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- 1. APPROACH TO HEART FAILURE IN INTENSIVE CARE UNIT PART-1 Dr ASHISH NAIR MBBS,MD ANAESTHESIA, IDCCM, DrNB CRITICAL CARE(SR)
- 2. Statistics Leading cause of hospitalization The incidence: 1 in 1000 population per year; increasing by about 10% every year. In >85y incidence is 10 cases per 1000. The prevalence ranges from 3-20 cases per 1000 population Overall prevalence- developed country-2% Prevalence in Age> 65yrs – 6-10% The male to female ratio is about 2:1. The median age of presentation is 76 years. The prevalence of heart failure is increasing because of the improved treatment of coronary heart disease Developed country – risk of HF by 49yrs of age ONE IN FIVE
- 3. Morbidity/Mortality Approximately 30-40% of patients with CHF are hospitalized each year. 50% of patients with heart failure over a 4-year period will die of the disease 287,000 people die annually of heart failure 40% of patient’s admitted to the hospital die or are readmitted within 1 year • The 5 year mortality after Dx was reported as 60% in men and 45% in women • Median survival of 3.2 years for men, and 5.4 years for women, post diagnosis. • The most common cause of death is progressive heart failure, but sudden death may account for up to 45% of all deaths. • Patients with coexisting IDDM have a significantly higher mortality rate.
- 4. Definition Persistent NYHA functional class IIIB or IV symptoms that limit daily activities and occur despite adequate pharmacologic treatment and is usually associated with a left ventricular ejection fracture below 30% The heart’s inability to pump enough blood to meet the body’s oxygen and nutrient demands
- 5. ESC guidelines (2016) HFREf vs HFmrEf vs HFpEf based on ejection fraction + symptoms & signs(Framingham criteria)
- 8. Types Systolic (pumping problem)—inability of the heart to contract to provide enough blood flow forward Diastolic (filling problem)—inability of the left ventricle to relax normally, resulting in fluid back up into the lungs Left-sided—inability of the left ventricle to pump enough blood, causing fluid back up into the lungs Right-sided—inefficient pumping of the right side of the heart, causing fluid buildup in the abdomen, legs, and feet
- 9. 2
- 10. The BERNHEIM EFFECT occurs when left heart failure and left ventricular hypertrophy causes the interventricular septum to bulge towards the right ventricle causing right heart failure that sometimes precedes left heart failure. This classically occurs in aortic valve stenosis. The REVERSE BERNHEIM EFFECT occurs when there is right ventricular pressure and volume overload that results in the interventricular septum bulging toward the left ventricle causing left ventricular diastolic impairment.
- 11. Acute vs. Chronic Acute—an emergency situation in which a patient was completely asymptomatic before the onset of heart failure; seen in acute heart injury such as MI Chronic—long-term syndrome in which a patient exhibits symptoms over a long period of time, usually as a result of a preexisting cardiac condition
- 15. Etiology Most common causes Hypertension (mc comorbidity) HFrEF- mc cause CAD Alcohol abuse(80gms of alcohol/day for 5-10yrs) dilated cardiomyopathy Non-cardiac diseases causing high- output cardiac failure Anaemia(mc HOS) Obesity(mc HOS causing hf) Thyrotoxicosis Chronic lung diseases Cirrhosis Vit B def(beri beri) Myeloproliferative disorder Septicaemia Paget's disease of bone Arteriovenous fistulae The activity of erythrocyte transketolase induced by thiamine pyrophosphate and normalized to age of the patient is a marker of thiamine metabolism disturbances with pathological consequences in the central and peripheral nervous system. High o/p states are seldom responsible for HF, but their development in the presence of underlying cardiovascular disease can precipitate HF Obesity-31% Liver disease-23% Av fistula- 23% Lung disease- 16% Myeloproliferative disorder-8% Obesity paradox-obese pt with HF have btr prognosis than pt with low or normal BMI
- 17. Pathophysiology Summarized as an imbalance in Starlings forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work. When the capacity of the lymphatic drainage is exceeded, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema
- 19. Preload— The amount of blood the heart must pump with each beat Determined by: Venous return to heart Accompanying stretch of the muscle fibers Increasing preload increase stroke volume in normal heart Increasing preload impaired heart decreased SV. Blood is trapped chamber enlargement Afterload— The pressure that must be overcome for the heart to pump blood into the arterial system. Dependent on the systemic vascular resistance With increased afterload, the heart muscles must work harder to overcome the constricted vascular bed chamber enlargement Increasing the afterload will eventually decrease the cardiac output.
