Cardiology JC009: Shortness Of Breath On Exertion: Heart Failure Flashcards

1
Q

Shortness of Breath (氣促, 呼吸急促, 氣喘, 抖唔到氣)

A

SOB:
- a ***Very sensitive symptom indicating interruption of following bodily function (Sensitivity for SOB on exertion: 66%):
1. Bring O2 into body
2. Remove CO2 from body
3. Deliver O2 to tissues
4. Maintain bodily pH
5. Psychological

  • But ***NOT specific for individual disease processes for SOB
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2
Q

Heart failure

A

Heart function:
- Pump blood at a rate (CO) commensurate with requirements of metabolising tissues

Heart failure:
- a Clinical state (not a disease)
- causes:
—> **
Hypoperfusion (
forward failure): unable to pump blood at a rate (CO) commensurate with requirements of metabolising tissues despite **adequate filling pressure (less common)
OR
—> Congestion (backward failure): can do so only from an ***elevated filling pressure (more common)

Epidemiology:
- Incidence ↑ exponentially after 65 yo (Transitional zone from healthy to sick)
- 1 year mortality: 14%
- 5 year mortality: 50%

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3
Q

Concept of Heart failure

A

Normal CO: 70 ml/kg/min
Body weight: 70 kg
—> CO: 4.9 L/min (~5 L/min)

Normal heart, Normal pumping function:
- Preload: 5 L/min
- CO: 5 L/min

Congestive HF (Backward failure), Reduced pumping function:
- Preload: 8 L/min
- CO: 5 L/min
—> i.e. require higher filling pressure for same CO
—> ↑ Right heart pressure: ↑ JVP
—> ↑ Left heart pressure: Loud P2 (Pulmonary hypertension), Basal crackles

Hypoperfusion / Cardiogenic shock (Forward failure), Reduced pumping function:
- Preload: 8 L/min
- CO: 3 L/min
—> i.e. no matter how much preload still cannot maintain CO
—> Low BP, Hypoperfusion, Syncope, Cardiogenic shock

Left heart forward failure (Less common):
- Syncope, Cardiogenic shock

Left heart backward failure (More common):
- Pulmonary congestion, SOB

Right heart forward failure (Less common):
- Syncope, Cardiogenic shock

Right heart backward failure (More common):
- Peripheral congestion, Liver congestion, Ascites, Pleural effusion

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4
Q

***Clinical features of HF

A

Low output symptoms (Forward HF):
Symptoms:
- Dizziness (Pre-syncope) (∵ cerebral hypoperfusion)
- Disturbance of consciousness (∵ cerebral hypoperfusion)
- Memory disorder (∵ cerebral hypoperfusion)
- Restlessness (∵ high sympathetic tone due to low perfusion pressure)

Signs:
- Cyanosis
- Hypotension
- Cold sweat (∵ sympathetic overactivity)
- Cold extremities (∵ sympathetic overactivity)
- Oliguria (∵ ↓ renal perfusion)
- Agitation
- Confusion

Congestive symptoms (Backward HF):
Right heart failure
Symptoms:
- Ankle swelling (esp. evening)
- Abdominal distension
- RUQ abdominal pain (∵ liver congestion)
- Anorexia (∵ GI edema)

Signs:
- ↑ JVP
- Hepatojugular reflux
- Bilateral pitting ankle edema
- Hepatomegaly
- ↑ Hepatobiliary enzymes
- Pleural effusion

Left heart failure
Symptoms:
- SOB on exertion (∵ lung congestion)
- Nocturnal cough (maybe features of Orthopnea / PND)
- Pinky frothy sputum
- Orthopnea (端坐呼吸) / PND (陣發性夜間呼吸困難)
- Palpitation

Signs:
- Tachycardia
- Lung crackles
- S3 / S4
- Cardiomegaly

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5
Q

Frank Starling Law for Heart Failure

A

Normal heart:
- ↑ Preload (VR) —> Stretch out Actin / Myosin —> ↑ Overlapping —> Greater contractile force —> ↑ SV
- If past optimal point —> too stretched out beyond maximal overlapping between Actin / Myosin —> ↓ SV, blood stays in Ventricle

Heart failure:
- Much flatter curve —> require a **higher Preload to maintain **same SV (Compensated HF)
- Past optimal point —> ↓ SV, blood stays in Ventricle (Decompensated HF)

