e.g amiodarone or flecainide

Surgical

  • Radiofrequency catheter ablation (radiofrequency energy is used to destroy an area of heart tissue that is causing the irregular contractions)
232
Q

Complication premature beats

A
  • Increased risk of Arrhythmias
  • Cardiomyopathy
  • Sudden Cardiac death
233
Q

What is paroxysmal supraventricular tachycardia

A

a type of abnormal heart Rythm

234
Q

Pathophysiology of paroxysmal supraventricular tachycardia

A
  • The cause is not known
  • Underlying mechanism typically involves an accessory pathway that results in re-entry
235
Q

RF for paroxysmal supraventricular tachycardia

A
  • Alcohol intake
  • Caffeine
  • Nicotine
  • Psychological stress
  • Wolff-Parkinson-White syndrome
236
Q

SS for paroxysmal supraventricular tachycardia

A

Often patients have no symptoms. Otherwise symptoms may include:

  • Palpitations
  • Feeling lightheaded
  • Sweating
  • SOB
  • Chest Pain
  • Episodes start and end suddenly
237
Q

Ix for paroxysmal supraventricular tachycardia

A

ECG:

Narrow QRS and a fast rhythm typically between 150 and 240 bpm

238
Q

Management for paroxysmal supraventricular tachycardia

A
  • If patient has normal BP,

1) Adenosine

2) CCB or BB

3) Synchronized cardioversion

4) Catheter ablation

239
Q

What is Pulmonary stenosis/insufficiency

A

Pulmonic valve diseases are rare

Pulmonary stenosis are usually congenital diseases when they happen. Pulmonary regurgitation commonly occur as a complication of surgical procedures e.g to relieve symptoms of pulmonic stenosis. Can also occur due to pulmonary hypertension or marfans

240
Q

pathophysiology for Pulmonary stenosis/insufficiency

A
  • Pulmonic valves have three cusps and they regulate blood flow from the right ventricle into the lungs
  • Pulmonic stenosis causes an obstruction of blood flow to the lungs which lead to right ventricular dilation due to volume overload
  • Pulmonary regurgitation also cause volume overload during diastole causing right ventricular dilation
241
Q

RF for Pulmonary stenosis/insufficiency

A
  • Rheumatic disease
  • Congenital heart disease
242
Q

SS for Pulmonary stenosis/insufficiency

A
  • Sudden death
  • SOB
  • Exertional syncope
  • Parasternal heaves/thrills
  • Ascites/pedal oedema
  • In pulmonic stenosis, Systolic murmur can be heard best lying down (can be physiological in healthy individuals). Ejection pulmonic click can also be heard
  • Loud P2 (Pulmonic component may be heard in pulmonary regurgitation). Diastolic murmur also heard in pulmonary regurgitation
243
Q

Ix for Pulmonary stenosis/insufficiency

A

Bloods

  • FBC (Look for anaemia), Us and Es (Look for dilutional electrolyte problems), BNP (Might be raised in heart failure), LFTs (Might be deranged due to liver congestion)

X-ray/Imaging

  • CXR might show cardiomegaly. Echocardiogram is useful in seeing valvular function

ECG

  • Right ventricular hypertrophy. Right bundle branch block
244
Q

Managment Pulmonary stenosis/insufficiency

A
  • Manage cause as appropriate eg antibiotics for rheumatic fever
  • Resuscitation if acutely unwell. In neonates with pulmonic stenosis, prostaglandin infusion can be used to dilate the ductus arteriosus
  • Refer all symptomatic cases of pulmonic stenosis/regurgitation to cardiology. Mild Pulmonary regurgitation doesn’t require any specific intervention other than for cardiologist to monitor every 1-3 years
  • If intervention required, patient might undergo valve replacement depending on severity
245
Q

Complication Pulmonary stenosis/insufficiency

A
  • Heart failure
  • Arrhythmia
246
Q

what is Shock

A

Hypoperfusion associated with low or declining blood pressure

3 types:

  • cardiogenic - pump failure
  • Hypovolemic - loss of intravascular volume
  • failure of vasoregulation and obtruction to blood flow
247
Q

pathophys of shock

A

cardiogenic:
MI, Cardiomyopathy, valve issue and arrythmias
Hypovolemic causes:
Haemorrhage, burns, heat stress, GI losses
Distributive causes:
Sepsis, anaphylaxis, poising, Addison’s disease
Obstructive causes:
Pulmonary embolus, cardiac tamponade, tension pneumothorax