- 20. Other Conditions That Contribute to Heart Failure Increased metabolic rate Iron overload Hypoxia Severe anemia Electrolyte abnormalities Cardiac dysrhythmias Diabetes
- 22. LV Failure with PE • Left ventricle fails as an effective forward pump • Back pressure of blood into the pulmonary circulation • Pulmonary edema • Left atrial pressure rises • Increased pressure in the pulmonary veins and capillaries • When pressure becomes to high, the fluid portion of the blood is forced into the alveoli. • Decreased oxygenation capacity of the lungs
- 23. Signs and symptoms Unexplained cough Low oxygen saturation Cyanosis Diaphoresis Third heart sound(S3) Reduced urine output Severe resp. distress (orthopnea, dyspnea, PND) Severe apprehension, agitation, confusion Dizziness and light-headedness Fatigue and weakness Pulmonary congestion Rales—especially at the bases. Rhonchi—associated with fluid in the larger airways
- 28. Jugular Venous Distention—not directly related to LVF. Comes from back pressure building from right heart into venous circulation Vital Signs— Significant increase in sympathetic discharge to compensate. BP—elevated Pulse rate—elevated to compensate for decreased stroke volume. Respirations—rapid and labored RAP = 5+JVP 1.36 (1.36 converts venous pressure in cmH2O to mmHg) 5 is the JVP up to the angle of louis Calculate the estimated RAP if jvp is found to be 10cm? • 11mmHg • 12mmHg • 13mmHg • 14mmHg
- 29. The classic ‘a, c, v’ pattern may not always be obvious. JVP CLASSIC TRACE- systole diastole
- 31. LANCISI SIGN(cv waves) Y WAVE > X WAVE Friedreich’s sign
- 32. KUSSMAUL’S SIGN -Mean JVP increases during inspiration • Constrictive pericarditis • RV infarction • Severe RHF • Restrictive cardiomyopathy • Impaired RV compliance ABDOMINAL-JUGULAR REFLUX • Hepatojugular reflux- RONDOT(1898) • Done In patient suspected to be in RHF but no raised JVP(incipient RHF) • Apply firm pressure to periumbilical region 30-60sec(right upper quadrant) • Normally JVP rises transiently to <1cm while abdominal pressure is continued. • If JVP remains elevated >3cm in venous pressure for atleast 15sec after resumption of spontaneous respiration – positive AJR • Abd compression forces venous blood into thorax • A failing/dilated RV is not able to receive venous return without rise in mean venous pressure. • Predicts HF and pcwp >15 mmHg • Not usefull if Valsalva/breath holding • Positive AJR – RVF/TR/COPD
- 33. Right HF Etiology Acute MI— Inferior MI Pulmonary disease COPD, fibrosis, HTN Cardiac disease involving the left or both ventricles Results from LVF Pathophysiology Decreased right-sided cardiac output or increased pulmonary vascular resistance increased right vent. Pressures. As pressures rise, this increased pressure in the right atrium and venous system Higher right atrium pressures JVP
- 34. • In the peripheral veins, pressures rise and the capillary pressures increase, hydrostatic pressure exceeds that of interstitial pressure. • Fluid leaks from the capillaries into the surrounding tissues causing peripheral edema
- 37. History of HF is the most useful historical parameter(Sn60% and Sp90%)-tintinalli’s EM Most specific symptoms are 1. PND 2. Orthopnoea 3. Oedema Abdominal-jugular reflex and JVP are the only 2 signs other than S3 which is diagnostic.
