Heart Failure Flashcards
How can we define heart failure?
It is a state in which the heart isn’t able to provide sufficient cardiac output to match the metabolic demands of heart and other tissues. There are many different symptoms with different presentations with many DDX. It is therefore important to follow a certain reasoning when there is suspicion of HF.
What are some common signs and symptoms of heart failure?
Shortness of breath DDX with respiratory disease, memory problems worsening, waking up many times during the night DDX with renal issues, cough DDX with many respiratory diseases, swollen or tender abdomen, swelling of feet DDX peripheral vein issues.
None of these symptoms will guarantee HF diagnosis although may help with other gathered information to give diagnoses.
What are some congestive events caused by HF?
Impact on liver : stasis of blood, impairment of liver function will change levels of liver proteins as lower albumin, changes in ALT and AST, and alteration of coagulation factors.
Impact on intestine : intestinal edema, tenderness, congestion.
Impact on legs : peripheral edema of different entities.
What are some abnormal perfusion events caused by HF?
Impact on brain : temporary hypo-perfusion.
Impact on kidneys : 25% of cardiac output goes to kidneys, if it decreases they will respond activating RAAS.
What are some compensatory mechanisms against HF?
Decreased blood flow to the kidney activates the RAAS to increase blood pressure and water reabsorption to increase blood volume. This is called vascular congestion which may turn into tissue congestion.
Sympathetic activation will increase HR to increase cardiac output since EF is decreasing.
These mechanism are only helpful at the beginning but are harmful long term.
Why is EF important in HF?
If EF is decreased than it is a sure sign of HF. If it is not decreased it doesn’t mean there isn’t HF as the stroke volume could be decreased due to hypertrophy leading to a decreased CO.
How can we suspect HF?
We asses risk factors such as hypertension, lipid levels and coronary artery disease. Look out for signs and symptoms indicating possible HF. Analyze ECG for any abnormalities.
Check for BNP which is B type Natriuretic peptide. If normal unlikely HF if not it can strongly suggest HF.
What are the different causes of HF clustering them based on importance?
IHD : myocardial scarring after necrosis or fibrosis, myocardial stunning after prolonged ischemia, epicardial coronary artery disease, abnormal coronary micro circulation and endothelial dysfunction.
Toxic damage : recreational substance abuse such as cocaine and anabolic steroids, heavy metals like copper and lead, medications like transtuzumab and cetuximab, radiation.
Infiltration : related to malignancies, related to metabolic disorders like hemochromatosis or other systemic diseases like amyloidosis and sarcoidosis.
Metabolic changes : obesity, it is a direct cause of HF without reduced EF.
Abnormal loading conditions : hypertension, valvular defects, myocardium structural defects, constrictive pericarditis, severe anemia.
Arrhythmias such as tachyarrhythmias and bradyarrhythmias.
How do myocytes adapt to increased stress? How is it related to HF?
Myocytes need to adapt to maintain sufficient CO during stress. To increase the EF concentric hypertrophy can occur, to combat volume overload eccentric hypertrophy can occur.
These compensatory mechanisms will eventually worsen HF.
What is the epidemiology of HF?
HF is a chronic progressive disease with same prognosis of lung cancer, it is a very severe condition and can cause sudden death despite sometimes being asymptomatic and worsening within few days. Prevalence: 1-3% in general population.
Mortality after an acute event after 5 years is 50%.
Why are paroxysmal nocturnal dyspnea and orthopnea among the most important symptoms of HF?
Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing. Paroxysmal nocturnal dyspnea is the sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep.
This occurs because when laying down gravity is no longer working against venous flow therefore increase venous flow to the RV. In a normal heart because of the frank sterling mechanism the heart can manage by increasing stroke volume. In a person with heart failure, the left ventricle has an inadequate capacity to respond to increased arrival of blood from the pulmonary circulation leading to congestion. Which could in turn lead to interstitial trasudation or even alveolar trasudation.
How can we examine the jugular venous pressure? Why is it helpful to diagnose HF?
Patient must be recumbent on his back at a 45 degree angle. Measure the vertical distance between the angle of louis (palpable anatomical feature formed from the manubriosternal junction) and the most cranial visible part of the external jugular vein in cm. Add that to 5 cm as that is the distance from the angle of Louis to the right atrium. This roughly gives us the pressure in cm of water, cmH2O. Should be between 4 and 8.
A high JVD indicates backed up blood in the vein, a common symptom of HF.
What are some treatments for congestion?
Loop diuretics : they are the standard for treatment of congested patient. They are natriuretics, facilitating Na+ outflow and thereby reducing circulating volume and intravascular congestion. Aren’t very effective on tissue congestion.
Aquaretics : vasopressin antagonists, not standard treatment, they cause pure water excretion at the level fo the kidney. They are better to recall water from tissues.
What is the pathophysiology of congestion?
Under normal condition the hydrostatic pressures (outward pressure) and oncotic pressures (inward pressure) in the capillaries are in equilibrium. During compensated HF hydrostatic pressures rise and oncotic pressures decrease. This causes fluid to build up in the interstitial space.
Hydrostatic pressures decreases because of right side heart failure for example increasing pressure in venous system.
Oncontic pressure decreases because liver function is decreasing for example. Proteinsthat are meant to bring fluid in aren’t enough.
What are the signs and symptoms of intravascular congestion? How is it diagnosed?
Clinical signs : Increased jugular venous pressure, orthopnea, 3rd heart sound, acute distention of ventricle, sign of impaired filling.
Biomarkers : NT-proBNP and hemoconcentration.
Techniques : Inferior vena cava ultrasonography to check diameter, jugular vein ultrasonography to check JV pulse, renal ultrasonography and implantable pressure sensors.
