Cardiovascular System 1 PDF

Cardiovascular System 1  Right AV (Tricuspid) Pulmonary Valve semilunar valve SVC, IVC RIGHT atrium RIGHT Pulmonary coronary sinus ventricle trunk & ant. cardiac...

Cardiovascular System 1  Right AV (Tricuspid) Pulmonary Valve semilunar valve SVC, IVC RIGHT atrium RIGHT Pulmonary coronary sinus ventricle trunk & ant. cardiac Pulmonary veins arteries Lungs Body AORTA LEFT LEFT atrium Pulmonary ventricle veins ascending aorta Aortic Left AV semilunar valve (Mitral) valve  What makes blood flow? Pressure differential! OD BLO  Fluids always flow DOWN their pressure gradient! More gradient = more flow! High pressure Low(er) pressure F = ∆P/R And what is our -If ∆P ↑ = F ↑ pressure source? -If ∆P ↓ = F ↓ -If R ↑ = F ↓ -If R ↓ = F ↑ relaxation contraction  Cardiac Output (CO) Total volume of blood pumped by each ventricle per minute (mL / min) = to “blood flow” Under normal circumstances, both ventricles CO is equal (each ventricle will pump out what it receives from the other Stroke Determined by: volume (mL per beat) Heart rate (beats/min) CO = heart rate (HR) x stroke  CARDIAC RESERVE = CO (max) – CO (resting) (= amount that a heart can pump above its resting CO) Reserve is usually 4X (untrained) – 7X (trained) resting CO t even at rest, CO/min typically > or = to a person’s entire blood volume  Factors related to stroke volume ESV = End-Systolic Volume (amount of blood in chamber at end of systole) EDV = End-Diastolic Volume (amount of blood in chamber at end of diastole) SV = EDV – ESV (in mL) Ejection Fraction = % of EDV ejected EF = SV / EDV Healthy EF = 50 - 70% (-ish)  Textbook t res t SV a THIS IS A MEAN! sez: = 7 0 mL Heart size correlated with body size and obviously there is a wide range of human body size CO for someone 5’ tall vs 6’ tall, what do you think? EF is a much better clinical assessment tool because eliminates body size as a factor, regarding health of heart! (IT’S RELATIVE!) 3 Factors Regulating SV 1) Preload: The tension/force (degree of stretch) in the left ventricle at end- diastole (immediately before contraction). Preload is determined by blood VOLUME in the ventricle at end-diastole = ↑ venous return = ↑ EDV = ↑ SV & CO (Frank-Starling Law of the Heart) 2) Contractility: the heart muscle’s ability to generate force based on sympathetic & hormonal input to heart. 3) Afterload: pressure that must be overcome for ventricles to eject blood Hypertension (w/ high BP= more blood left after systole) = heart wall is thicker ength-tension relationship = Goldilocks zone of force Muscles that are too Muscles that are shortened, stretched too much, few Z-discs can’t get closer to myosin heads able to each other grab on to actin LOOKING AT PRELOAD! Between 80-120% resting length, maximal force can be generated  PRELOAD! Frank-Starling Law and Skeletal muscles normally Cardiac Muscle kept near optimal length Length-tension So as they stretch, they Typical cardiac operating zone weaken Cardiac muscle fibers = THE MORE BLOOD IS IN normally kept SHORTER than THE HEART (stretching it to optimal length optimal length), So as they stretch, they CAN THE HARDER THE HEART  Frank-Starling Law: As preload increases, CO also increases! I.E., the heart pumps what it gets! What causes increased preload? Remember, higher preload = higher EDV What does Frank-Starling “mechanism” mean for Left vs Right CO?  CONTRACTILITY - Factors that influence the force of each contraction, INDEPENDENT of EDV - I.e., EXTRINSIC factors - PRIMARILY WE ARE DEALING WITH ALTERING MEMBRANE POTENTIALS TO INCREASE OR DECREASE CONTRACTION FORCE  junctions between cells anchor cardiac cells Nucleus Intercalated discs Cardiac muscle cell Gap junctions Desmosomes : prevent allow ions to cells from pass; separating adjacent cells during are contraction interconnecte d (a) Cardiac muscle contractio is pretty similar to skeletal mm. But there are some important difference …  parasympathetic GVE = ? 