Cardiovascular System Flashcards
(105 cards)
1
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The Cardiovascular System
A
A circulating transport system - A pump (the heart) - A conducting system (blood vessels0 - A fluid medium (blood) Functions to transport materials to and from cells
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5 Functions of Blood
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- Transport of dissolved substances
- Regulation of pH and ions
- Restriction of fluids losses at injury sites
- Defence against toxins and pathogens
- Stabilisation of body temperature
3
Q
Characteristics of Blood
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- Blood volume:
M: 5-6L F: 4-5L - Blood is highly viscous, slightly alkaline (7.35-7.45), temp 38°C
- Blood consists of: ~55% plasma and ~45% formed elements (erythrocytes: RBC, Leukocytes: WBC, Thrombocytes: Platelets)
- Hematocrit: Measure of % of RBC in whole blood
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Q
Formation of Blood Cells
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- Formed elements develop by Hematopoiesis in red bone marrow
- Hemocytoblasts differentiate into:
1) Myeloid stem cells: give rise to RBC platelets, eosinophils, basophils, neutrophils, monocytes
2) Lymphoid stem cells: give rise to lymphocytes - migrate to lymphatic system to complete maturation
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Q
Erythrocytes (RBCs)
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- RBC’s = 99% of blood’s formed elements
- Approx 5 million RBC per microlitre of blood (1 drop ~50 microlites):
- High SA:V (quick absorption and release of oxygen)
- Bioconcave discs
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Blood Typing
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- Cell surface proteins that identify cells to immune system
- Normal cells are ignored and foreign cells attacked
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4 Basic blood types
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- Type A (surface antigen A) has antibodies to B
- Type B (surface antigen B) has antibodies to A
- Type AB (surface antigens A and B) neither antibodies
- Type O (neither A nor B surface antigens) antibodies to A and B
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Q
Rhesus (Rh) Factor
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- 5 Rh antigens
- refers only to the D antigen
- Rh positive (Rh+): presence of surface antigen
- Rh negative (Rh-): absence of surface antigen
- RBC: surface antigen A and Rh antigen - A+
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Cross-Reactions
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- Normal cells are ignored and foreign cells attacked
- Plasma antibody meets its specific surface antigen
- Blood will agglutinate and hemolyze
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Functions of LEukocytes
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- WBCs accumulate at the sites of infection/inflammation: lymphocytes recirculate between blood and tissues
- WBCs ‘emigrate’ from blood compartment: adhesion molecules on WBC and endothelial cells allow WBCs to ‘stick’ to endothelium then move to site of infection/inflammation via chemotaxis
- Once at the site of infection/inflammation WBCs carrout out various functions in the inflammatory/immune response
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Thrombocytes (Platelets)
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- Cell fragments involved in human clotting system
- Disc-shaped structures, no nuclei
- Release important clotting chemicals
- Temporarily patch damaged vessel walls
- Actively contract tissue after clot formation
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Platelet production
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- Thrombocytopoiesis
- Occurs in bone marrow
- Megakaryocytes break into 2000-3000 cell fragments in red bone marrow
13
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Hemostasis
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- The cessation of bleeding
- Three phases
1) Vascular phase
2) Platelet phase
3) coagulation phase
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Q
Vascular phase (Hemostasis)
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- Vascular spasm: lasts about 30 mins
- Contraction of smooth muscle of damaged blood vessel wall caused by: Damage to smooth muscle and endothelial cells, activation of platelets (release vasocontrictors) and reflexes are initiated by pain receptors
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Q
Platelet Phase (Hemostasis)
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- Begins within 15 seconds after injury
- Platelet plug formation
- Platelets contact and adhere to damaged tissue in blood vessel wall. Platelets become activated, extend projections to attach to one another, positive feedback loop of aggregration. Activated platelets release clotting compounds, plug size restricted by inhibitory compounds, negative feedback and formation of blood clot
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Q
Coagulation Phase (Hemostasis)
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- Begins 30 seconds or more after injury
- Converts prothrombin (enzyme produced by liver) into thrombin.
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Q
Clot retraction and repair
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Platelets pull on fibrin threads - clot contracts drawing wound edges closer together.
