Cardiology Flashcards

1
Q

Midline sternotomy +…

Metallic click

A

Mechanical valve replacement

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2
Q

Midline sternotomy +…

Murmur

A

Tissue valve

Valvotomy

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3
Q

Midline sternotomy +…

Vein harvest scars

A

CABG

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4
Q

Midline sternotomy +…

Old scar, young patient

A

Repair of congenital defect

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5
Q

Midline sternotomy +…

Immunosuppression

A

Heart transplant

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6
Q

Midline sternotomy +…

No other findings

A

Trauma: tamponade,

Internal mammary artery CABG

Tissue valve

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7
Q

Cardiac Causes of Clubbing

A

Infective endocarditis

Congenital cyanotic heart disease

  • Fallot’s tetralogy
    1. VSD
    2. Pulmonary stenosis
    3. Right ventricular hypertrophy
    4. Overriding aorta
  • Transposition of the Great Vessels

Atrial myxoma

Associated with Carney Complex LAMES syndrome

Lentigines: spotty skin pigmentation

Atrial Myxoma

Endocrine tumours: pituitary

Schwannomas

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8
Q

Causes of Collapsing Pulse

A

Caused by hyperdynamic circulation

ATAP

Aortic regurgitation

Thyrotoxicosis

Anaemia

Pregnancy

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9
Q

Causes of Absent Radial Pulse

A

Arrest

Trauma

Thrombosis/ embolism

Co-arctation of aorta

Takayasu’s arteritis

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10
Q

Impalpable Apex Beat

A

COPD

COPD

Obesity

Pericardial effusion

Dextrocardia

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11
Q

Features of Pulmonary Hypertension

A

Increased JVP

Left parasternal heave

Loud P2 + Pan-systolic murmur of Tricuspid regurgitation

Pulsatile hepatomegaly

Ascites and peripheral oedema

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12
Q

Heart sounds

A

S1 = mirtal valve closure

S2 = aortic valve closure

S3 = rapid venitrcular filling of dilated left ventricle

S4 = atrial contraction against stiff ventricle

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13
Q

Signs on Examination of Aortic Stenosis

A

Slow-rising pulse

Narrow pulse pressure <30mmHg

Precordium

Pacemaker

Aortic thrill

Apex: forecful, non-displaced

HS: Quiet A2, S4 (forceful atrial contaction against hypertrophied left ventricle)

Murmur

Early, ejection systolic murmur

Right 2nd ICS

Loudest sitting forward at end-expiration

Radiates to carotids

SEVERE AS
Quiet, absent A2

S4

Narrow pulse pressure

Decompensation: LVF

Significant negatives

Infective endocarditis

LVF

Indicators of severity

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14
Q

Clinical Signs of Severe Aortic Stenosis

A

Quiet A2

S4

Narrowed pulse pressure

LVF

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15
Q

Differential for Aortic Stenosis

A

Aortic sclerosis: no radiation to carotids, normal pulse character

Mitral regurgitation (also, systolic murmur)

HOCM: valsalva increases murmur, squatting decreases murmur

Pulmonary stenosis: right sided

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16
Q

Causes of Aortic Stenosis

A

Age-related senile calcification

Biscuspid aortic valve

Rheumatic heart disease

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17
Q

Clinical symptoms of Severe Aortic Stenosis

A

Angina: 50% dead in 5 years

Syncope: 50% dead in 3 years

Dyspnoea: 50% dead in 2 years

Clinical signs

Quiet A2

S4

LVF

Narrowed pulse pressure

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18
Q

Echo features of severe Aortic stenosis

A

Valve area <1cm2

Pressure gradient >40mmHg

Jet velocity >4m/s

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19
Q

Management of Aortic Stenosis

A

MDT: GP, Cardiologist, Cardiothoracic surgeons, dietician, specialist nurse

Conservative

  • Monitor, regular follow-ups with echo

Medical

  • Optimise CV risk factors: atorvastatin, Anti-HTN, DM, anti-platelets

Surgical

  • if symptomatic then valve replacement
  • if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
  • balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
  • TAVI
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20
Q

Signs of Mitral Regurgitation on Examination

A

Peripheral inspection: warfarin bracelet

Pulse: Atrial fibrillation

Precordium

Left parasternal heave

Apex: THRUSTING displaced - volume oberload as ventricle has to pump forward systolic volume and regurgitant volume —> eccentric hypertrophy

HS: Soft S1, S2 not heard separately from the murmur (+/- loud P2 if pulmonary hypertension)