248
Q

SS for shock

A

cold, unwell, anxious, faint, SOB
Oliguria
Pale and sweaty
Tachypnoea
Cold peripheries
Tachycardia
postural hypotension
confusion
coma

249
Q

Ix for shock

A

FBC, U&E, LFT, group and cross-match, coagulation, blood gasses, monitor urine output, CRP, ESR, lactate, blood glucose, pregnancy test?, CXR, ECG

250
Q

Management for shock

A
  • Remember ABC. Regular OBS
  • Oxygen. Venous access. Resuscitation with fluid. Blood transfusion?
  • Vasodilators? Analgesia? Surgery if needed (ectopic pregnancy), vasopressors?
251
Q

What is stroke

A

Stroke is a sudden onset of brain dysfunction, caused byan alteration in cerebrovascular blood supply.It is characterised by:

  • Rapid, acute onset – within a few minutes
  • Focal neurological defect

Classification for stroke:

  • Haemorrhage
  • Brain ischaemia
  • TIA
252
Q

Pathophysiology of stroke

A
  • Arterial embolism –from a distant site; e.g. carotids, vertebral or basilar arteries. The embolus will occlude an artery of the brain resulting in infarction. May also come fromheart valves in endocarditis.
  • Haemorrhage –can be in the cerebrum itself, or also asubarachnoid haemorrhagemay cause a similar effect
253
Q

RF for stroke

A

HTN

Smoking

Exercise and diet

Afib

Diabetes

Alcohol

Cholesterol

sleep apnoea

carotid artery stenosis

obesity

ethnicity

age

heart disease

Family Hx

sex-male

254
Q

Anterior circulationstroke common presentation:

A
  • Limb and/or facial weakness
  • Paraesthesia or numbness
  • Speech difficulty (aphasia/dysarthria/dysphasia)
  • Headache
255
Q

Investigation for stroke

A
  • Non-contrast CT head on admission, can be followed by CT angiogram for vascular causes.
  • MRI brain with diffusion weighted imaging to provide more accurate imaging about stroke lesion and/or haemorrhage.

Bloods

  • FBC – to exclude anaemia or thrombocytopaenia prior to possible initiation of thrombolytic agents.
  • U&Es – to exclude electrolyte disturbance and renal failure
  • PT + PTT - coagulopathy
  • INR
  • Serum Glucose – to exclude hypoglycaemic cause
  • Cholesterol HDL/LDL -
  • Cardiac enzymes – concomitant MI

ECG

  • To exclude cardiac arrhythmia or ischaemia, to identify AF/pAF

Special Tests

  • ECHO – in subacute stage to investigate cardioembolic cause
  • Carotid and/or Vertebral Dopplers – in subacute stage to investigate for carotid stenosis
256
Q

Acute Management for stroke

A

Acute management of Ischaemic stroke:

  • If patient presents within 4.5 hours of onset of neurological symptoms – r-tPA (alteplase 0.9mg/kg)
  • Aspirin 300mg OD to be commenced 24 hours post administration of r-tPA
  • Endovascular intervention (Thrombectomy) – patients must meet the following criteria:
    • mRS 0
    • occlusion of ICA or proximal M1
    • Age ≥18 years old
    • NIHSS ≥6
    • ASPECTS ≥6
  • Thrombectomy with stent retriever should be undertaken within 6 hours of onset.
  • Admission to stroke unit for ongoing medical care, treatment of any complications and early initiation of rehabilitation therapy. Encourage VTE prophylaxis and early mobilisation
257
Q

Complication for stroke

A
  • Increased risk of further event (Stroke or TIA)
  • Increased risk of haemorrhagic transformation of infarct
  • Sepsis
  • CKD
  • Death
258
Q

Posterior circulationstroke common presentation:

A
  • Visual loss or double vision
  • Confusion
  • Dizziness
  • Vertigo
  • Nausea
259
Q

Arterial dissectionscommon presentation:

A
  • Neck or facial pain.
260
Q

Lacunar strokescommon presentation:

A
  • Limb and/or facial weakness (typically affects face, leg and arm)
  • Speech difficulty
  • Ataxia
  • Paraesthesias or numbness (typically affects face, leg and arm).
261
Q

