Definition of circulatory failure
Inability of cardiovascular system to nourish the body's cells, supply oxygen and remove metabolic products.
Causes of circulatory failure
Heart failure, Low cardiac output, High Output Cardiac Failure
Defintion/diagnosis of heart failure
1. Symptoms of HF (dyspnea-SOB, fatigue, ankle swelling). 2. Signs of HF (tachycardia, tachypnea, increased venous pressure, edema, hepatomegaly, murmurs). 3. Objective evidence of a structural or functional heart abnormality at rest (cardiomegaly, S3, murmur, abnormal echo, increased BNP).
Types of heart failure
1. Systolic/Diastolic (main distinction relevant for prognosis and treatment, the rest semantic), 2. Forward/backward, 3. Left/Right, 4. Low output/high output
What are the elements of systolic HF that distinguish it from diastolic HF?
Damage to/reduction of contractile function. Usually will also have diastolic dysfunction.
Diastolic HF as distinguished from systolic HF
Problem occurs during diastolic phase/relaxation/filling impairment to ventricle. No actual problem with contractile function of the heart. Implication that systolic fxn is normal.
Forward HF as distinguished from backwards HF
Underperfusion of systemic tissues. Patient presents with weakness/tiredness with even mild exertion. Reduction in perfusion of skeletal muscle.
Backwards HF as distinguished from forward HF
Increased in LVEDP. Reflected backwards into the lungs. Pulmonary pressure goes up, SOB.
Left HF as compared to right HF
Complains of SOB and weakness upon exertion. Crepitations and fluid in lungs on examination.
Right HF as compared to left HF
RV not working. Peripheral edema. High jugular venous pressure. If only right with no left: due to severe lung disease.
Low output vs high output
Reduced cardiac output, sign of severe LV damage and systolic dysfunction severe HF patients.
High output vs low output
Rare and unusual. Heart has to pump an abnormally large amount of blood through the body to supply oxygen. Heart functions normally or above normal
When does high output heart failure occur?
1. Increased blood volume (or fluid)/excess salt and water accumulation. No intrinsic circulatory problem. 2. Abnormally high venous return and/or decreased peripheral vascular resistance.
What is the definition of oliguria?
What are causes of increased blood volume/fluid?
IV fluids, blood transfusion, steriods (or NSAIDs, a lot over a long period of time), oliguria/anuria.
What are the causes of abnormally high venous return or high PVR?
Pregnancy (rare), hyperthyroidism, Severe anemia (most common, developed over a long period when compensation fails), AV fistulae/shunts, Beri-beri. Eventually chronic pressure/volume overload-->pump failure.
What is an AV fistula?
AV fistula: patients on hemodialysis from chronic renal failure. In dialysis doctors fashion a huge BV but joining radial or brachial artery and vein-looks like a snake under the skin. Sometimes BV are so big that get a huge venous return back to heart and can unusually put patients into HF from huge preload they can't deal with.
What are the 3 basic categories of heart failure?
1. Mechanical abnormalities, 2. Loss of myocyte function, 3. Alteration of cardiac rhythm
What are the mechanical abnormalities that can lead to HF?
1. Increased worload, 2. Increase pressure load/afterload (Central: aortic stenosis, or peripheral: HTN). 3. Volume overload/increased preload (mitral regurgitation), 4. Pericardial constriction/tamponade (rare)
How does mitral regurgitation lead to heart failure?
Heart pumps blood in systole, some blood goes out through aorta. But because there is a backup, pressure is lower in the LA and blood goes back. In diastole you get blood from venous side of lungs and regurgitated from LV. Each time there is more blood. Gets worse and worse. "MR begets MR." gradually the LV will start to dilate. Can stretch to a large degree with no loss of systolic function until there is a significant drop-->HF.
Types of loss of myocyte function
1. Cardiomyopathy, 2. Toxic (alcoholic), genetic, medical (anthrocyclines), other rare ones. 2. Ischemic heart failure, 3. Negative inotropes
What is cardiomyopathy as relating to HF?
roup of heart muscle diseases. Implication that there is a disease of the myocardial tissue, myocytes themselves, of unknown etiology.
What are the 3 main groups of cardiomyopathy?
1. Hypertrophic, 2. Dilated, 3. Restrictive.
What is hypertrophic cardiomyopathy?
Significant hypertrophy. Genetic condition with mutations of different genes affecting myosin, actin, or other pieces in the heart itself. Massive hypertrophy. Good function but very stiff so diastolic dysfunction.
What is dilated cardiomyopathy?
Significant systolic dysfunction, destruction of myocytes.
What is restrictive cardiomyopathy?
Smaller and more uncommon. Infiltrate into cardiac muscle. Heart doesn't actually dilate but reduction in systolic function. Stiff and noncompliant.
What is ischemic heart failure?
Problem in blood supply from coronary arteries blocked off. Can be result of one big MI or a bunch of small ones.
How do negative inotropes relate to heart failure?
Reduce heart function to some extent. Beta blockers and calcium channel blockers. Paradox: beta blockers treat HF.
How does alteration of cardiac rhythm cause heart failure?
Fast heart rates or slow heart rates cause HF because reduce efficacy in HF. Asynchrony: heart block, detachment between atrial and ventricular contraction, ventricles aren't being properly filled by atria.
What are the components in the etiology of heart failure?
Most common in western lifestyle and low rheumatic fever: coronary artery disease and dilated cardiomyopathy. Most common with rheumatic fever: valvular heart disease. Others: hypertension (not direct but will contribute to others) and congenital heart disease (more children survive now so higher prevalence).
What are compensatory mechanisms in heart failure?
Reduction of perfusion to peripheral organs. May cuase more damage than good. 1. Autonomic increase in HR and contractility, 2. decrease renal perfusion-more fluid preservation, 3. increased adrenal stimulation, 4. more renin and angiotensin
How do ACE inhibitors affect HF?
They are vasodilators but also blocks all these negative effects of HF from angiotensin II. No other vasodilators improve prognosis similarly.
Compensatory hormone mechanisms against HF
1. ANP (released in atrial distension: vasodilation, sodium and water excretion, reduced preload), 2. Prostaglandin vasodilation, 3. Peptides: bradykinin, 4. endothelin (raise BP)
What are the 2 patterns of left ventricular hypertrophy (LVH)?
1. Concentric (pressure overload): hypertrophy without change in volume (Aortic stenosis), 2. Eccentric (volume overload): hypertrophy with increased volume of LV (aortic regurgitation).
When does hypertrophy lead to heart failure?
When it is chronic overload with increased wall stress and depressed contractility. At first compensated but when necrosis leads to overload and wall stress increases further.
Law of Laplace equation
Wall stress=Pxr/2*(wall thickness)
How much blood to the ventricles is provided by the atrial kick?
15-20% but decreased with tachycardia
How is the blood affinity for oxygen altered in HF?
Increased 2,3DPG-reduced affinity of Hb for O2. Rightward shift. Increased oxygen extraction.