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HAP2_L9

Cardiovascular Physiology

QuestionAnswer
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
Created by: 1092422624234171
 

 



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