Murmur

Blowing: pansystolic murmur

Loudest at apex, left lateral position and on end-expiration

Radiates to axilla

Clinical signs of severe Mitral Regurgitation

Left ventricular failure

Atrial fibrillation

Significant negatives: Infective endocarditis, AF, LVF (indicators of severity)

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21
Q

Differential for Mitral Regurgitation

A

Aortic stenosis (systolic)

Ventricular septal defect

Tricuspid regurgitation: right-sided

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22
Q

Clinical Signs of Severe Mitral Regurgitation

A

LVF

AF

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23
Q

Causes of Mitral Regurgitation

A

Functional: Left ventricular dilatation secondary to hypertension or idiopathic

Annular calcification —> contraction

Rheumatic heart disease

Mitral valve prolapse

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24
Q

ECG changes in Mitral Regurgitation

A

P-mitrale (atrial hypertrophy)

Arrhythmias

  • Atrial premature beats
  • Paroxysmal supraventricular tachycardia
  • Ventricular premature beats
  • Complex ventricular ectopy

Left ventricular hypertrophy

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25
Echo features of severe Mitral Regurgitation
Jet width of \>0.6cm Systolic pulmonary flow reversal Regurgitant volume \>60ml
26
Management of Mitral Regurgitation
MDT: GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM **Specific** **AF**: rate control and **anti**-**coagulate** Reduce afterload: ACE-inhibitor or b-blocker (esp Carvedilol) **Surgical:** Valve replacement or repair If unfit: ?Percutaneous mitral valve leaflet repair for mitral regurgitation Aim to replace the valve before significant LV dilatation and dysfunction Indications for surgery: symptomatic
27
Eponymous signs of Aortic Regurgitation
Quincke's sign: capillary pulsation in nail beds Corrigan's: visible vigorous carotid pulsation De Musset's: head bopping Traube's: pistol-shot femorals (pistol-sound heard over femorals) Durozieze's: systolic murmur over femoral artery with proximal compression, diastolic murmur with distal compression Mueller's: systolic pulsations of uvula Rosenbach's: systolic pulsations of the liver
28
Causes of Aortic Regurgitation
**Marfan's** Tall, thin, long arms, high-arched palate **Ankylosing spondylitis:** cervical kyphosis
29
Signs of Aortic Regurgitation on Examination
**Pulse:** Collapsing Wide pulse pressure e.g. 180/45 **Precordium** Aortic thrill Apex: displaced (volume overload) **HS:** soft S2, +/- S3 **Murmur** **High-pitched early diastolic murmur** Loudest on lower left sternal edge (parasternal 3rd IC), sitting forward in end-expiration Additional murmurs: Ejection systolic flow murmur **Austin-flint murmur** = **rumbling mid-diastolic murmur** secondary to regurgitant jet fluttering the anterior of mitral valve **Clinical Signs of Severe Aortic Regurgitation** Collapsing pulse Wide pulse pressure Left ventricular failure **Significant negatives:** infective endocarditis, indicators of severity (LVF, wide pulse pressure, collapsing pulse)
30
Clinical Signs of Severe Aortic Regurgitation
Collapsing Pulse Wide pulse pressure Left ventricular failure
31
Causes of Aortic Regurgitation
**Chronic** Bicuspid aortic valve Rheumatic heart disease Autoimmune: ankylosing spondylitis Connective tissue disease: Marfan's, Ehlers-Danlos **Acute** Infective endocarditis Type A aortic dissection
32
Differential for Aortic Regurgitation
Mitral stenosis Pulmonary regurgitation, tricuspid stenosis: right-sided
33
Echo findings in Aortic Regurgitation
**Severe** Jet width \>65% of outflow tract Regurgitant jet volume Premature closure of mitral valve
34
Management of Aortic Regurgitation
**MDT:** GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse Optimise cardiovascular risk factors: Atorvastatin, anti-platelet, anti-HTN, DM **Specific** **Reduce afterload:** ACE-inhibitor, or b-blockers (carvedilol) OR diuretics **Surgical: valve replacement (before LV dilatation)** Indications: NYHA \>2, LV dysfunction Pulse pressure \>100mmHg ECG changes: T invesion in lateral leads LV enlargement on CXR or EF \<50%
35
Signs of Mitral Stenosis on Examination