SS for Anterior circulation infarct stroke

A
  • Partial or total loss of tone in face and upper and/or lower limbs (usually unilateral)
  • Expressive and/or receptive dysphasia (or aphasia)
  • Decreased or loss of sensation in face and upper and/or lower limbs (associated sensory neglect if non-dominant hemisphere stroke)
  • Gaze paresis (often horizontal and unidirectional).
  • Gaze deviation (away from the side of lesion, towards the hemiparetic side) this should prompt consideration of seizure but can also occur infarcts in the pons or thalamus.
  • Horner’s syndrome (suggests ipsilateral carotid dissection.)
262
Q

SS of Posterior circulation infarct stroke

A

:

  • Specific cranial nerve deficits (unilateral tongue weakness, diplopia)
  • Horner’s syndrome (hemilateral triad of miosis, ptosis, and facial anhidrosis)
  • Loss of visual fields
  • Dysarthria
  • Nausea and/or vomiting
  • Difficulty with gait and fine motor co-ordination
  • Altered level of consciousness
263
Q

SS of Lacunar infarct stroke:

A
  • Pure motor hemiparesis
  • Pure sensory hemiparesis
  • Ataxia
  • Mixed motor and sensory signs
  • Dysarthria.
264
Q

SS of Haemorrhagic stroke:

A
  • Headache of gradually increasing intensity
  • Neck stiffness
  • Visual changes
  • Photophobia
  • Sudden onset of symptoms with progression over time
  • Aphaisa
  • Dysarthria
  • Ataxia
  • Sensory loss
  • Altered level of conciousness
  • NIHSS to calculate severity of stroke
265
Q

Long term Management for stroke

A
  • Lifelong anticoagulation with warfarin in patients with aetiology of AF
  • Antiplatelet therapy with clopidogrel is indicated in patients who do not have AF.
  • Carotid endarterectomy should be considered for patients with symptomatic carotid artery stenosis – no evidence for benefit of CEA in patients with near-occlusion.
  • Treat underlying aeitiology accordingly.
  • In patients with an embolic stroke of undetermined source and a patent foramen ovale (PFO) and high ROPE score, closure of the PFO may be of benefit for secondary prevention.

Acute management of haemorrhagic strokes:

  • Neurosurgical review for potential need for surgical intervention (craniectomy/craniotomy)
  • Larger haemorrhages warrant ITU admission for intubation and invasive BP/ICP control
  • Stable haemorrhages warrant HASU admission to monitor haemorrhage, blood pressure control, DVT prophylaxis and correction of coagulopathy
266
Q

What is tetralogy of fallot

A

Common cyanotic congenital heart disease

Hole between ventricles → oxygen rich blood mixes with oxygen poor blood

Overriding aorta = aorta is deeper in heart overlying the hole = the oxygen poor blood flows into the aorta too

Pulmonary artery is narrowed = less blood reaches lungs = right ventricle works harder = hypertrophy

267
Q

SS of tetralogy of Fallot

A

4 main anatomical features:

  • Large ventricular septal defect
  • Overriding aorta
  • Right ventricular outflow obstruction
  • Right ventricular hypertrophy

Baby is blue due to lack of oxygenated blood

268
Q

Investigations for tetralogy of fallot

A

Foetal screening and ECHO have led to an increase in prenatal diagnosis

Squatting to rest whilst exercising is characteristic of a right-to-left shunt and presents in an older child

269
Q

Management for tetralogy of fallot

A

Surgery

270
Q

What is Tricuspid stenosis/insufficiency

A

Right heart valvular problems

Tricuspid stenosis is rare. Tricuspid regurgitation is more common

271
Q

Pathophysiology of Tricuspid stenosis/insufficiency

A
  • The tricuspid valve is in between the right atrium and ventricle
  • Tricuspid stenosis is commonly caused by rheumatic fever. Other causes include SLE, right atrial myxoma
  • In tricuspid stenosis the valves become thickened and narrow. This increases pressure in the right atrium causing dilation
  • Tricuspid regurgitation commonly occurs due to infective endocarditis. This causes an incompetency of the valve causing blood to flow back into the right atrium during ventricular systole
  • Tricuspid regurgitation may occur with mitral stenosis/regurgitation
272
Q

RF Tricuspid stenosis/insufficiency

A
  • Congenital heart disease
  • Streptococcal infection
273
Q

SS of Tricuspid stenosis/insufficiency

A
  • Fever/history of previous untreated bacterial infection
  • Fatigue
  • SOB/exercise intolerance
  • Pulmonary oedema/crackles (if biventricular heart failure)
  • Hepatomegaly
  • Ankle oedema
  • Raised JVP
  • Diastolic murmur in tricuspid stenosis. Pansystolic murmur in regurgitation (Accentuated by pressing the liver, inspiration or raising legs up)
  • Split S1 or S2 only heard
  • Ascites
  • Chest Pain
274
Q

