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HAP2_L9
Cardiovascular Physiology
| Question | Answer |
|---|---|
| receives oxygen-poor blood from tissues Pumps blood to lungs to get rid of CO2, pick up O2, via pulmonary circuit | right side |
| receives oxygenated blood from lungs Pumps blood to body tissues via systemic circuit | left side |
| Receives blood returning from systemic circuit | Right atrium |
| Receives blood returning from pulmonary circuit | Left atrium |
| Pumps blood through pulmonary circuit | right ventricle |
| Pumps blood through systemic circuit | left ventricle |
| prevent adjacent cells separating during contraction | desmosomes |
| transmit current across the entire heart and the myocardium behaves as a single coordinated unit | gap junctions |
| L) ventricle | receives most of the coronary blood supply |
| located at the base of the aorta and above the aortic valve | L) and R) coronary arteries |
| Coronary arteries branch and become | coronary capillaries then coronary veins |
| Coronary veins merge on | posterior into the coronary sinus |
| Coronary sinus empties into | R) atrium |
| Heart rhythm controlled by the | intrinsic conducting system and the extrinsic innervation of the heart |
| = less than 60 bpm | Sinus bradycardia |
| = greater than 100 – 150-180 bpm | Sinus tachycardia |
| = greater than 150+ bpm | Supra-ventricular tachycardia |
| = irregularly irregular from 50-150+ bpm | Atrial fibrillation |
| = greater than 150 bpm | Ventricular fibrillation |
| = 40-60 bpm or less | Heart block |
| = 60-100 beats per minute (bpm) | Sinus rhythm |
| – K+ ion channels close and Na+ ion channels open. The interior of pacemaker cells becomes more positive. | Pacemaker potential |
| -40 mV, Ca2+ -> SA node. action potential across both atria-> atria contract. Impulse delay at AV node. Ventricular action potential at apex. | depolarisation |
| Ca2+ inactive, and K+ open with efflux of K+ ions. memb potential -60 mV. | repolarisation |
| spontaneously depolarise and initiate heart rate | pacemaker cells |
| increases (↑) rate & force of heartbeat in response to fright, anxiety or exercise | Sympathetic nervous system |
| decreases (↓) heart rate when a stressful situation has passed. | Parasympathetic nervous system |
| The dominant influence of the autonomic nervous system is | inhibitory |
| Sympathetic cardiac nerves initiated in the | cardioacceleratory centre of the medulla |
| Sympathetic cardiac nerves release norepinephrine into | β1 adrenergic receptors (β1) shaped like ꓴ |
| Cardioacceleratory centre within the medulla oblongata projects sympathetic neurones to | Thoracic 1 – Thoracic5 (T1-T5) region of the spinal cord. |
| sympathetic neurones synapse with other sympathetic neurones in the | neck & thorax |
| Sympathetic fibres then run to the heart and release norepinephrine on β1 adrenergic receptors (β1 - ꓴ) in the | SA node AV node Heart muscle Coronary arteries |
| Cardioinhibitory centre within the medulla oblongata, sends impulses to | long preganglionic parasympathetic neurones via branches of the vagus nerve to the heart |
| Short parasympathetic fibres release acetylcholine (ACh) to act on | cholinergic (muscarinic type) receptors (ꓴ) in the: SA node AV node Heart muscle |
| period of heart contraction | Systole |
| period of heart relaxation | Diastole |
| blood flow through the heart in one heartbeat, with approximately 70 ml ejected from each ventricle after systole. | Cardiac cycle |
| Stroke volume (SV) x Heart rate (HR) | Cardiac output (CO) |
| 120 ml of blood that has collected in a ventricle during diastole | End Diastolic Volume (EDV) |
| 50 ml of blood that remains in a ventricle after it has contracted | End Systolic Volume (ESV) |
| 70ml of blood ejected from each ventricle | Stroke Volume (SV) |
| Preload 2. Contractility 3. Afterload | Stroke volume of 70ml affected by: |
| the degree to which cardiac muscles are stretched just before they contract | Preload |