Fibroblasts form connective tissue and new endothelial cells repair vessel lining - clot eventually dissolved through action of plasmin (plasma enzyme)
18
Q
Organisation of the CV system
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The CV System is a closed loop. The heart is a pump that circulates blood through the system. Arteries take blood away from the heart and veins carry blood back to the heart
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Q
Pulmonary Circuit
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Carries blood to and from gas exchange surfaces of lungs
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Systemic Circuit
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Carries blood to and from the rest of the body
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Location of the Heart
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- Rests on diaphragm
- Situated in the mediastinum
- Two-thirds lies to left of midline
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Pericardium
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- Heart enclosed and stabilised by pericardium: fibrous network of collagen fibres - lined by serous membrane with 2 layers
1) Outer = parietal pericardium - lines inner surface of tough pericardial sac
2) Inner = visceral layer (epicardium) - attached to outer surface of heart - Pericardial cavity filled with fluid: reduces friction
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Q
Heart Wall
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1) Epicardium (visceral layer of serous pericardium)
2) Myocardium (cardiac muscle tissue): bulk of heart tissue, provides pumping action
3) Endocardium: continuous with endothelial lining of great vessels
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Q
Myocardium
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- Cardiomyocytes or cardiac muscle
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Cardiac muscle fibres
- Contain single central nucleus
- Connected via gap junctions
- Have very high aerobic capacity
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Intercalated discs
- Specialised contact points between cardiomyocytes
| - Join cells via gap junction and desmosomes
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Functions of intercalated discs
- Maintain structure
- Enhance molecular and electrical connections (transfer force of contraction)
- Conduct action potentials
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Superficial Anatomy of Heart
- Great veins and arteries at the base
- Pointed tip is apex
- Coronary sulcus: divides upper atria from ventricles
- Interventricular Sulus: Separate R & L ventricles
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Chambers of the Heart
- 4 chambers: upper 2 atria, lower 2 ventricles
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Atria
- Receive blood into the heart
- R and L atria separated by inter-atrial septum
- Septum has fossa ovalis (shallow depression in wall where foramen ovale of foetal heart was - closes over at birth)
- Auricle = 'flap' of expandable atrium visible when not filled
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Ventricles
- Right ventricle pumps blood to pulmonary circulation: thinner wall, less pressure than left ventricle
- Left ventricle pumps blood to systemic circulation: thicker wall, greater pressure, rounder in shape
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Blood flow through the heart
- Right atrium receives blood from systemic circulation via: superior vena cava (SVC), inferior vena cava (IVC), colonary sinus
- right atrium to right ventricle through AV valve
- right ventricle to pulmonary trunk and pulmonary arteries
- then into pulmonary circulation
- blood passes through lungs and returns to heart through 4 pulmonary veins
- pulmonary veins into left atrium
- left atrium to left ventricle through AV valve
- then into systemic circulation via aorta
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Valves of the heart
- direct blood flow through and out of the heart
- valves prevent backflow of blood
- composed of dense connective tissue covered by endothelium
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Atrioventricular (AV) Valves: Valves of the Heart
- Lie between atria and ventricles: right AV and left AV
- Cusps linked by chordae tendinae to papillary muscle
- Pressure in atria > pressure in ventricles: valves open and blood flows in ventricles
- Pressure in ventricles > pressure in atria: valves close and blood flows into aorta or PA
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Semilunar Valves: Valves of the Heart
- Between ventricles and major arteries (aorta and PA)
- Prevent blood flowing back into heart
- Pulmonary semilunar valve: at base of pulmonary arterial trunk
- Aortic semilunar valve: at base of aorta
- No valves between veins and atria
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Coronary Circulation: Coronary Arteries
- branch from ascending aorta
- Fill upon diastole
- Carry oxygenated blood to the myocardium: pulsatile blood flow, little flow during systole
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Coronary Circulation: Coronary Sinus
- Carries deoxygenated blood back to right atrium
| - Thin walled vein with no smooth muscle to alter diameter
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Clinical Note: Myocardial Infarction
- Blockage of coronary artery
- Lack of oxygen to muscle > muscle death
- causes: atherosclerosis
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Cardiac Muscle Fibres: Autorhythmic fibres
- Specialised muscle fibres
- Initiate and conduct AP
- Form conduction system
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Cardiac Muscle Fibres: Contractile fibres
- 99% of all muscle fibres
| - Provide mechanical work of the pump
