PSIO FINAL EXAM STUDY GUIDEUNIT 1Path of blood flow through the heart and the lungs:1. Right Atrium (deoxygenated blood)2. Tricuspid valve3. Right ventricle4. Pulmonary valve5. Pulmonary trunk and pulmonary arteries6. In pulmonary capillaries, blood loses Co2 and gains O27. Pulmonary veins (oxygenated blood)8. Left atrium9. Bicuspid valve10. Left ventricle11. Aortic valve12. Aorta and systemic arteries13. In systemic capillaries, blood loses O2 and gains CO214. Superior vena cava/ Inferior Vena Cava/ Coronary sinusSequence of excitation of the cardiac conduction system:1. P-Wave: atrial depolarization2. QRS complex: Ventricular depolarization3. T-wave Ventricular repolarization4. P-Q Interval: time it takes fro electrical excitation to travel through atria5. S-T Segment: time ventricular fibers fully depolarized6. Q-T intervals: time from ventricular depolarization to ventricular repolarizationMajor determinants of stroke volume, and the underlying mechanisms of each:1. Aortic (or pulmonary artery) blood pressure “afterload”a. Ventricles cannot eject blood into aorta or pulmonary artery until the pressure in the ventricle exceeds the pressure in the arteryb. Thus, an increase in pressure will have a major impact on the work of the heart and on the stroke volume. 2. End-diastolic volume “preload”a. The cardiac chambers are mechanical pumps, and therefore can pumponly what is delivered to themb. Preload = end-diastolic volumec. Major impact on the stroke volumed. Stroke volume cannot increase unless the rate of cardiac filling also increases3. Active or passive contractilitya. Refers to the strength of cardiac muscle contractionb. Active and passive i. Active: stimulation of the sympathetic nerves to the heart1. Norepinephrine or epinephrine2. Increased rate of pacemaker activity3. Increased force of cardiac muscle contractionii. Passive: the result of changing the length of the cardiac muscle fibers “Frank-Starling mechanism”1. Relationship between the rise in stroke volume and the rise in preload2. If the preload is increased – even in a heart with now nerve supply – the stroke volume will increase systemically.Autonomic nervous system (ANS) controls heart rate:1. The heart rate is modified by changes in the ANS2. The effects are called “chronotropic effects”3. ANS activity can be modified by circulatin hormones and by higher brain structures4. The sympathetic neurons that send nerve fibers to the heart are located in the caudal portions of the medulla oblongata (the “cardiovascular center”)5. Neurons in the CV center synapse upon preganglionic neurons in the intermediolateral cell columns (lateral gray horns) of the thoracic spinal cord6. The preganglionic neurons then synapse on postganglionic neurons, which are located in the ganglia of the sympathetic chain7. The postganglionic neurons then send their axons to the SA and AV nodes, and the cardiac muscle fibers8. Preganglionic neurons release acetylcholine (Ach) onto postganglionic neurons9. The postganlionic neurons then release norepinephrine (NE) onto the target cells10. NE is the postganglionic neurotransmitter for the sympathetic nervous system11. NE activates beta-1 receptors, which have wde-spread effects on the cardiac nervous and muscle tissueDescribe the forces that result in movement of fluid into and out of capillaries:1. Diffusion: movement of molecules or ions from a region of higher concentration to one of lower concentration until equilibrium is reached PASSIVE PROCESS2. Bulk Flow: bulk flow refers to the movement of a fluid from a region of higherpressure to one of lower pressure PASSIVE PROCESSa. Fluid exchange primarily based on bulk flowi. Blood hydrostatic pressure (BHP): pushes fluid out through thecapillary poresii. Interstital fluid osmotic pressure (IFOP): pulls fluid out via osmosis; this pressure is very small compared to the BHPiii. The blood colloid osmotic pressure (BCOP): the BCOP is tehresult of difference in protein concentration between plasma and ISF, which tends to pull water from the ISF and intothe capillariesiv. Interstitial fluid hydrostatic pressure (IFHP): sue to the pressure exerted by interstitial fluid, but it is normally very smallb. NFP = (BHP + IFOP) – (BCOP+ IFHP)c. Outward (filtration) – Inward (reabsorption)d. BHP and BCOP are the major factors that determine fluid movement across the capillary wall3. Transcytosis: substances enter pinocytotic vesicles, move to endothelial cells via endocytosis and exit on opposite side via exocytosis ACTIVE PROCESSDescribe principal components of vascular resistance, and explain why vessel diameter has such a large impact on resistance:1. Blood flow is proportional to the driving pressure, and inversely proportionalto the resistance to flowa. Flow = driving pressure / Resistance2. Resistance is calculated after flow and pressure are measured3. Resistance is the sum of all forces that retard flow4. Resistance = (viscosity)(vessel length)/radius to the 4th powera. Halving the radius results in 16-fold increase in resistance. Describe how hormones can either decease or increase blood pressure:1. Catecholamines (NE and Epinephrine)a. Circulate, and bind directly to cardiac muscle fibers and to blood vessel smooth muscle cellsb. The effect is an increase in HR and SV and constriction of veins and arteriolesc. NOTE: ateries supplying the brain and heart have little smooth muscle and are not subject to vasoconstriction by the sympathetic DIv. or catecholaminesd. The vessels autoregulate2. Antidiuretic Hormone (ADH): a. causes intense vasoconstriction in cases of extremely low BPb. produce by hypothalamus and released form posterior pituitary when blood loss is severe, and blood pressure is reduces. c. Kidney retain more water (decreases urine output), arterioles constrict (increases blood pressure), sudoriferous glands decrease water loss by perspiration from skin. 3. Angiotensin II:a. Causes instense vasoconstriction when renal perfusion is inadequateb. One of the most powerful vasoconstrictorsc. Acts on all arterioles simultaneously when it is released into the bloodd. Results in increase in vasucal resistance when blood pressure is too lowe. Low blood pressure results in the release of renin by the kidney 4. Aldosterone: causes water retention and increases blood volumea. Controls aldosterone secretionb. When angiotensin II levels are increased, aldosterone is secretes by adrenal cortex, which increases salt and