Prior to Optimal point:
- ↑ VR —> ↑ SV

After Optimal point:
- ↑ VR —> ↓ SV
—> ↑ LV End-diastolic volume
—> ↑ LV End-diastolic pressure
—> ↑ LA pressure
—> ↑ Pulmonary venous pressure
—> Pulmonary congestion

Effects of Postural change on Preload (Orthopnea / PND):
- Standing: Gravitational venous blood pooling to lower limbs (300-600 ml)
- Lying down: Loss of gravitational pooling —> ↑ 300-600 ml VR to heart —> if heart already near optimal point (∵ 一直at a high preload to maintain low SV) —> cannot accommodate sudden ↑ in blood volume —> SOB
- Sitting back up: Partial restoration of gravitational pooling —> ↓ VR to heart —> resolving SOB

Orthopnea vs PND:
- Orthopnea: VR from lower limb vein
- PND: VR from interstitium (take much longer from interstitium back to circulation)

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6
Q

Pulmonary congestion

A

↑ Pulmonary venous pressure
—> ↑ Hydrostatic pressure in pulmonary circulation

Normal setting:
- Pulmonary capillary hydrostatic pressure (i.e. LA pressure): ~7 mmHg
- Plasma oncotic pressure (e.g. Albumin, Globulin): ~28 mmHg
—> Osmotic tendency to ***dehydrate interstitium + alveoli

Left heart failure:
- Pulmonary capillary hydrostatic pressure: ~25-30 mmHg
- Plasma oncotic pressure: ~28 mmHg
—> ↑ LVEDP —> ↑ Hydrostatic pressure to ***force fluid into interstitium + alveoli

Specificity for Left heart failure:
- Orthopnea: 81%
- PND: 76%
- Tachycardia: 99%
- Basal crackles: 91%

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7
Q

Diagnosis of Heart failure

A

Clinical diagnosis

  1. ***Framingham criteria for Heart failure
    Major criteria:
    - PND
    - ↑ JVP
    - Basal crackles
    - Cardiomegaly on X-ray
    - Acute pulmonary edema
    - S3 gallop (Protodiastolic gallop)
    - ↑ CVP (>=16 cm H2O)
    - ↑ Circulation time (>=25 sec)
    - Hepatojugular reflux
    (- Pulmonary edema, visceral congestion of Cardiomegaly on autopsy)

Major or Minor criteria:
- Weight loss of >=4.5 kg in 5 days in response to treatment
—> when weight loss attributable to treatment of HF —> considered major criteria (otherwise considered minor criteria)

Minor criteria:
- Lower limb edema
- Nocturnal cough
- Dyspnea on ordinary exertion
- Hepatomegaly
- Pleural effusion
- ↓ in vital capacity by 1/3 from maximum recorded
- Tachycardia (HR >=120 bpm)

  1. ***Boston criteria for HF
    - Definite HF: total score >7
    - Possible HF: total score 5-7
    - Unlikely HF: total score <5
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8
Q

Killips classification

A
  • To stratify severity of LV dysfunction
  • To determine clinical status of post MI patients

Class 1: No crackles, No S3
Class 2: Crackles <50% lung field / Presence of S3
Class 3: Crackles >50% lung field (i.e. Pulmonary edema)
Class 4: Cardiogenic shock

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9
Q

LA pressure correlated with pathological findings

A

CXR findings to estimate LA pressure:
- Normal: 5-10 mmHg

  • Upper lobe diversion: 10-15 mmHg
    —> Pulmonary venous HT
    —> Engorgement of upper pulmonary veins / Cephalisation (radiopaedia: upper lobe veins are of same / larger diameter than lower lobe veins when measured equidistant from hilar point)
    —> proposed mechanism: hydrostatic pressure >10 mmHg —> fluid leaks into interstitium, compressing lower lobe vessels due to gravity? —> recruiting upper vessels OR hypoxia leading to vasoconstriction in lower vessels
  • Kerley B lines: 15-20 mmHg
    —> Short, white lines perpendicular to pleural surface at lung base
    —> indicate interstitial edema but not in alveoli: SpO2 still normal but take harder for alveoli to expand
  • Peri-bronchial cuffing: 15-20 mmHg
    —> indicate interstitial edema
    —> same septal lines as Kerley B but just around bronchi
    —> fluid accumulate around bronchi causing thickening of wall
    —> fluid-thickened bronchial walls that visible producing “doughnut-like” densities in the lung parenchyma
  • Pulmonary alveolar edema (Batwing, start to see O2 desaturation): >25 mmHg
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10
Q

