Cardiology JC009: Shortness Of Breath On Exertion: Heart Failure Flashcards
Shortness of Breath (氣促, 呼吸急促, 氣喘, 抖唔到氣)
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
Heart failure
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%
Concept of Heart failure
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
***Clinical features of HF
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
Frank Starling Law for Heart Failure
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)
Pulmonary congestion
↑ 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%
Diagnosis of Heart failure
Clinical diagnosis
- ***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)
- ***Boston criteria for HF
- Definite HF: total score >7
- Possible HF: total score 5-7
- Unlikely HF: total score <5
Killips classification
- 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
LA pressure correlated with pathological findings
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
Biomarkers for HF
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
***Diagnostic flowchart for HF
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
History taking of HF
- Established CVD
- CAD
- PVD
- Stroke - Risk factors for CVS
- HT
- Smoking
- DM
- Obesity
- Dyslipidaemia - Exposure to cardiotoxic agents
- Chemotherapy
- RT
- Alcohol
- Substance abuse - Valvular diseases
- Rheumatic fever
- CT diseases - Systemic disorders
- Thyroid
- Myopathy
- STD
- Phaeochromocytoma - Family history
- CMP
- Sudden death
- Myopathy
- Arrhythmia
- Premature CVD
***Investigations for HF
- CBC
- Serum K, Ca, PO4, Creatinine, Urea, fasting glucose
- Urine
- Protein
- Blood
- Glucose
- Microscopic urinalysis - ECG
- LVH
- Arrhythmia - TFT
- TSH - CXR
- BNP / Pro-BNP
- Echocardiography
Staging of Heart failure
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
***Causes of Heart failure
Everything! Final common path of all cardiac diseases
- Myocardial disease
- Loss of contractile force (Systolic)
- Impaired relaxation (Diastolic) - Heart rhythm disorders
- Bradycardia
- Tachycardia
- Loss of AV synchronicity
- Loss of VV synchronicity - Systemic pressure overload
- Hypertension - Pulmonary pressure overload
- Pulmonary HT - Valvular disease (Pressure / Volume overload)
- MS / MR
- AS / AR - Congenital anomalies (Pressure / Volume overload)
- ASD / VSD / PDA
- HOCM - 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)
Myocardial causes of HF
- IHD
- Cardiomyopathy
- HCM
- DCM
- RCM - Cardiotoxic substance
- Substance abuse
- Heavy metals
- Anthracyclines
- Radiation damage - Infectious disease
- Myocarditis: Viral / Bacterial / Rickettsial infections - Autoimmune disease
- RA
- SLE
- Polymyositis - Infiltrative disease
- Sarcoidosis
- Amyloidosis
- Haemochromatosis - Metabolic / Enzyme abnormality
- DM
- Hunter syndrome - Endocrine disorder
- Hyperthyroidism
- Cushing disease
- Phaeochromocytoma
HFpEF vs HFrEF
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
Management considerations of HF
- Acute?
- Severity
- Precipitating causes
- Haemodynamic subtype
- Treatment options
Acute HF
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
Haemodynamic assessment of ADHF (Acute decompensated HF)
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)
***Management of Acute HF
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
Patient monitoring in Acute HF
- Weight
- determine after voiding in morning - Fluid intake + output
- Vital
- Orthostatic BP
- O2 saturation - Signs
- Edema, Ascites, Pulmonary crackles, Hepatomegaly, JVP, Hepatojugular reflux, Liver tenderness - Symptoms
- Orthopnea, PND, cough, nocturnal cough, dyspnea, fatigue, lightheadedness - Electrolytes
- K, Na - RFT
- BUN, serum creatinine
Chronic HF
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
Management of Chronic HF
***Treat underlying cause
- Whip the horse (Inotropes) —> CI to be used now (∵ die much faster)
- Unload the wagon (ACEI, ARB, Mineralocorticoid receptor antagonist) —> ↓ preload + afterload —> ↓ workload of heart
- Slow the horse (β-blockers, Ivabradine) (—> ↓ preload) —> ↓ workload of heart
- Get a new horse (Heart transplant)
- Get a tractor (LVAD, ICD)
- 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
