B3W3 Cardiac Regulation Flashcards
Afferent Cardio Receptors
Arterial Baroreceptor (Inhibitory)
Arterial Chemoreceptors (Excitatory)
Cardiopulmonary Baroreceptors (Inhibitory)
Muscle Metaboreceptors (Excitatory)
Parasympathetic Innervation of the heart
Parasympathetics are always on at the heart at the SA and VA nodes
Parasympathetics decrease sympathetic NE release
Causes decreased heart rate, conduction velocity, and contractility
Sympathetic Innervation of the Heart
NE binds to beta-1 receptors on the SA node, AV node, and Cardiac Muscle
Causes increased heart rate, conduction velocity, and contractility
Innervation of Vasculature
Arteries and Vein mainly innervated by the sympathetic Nervous System
Arteries have more Alpha 1 than Beta 2
Arteries are vasoconstricted
Pulmonary Arteries have more Beta 2
Pulmonary Arteries are vasodilated
Alpha Receptor Effects
Vasoconstriction
Beta Receptor Effects
Beta 1 increase heart function
Beta 2 vasodilation
Arterial Baroreceptor
Detects arterial pressure in the carotid sinus and aortic arch
Decreases sympathetic outflow to decrease pressure and maintain high blood flow
Aortic Arch Baroreceptor
High threshold and mainly only responds when the carotid baroreceptors are saturated
Afferent through Vagus Nerve
Carotid Sinus Baroreceptors
low threshold and highly sensitive to change in MAP
Afferent through glossopharyngeal nerve
Baroreceptors
Stretch Receptors
Cardiopulmonary Baroreflex
Sensitive to pressure during diastole, low pressure baroreceptor based on the amount of cardiac filling
Increased sympathetic outflow to heart
Decreased sympathetic outflow to kidneys
Decreased Sympathetic outflow to Kidney
Inhibits ADH causing increased H2O excretion
ANP release causes increased Na+ excretion
This lowers blood volume overall
Peripheral Chemoreceptors
Triggered by low pO2 and high CO2
Chemosensitive fibers that signal through the carotid sinus nerve and aortic depressor nerve
Increases sympathetic and vagal response
Central Chemoreceptors
Triggered by only high pCO2 and low pH
Increases sympathetic outflow
Skeletal Muscle During Exercise
Stimulated by H+ and K+ ions
Signal goes through muscle afferents
Increases Sympathetic Tone and decreases parasympathetic
Active muscle site however are effected more by local vasodilators than the sympathetic nervous system
Reflex from Lung
Stimulated by lung inflation
Signal through the vagal nerve
Decreases Vagal and sympathetic signal
Mutual Inhibition
Combined signal is less than the sum of two signals
Additive Summation
Output is equal to the sum of two inputs
Mutual Facilitation
Combined signal is larger than the sum of two inputs
Heart Failure
Syndrome characterized by elevated cardiac filling pressure or inadequate peripheral oxygen delivery, at rest or during stress caused by cardiac dysfunction
P-V Relationship Systolic Dysfunction
End Systolic point has the heart at a higher volume and lower pressure and lower contractility by shifting it downward and to the right
P-V Relationship Diastolic Dysfunction
Ventricle can only fill at a higher pressure resulting in higher pressure at the end of diastole and a smaller stroke volume
Causes of Left Sided Heart Failure
Systolic dysfunction
Impaired Contractility
Increased Afterload
Diastolic Dysfunction
Impaired LV Relaxation
Obstruction of LV Filling
Pathogenesis of Chronic Heart Failure
Coronary heart disease, hypertension, or cardiomyopathy
Effects of left ventricle lack of function
Lower Cardiac output, abnormal reflexes, chronic activation of the sympathetic nervous system
Index Event
An event that triggers the progressive onset of heart failure
Secondary Damage
Permanent damage caused by excessive activation of neural hormonal symptoms
Compensatory Mechanisms
Mechanisms that attempt to undo detrimental effects caused by secondary damage
Angiotensin II
Active form of Angiotensin
Very powerful abnormal vasoconstrictor
Further Constriction effects of Angiotensin II
Activation of the sympathetic nervous system, increased aldosterone, increased vasopressin, and increased endothelin
Clotting effects of Angiotensin II
Increased Pa-1 (causes thrombosis), platelet aggregation, and superoxide production
Smooth Muscle Remodeling effects of Angiotensin II
Myocyte growth, increased vascular muscle growth, and increased collagen
Functional Classification of Heart Failure
Class I
-No limitations
-no symptoms with ordinary activity
Class II
-Slight limitations
-Symptoms with ordinary activity
Class III
- Marked Limitations
- Symptoms with less than ordinary activity
Class IV
- Symptoms of cardiac insufficiency at rest
Symptoms of Heart Failure
Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, Fatigue, RUQ Fullness/Pain, anorexia, nausea, or vomiting
Heart Failure Treatment
Neurohormonal treatment with ace inhibitors beta blockers and other agents to block neurohormonal activation
