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The Cardiovascular System
Compare and contrast the systemic and pulmonary systems Systemic:Left side of the heart receives oxygenated blood retiring from they lungs and pumps this blood thru’out the body to supply oxygen and nutrients to tissue. Blood vessels carrying blood to and away from the body tissue are ALL part of the SYSTEMIC circuit. -venae cavae , L +R atrium, ventricle, aorta and capillaries Pulmonary: The right side of the heart receives deoxygenated blood from the body tissue and pumps it to the lungs to be re-oxygenated and dispel CO2 .The blood vessels carrying blood to and from the lungs are part of the pulmonary circuit.
- Pulmonary arteries and Veins Describe the coordinated electrical activity of the heart: § Trace an impulse from the SA node to thee end of repolarisation
Depolarisation: The AP begins when the pacemaker potential reaches threshold -40mV. Ca2+ channels open allowing excess entry of Ca2+ from the ECF
Repolarisation: due to Ca2+ channels inactivating and K+ channels opening allows EFFLUX of K+ bring membrane back to it’s most NEGATIVE voltag
§ Define pacemaker: 1% of cardiac fibbers have auto rhythmic ability to depolarise ( more +’ve) spontaneously and thus pace the heart. Initiate AP that spread throughout the heart compare resting membrane potential with pacemaker potential Pacemaker Potential: Due to the special properties of the ion channels in the sarcomlema, in hyper polarisation closes K+ channels and opens Na+ channels ( at the end of an AP)The Na+ influx makes the membrane more POSITIVE
Resting membrane potential: -90mV in cardiac muscle , potentail difference across a membrane § Define spontaneous depolarisation of cardiac tissue and list they ionic currents responsible for this electrical activity of the heart Depolarisation is due to Na+ influx thur’ the fast voltage-gated Na+ channels. A +’ve feedback cycle rapidly opens many Na+ channels reversing the membrane potential. § Describe the role of the AV node in transmitting and filtering impulses From the SA node the depol. wave spreads vis gap junctions thru’out the atria via the internal p.way to the AV node-in the intertribal septum above the tricuspid valve. Impulse is delayed for 0.1s so that atria can respond and complete their contraction before ventricles contract.AV node conducts impulses slowly. § Compare the rates of depolarization and action potentials of the different cardiac conduction cells
§ Describe the valvular events in the cycle,the trans-valvular pressure gradients and the generation and timing of the first and second heart sounds LUB ->pause: indicates period when heart is relaxing -> DUB lub: occurs as AV valves closing - loud and long point at which ventricular P’> atrial pressure- beginning of ventricular systole DUB: occurs as SL valves snap shut - short and sharp sound Discuss the electrocardiograph (ECG): § Describe the cardiac electrical events that correspond to the Pwave,P-Rinterval,QRScomplex,Q- Tinterval and T wave of the ECG recording Refer to figure above: § Identify atrial depolarisation on the electrocardiogram P-R interval includes atrial depolarisation and contraction § Describe the relationship between the ECG recording and the cardiac cycle Ref. to figure above Discuss cardiac function: § Define cardiac output stroke volume and the relationship between cardiac output,stroke volume and heart rate Cardiac output (CO) is the amount of blood pumped out by each ventricle in 1 min CO=SV x HR
WAVE TIME P 0.08s depol. from SA node thru’atria atrial depolarization ORS-complex 0.08s vent. DEpol T 0.16 vent.REpol slower and lower amplitude P-R interval 0.16s begininng of atrial excitation to ben. excitation includes atrial depol. and contraction Q-T interval 0.38s beg. of ven DEPOL to ven. REpol
Stroke Volume ( SV): vol of blood pumped out by one ventricle with each beat- correlated with force of ventricular contraction § Define inotropic:contraction of myocardium lusitropic: relaxation of myocardium chronotropic : firing of SA node- Heart Rate § Define preload: Degree to which cardiac muscle cells are stretched prior to contraction- ^ EDV ^ SV( Frank-starling Law) contractility: contractile strength achieved at a given muscle length- can enhance SV afterload: the pressure that the ventricles must overcome to eject blood-reduced SV ,and describe how stroke volume is regulated in terms of these three § Explain how changes in ventricular pressure, volume, radius and wall thickness affect ventricular wall tension/ stress
§ Explain how stretching cardiacmyofilaments can increase stroke volume(Frank- Starlingrelationship) Relationship between preload and SV is F-S law, optimal length of muscles is max no. of active cross bridges between actin and myosin and the contraction force is max. Exhibit length- tension relationship. Stretching cell + increase in contractile force. VR increase amount of blood retiring to heart ^ EDV and SV and CO and force of contraction § Explain how changes in wall stress affect myocardial oxygen demand
§ Explain how sympathetic activation affects myocardial contractility/ inotropy, in terms of circulating adrenaline, the receptors involved, cAMP and calcium ion movement ^SNS stimulation ^ contractility , NE or E binding to B-adrenergic receptor and innate cAMP second-messenger system that ^ Ca2+ entry which promotes cross-bridge formation and enhances ventricular contraction. POSITIVE inotrophic agents
§ Explain the effect of parasympathetic activation on the heart and the ‘normal’ vagal tone of the heart The parasympathetic nervous system (PNS) releases the hormone acetylcholine to slow the heart rate.