- 38. Compensatory Mechanisms • Neurohormonal system • Renin-angiotensin-aldosterone system • Ventricular hypertrophy
- 39. Neurohormonal System • Stimulated by decreased perfusion secretion of hormones Epinephrine— • Increases contractility • Increases rate and pressure • Vasoconstriction SVR Vasopressin— • Pituitary gland • Mild vasoconstriction, renal water retention
- 41. RAAS • Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys Aldosterone is released increase in Na+ retention water retention Preload increases Worsening failure
- 42. Compensatory Mechanisms: Renin-Angiotensin-Aldosterone System Renin + Angiotensinogen Angiotensin I Angiotensin II Peripheral Vasoconstriction Afterload Cardiac Output Heart Failure Cardiac Workload Preload Plasma Volume Salt & Water Retention Edema Aldosterone Secretion ACE Kaliuresis Beta Stimulation • CO • Na+ Fibrosis
- 43. Ventricular Hypertrophy • Long term compensatory mechanism • Increases in size due to increase in work load of skeletal muscle
- 45. VICIOUS CYCLE OF READMISSION
- 46. In men, the 1-year survival rate was 7% and the 5-year survival rate was 35%. In women, the 1- and 5-year survival rates were 88% and 53%, respectively
- 47. Weight loss>4.5 kg in 5 days in response to treatment
- 48. Diagnostic Tests Medical history and physical exam Brain natriuretic peptide measurement Lab tests: complete blood cell count, metabolic panel, liver function studies, and urinalysis Other tests: thyroid function tests and fasting lipid profile
- 51. • B-type natriuretic peptide, also called brain-type natriuretic peptide (BNP), was first described in 1988 after isolation from porcine brain. • However, it was soon found to originate mainly from the heart, representing a cardiac hormone. • Major source of BNP synthesis and secretion is the ventricular myocardium. • Small amounts of BNP are stored in granules and rapid gene expression with de novo synthesis of the peptide is the underlying mechanism for the regulation of BNP secretion
- 52. CLINICAL APPLICATIONS DIAGNOSIS IN HEART FAILURE Emergency room setting: BREATHING NOT PROPERLY STUDY
- 54. N-terminal pro BNP has a diagnostic accuracy similar to that of BNP. N-terminal proBNP Investigation of Dyspnoea in the Emergency department (PRIDE) study and The International Collaboration of NT-proBNP (ICON) study The diagnostic role of NT-proBNP in patients presenting with the cardinal symptom of shortness of breath has been established. In these studies, a cut-off value for NTpro BNP of 300 pg/ml to exclude heart failure was determined.
- 58. FOR HFpEF AND OTHER HF - BNP>35pg/ml AND NT-proBNP >125pg/ml – ESC 2021 GUIDELINES
- 60. INCREASED LEVELS Increasing age Acute coronary syndrome Pulmonary hypertension Pulmonary embolism Anaemia Severe burns copd Atrial fibrillation Renal Failure SAH/stroke Thyrotox/DKA DECREASED LEVELS Obesity Burnt out cardiomyopathy (myocardium is thinned out already) Flash pulmonary edema. Acute MR Constrictive pericarditis(Braunwald 11th edition) NEET SS 2021
- 61. Caveats in using Natriuretic peptide levels Other causes • Pulmonary hypertension , RV dysfunction secondary to pulmonary embolism, and cor pulmonale. • Interpret with History and clinical features of HF/Prior diuretic use
- 62. Causes for Elevated Natriuretic Peptide Levels Cardiac Noncardiac Heart failure, including RV syndromes Acute coronary syndrome Heart muscle disease, including LVH Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Cardioversion Advancing age Anemia Renal failure Pulmonary causes: obstructive sleep apnea, severe pneumonia, pulmonary hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults, including cancer chemotherapy and envenomation
- 63. Renal disease Cut-off concentrations for detecting HF to be raised when estimated glomerular filtration rate (eGFR) is < 60 ml/min. No additional adjustment seems necessary for NT- proBNP once using age-adjusted rule in cut off. For BNP, the effect of renal dysfunction overall is smaller, and increasing the rule-out cut-off to 200 pg/mL rather than 100 pg/mL seems sufficient.
