Cardiac Output Flashcards
Cardiac Output Def.
Volume ejected from ventricle per min (L/m). Volume ejected per beat (stroke volume) X no. of beats per min (Heart rate). Average ~ 5 L/min
What system regulates cardiac output
Autonomic Nervous System
RMP of Cardiac Cell
~ -55 mV
Action Potential Activation
~ -40mV
Parasympathetic effect on heart rate
Choline activates cholinergic receptors. This decreases cAMP and decreases heart rate
Sympathetic effect on heart rate
Androgenic receptors increase cAMP, increasing heart rate
What antagonist decreases heart rate
Beta Blockers
What antagonist increases heart rate
Atropine
Tachycardia Def.
Increase in heart rate, sympathetic nervous system effect
Adrenegeric Action Def.
Beta-adrenoreceptor (g-protein couple) stimulate cAMP which activates PKA. Increases Ca^2+ entry (depolarisation). Ca^2+ binds to troponoin to activate cross bridging
Sympathetic Agonists
Positive (promoting) chronotropes (faster acting) and inotropes (increase output force)
Para synthetic Chronotypes
Negative chronotropes ( slow down rate). No ionotropic effects
Beta-blockers (atenolol and propranol) Outline
Negative chronotropes and ionotropes
Relationship between cardiac output and blood re-entering heart
Blood volume exiting heart = blood volume entering heart
Intrinsic Regulation of Heart Outline
Heart can adapt to changes in blood volume without reference to nerves or hormones
Frank Sterling Law of Heart Outline
Greater stretch of cardiac muscle = greater force of contraction. Thus increasing preload (volume of blood stretching muscle) = increasing stroke volume (force pushing blood out of heart)
What happens when cardiac muscle is understretched
Myosin and actin in muscle are imperfectly aligned. Cross bridges aren’t as efficient. The more the myocardium is stretched = more efficent cross bridge overlap (greater force generated)
Relationship between stretching and stroke volume
Closely positively associated until heart muscle is stretched past a ceratin stage where cross bridges can no longer overlap and force that generates stroke volume decreases
Preload Outline
Ventricular filling during diastole. Affected by atria and venous pressure, gravity and circulation blood pressure
Blood Volume + Venous Tone
Great veins tore blood at any time, increased blood volume = increased central venous pressure. Increased central venous pressure = increased preload
Gravity Realtionship to pressure
Increased gravity force = decreased blood pressure. Low blood pressure at head (when standing). Hypotension occasionally occurs when standing up
How blood flows against gravity
Vein’s valves (preventing backflow) and skeletal muscle blocks (compress against veins, only active by movement). These push blood towards heart
Inspiration Thoracic Pump Outline
Inspiration raises abdominal (stomach) pressure and
lowers thoracic (chest) pressure. Blood in abdomen moves to thorax, blood in legs remains there
Expiration Thoracic Pump Outline
Lowers abdominal pressure and decreases thoracic pressure. Blood moves from legs to abdomen
Starling and Contractility
Stroke volume increases by changing orientation. Inotropes increase Ca, increasing contractility
Consequences of Too Low Blood Pressure
Low tissue perfusion. Organ failure (noticeably brain and kidney filtration)
Consequences of Too High Blood Pressure
High perfusion. Damage to cells causing damage to cells
Mean Arterial equation Factors
Mean Arterial Output = Net Peripheral Ressistance x Cardiac Output
Distribution of Water
67% intracellular and 33% extracellular. 1/9 is vascular and 2/9 = interstitial
Renin-Angionestic System Def
Potent vasoconstricting (increase ressistance). Stimulates adelsterone increased absorption from kidney = increased blood volume
Arginine Vasopressin
ADH released due to high osmolality and low blood volume. Increase reabsorption
Atrial Natriuretic Peptide
Inhibits absorption from kidneys. Lowers blood volume
Baroreceptor Reflex Outline
Short term blood pressure regulation via negative reflex. Mechanoreceptors (sense pressure changes), central relays (brain stem and medulla oblongata) and effector efferent (innervates heart and vessels). Signals nucleus tractus soliteras in medulla
Baroreceptor Nerve Fibres
Increase aterial pressure = increase firing rate. Rate = dynamic, magnitude = static senitivity. Regulate sympathetic and parasympathetic
Blood Pressure Dropping
decreased pressure = less vessel stretching = decreased baroreceptor firing to NTS = decreased PNS and increased SNS = increased heart rate
Heart Failure Outline
Inability to maintain cardiac output. Decreasing output = decreasing pressure = increased SNS via baroreceptors = increase renin-angiotenion