Peripheral inspection: middle-aged female, wafarin bracelet, malar flush **Pulse**: Atrial fibrillation **Precordium** Left parasternal heave: Right ventricular hypertrophy secondary to pulmonary hypertension Apex: Tapping (palpable S1), non-displaced **HS:** Loud S1, +/- Loud S2 if Pulmonary hypertension **Murmur** **Rumbling mid-diastolic murmur** Loudest at the apex, left lateral position, with the bell, radiating to axilla +/- **Graham Steell** (early diastolic) murmur due to pulmonary regurgitation secondary to pulmonary hypertension **Clinical Signs of Severe Mitral Stenosis** Malar flush Long murmur LVF **Significant Negatives:** infective endocarditis, indicators of seveirty, evidence of pulmonary hypertension (raised JVP with large v waves, left parasternal heave, loud P2)
36
Causes of Mitral Stenosis
Rheumatic heart disease Other rarer causes: prosthetic valve, congenital
37
Echo features of Severe Mitral Stenosis
Valve orifice \<1cm2 Pressure gradient \>10mmHg Pulmonary artery systolic pressure \>50mmHg (pulmonary hypertension)
38
Management of Mitral Stenosis
**MDT:** GP, cardiologist, cardiothoracic surgeon, dietician, specialist nurse **Optimise cardiovascular risk factors:** Atorvastatin, anti-platelet, anti-HTN, DM **Specific** **AF:** Rate control with b-blockers, anti-coagulate Diuretics for symptomatic relief **Surgical** Indicated in mod-severe mitral stenosis Percutaneous balloon valvuloplasty CI: atrial mural thrombus Valve replacement
39
Pathophysiology of Rheumatic Fever
Antibiody cross-reactivity following **_Strep pyogenes_** infection Leading to a **Type II** hypersensitivity reaction (molecular mimicry) **Antibodies cross-react with myosin, muscle glycogen and smooth muscle cells** **Histology: Aschoff bodies and Anitschkow myocytes**
40
Revised Jones Criteria
**Evidence of Group A strep infection** **AND** either **2 major criteria** **OR** **1 major + 2 minor criteria**
41
``` Major Criteria (Jones) Rheumatic Fever **PASES** ```
**PASES** **P**ancarditis **A**rthritis **S**ubcutaneous nodules **E**rythema marginatum **S**ydenham's chorea
42
Minor Criteria (Jones) Rheumatic Fever
**FEPAP** **F**ever **E**SR / CRP raised **P**rolonged PR interval (not if carditis is major) **A**rthralgia (not if arthritis is major) **P**revious rheumatic fever
43
Management of Rheumatic Fever
Bed rest for 2 weeks Benpen for strep throat Naproxen for arthritis Diazepam if chorea not settling
44
Causes of recurrence of rheumatic fever
Strep throat infection again Pregnancy OCP
45
Valve disease in rheumatic heart disease
**Mitral: 70%** Aortic: 40% Tricuspid: 10% Pulmonary: 2% Regurgitation ---\> stenosis
46
Rheumatic fever prognosis
resolves within ~3 months **60% of those with carditis will have rheumatic heart disease**
47
Secondary prophylaxis against rheumatic fever
**Pen V 250mg / 12h** For at least **five years** or until age 21 years, whichever is longer. This should be for ten years for RF with carditis but no valvular disease (or well into adulthood, whichever is longer). However, with substantial valvular disease this should be continued longer. In severe valvular damage, or with valve surgery, prophylaxis should be continued for life
48
Signs of Valve Replacement on Examination
General: audible click, bruising from anti-coagulation, warfarin bracelet, anaemia **Scars** * Midline sternotomy: CABG, aortic valve replacement, mitral valve replacement * Left lateral inferior thoracotomy: mitral valve replacement, mitral valvotomy * Neck scars: central line insertion * Groin / femoral / **wrist** scars from angiography * Vein harvesting **Pulse:** **AF** suggestive of mitral replacement due to mitral stenosis Time click with pulse, occurs in time = mitral valve (systole --\> mitral closure) **Precordium** 3 artifical sounds = Starr-Edwards 1 artifical sound = tilting disc or bileaflet No sounds - biological valve Aortic replacement: **lub-click** +/- systolic flow murmur Mitral replacement: **click-dub** +/- diastolic flow murmur **Murmurs** **well-seated valves --\> flow murmurs** Aortic: systolic Mitral: diastolic **Poorly seated valves --\> regurgitation** Aortic: diastolic Mitral: systolic
49
Starr-Edwards Valve
**3 artifical sounds** **Quiter** click as valve opens **Loud** thud as valve closes **Rumbling** sound as ball rolls in cage
50
Tilting disc valve Bileaflet valve
1 artificial sound high-pitched click as valve closes
51
Complications of valve replacement