- 64. OBESITY Concentrations of BNP, NT-proBNP and are lower in obese persons (BMI ≥30 kg/m2) both with and without HF. This may be due to suppression of the bnp gene by circulating factors such as androgens that produced by adipose tissue. To optimize diagnostic accuracy, lowering the established cut-off concentrations by up to 50% in obese patients is reasonable.
- 66. OTHER Diagnostic Tests Echocardiogram to assess ejection fraction (LVEF)- most imp parameter Chest X-ray(KERLEY LINES) ECG Cardiac stress test Cardiac catheterization Cardiac computed tomography scan or magnetic resonance imaging Radionuclide ventriculography Ambulatory ECG monitoring (Holter monitor) Pulmonary function tests Heart biopsy Exercise testing (6-minute walk) CARDIAC MRI- gold standard for LV mass and volume assessment
- 69. A diagnosis of diastolic heart failure requires the presence of all the following features: The presence of symptoms or signs of heart failure. The presence of normal or slightly reduced left ventricular (LV) systolic function. Evidence of abnormal LV relaxation and filling, diastolic distensibility, and diastolic stiffness. The second feature is readily diagnosed by routine echocardiography. The third, however, can only be diagnosed by Doppler echocardiography, which is not routinely available, or by cardiac catheterization.
- 70. Differential Diagnosis Other causes of shortness of breath on exertion - e.g. pulmonary disease, obesity, unfitness, volume overload from renal failure or nephrotic syndrome, angina, anxiety. Other causes of peripheral oedema - e.g. dependent oedema, nephrotic syndrome. Non-cardiac diseases causing high-output cardiac failure
- 71. Mc cause of death in NYHA2- sudden cardiac arrest Mc cause of death in NYHA4- progressive pump failure
- 72. Prognostic Features Demographic: Advanced age, sex, Ischemic etiology Symptoms: NYHA class IV, Syncope Signs: Chronic S3, Right heart Failure, ↑ JVP, Mod-Severe MR/TR Laboratory: Na+, Creatinine, Anemia, Cardiothoracic Ratio, LVEDD ECG: QRS or QT prolongation, NSVT, VT Hemodynamic: LVEF, PCWP, CI Excersice: 6 MWT, Peak VO2 Neurohormonal: Plasma Norepinephrine, ANP, BNP
- 73. A total of 245 prevalent heart failure cases (88 men, 157 women) were identified at baseline in the Rotterdam Study. In the remaining study population (n=7734), we identified 725 incident cases of heart failure (335 men, 390 women), of whom 673 were classified as definite, and 52 as probable cases. 5 yr mortality- 50%
- 74. Staging & Severity After all data are gathered, cause and classification can be determined and an appropriate treatment plan Two well-accepted classification systems used: ACC/AHA stages of heart failure and NYHA functional classifications
- 75. NYHA Grading Not used unless heart disease is present. 1 year mortality rate: Class I - <5% Class II – 10-15% Class III – 20-30% Class IV – 30-70% Orthopnoea is included in NYHA and not PND NYHA vs WHO-FC FDPA vs FDSA
- 76. Classification of Heart Failure ACCF/AHA Stages of HF A At high risk for HF but without structural heart disease or symptoms of HF. B Structural heart disease but without signs or symptoms of HF. C Structural heart disease with prior or current symptoms of HF. D Refractory HF requiring specialized interventions.
- 78. Clinical Events and Findings Useful for Identifying Patients With Advanced HF Repeated (≥2) hospitalizations or ED visits for HF in the past year Progressive deterioration in renal function (e.g., rise in BUN and creatinine) Weight loss without other cause (e.g., cardiac cachexia) Intolerance to ACE inhibitors due to hypotension and/or worsening renal function Intolerance to beta blockers due to worsening HF or hypotension Frequent systolic blood pressure <90 mm Hg Persistent dyspnea with dressing or bathing requiring rest Inability to walk 1 block on the level ground due to dyspnea or fatigue Recent need to escalate diuretics to maintain volume status, often reaching daily furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy Progressive decline in serum sodium, usually to <133 mEq/L Frequent ICD shocks Adapted from Russell et al. Congest Heart Fail. 2008;14:316-21.
- 79. 2016-2017 DATA