| What is HF? | Complex clinical syndrome, resulting from structural/functional impairment of ventricular filling or ejection of blood
Leads to dyspnea, fatigue, signs of HF (edema/ rales) |
| How is epidemiology of HF? | Growing global condition, 64 million pt and increases with age, 1 in 5 people develop it, number 1 cause of hospitalization in elderly
It has worse survival rate compared with some other cancers (still more than lung and colorectal cancer males, and ovarian in females)
Risk never rests (9 out of 10 remain symptomatic with HF SoC, 5 out of 10 die within 5 years of dx) |
| What are the different characteristics of HFpEF and HFrEF? | HF could be reduced, midrange or preserved (HFpEF, HFmrEF and HFrEF)
HFpEF (dysfunction is diastolic, LVEF >50%, concentric LV remodeling, increased wall thickness and mass with high ratio of mass:volume and no prognostic improvement with HF therapy)
HFmrEF (mild systolic and features of diastolic, LVEF 40-49%)
HFrEF (dysfunction is systolic, LVEF <40%, eccentric LV remodeling, increased EDV, decreased wall thickness and low mass:volume ratio, and improves with HF therapy (but same mortality) |
| How is the prevalence of HFpEF vs HFrEF? | 50% of pt with HF have HFpEF, older pt and females (for HFpEF) |
| Why is chronic HF a complex clinical syndrome? | Different pathophysiologies, variable systolic and diastolic dysfunction (as LVEF increases: more HFpEF and diastolic dysfunction, as LVEF decreases: more HFrEF and systolic dysfunction) |
| What are etiologies causing HF? | Depressed EF (<40%) (CAD [MI], chronic pressure overload [HTN, obstructive valve disease], chronic volume overload [regurg, shunting], chronic lung disease [cor pulmonale, pulmonary vascular disorders], Chaga's disease, disorders of rate and rhythm, toxic induced damage, non-ischemic dilated cadiomyopathy [familial/infiltrative disorders])
Preserved EF (>50%) (Pathologic hypertrophy [primary or secondary HTN], aging, fibrosis, endomyocardial disorders, restrictive cardiomyopathy [infiltrative, storage disorders (hemochromatosis)])
High output state (metabolic disorders [thyrotoxicosis, beriberi], excessive blood flow [AV shunt, chronic anemia]) |
| What is the new york association classification (NYHA) of heart failure? | Class I (pt with HF with no limitation of physical activity, no fatigue/palpitation/dyspnea/angina)
Class II (slight limitation with physical activity)
Class III (marked limitation with activity, comfortable at rest)
Class IV (inability to carry out any physical activity without discomfort
All are at risk for death (34% of NYHA class I and II die, 42% of class III and IV die) |
| How is pathogenesis of HF? | Baroreceptor dysfunction, decreased afferent inhibitory signals, increased sympathetic NS and decreased limb blood flow with increased vasopressin secretion, renin secretion, aldosterone, sodium reabsorption and water retention
This causes HFrEF caused by increased BP, hypertrophy,fibrosis (by RAAS), HR, vasopressin, contractility (SNS). |
| What is the basic mechanism of HF? | HFrEF: myocyte hypertrophy, alteration of contractile properties, loss of myocytes by necrosis and apoptosis, beta adrenergic desensitization, abnormal energy of myocytes, reorganization of matrix dissolution of structural collagen replaced by interstitial collagen matrix not structural type.
Reduced ATP (in ischemia, slowed myocardial relaxation)
Decreased LV compliance so decrease LV filling due to hypertrophy/fibrosis thus elevated EDV and EDP ->increased pulmonary capillary pressure -> dyspnea
Hypertrophy will cause diastolic dysfunction |
| What is left ventricular remodeling? | Changes in LV mass, volume, shape, composition after cardiac injury
May contribute in progression to HF, can be reversed by medical therapy/device to get better outcomes of HFrEF, so our goal is to prevent remodeling which will cause overactivation of neurohormones, apoptosis, hemodynamic alterations leading to heart failure
Predictors of reverse remodeling is seen by LVEF and HF onset (reverse if non-ischemic, shorter time of HF, lower LVEF, and biomarkers low) |
| What are clinical manifestations of HF? | Fatigue, dyspnea (due to reduction of pulmonary compliance, increased resistance, muscle fatigue, anemia, pulmonary congestion with fluid accumulation, less frequent for RV failure and tricuspid regurg)
Orthopnea (nocturnal cough, sleeping with many pillows, due to redistribution of fluid from lower limbs to central circulation increasing capillary pulmonary pressure)
Paroxysmal nocturnal dyspnea (episodes of SoB at night awaken pt, maybe cough or wheeze)
Cardiac asthma (closely related to PND, secondary to bronchospasm)
Cheyen-Stokes respiration
Acute pulmonary edema
GI symptoms |
| What are the PE done for HF? | General appearance and vitals, jugular vein, pulmonary exam, cardiac exam, abdomen and extremities exam
Cardiac cachexia |
| How is dx of HF? | Routine labs, ECG, CXR, LV function assessment, biomarkers (BNP, NT-proBNP for chronic HF) |
| What is cor Pulmonale? | Altered RV structure/ function with chronic lung disease, triggered by onset of pulmonary HTN (not RV dysfunction)
It occurs due to acute/ chronic pulmonary vascular and parenchyma disorder causing pulmonary HTN, COPD, chronic bronchitis (50% of cor pulmonale) |
| How is pathophysio of cor pulmonale? | Pulmonary HTN sufficient to alter RV structure (dilation w/ or w/out hypertrophy) and function
Pressure overload causes increased resistance causing eventual RV failure |
| What are symptoms of cor pulmonale? | Ones related to underlying pulmonary disease, abdominal pain and ascites, lower extremities edema (secondary to neurohormonal activation, elevated RV filling pressure or increased CO2 and hypoxemia) leads to peripheral vasodilation and edema formation |
| How is dx of cor pulmonale? | TTE, CT, R/O left heart failure/ embolic disease, right heart catheterization confirming pulmonary HTN |
| How is management of HFrEF? | To reduce mortality (ACE I, BB, MRA, SGLT2i (most imp)) for all pt
To reduce hospitalization (SR w/LBBB: use CRT-P/D)
Ischaemic etiology (give ICD), A.fib (anticoagulant, digoxin, PVI) CAD (CABG), iron deficiency (ferric carboxymaltose)
If advanced pt (heart transplant, MCS as BTT/BTC, long term MCS.
As prophylaxis: exercise rehab and multiprofessional disease management |
| How is management of HFpEF and HFmrEF? | SGLT2i, ARNI, MRA, Beta blocker (mr) and ARB (p)
We should reduce congestive state, control BP, maintain atrial contraction and prevent tachycardia, treat and prevent MI, detect and treat sleep apnea
Usually RAAS management, digoxin and BB are ineffective but may reduce hospitalization |
| What is acute decompensated HF? | ADHF is a heterogeneous clinical syndrome most often resulting in
need for hospitalization due to confluence of interrelated
abnormali-ties of decreased cardiac performance， renal dysfunction
， and altera-tions in vascular compliance.
• The first principle of management of these patients is identify and
tackle known precipitants of decompensation. |
| What is volume management of HF? | • Intravenous diuretic agents
• Vascular therapy
• Inotrop |