Diastolic blood pressure (DBP):It’s defined as the lowest pressure measured in a systemic artery during the cardiac cycle. This lowest pressure coincides with ventricular diastole phase of the cardiac cycle. In a normal healthy individual the DBP is measured to be 80 mm of Hg. mean arterial blood pressure (MAP) :MAP is the average pressure within a blood vessel during one cardiac cycle. MAP=CO x TPR MAP=DBP+1/3(SBP-DBP) total peripheral vascular resistance (TPR) :Total resistance offered by systemic arteries to the blood flow across them is referred to as TPR. TPR is responsible for maintaining the diastolic blood pressure. The major contribution to the TPR is provided by the systemic arterioles. § Describe changes in blood pressures noted in the systemic circulation from aorta to capillaries to veins
§ Explain the pulsatile nature of aortic and small artery pressures and non-pulsatile nature of smaller vessel pressures Aortic pressure is highest at the aorta and becomes less pulsatile and lower pressure as blood vessels divide into arteries, arterioles, and capillaries such that flow is slow and smooth for gases and nutrient exchange. § Define auto-regulation of blood flow by body tissues and list the common mechanisms of such control. Local manifestation of blood flow in the body, the intrinsic ability of of an organ to maintain constant blood flow despite changes in perfusion pressure. Occurs in the absence of neural or humoural responses
metabolic, myogenic and endothelial responsible for the vasoconstriction
§ List the extrinsic and extrinsic mechanisms controlling arteriolar smooth muscle in the systemic circulation
Describe the control of arterial blood pressure: § Summarise the factors involved in maintaining systemic arterial blood pressure. -Peripheral resistance - vessel elasticity - blood volume -cardiac output § List the four neural short-term control mechanisms and briefly explain their mechanisms of action (what stimulates them and what effect they have)
- Baroreceptor reflex: change peripheral resistance, HR and SV in response to changes in BP
- Chemoreceptor Reflexes: senscory receptors senstive to O2, CO2 and pH levels of blood
- CNS ischemic response: results from high CO2 or low pH in medulla and increases peripheral resistance
Describe the functioning of the venous system: § Explain why the venous system is called a capacitance system: contains 60% of the body’s blood volume § Describe how changes in venous return affect cardiac output with reference to the Frank-Starling relationship Ref to F-S curve above § Describe and explain the effect on venous return (and hence cardiac output) of changes in blood volume and in systemic arteriolar and venous smooth muscle tone Ref. to image below § Describe and explain the effect on venous return of changes in posture On the transition from sitting in a chair to standing, blood is pooled in the lower extremities as a result of gravitational forces. Venous return is reduced, which leads to a decrease in cardiac stroke volume, a decline in arterial blood pressure, and an immediate decrease in blood flow to the brain. § Describe how normal inspiration,contraction of skeletal muscle and venous valves affect venous return Ref.to image below
Describe the changes in cardiac output that occur with exercise, with reference to: § Alterations in contraction of skeletal muscle around veins § Venous return on the Frank-Starling relationship Exercise ^ SNS activity and ^ skeletal respiratory pumps^Ventricular filling time due to decreed HR thus ^VR, EDV and SV § Autonomic effects on cardiac contractility and heart rate CNS response to exercise ^SNS and decrease PNS activity thus ^contractility and HR but decrease ESV ultimately ^CO
