Lecture

• Heart failure: inability of the heart to pump adequate blood to meet needs; generally occurs because of impaired CO or SV or cuz not enough supply to meet the demands
• Heart failure causes increased myocardial infarct and decreased CO as time and compensatory mechanisms prolong
• Scarring changes heart tissue to fibrin, making it stiffer
• In HF, SV can be decreased because of cellular injury but can also be increased of dilation without having an increased strength in contraction
• EDV does not change in accordance to SV; preload(EDV) will not change regardless of whether someone's having an MI or if they're CO is shit cuz of decreased SV
• Contractility is affected by: amount of contractile proteins present(Sarcomeres/ischemia/scarring), ATP, Ca+(majority of movement is done thru active transport), increased MVO2, ischemia and electrolytes.
• Prolonged ischemia can decrease contractile proteins because they it causes cell death
• Inotropy has a relationship with afterload however it has no relation to preload
• Types of heart failure: Systolic, Diastolic, Left sided and right sided
• Systolic heart failure: weakened EF and low output. It's a contracting problem that usually presents with hypertrophy and cardiomegaly.
• Diastolic heart failure: filling problem and the heart is stiff. Still has high output
• Hallmark S/S of heart failure: PE, dyspnea on exertion, some type of megaly, systemic edema and orthopnea
• Systolic heart failure: decreased contractility leading to decreased stroke volume. Increased piled up preload. It can be caused by CAD(very systemic rxn), AMIs(very local rxn and most common cause of systolic heart failure) and dilated cardiomyopathy(floppy ventricle walls via apoptosis/necrosis) that occurs due to mitral/aortic regurgitation.
• Could have tricuspid and pulmonary regurgitation but its a lot more rare than mitral/aortic regurgitation.
• Generally systolic heart failure is seen with an EF of 40 % and life threatening HF is seen with an EF of 35% of less
• Systolic heart failure causes these things sequentially: Decreased EF causes increases EDV -> ventricular dilation/stretching -> increased ventricular wall tension->increased workload/MVO2 -> pressure from increased EDV causes blood to backflow into supplying circulation -> pulmonary/peripheral edema
• Diastolic heart failure is a filling, relaxing and compliance problem; decreased chamber space and compliance. Beforehand, myocytes have undergone hypertrophy which causes reduced chamber space. Causes decreased EDV but increased pressure.
• In diastolic heart failure: contractility is generally unaffected but SV decreases bcuz chamber volume has decreased. EF stays the same bcuz EDV also decreases so the ratio stays the same
• Ejection fraction can stay the same but one may still have heart failure problems
• Most common causes of diastolic heart failures: ischemic heart disease/CAD and long standing increased afterload. A less common cause is aortic stenosis.
• Long standing hypertension causes increased afterload; this may cause LVH which causes less compliance and more MVO2
• Chronic hypertension is the most common cause of LVH
• Other causes of diastolic heart failure are obstructed expansion and reduced Lusitropy
• Hypertrophy of the ventricles is early compensation while dilation is late
• Obstructed expansion consists of: pericardial effusion(chest trauma, post CABG, CHF), cardiac tamponade(acute inhibition of heart's ability to expand; typically trauma but could occur post MI), constrictive pericarditis(long term complicated of pericardial effusion that is caused by tuberculosis) and restrictive cardiomyopathy(damage of myocardium causing rigidity; caused by cancers, chemotherapy meds, hemochromatosis/infiltration of iron)
• Reduced Lusitropy: decreased ability in being able to relax the myocardium; Ca+ must be actively removed for the muscles to relax, meaning its an aerobic process. If ventricles aren't relaxed enough, filling is also reduced
• Non cardiac causes of diastolic failure: Severe anemia(hypertrophy due to lack of O2), hyperthyroidism(increases MVO2) and pregnancy(fluid overload, which causes increase MVO2); Generally occurs if there's an underlying cardiovascular disease present.
• Backing up of pressure due to piled up EDV increases hydrostatic pressure
• High hydrostatic pressure causes blood to back up into alveoli and capillaries which causes pulmonary and peripheral edema
• Ascites: edema in the abdomen
• Chronic heart failure will cause chronic SNS stimulation; this causes downregulation which is a big issue in a moment of stress such as the flu
• Left ventricular heart failure can cause right sided heart failure but it cannot cause Cor Pulmonale
• Cor Pulmonale is right atrial and ventricular enlargement secondary to a lung disorder. Produces pulmonary hypertension. Exacerbated by vasoconstrictors and lack of vasodilators. Hypercapnia and hypoxia are major S/S.
• Pulmonary hypertension causes Right sided hypertrophy which causes venous blood to back up; causes JVD, Ascites, edema in the liver/intestines and extremities.
• Pts with diastolic heart failure are very sensitive to tachycardia as there's already very little space for filling and then positive chronotropy exacerbates this
• Right heart failure is less common than left heart failure
• Left heart failure can become right and vice-versa; same with systolic/diastolic
• Left heart failure is more common bcuz its caused by a lot more common causes
• Common causes of HF: CAD, AMI, Hypertension, Cardiomyopathies and valvular heart disease
• Cardiomyopathies: pathological changes to myocardium resulting in thickening/thinning/weakening all resulting in decreased cardiac output. Causes are: genetic, alcohol, cocaine(potent vasoconstrictor), CAD, broken heart syndrome/Takotsubo(caused by influx catecholamines)