Biomarkers for HF

A

Brain natriuretic peptide (BNP) + NT-proBNP (N-terminal portion of BNP)

Causes of ↑ BNP:
Cardiac:
- HF, RV syndromes
- ACS
- Heart muscle disease (including LVH)
- Valvular heart disease
- Pericardial disease
- AF
- Myocarditis
- Cardiac surgery
- Cardioversion

Non-cardiac:
- Advancing age
- Anaemia
- Renal failure
- Pulmonary causes: OSA, Severe pneumonia, Pulmonary HT
- Critical illness
- Bacterial sepsis
- Severe burns
- Toxic-metabolic insults, including cancer chemotherapy + envenomation

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11
Q

***Diagnostic flowchart for HF

A

SOB on exertion (SOBOE)
—> DDx (Cardiac, Respiratory, Systemic (anaemia, hyperthyroidism, CKD, acidosis, deconditioning), Psychological)
—> History, P/E, Investigations
—> HF
—> Staging of HF
—> Cause of HF
—> Treatment of HF
—> 1. Drug treatment + 2. Device therapy + 3. Surgical therapy

Device therapy:
- Pacemaker
- Cardiac resynchronisation therapy (CRT)
- ICD

Surgical therapy:
- Revascularisation
- Valvular intervention
- LVAD (left ventricular assist device)
- Cardiac transplant

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12
Q

History taking of HF

A
  1. Established CVD
    - CAD
    - PVD
    - Stroke
  2. Risk factors for CVS
    - HT
    - Smoking
    - DM
    - Obesity
    - Dyslipidaemia
  3. Exposure to cardiotoxic agents
    - Chemotherapy
    - RT
    - Alcohol
    - Substance abuse
  4. Valvular diseases
    - Rheumatic fever
    - CT diseases
  5. Systemic disorders
    - Thyroid
    - Myopathy
    - STD
    - Phaeochromocytoma
  6. Family history
    - CMP
    - Sudden death
    - Myopathy
    - Arrhythmia
    - Premature CVD
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13
Q

***Investigations for HF

A
  1. CBC
  2. Serum K, Ca, PO4, Creatinine, Urea, fasting glucose
  3. Urine
    - Protein
    - Blood
    - Glucose
    - Microscopic urinalysis
  4. ECG
    - LVH
    - Arrhythmia
  5. TFT
    - TSH
  6. CXR
  7. BNP / Pro-BNP
  8. Echocardiography
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14
Q

Staging of Heart failure

A

New York Heart Association functional classification:
Class 1:
- ***No limitations
- Ordinary physical activity NOT cause fatigue, dyspnea, palpitation (Asymptomatic LV dysfunction)

Class 2:
- ***Slight limitation of physical activity
- Comfortable at rest
- Ordinary physical activity results in fatigue, palpitation, dyspnea, angina pectoris (Symptomatically “mild” heart failure)

Class 3:
- ***Marked limitation of physical activity
- Less than ordinary physical activity will lead to symptoms (Symptomatically “moderate” heart failure)

Class 4:
- Symptoms of congestive heart failure are present, even ***at rest
- With any physical activity, increased discomfort is experienced (Symptomatically “severe” heart failure)

American College of Cardiology Foundation (ACCF) / American Heart Association (AHA) stages of HF:
Stage A:
- At high risk for HF but ***without structural heart disease / symptoms of HF (e.g. HT, DM, CAD, Family history of CMP)

Stage B;
- **Structural heart disease but **without signs / symptoms of HF (e.g. previous MI, LV systolic dysfunction, LVH, asymptomatic valvular disease)