Ix for Tricuspid stenosis/insufficiency

A

Bloods

  • FBC-Might show leucocytosis/Anaemia
  • LFT-Might show deranged LFTs
  • BNP-Raised in heart failure
  • Us and Es-might show dilutional electrolyte imbalance

X-ray/Imaging

  • Echocardiogram to see valvular pathologies and pressure
  • CXR-may show right atrial enlargement/cardiomegaly/pleural effusion

ECG

  • Tall P waves due to right atrial hypertrophy

Special Tests

  • Cardiac catheterisation might be used to determine severity and associated congenital defects
275
Q

Management for Tricuspid stenosis/insufficiency

A
  • Manage underlying conditions eg Bacteria infections with antibiotics
  • Manage arrhythmias
  • Manage heart failure (see heart failure matrix condition)
  • Valve replacement in severe cases or if refractory to medical management (MIld cases of tricuspid stenosis/regurgitation does not need surgical input)
276
Q

Complication Tricuspid stenosis/insufficiency

A
  • Arrhythmia
  • Heart failure
277
Q

What is ventricular septal defect

A

One or more holes in the septum

Communication between left and right ventricles of the heart

278
Q

ss ventricular septal defect

A

Symptoms depend on size of hole

Not obvious at birth

Exercise intolerance – impacts feeding  poor weight gain

279
Q

Ix ventricular septal defect

A

Splitting of second heart sound, harsh pansystolic murmur

ECHO

280
Q

Management ventricular septal defect

A

No treatment/ medical management/ surgical management

281
Q

What is varicose vein

A

dilated and tortuous veins mainly occurring in the superficial venous system of the legs

282
Q

Pathophysiology of varicose vein

A

occurs due to incompetence of the one-way valve → leakage →pooling of blood

The weaker thinner walls make it more prone to the effects of high pressure build up leading to distension of the venous walls and tortuosity

283
Q

RF of varicose vein

A

increase with age

pregnancy

long periods of standing

FHx

common in female

Hx DVT

284
Q

SS of varicose vein

A

often asymptomatic

pain

leg fatigue

nocturnal leg cramps

discoloration

285
Q

Ix of varicose vein

A

clinically diagnosed

doppler used to confirm diagnosis

286
Q

Management of varicose vein

A

exercise and weight loss

refer to vascular Serivices

compression therapy - IMPORTANT to exclude arterial insufficiency

Endothermal ablation
(first line for surgery)

287
Q

Complication of varicose vein

A

bleeding

DVT

288
Q

What is venous thrombosis

A

Blood clot in the deep vein in the leg

289
Q

Pathophysiology of venous thrombosis

A

DVT in leg, thighs, pelvis or abdomen → impaired venous flow and consequent oedema and pain

290
Q

RF venous thrombosis

A
  • Bedbound
  • Hospitalisation within 2 months
  • Major surgery within 3 months
  • Active Ca
  • History of trauma
  • Age
  • Pregnancy
  • Factor V Leiden
  • Obesity
  • Recent long-distance air travel
  • Family history
291
Q

SS venous thrombosis

A
  • On history taking note presence of risk factors and social history.
  • History of DVT or PE
  • Wells’ score <2 15% probability of DVT
  • Wells’ score >2 40% probability of DVT
  • unilateral swelling and difference in circumference more than 3 cm
  • Pain
292
Q

Ix venous thrombosis

A
  • Wells’ Score - >2 = likely DVT
  • D-Dimer – Consider in patients with a wells’ score of 2 or above.
  • Elevated d-dimer: >500ng/mL – however d-dimer is non-specific and can be raised in patients who are older, acutely ill, have an underlying hepatic disease, have an infection, or are pregnant.
  • USS Lower Limbs – whole leg or proximal USS performed to assess the presence of a thrombus by compressibility and venous flow, the presence of a thrombus prevents compression, reduced or absent spontaneous flow, lack of respiratory variation, intraluminal echoes, or colour flow patency abnormalities.
  • CTPA – in patients with a confirmed DVT a CT pulmonary angiogram can be undertaken to exclude pulmonary emboli if clinically indicated.
293
Q