Thromboembolism: 1-2% per annum despite warfarin Anaemia: haemolysis Bleeding Infective endocarditis Failure Acute: breakage, thrombus, dehiscence Chronic: stenosis or incompetence
52
Risk Factors for Infective Endocarditis
IVDU Skin wounds Immunosuppression: Chronic Renal Failure, Diabetes Melitus
53
Organisms causing Infectiv Endocarditis
**Strep viridans (most common)** **Staph aureus (IVDU)** S.epidermidis S. bovis (needs colonoscopy for colonic neoplasm) HACEK = culture negative IE
54
Clinical Features of Infective Endocarditis
**Hands** Clubbing Splinter haemorrhages Janeway lesions Osler nodes **Cardiac** New/changing murmur Mitral regurgitation: 85% Aortic regurgitation: 55% **Other** Fever Roth spots Splenomegaly **Haematuria**
55
Duke Criteria for Infective Endocarditis
2 major OR 1 major AND **3** **minor** OR **All 5 minor**
56
Major Duke Criteria
**1) Positive blood culture** **Typical** organism in **2 separate** cultures **OR persistently +ve cultures** e.g. 3 \>12 h apart **2) Endocardial involvement** +ve echo vegetation, abscess, dehiscence OR New valvular regurgitation
57
Minor Duke Criteria (5)
1. **Predisposition**: IVDU, cardiac lesion 2. **Fever** \>38 3. **Emboli: septic i**nfarcts, splinters, janeway lesions 4. I**mmunological phenomena:** Glomerulonephritis, Osler nodes, Roth spots, RF 5. **+ve blood culture** not meeting major criteria
58
Treatment of Infective Endocarditis
**Acute severe:** Flucloxacillin OR Vancomycin IV + Gentamicin IV **Subacute:** Benpen + Gentamicin IV
59
Apex Beat Displacement
**Thrusting displaced apex beat** is caused by volume overload: an active large stroke volume ventricle eg aortic or mitral regurgitation or left to right shunts. **Sustained apex beat** is caused by pressure overload eg aortic stenosis, gross hypertension. **Tapping apex beat** - mitral stenosis. **Diffuse pulsation asynchronous with apex beat** - left ventricular aneurysm. **Double or triple impulse** may occur in hypertrophic obstructive myopathy. **Impalpable apex beat -** obesity, overinflated chest, pericardial effusion. Also consider dextrocardia.
60
Signs of Atrial Fibrillation on Exmaination
**On inspection:** Hyperthyroidism: tremor, thin, palmar erythema, sweating, eye signs Mitral stenosis: malar flush Pneumonia: bronchial breath sounds + added sounds **Pulse:** irregularly irregular **Precordium** Mitral stenosis: mid-diastolic murmur Mitral regurgitation: pan-systolic murmur Significant negatives: murmur, evidence of hyperthyroidism, LVF, bruising from warfarin
61
Causes of Atrial Fibrillation
**Common** IHD Rheumatic herat disease Thyrotoxicosis HTN **Other** Pneumonia PE Post-op Potassium: hypokalaemia Poison: alcohol Painful joints: rheumatoid arthritis
62
Differential diagnosis of irregularly irregular pulse
**AF** Remains when exercising the patient Multiple ventricular ectopics As patient exercises, pulse appears regular as there is reduced window for ectopics
63
Pulse deficit
Difference ub HR at the wrist and at the apex
64
CHA2DS2-VASc Score
Determine the necessity of anticoagulation in AF **C**ongestive heart failure/left ventricular dysfunction (heart failure with reduced ejection fraction, or people with recent decompensated heart failure requiring hospitalization, irrespective of ejection fraction) = 1 **H**ypertension (defined as a resting blood pressure greater than 140 mmHg systolic and/or greater than 90 mmHg diastolic on at least 2 occasions _or current antihypertensive pharmacologic treatment_) = 1 **A2**ge older than or equal to 75 years = 2 **D**iabetes mellitus (defined as fasting plasma glucose level of 7.0 mmol/L [126 mg/dL] or more or treatment with oral hypoglycaemic drugs and/or insulin) = 1 **S****2**troke/TIA/thromboembolism = 2 **V**ascular disease (prior myocardial infarction, peripheral arterial disease, or aortic plaque) = 1 **A**ge 65–74 years = 1 **S**ex category (female) = 1 Anticoagulation treatment = **CHA2DS2VASc score of** 2 or above, Consider offering it to men with a CHA2DS2VASc score of 1 **Weigh up with HASBLED**
65
HAS-BLED Score