Stage C:
- Structural heart disease ***with prior / current symptoms of HF

Stage D:
- Refractory HF requiring specialised treatment

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15
Q

***Causes of Heart failure

A

Everything! Final common path of all cardiac diseases

  1. Myocardial disease
    - Loss of contractile force (Systolic)
    - Impaired relaxation (Diastolic)
  2. Heart rhythm disorders
    - Bradycardia
    - Tachycardia
    - Loss of AV synchronicity
    - Loss of VV synchronicity
  3. Systemic pressure overload
    - Hypertension
  4. Pulmonary pressure overload
    - Pulmonary HT
  5. Valvular disease (Pressure / Volume overload)
    - MS / MR
    - AS / AR
  6. Congenital anomalies (Pressure / Volume overload)
    - ASD / VSD / PDA
    - HOCM
  7. Pericardial disease (Constrictive filling)
    - Constrictive pericarditis
    - Pericardial effusion

How to investigate:
- Echocardiogram
—> for Myocardial disease: HF with preserved EF (HFpEF) (LV stiffer —> cannot accommodate ↑ preload —> congestive symptoms) / HF with reduced EF (HFrEF) (pumping function / contractile force jeopardised)

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16
Q

Myocardial causes of HF

A
  1. IHD
  2. Cardiomyopathy
    - HCM
    - DCM
    - RCM
  3. Cardiotoxic substance
    - Substance abuse
    - Heavy metals
    - Anthracyclines
    - Radiation damage
  4. Infectious disease
    - Myocarditis: Viral / Bacterial / Rickettsial infections
  5. Autoimmune disease
    - RA
    - SLE
    - Polymyositis
  6. Infiltrative disease
    - Sarcoidosis
    - Amyloidosis
    - Haemochromatosis
  7. Metabolic / Enzyme abnormality
    - DM
    - Hunter syndrome
  8. Endocrine disorder
    - Hyperthyroidism
    - Cushing disease
    - Phaeochromocytoma
17
Q

HFpEF vs HFrEF

A

HFpEF:
- >=50%
- **Diastolic HF
- frequently female, elderly
- normal LV size, often LVH, ECG showing LVH
- CXR: Congested with NO Cardiomegaly
- S4
- Comorbidities: **
HT, Obesity, DM
- NO efficacious therapy

HFrEF:
- <=40%
- **Systolic HF
- more often male, 50-70
- LV dilated
- CXR: Congested with Cardiomegaly
- S3
- Comorbidities: **
Old MI
- Effacious therapy demonstrated / available

18
Q

Management considerations of HF

A
  1. Acute?
  2. Severity
  3. Precipitating causes
  4. Haemodynamic subtype
  5. Treatment options
19
Q

Acute HF

A

Diagnosis: Clinical (based on S/S)
- determination of BNP / NT-proBNP concentration if diagnosis uncertain

Treatment aim:
1. **Improve symptoms (esp. congestion + low output symptoms)
2. **
Restore normal oxygenation
3. ***Optimise volume status
- identity etiology
—> Haemodynamic assessment of ADHF: Congestive / Hypoperfusion

  • identify + address precipitating factors
    —> ***CHAMP (ACS, Hypertension emergency, Arrhythmia, Mechanical causes (e.g. aortic lesion, papillary rupture causing MR), Pulmonary embolism)
    —> Systemic causes: Anaemia, Endocrine (thyroid, phaeochromocytoma), Adverse drug effects
  • optimise chronic oral therapy
  • minimise SE
  • identify patients who might benefit from revascularisation / device therapy
  • identify risk of thromboembolism + need for anticoagulant therapy
20
Q

Haemodynamic assessment of ADHF (Acute decompensated HF)

A

Warm vs Cold + Dry vs Wet
- Warm + Dry: High perfusion + Low congestion
- Warm + Wet: High perfusion + High congestion
- Cold + Dry: Low perfusion + Low congestion
- Cold + Wet: Low perfusion + High congestion

Cold: Vasodilator (↓ afterload) + Inotropes
Wet: Diuretics (↓ preload)

21
Q

***Management of Acute HF

A

General measures (↓ preload)
1. Complete bed rest
2. Oxygen
3. Low salt diet
4. Fluid restriction

Medications (if BP stable)
1. IV Furosemide (↓ preload + afterload)
2. IV Nitrate (↓ preload (∵ venous dilatation))
3. Morphine (↓ preload (histamine release) + afterload (anxiolytic —>↓ sympathetic activity))