| relationship between preload and SV | Frank-Starling law of the heart |
| increases venous return because of ↑ Sympathetic NS action and skeletal muscles squeezing and compressing veins. This results in less blood in muscles and more blood returning to the heart | Exercise |
| Severe blood loss or very rapid heart rate can cause | ↓ed venous return |
| defined as the contractile strength achieved at a certain muscle length | Contractility |
| ↑’s contractility, due to action of norepinephrine encouraging more Ca2+ ions to enter myocardial cells and more blood (SV) ejected from the heart. | Increase sympathetic NS activity |
| ↑ contractility, e.g. epinephrine, thyroxine, glucagon, digitalis, ↑ levels of extracellular Ca2+ ions | Positive inotropic agents |
| ↓ contractility, e.g. excess H+ ions (acidosis), ↑ levels of extracellular K+ ions and calcium channel blocker medicines. | Negative inotropic agents |
| the pressure that the ventricle must overcome to eject blood. … essentially the backpressure that arterial blood exerts on the aortic and pulmonary valves | Afterload |
| Backpressure of arterial blood in: Aorta | approximately 80 mm Hg |
| Backpressure of arterial blood in: Pulmonary trunk | approx. 10 mm Hg |
| in people with hypertension (↑ed BP) | afterload is important because it reduces the ability of the ventricles to eject blood |
| force exerted on the inside of a blood vessel wall where blood is contained. | Blood pressure |
| Cardiovascular centre in medulla oblongata Baroreceptors Chemoreceptors Higher brain centres | Short-term regulation – neural controls |
| Blood volume Effectiveness of heart as a pump . Resistance. Distribution | Blood pressure is determined by |
| the amount of friction the blood encounters as it passes through blood vessels, which occurs mostly in the systemic (peripheral) circulation | Resistance/Peripheral resistance |
| stickiness of the fluid, if ↑ed viscosity = ↓ blood flow | Blood viscosity |
| longer the vessel then ↑ed resistance | Total blood vessel length |
| changes frequently in smaller vessels, e.g. arterioles responding to neural or chemical controls by vasodilation (enlarge) or vasoconstriction (narrow) | Blood vessel diameter |
| Aortic arch Carotid sinuses within internal carotid arteries | Baroreceptors Location |
| Stretched in response to ↑ arterial BP Inhibits vasomotor & cardio-acceleratory centre Cardio-inhibitory centre stimulated Vasodilation and ↓ heart rate & contractile force then decrease BP | Baroreceptors Action |
| in aortic arch (located near baroreceptors) | Aortic bodies |
| in large arteries in the neck (located near baroreceptors) | Carotid bodies |
| Respond to ↑CO2, ↓O2, ↓pH | Chemoreceptors |
| cardio-acceleratory centre and cardiac output increased Vasomotor centre & vasoconstriction occurs BP ↑’s and blood sent rapidly to heart and lungs | Chemoreceptors Impulses sent to |
| ↑ blood volume or ↑BP and glomerular capillaries filters fluid from blood | direct renal mechanism |
| ↓ arterial blood pressure stimulate response | indirect renal mechanism |
| renin acts on | plasma protein angiotensinogen |
| angiotensinogen converts to | angiotensin I |
| angiotensin I acted on by | angiotensin-converting enzyme |
| angiotensin I converts to | angiotensin II |
| long nephron loop, glomerulus closer to the cortex-medulla junction, efferent arteriole supples vasa recta | juxtamedullary nephron |
| short nephron loop. glomerulus further from the cortex-medulla junction, efferent arteriole supplies peritubular capillaries | cortical nephron |
| chemoreceptors for NaCl content of filtrate entering distal convoluted tubule | macula densa cells |
| mechanoreceptors in afferent arteriole wall that detect BP | granular cells |
| granular cells of JGA release | renin |
| in the lungs, blood of the pulmonary capillaries is rich in | ACE |
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