Identify people at high risk of bleeding who could benefit from increased vigilance and a specific focus on correction of modifiable risk factors * Uncontrolled hypertension * Poor control of INR * Concurrent medication (for example concurrent use of aspirin or a nonsteroidal anti-inflammatory drug) * Harmful alcohol consumption **H**ypertension (uncontrolled, greater than 160 mmHg systolic) **A**bnormal liver function **/ A**bnormal renal function **S**troke (previous history, particularly lacunar) **B**leeding (bleeding history or predisposition) **L**abile international normalized ratios (INRs, therapeutic time in range less than 60%) **E**lderly (aged over 65 years) **D**rugs (antiplatelet agents or nonsteroidal anti-inflammatory drugs) **H**armful alcohol consumption
66
Management of new-onset AF
Admit if they present with severe symptoms or a serious complication of AF. * Identify and manage any underlying causes or triggers of AF. * Treat the arrhythmia : * rate-control treatment (beta-blocker or a rate-limiting calcium-channel blocker) is recommended for most people with AF * Referral for rhythm-control treatment (cardioversion) may be appropriate for people: * With new-onset AF. * Whose AF has a reversible cause (for example a chest infection). * Who have heart failure thought to be primarily caused, or worsened, by AF. * With atrial flutter and is considered suitable for an ablation strategy to restore sinus rhythm. * Rate-control or rhythm-control treatment should be considered for people with AF presenting acutely with non-life threatening haemodynamic instability, depending on the time of onset of arrhythmia. * Assess stroke risk using the CHA2DS2VASc assessment tool. * Assess risks and benefits of anticoagulation , and start treatment if appropriate. * The HAS-BLED assessment tool should be used to assess the risk of a major bleed and to identify and manage modifiable risk factors for bleeding, such as uncontrolled hypertension, harmful alcohol consumption, and concurrent use of aspirin or a nonsteroidal anti-inflammatory drug. Arrange follow up : * After starting rate-control treatments — to assess their effectiveness and tolerability. * After starting anticoagulation treatment — to assess compliance and adverse effects. Provide advice and information on AF, its treatments, and where to find support groups.
67
Management of AF
**1st Line** * Offer a rate-control treatment to most people with atrial fibrillation * Offer a beta-blocker (see Choice of beta-blocker) or a rate-limiting calcium-channel blocker (diltiazem [off-label use] or verapamil) * Consider digoxin monotherapy for people with non-paroxysmal AF only if they have a sedentary lifestyle (that is, they do little or no exercise)Follow up within 1 week of starting rate-control treatment to assess tolerance to treatment and to review symptom control, heart rate, and blood pressure. **Refer to a cardiologist for consideration of rhythm-control treatment (cardioversion), people:** * With new-onset AF. * Whose AF has a reversible cause (for example a chest infection). * Who have heart failure thought to be primarily caused, or worsened, by AF. * With atrial flutter who are considered suitable for an ablation strategy to restore sinus rhythm. * For whom a rhythm-control strategy would be more suitable based on clinical judgement. **For people with AF presenting acutely with non-life threatening haemodynamic instability, rate-control or rhythm-control treatment should be considered, depending on the time of onset of arrhythmia.** * If the onset of arrhythmia is within 48 hours, offer rate-control treatment or refer the person to an acute medical unit for consideration of immediate cardioversion (without the need for anticoagulation treatment). * If the onset of arrhythmia is more than 48 hours or uncertain, start rate-control treatment. If referral for consideration for rhythm-control treatment (cardioversion) is thought to be necessary using clinical judgement, cardioversion should be delayed until the person has been maintained on therapeutic anticoagulation for a minimum of 3 weeks. **Rhythm-control treatments used by specialists include:** * Electrical cardioversion. * Pharmacological cardioversion with antiarrhythmic drugs (such as amiodarone or sotalol). * For people having cardioversion for atrial fibrillation (AF) that has persisted for longer than 48 hours, electrical (rather than pharmacological) cardioversion is used
68
Contrainidcations to Warfarin
Coagulopathues Compliance issues Risk of falls PUD Pregnancy Patient choice
69