Inotropic agents (if BP unstable)
1. Dopamine
2. Dobutamine

—> BP not stabilised / refractory APO
1. Intra-aortic balloon pump
2. ECMO

—> Ventilatory support (if desaturation / exhaustion / cardiogenic shock) (↓ preload + afterload)
1. Non-invasive CPAP
2. Intubation, mechanical ventilation

22
Q

Patient monitoring in Acute HF

A
  1. Weight
    - determine after voiding in morning
  2. Fluid intake + output
  3. Vital
    - Orthostatic BP
    - O2 saturation
  4. Signs
    - Edema, Ascites, Pulmonary crackles, Hepatomegaly, JVP, Hepatojugular reflux, Liver tenderness
  5. Symptoms
    - Orthopnea, PND, cough, nocturnal cough, dyspnea, fatigue, lightheadedness
  6. Electrolytes
    - K, Na
  7. RFT
    - BUN, serum creatinine
23
Q

Chronic HF

A

Treatment aim:
1. **Relieve symptoms
2. **
Improve exercise capacity + QoL
3. Prevent + Treat complication (↓ morbidity)
4. Prevent / Modify disease progression
5. Improve prognosis (↓ mortality)

Vicious cycle of HF:
LV dysfunction
—> ↓ CO + ↓ BP
—> Frank-Starling mechanism, Remodeling, Neurohormonal activation
—> ↑ CO (via ↑ contractility + HR) + ↑ BP (via vasoconstriction, ↑ blood volume)
—> ↑ Cardiac workload (↑ preload + afterload)
—> LV dysfunction

Details:
↓ CO
—> SNS activation (↑ HR, vasoconstriction to maintain perfusion) + RAAS activation (vasoconstriction, salt + H2O retention) + Vasopressor system activation (H2O retention)
—> ↑ preload + afterload
—> Improve perfusion / maintain BP (good in short run)
—> chronic ↑ preload + afterload (bad in long run)
—> maladaptation of heart
—> congestion

Natriuretic peptide system (ANP + BNP from cardiomyocytes)
- Compensatory mechanism to protect heart
—> vasodilation
—> ↓ BP
—> ↓ sympathetic tone
—> natriuresis, diuresis
—> ↓ ADH
—> ↓ aldosterone
—> ↓ fibrosis
—> ↓ hypertrophy

24
Q

Management of Chronic HF

A

***Treat underlying cause

  1. Whip the horse (Inotropes) —> CI to be used now (∵ die much faster)
  2. Unload the wagon (ACEI, ARB, Mineralocorticoid receptor antagonist) —> ↓ preload + afterload —> ↓ workload of heart
  3. Slow the horse (β-blockers, Ivabradine) (—> ↓ preload) —> ↓ workload of heart
  4. Get a new horse (Heart transplant)
  5. Get a tractor (LVAD, ICD)
  6. Heal the horse (Regenerative medicine?)

Drugs:
1. ACEI / ARB
2. β-blockers / Ivabradine
3. Mineralocorticoid receptor antagonists (Spironolactone)
4. Others
- ARNi (angiotensin receptor neprilysin inhibitor) (Entresto)
- CRT (Cardiac resynchronization therapy)
- Empagliflozin, Dapagliflozin
- Nitrates, Hydralazine

25
Q
  1. ACEI / ARB
A

ACEI:
- blocks conversion of angiotensin 1 to angiotensin 2 —> prevent functional deterioration
—> Vasodilation —> ↓ afterload
—> ↓ Aldosterone —> ↓ preload + afterload
- recommended for all HFrEF patients
- relieves symptoms, improves exercise tolerance, ↓ risk of death, ↓ disease progression

ARB (Valsartan, Candesartan, Losartan):
- block AT1 receptors, which binds to circulating angiotensin 2
- should not be considered equivalent / superior to ACEI
- for ACEI intolerant patients due to cough / angioedema
- should ***NOT be considered equivalent to ACEI

26
Q
  1. β-blockers
A
  • Carvedilol, Bisoprolol, Metoprolol
  • ***Cardioprotective effects due to blockade of excessive SNS stimulation