Management venous thrombosis

A

Refer immediately for same day management for a woman who is pregnant or has given birth within past 6 weeks

For people who arelikelyto have DVT:

offer leg vein ultrasound

For people who areunlikelyto have DVT:

D-dimer

If interim therapeutic anticoagulation is required:

offer apixaban or rivaroxaban

carry out baseline blood test e.g. FBC eGFR LFT PT and APTT

294
Q

Complication venous thrombosis

A
  • Pulmonary Embolism (PE)
  • Risk of bleeding
  • Heparin-induced thrombocytopenia (HIT)
  • Heparin resistance/aPTT confounding
  • Post-thrombotic syndrome
  • Osteoporosis (if being treated with unfractionated heparin)
295
Q

What is ventricular tachycardia

A

VT is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart

296
Q

Pathophysiology of ventricular tachycardia

A

VT can occur due to

  • CAD
  • Aortic stenosis
  • Cardiomyopathy
  • Electrolyte problems
  • Morphology of the VT depends on its cause and the origin of the re-entry electrical circuit in the heart
  • Monomorphic VT - scarring of the heart muscle from previous MI. This scar cannot conduct electrical activity
  • Polymorphic VT - abnormalities of ventricular muscle repolarization
297
Q

RF ventricular tachycardia

A
  • CAD
  • Structural heart disease
  • Electrolyte deficiencies e.g hypokalaemia, hypocalcaemia, hypomagnesaemia
  • Sympathomimetic agents (e.g caffeine or cocaine) may stimulate VT in vulnerable hearts
298
Q

SS ventricular tachycardia

A
  • Lightheadedness
  • Palpitations
  • Chest Pain
  • Dyspnoea
  • Syncope
  • Symptoms of HF
  • Signs reflect degree of haemodynamic instability
  • Basal fine lung crepitations
  • raised JVP
  • Hypotension
  • anxiety
  • Agitation
  • lethargy
299
Q

Ix ventricular tachycardia

A

Bloods

  • electrolytes, including serum calcium, magnesium and phosphate levels. Serum troponin levels

X-ray/Imaging

  • CXR if there is a possibility of CHF or other cardiopulmonary pathology as contributing factors

ECG

  • showing a rate of greater than 120bpm and at least 3 wide QRS complexes in a row

Special Tests

  • Levels of therapeutic drugs - e.g, digoxin
300
Q

Management for ventricular tachycardia

A
  • Address the ABCs of resuscitation and provide BLS and ALS
  • VF or pulseless VT - unsynchronised defibrillation
  • VT - synchronised cardioversion
  • Defibrillation is followed by airway management if required, supplemental oxygen, vascular access
301
Q

Complication ventricular tachycardia

A
  • Ventricular fibrillation
  • Cardiac Arrest
302
Q

What is Ventricular fibrillation/flutter

A

Fibrillation: disorganised electrical impulses causing the heart to quiver rather than contract

Flutter: tachycardic arrhythmia affects the ventricles, considered as transition phase between ventricular tachycardia and ventricular fibrillation

303
Q

Pathophysiology Ventricular fibrillation/flutter

A
  • Ventricular Flutter is an arrhythmia characterised with a typical sinusoidal pattern on an ECG
  • With a frequency of 250-300 bpm, Ventricular Flutter, due to its repolarisation, results in minimal cardiac output and subsequent ischaemia
  • This can then lead to flutter becoming fibrillation
  • Ventricular Fibrillation is a life threatening condition caused by the disorganised excitation replacing organised electrical activity to the ventricles
  • The most common arrhythmia identified in cardiac arrest
  • The inability of the ventricles to contract efficiently reducing the cardiac output is what leads to cardiac arrest and eventually death if not treated within the time frame
304
Q

RF Ventricular fibrillation/flutter

A
  • Previous ventricular fibrillation
  • Previous myocardial infarction
  • Cardiomyopathy
  • Drug toxicity
  • Electrocution
  • Congenital heart diseases
  • Sepsis
305
Q

ss Ventricular fibrillation/flutter

A
  • Nausea
  • Vomiting
  • Tachycardia
  • Shortness of breath
  • Chest pain
  • Syncope
306
Q