Signs of Pacemaker on Examination
**Inspection:** groin scars from insertion, Medic alert bracelet **Pulse:** AF **Precordium** Left infraclavicular incisional scar Palpable pacemaker: if large ? defibrillator Murmur ?aortic stenosis **Significant negatives**: AF, LVF, valvuar pathology, complications of pacemaker (infection or erosions)
70
Signs of pacemaker on ECG
**Pacing spikes** Physiological ECG trace does not include vertical signals Evidence of ischaemia
71
Permanent pacemaker indications
Complete AV block Mobitz type II Symptomatic bradycardia e.g. sick sinus syndrome Drug-resistant tacharrhythmias **Biventricular pacing in chronic heart failure**
72
Letters of pacemaker
1st: chamber paced (A, V, or D) 2nd: chamber sensed (A, V, or D) 3rd: Response (**I**nhibited, **T**riggered, **D**ual)
73
Number of Pacemaker Leads
**Single lead:** one lead senses and responds e.g. VVI **Dual lead**: sense and respond in either chamber **Biventricular**: leads to both ventricles +/- right atrium Used for cardiac resynchronisation therapy in HF
74
Dual lead pacemaker One lead in rigth atrium One in right ventricle
75
Single lead pacemaker
76
**Biventricular pacemaker** Right atrium and right venbtricle lead inserted intravenously Left ventricle lead was placed epicardially via mini-sternotomy and tunneled up to the prepectoral pocket
77
Implantable defibrillator
Can be incorporated into any pacemaker
78
Complications of a Pacemaker
**Insertion** Bleeding Arrhythmia **Post-insertion** Erosion Lead migration Pocket infection Malfunction
79
Definition of Chronic Heart Failure
**Cardiac output is inadequate** for the body's requirments **despite adequate filling pressures**
80
Caues of Left-sided heart failure
Ischaemic heart disease Idiopathic dilatated cardiomyopathy Systemic hypertension Mitral and aortic valve disease
81
Signs and Symptoms of Left-Sided Heart Failure
**Signs** Cold peipheries +/- cyanosis AF Cardiomegaly with displaced apex beat S3 + tachycardia = gallop rhythm Wheeze (cardiac asthma) **Bibasal crepitations** **Symptoms** Fatigue Exertional dyspnoea Orthopnoea and paroxysmal nocturnal dyspnoea Nocturnal cough (+forthy pink sputum) Weight loss and muscle wasting
82
Causes of Right-Sided Heart Failure
Left ventricular failure Cor pulmonale Tricuspid and pulmonary valve disease
83
Signs and Symptoms of Right-Sided Heart Failure
**Signs** **Increased JVP +** jugular venous distension Tender smooth hepatomegaly (may be pulsatile) Pitting oedema Ascites **Symptoms** Anorexia Nausea
84
New York Classification of Heart Failure
**I:** nil shortness of breath **II:**comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea **III:** marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms **IV:** Shortness of breath at rest
85
NT-proBNP
**Secreted from ventricles in response to stretch and increased HR** Increased levels are sensitive marker of HF If low, revise diagnosis
86
CXR changes in heart failure
**A**lveolar shadowing Kerley **B** lines **C**ardiomegaly Upper lobe **D**iversion **E**ffusions **F**luid in the fissures
87
ECG findings in chronic heart failure
Ischaemia Hypertrophy AF / arrhythmias
88
Echo findinds in CHF
Focal / global hypokinesia Hypertrophy Valve lesions Ejection fraction reduced (normally 60%) Can be normal HF PEF
89
Management of CHF
MDT: Gp, cardiologist, physio, dietician, specialist nurse Optimise CVS risk factors: statins, Anti-HTN, DM, anti-platelet **Specific** 1st-line treatment for all patients is both an **ACE-inhibitor** and a **beta-blocker** 2nd- line treatment is now either an **aldosterone antagonist, angiotensin II receptor blocker** or a **hydralazine** in combination with a nitrate 3rd -line: If symptoms persist **cardiac resynchronisation therapy** or **digoxin\*** should be considered. A n alternative supported by NICE in 2012 is ivabradine. The criteria for ivabradine include that the patient is already on suitable therapy (ACE-inhibitor, beta-blocker + aldosterone antagonist), has a heart rate \> 75/min and a left ventricular fraction \< 35% **Adjuncts** diuretics should be given for fluid overload offer annual influenza vaccine offer one-off\*\* pneumococcal vaccine
90
Trials for Heart Failure Drugs
ACE inhibitors (SAVE, SOLVD, CONSENSUS) spironolactone (RALES) beta-blockers (CIBIS) hydralazine with nitrates (VHEFT-1)
91