Short term:
- ↓ Myocardial contractility
- ↑ EF after 1-3 months of use

Start with low dose —> cautiously ↑ dose during initial titration

Long term:
- ***Symptomatic improvement

27
Q

Ivabradine

A

Funny channel blocker to ↓ SA node firing frequency (phase 4 depolarisation) to ↓ HR
- no significant BP effect
- ↓ hospitalisation (but not mortality)
- mostly for patients intolerant to β-blockers (
consider β-blockers first ∵ survival benefit)

Indication:
- NYHA 2-4
- Ischaemic / Non-ischaemic etiology, LVEF <=35%
- Sinus rhythm + HR >=70
- Documented hospitalisation for worsening HF <=12 months

28
Q
  1. Mineralocorticoid receptor antagonists (MRA)
A
  • Generally well-tolerated

Spironolactone:
- ↓ HF-related morbidity + mortality in patients with NYHA class 3-4
- SE: HyperK, gynaecomastia
- Monitor K, Creatinine

Eplerenone:
- ↓ mortality in MI + HF patients
- less hormonal SE

29
Q

ARNi (angiotensin receptor neprilysin inhibitor)

A

Entresto

Benefit based on BNP pathway
—> vasodilation
—> ↓ BP
—> ↓ sympathetic tone
—> natriuresis, diuresis
—> ↓ ADH
—> ↓ aldosterone
—> ↓ fibrosis
—> ↓ hypertrophy

30
Q

Empagliflozin, Dapagliflozin

A

SGLT2 inhibitor

Observed unintended benefit for HF patient to ↓ mortality

31
Q

Nitrates, Hydralazine

A

Nitrates:
- Venous vasodilation —> ↓ preload
- Coronary vasodilation —> ↑ myocardial perfusion

Hydralazine:
- Arterial vasodilation —> ↓ afterload

Both used together:
—> act just like ACEI / ARB
- ↓ Pulmonary congestion
- ↓ Ventricular size
- ↓ Ventricular wall stress
- ↓ MVO2 (Myocardial Volume Oxygen (consumption))

Indications:
- Patient cannot tolerate ACEI / ARB (e.g. renal failure)
- In combination with ACEI / ARB?

Benefit:
- ↓ Mortality before era of ACEI / ARB

32
Q

Treatment of HFpEF / Diastolic HF

A
  • Limited data, unsatisfactory
  • Treat underlying cause e.g. ***BP control, therapy for CAD
  • Treat ***precipitating factors e.g. AF, DM
  • Symptoms relieve: cautious use of Diuretic
  • Slowing of HR to ↑ time for diastolic filling: β-blockers, Verapamil, Diltiazem
  • Regression of LVH: BP control, ?ACEI, ARB
  • ↓ hospitalisation + mortality: ARB
33
Q

Non-pharmacological treatment of HF

A
  1. CABG / PCI
    - for ischaemic cardiomyopathy
  2. Cardiac resynchronisation therapy (CRT)
  3. ICD
    - secondary prevention of VT / VF
    - primary prevention in patients with low LVEF, CAD +/- inducible VT on electrophysiology study
  4. Cardiac transplantation / LVAD
    - for Refractory HF
34
Q

Cardiac resynchronisation therapy (CRT)

A

Biventricular pacing
—> resynchronise contraction of Lateral wall + Septum

Should be considered for all patients with all of following:
- NYHA 3 despite optimal medical therapy
- Sinus rhythm
- ***Widened QRS (>=120ms) (esp. LBBB)
- LVEF <=35% + LVD >5.5cm

35
Q

Prophylactic ICD placement (Primary prevention)

A

HF patients not only have pumping problem but also ***rhythm problem (VT, VF) —> sudden cardiac death

ICD:
- should be considered in patients with NYHA 2-3 (LVEF <=30%)
- may be considered in those with NYHA 2-3 (LVEF 31-35%)

36
Q

CXR findings of Chamber dilatation (Davidson)

A

LA dilatation:
- Straight left heart border (∵ prominence of LA appendage)
- Double cardiac shadow to right of sternum
- Widening of carina angle (∵ left main bronchus pushed upwards by enlarged LA)

RA dilatation:
- Projects from right heart border towards right lower lung field

LV dilatation:
- Prominence of left heart border
- Enlargement of cardiac silhouette

LV hypertrophy:
- Rounding of left heart border

RV dilatation:
- Increase heart size
- Displace apex upwards
- Straighten left heart border