Ix Ventricular fibrillation/flutter

A

Bloods

  • FBC
  • U&E
  • LFT
  • CRP
  • Troponin
  • BNP
  • Toxicology

X-ray/Imaging

  • CXR, Echocardiogram, CT, Angiogram

ECG

  • Ventricular Fibrillation: unsynchronised rapid irregular electrical activity between 400-500 bpm
  • Ventricular Flutter: sinusoidal waves without clearly defined QRS and T waves, with a rate of 250-350 bpm

Special Tests

  • Other comments: ECG will confirm the diagnosis of ventricular flutter/fibrillation. The rest of the work up is to determine possible cause of these arrhythmias and any damage caused as a result of the arrhythmias
307
Q

Management Ventricular fibrillation/flutter

A
  • Beta blockers and surgical treatment are considered after patient is stable

Medical

  • Defibrillation, CPR, Beta Blockers

Surgical

  • Angioplasty, Coronary Artery Bypass Graft, Implantable Cardioverter Defibrillator
308
Q

Complication Ventricular fibrillation/flutter

A

Sudden Cardiac Death

309
Q

what is Valvular cardiac failure

A

The heart is made up of 4 valves namely aortic, mitral, pulmonic, tricuspid

These valves ensure a unidirectional flow of blood normally during systole and diastole

310
Q

Pathophysiology of Valvular cardiac failure

A
  • Valvular heart failure can either be left or right sided depending on which valves are involved
  • Aortic and mitral valve heart failure are the two types of left sided valvular heart failure
  • Causes of left valvular heart failure includes idiopathic, SLE, Bicuspid aortic valve, rheumatic heart disease/infective endocarditis (can cause acute/chronic valvular heart failure)
  • Tricuspid and Pulmonic valve heart failure are the two types of right side heart failure
  • Pulmonic stenosis can cause valvular heart failure and they are usually congenital related heart failure caused by Tetralogy of fallot, congenital rubella syndrome
  • Tricuspid valve heart failure can be caused by rheumatic fever and it results in dilation of the right ventricle
  • Generally speaking, valvular heart failure results in either concentric or eccentric hypertrophy
311
Q

RF of Valvular cardiac failure

A
  • Rheumatic fever
  • IV drug use
  • Congenital heart disease
  • Autoimmune conditions
312
Q

SS of Valvular cardiac failure

A
  • SOB/reduced exercise intolerance
  • Orthopnea
  • Dizziness/LOC
  • Chest Pain
  • Lethargy/’blue spells’ in children
  • Haemoptysis-pressure in the bronchial veins
  • Tachycardia/Tachypnea
  • Raised JVP with hepatojugular reflux
  • Bilateral pedal oedema
  • Displaced apex beat
  • Abdominal distension
  • Heart murmurs (Can include Pansystolic, Mid systolic, Ejection systolic/Ejection clicks depending on which valves are involved)
  • Cardiac wheeze/reduced air entry
  • Framingham criteria is used to diagnose heart failure regardless of the cause. It uses full history, physical examination findings and CXR and it includes major and minor criteria
313
Q

Ix of Valvular cardiac failure

A

Bloods

  • FBC-For anaemia
  • BNP-marker of heart failure, LFT-heart failure can mildly affect liver function, Renal function tests-Deranged electrolytes
  • Thyroid function test
  • Blood cultures

X-ray/Imaging

  • CXR-Cardiomegaly/interstitial fluid
  • Echocardiogram - (Urgency depends on BNP levels and history of MI (request echo within 2 weeks and no need for BNP). If no hx of MI and BNP between 100-400 request echocardiogram within 6 weeks and if >400 request echo within 2 weeks). Echocardiogram will then categorise heart failure into either reduced ejection fraction or preserved ejection fraction

ECG

  • LVH. Arrhythmias. Bundle branch blocks depending on which valves are involved
314
Q

Management for Valvular cardiac failure

A
  • If acute presentation, use ABCDE
  • Treatment will depend on cause e.g IV antibiotics for rheumatic fever
  • Refer to cardiology-Symptomatic valvular problems might require TAVI or valvuloplasty depending which valves are involved
  • Chronic but stable management will involve the stepwise ladder of ACEi and Beta blockers (1st line), ARB/Hydralazine with nitrate/Aldosterone antagonist (2nd Line), Digoxin or cardiac resynchronisation therapy (3rd line)
  • See matrix condition on Aortic stenosis/Regurgitation, Mitral stenosis/regurgitation, Pulmonic stenosis/insufficiency, Tricuspid stenosis/insufficiency
315
Q

Complications for Valvular cardiac failure

A
  • Death
  • Arrhythmias