3) Can be directly Cardiac SA/AV excited OR nerves inhibited nodes sympathetic GVE = ? s er fib s) i n g er ct fib du e n nj co ki c ur i a (P rd Ca 1) INTRINSIC CONDUCTION 2) WHOLE ORGAN (w/ gap junctions) CONTRACTION (SYNCYTIUM)  Ca++ coming from extracellular space, flooding in using T-tubules in addition to sarcoplasmic reticulum ANYTHING INCREASING Ca++ INFLUX INCREASES Cardiac CONTRACTION FORCE! muscle cell Mitochondrion Intercalated Nucleus disc T tubule Mitochondrion Sarcoplasmic reticulum Z disc Nucleus Sarcolemma I band I band (b) A band Figure 18.11b Positive inotropics: Sympathetic neurons & norepinephrine (direct innervation) Circulating epinephrine / adrenaline Thyroxine On Beta-1 (T4), Glucagon adrenergics Digitalis extracts (drugs) Hypercalcemi a Negative inotropics: Acidosis (H+) Hypocalcemia Calcium channel blockers (drugs) Afterload… = Back pressure created by arterial blood (Newton’s 3rd law) Created by the mass (inertia) of blood and its resistance to flow - Viscosity of the blood - Vasoconstriction - Blood volume Are primary determinants of afterload typically More on this when we talk about blood pressure regulation OTHER COMMON EFFECTS: - Skeletal muscle contraction ( can temp increase create resistance ) - Peripheral vascular disease: ESP. ATHEROSCLEROSIS / ARTERIOSCLEROSIS Arteriosclerosis effects: What does it do to afterload? -distensibility lost -lumens of vessels shrink Both of these have what effect on pressure, and therefore afterload? This is resistance training for the heart What happens to any muscle required to exert more force? Hypertrophy! But against resistance, the myocardium hypertrophies inwardly. (CONCENTRIC HYPERT.) So more and more force required to pump less and less blood (High pressure, low SV!) Less blood into coronary AA, less healthy heart Heart failure may be in the cards, not to mention stroke, etc. Hard work against LOW resistance (like in healthy aerobic athletes) ECCENTRIC HYPERTROPHY: Myocardium thickens, but ventricle expands, allowing for increased SV and!  Regulation of the cardiac cycle -Some cardiac muscle cells exhibit AUTORHYTHMICITY i.e., unlike skeletal muscle, they depolarize ON THEIR OWN!) - Because of the syncytium, depolarization and AP in 1 cell rapidly is conducted to other cells - THEREFORE, THE HEART WILL BEAT ON ITS OWN, REGARDLESS OF AUTONOMIC INPUT! - The role of autonomics is to regulate the autorhythmicity so that its rate ( and therefore CO) matches the needs of the But first, what’s up with autorhythmicity? - Cells in SA node, AV node, and cardiac conducting fibers (e.g., Purkinje fibers) have unstable RMP - BC cell membranes LEAKY to Na+ - Therefore, RMP, always creeping toward AP threshold… - Spontaneous APs Pacemaker Potentials (SA, AV, Purkinje) Why is SA Node the PRIMARY pacemaker? Whichever cells have the fastest depolarization/repolarization rate, set the clock. Because they’re sending new action potential through the whole system so often, everybody else’s rate is forced to go along. So if SA node is SA node rate = 70-80 X / min busted, who typically (100X intrinsic, no neural takes over as input) pacemaker? 1) SA node depolarizes 2) AP conduction through atrial myocardium; ATRIA CONTRACT 3) AP reaches AV node (through myocardium) 4) AV node depolarizes 5) Signals conducted to ventricles through bundle branches, Purkinje fibers etc. 6) VENTRICLES CONTRACT (while Atria are relaxing) This pattern makes sure atria and ventricles alternate systole / diastole  ECG: Your window to the heart QRS complex Sinoatrial node Ventricular depolarization Atrial Ventricular depolarization repolarization Atrioventricular node P-Q S-T Interval Segment Atrial repolarizatio Q-T Interval n masked by QRS SA node R Depolarization Repolarization R P T Q P T S 1 Atrial depolarization, initiated by the SA node, causes the Q S P wave. 4 Ventricular depolarization AV node R is complete. R P T P T Q S 2 With atrial depolarization Q S complete, the impulse is 5 Ventricular repolarization delayed at the AV node. begins at apex, causing the R T wave. R P T P T Q S Q 3 Ventricular depolarization S begins at apex, causing the 6 Ventricular repolarization QRS complex. Atrial is complete. repolarization occurs. Figure 18.17  Abnormal ECG interpretation (a) Normal sinus rhythm. (b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min. (c) Second-degree heart block. (d) Ventricular fibrillation. These Some P waves are not conducted chaotic, grossly irregular ECG through the AV node; hence more deflections are seen in acute P than QRS waves are seen. In heart attack and electrical shock. this tracing, the ratio of P waves to QRS waves is mostly 2:1. Figure 18.18  Extrinsic Innervation 1) Parasympathetic: “rest and digest” CN X = Vagus Vagal tone: at rest dominant influence is inhibitory ACh; muscarinic receptors; K+ out (hyperpolarizes); Lowers RMP, so further from threshold, takes longer to reach AP  Extrinsic Innervation 2) Sympathetic: T1-T5 nerves via cervical & upper thoracic ganglia of sympathetic chain (synapse & then cardiac plexus) NE @ B1 adrenergic receptors ↑Ca2+ influx = threshold reached quicker ( + contractility) ↑ pacemaker; ↑ HR Note: if only ↑HR = SV ↓ b/c ↓EDV (less time ventricle filling) Adrenaline/epinephrine same effect!  Communication at subconscious level Cerebral cortex (frontal lobe) Hypothalamus, brainstem, and spinal reflexes all get to Limbic system make autonomic (emotional input) “decisions” Hypothalamus Overall integration But hypothalamus is of ANS, the boss the one ring… Brain stem (reticular formation, etc.) Regulation of pupil size, Sensory respiration, heart, blood pressure, swallowing, etc. input Spinal cord (GSA & GVA) Urination, defecation, erection, and ejaculation reflexes Figure 14.9  Limbic (emotional) input Sensory input (GSA & GVA) Hypothalamus (Hypothal neurons also direct access) Medull a Medulla and cord reflexes are the only DIRECT neural control!  Neural Control: Atrial (Bainbridge) reflex: sympathetic reflex b/c of ↑venous return stretch receptors (GVA) in atrial walls stimulates sympathetics to ↑ HR & SA node CONTROLLED VIA CARDIOVASCULAR CENTERS OF MEDULLA  Monkey pirate sez: There be also chemoreceptor and baroreceptor reflexes from arteries! More on that next week!  Exercise (by Heart rate Bloodborne Exercise, skeletal muscle and (allows more epinephrine, fright, anxiety respiratory pumps time for thyroxine, ventricular excess Ca2+ filling) Venous Sympathetic Parasympathetic Contractility return activity activity EDV ESV (preload) Stroke Heart volume rate Cardiac output Initial stimulus Physiological response Note: Stroke volume is controlled Result by venous return (EDV) Figure 18.22  Heart rates in infants SUPER high! (low body mass fx, it’s kind of a mammal thing…) Mean HR goes down through juvenile period “Maximal heart rate (HRmax) declines substantially with age, but the magnitude and possible modifying effect of gender, body composition, and physical activity are not fully established.” Nes et al, 2013 Several studies have shown that the “220- age” formula consistently underestimates Max HR, especially in people over 30 Whyte et al 2007 What they all look at is the slope, but not the CLUSTERING! (The strength of the relationship) Notice that athletes have much broader range. ALSO LOWER MaxHR (because Whyte et al 2007 hearts MORE FIT!)  In any case, these are better formulas for estimation: HRmax = 208 − 0.7 × age (Tanaka et al. 2001) HR Importantmax = 211 − 0.64·age (Nes et al. if HR max (or some target HR goal related to 2013) that) is part of your exercise plan for a client We can’t usually measure it directly, though of course this gives the best info for THAT INDIVIDUAL Good idea to ADJUST your estimate with more data on the client (their bodies may adapt, they may have congenitally  Homeostatic Imbalances Tachycardia: abnormally fast heart rate (>100 bpm) If persistent, may lead to fibrillation Ironically, can lead to low flow if fast enough (HEART CAN’T FILL BTW BEATS!) HOWEVER TACHYCARDIA IS NORMAL DURING EXERCISE! Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation Is desirable result of endurance training When pathological, both can lead to heart failure!  Congestive heart failure - “congestive” BC failure of either ventricle causes fluid back up on other side (LV failure causes backup in lungs (pleural effusion), RV failure in systemic aa (peripheral edema)) - Can be caused by a variety of factors (coronary a. disease, infarct, conduction/rhythmicity issues, etc., etc….) - Vicious cycle: reduced EF means less blood to coronary aa., means lower EF, means less blood to coronary aa…. - ULTIMATELY HEART WEAKENS, TYPICALLY UNTIL CARDIAC ARREST. Typically a long, slow process, defined by dropping EF  In CHF people want to move less… But they need to move more! Research shows EXERCISE is fantastic treatment and can even reverse