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Components of Conducting System: Sinoatrial Node (SN)
- Spontaneously depolarises (80-100 times/min)
- Rate of depolarization modified by neurotransmitters from ANS
- E.g. resting HR slower than rate of depolarisation of SA node due to parasympathetic tone
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Components of Conducting System: Atrioventricular (AV) Node
- Spontaneous depolarisation 40-60 times/min
- Conduction slows at AV node (AV nodal delay)
- Delay allows atria time to contract
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Other Components of Conducting System
- AV bundle
- Right and left bundle branches
- Purkinje fibres
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Action potential of autorhythmic cell
a) components of the conducting system
b) changes in the membrane potential of a pacemaker cell in the SA node that is establishing a heart rate of 72 beats per minutes
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Cardiac Action potential
- Resting membrane potential = -90mV
| - Excitation (neighbouring cell) > MP toward firing threshold (-75mV) > action potential - three phases
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Cardiac Action potential: Rapid Depolarization
- Voltage-gated sodium channels open
| - Rapid influx of Na+
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Cardiac Action potential: Plateau
- Na+ sodium channels close rapidly (+30mV) > Na+ efflux
- Voltage-gated slow Ca2+ channels open (slowly for a long time) > Ca2+ influx
- Balances slow Na+ outflow (0mV)
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Cardiac Action potential: Repolarization
- Voltage-gated slow Ca2+ channels close
| - Voltage-gated slow K+ channels open > K+ efflux
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Sequence of electrical events
1) SA node mass of cells (pacemaker): spontaneously generates an AP
2) Stimulus spreads across atria and reaches AV node
3) AV nodal delay ~ 100msecs: atrial contraction begins
4) AP spreads along AV bundles, bundle fibres and Purkinje fibres
5) AP relayed across ventricles: muscle of ventricles contract
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3 Criteria for Efficient Pumping
1) Atria must contract before ventricles
2) Coordinate excitation so that each heart chamber contracts a syncitium
3) Two atria should contract together; two ventricles should contract together
achieved via:
- interatrial pathway
- internodal pathway
- AV nodal delay
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Cardiac Cycle: Summary
- The period between the start of one heartbeat and the beginning of the next: includes both contraction and relaxation
- Phases of the cardiac cycle: within any one chamber (systole: contraction, diastole: relaxation)
- For HR 75 bpm: ventricular systole = 270msec, ventricular diastole = 530msec
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Cardiac Cycle: Process
a) atrial systole begins: atrial contraction forces a small amount of additional blood into relaxed ventricles
b) atrial systole ends, atrial diastole begins
c) ventricular systole - first phase: ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
d) ventricular systole - second phase: as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
e) ventricular diastole - early: as ventricles relax, pressure in ventricles drops; blood flows back against cusps of semilunar valves and forces them closed. Blood flows into the relaxed atria
f) ventricular diastole - late: all chambers are relaxed, ventricles fill passively
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Electrocardiogram
- Represents summed electrical activity of all cardiac cells recorded from skin's surface
- Each peak represents a different component of electrical events during cardiac cycle
- Mechanical events take place in between peak segment
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P Wave
Atrial depolarisation
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PR segment
AV nodal delay; atria contracted and emptying
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QRS wave
ventricular depolarisation
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ST Segment
ventricles contracting and emptying
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T wave
Ventricular repolarisation
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TP segment
Heart at rest and ventricles (and atria) are filling
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Cardiodynamics
Movement of blood and forces generated during cardiac contractions
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End-Diastolic Volume (EDV)
Volume of blood in each ventricle at end of ventricular diastole
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End-Systolic Volume (ESV)
Volume of blood remaining in each ventricle at the end of ventricular systole (=40% of EDV)
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Stroke Volume (SV)
Volume of blood pumped out of each ventricle during a single beat
SV = EDV-ESV
Most important factor in single cardiac cycle
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Ejection Fraction
The percentage of EDV represented by SV (=60% of EDV)
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Cardiac Output
The volume pumped by left ventricle in one minute
| CO = HR x SV
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Factors affecting HR: Autonomic Innervation of the Heart
- Both SNS and PNS innervate the SA and AV nodes and atrial and ventricular muscle cells
- In ventricles SNS > PNS
- Controlled by cardiac centres in medulla ablongata: cardioacceleratory centre (SNS ^ HR), cardioinhibitory centre (PNS decreases HR)
- Reflex pathways regulate cardiac centres, e.g. baroreceptors and chemoreceptors and higher order CNS
- Autonomic Tone: health, resting PNS activity > SNS activity
- Effects on the SA node: ANS changes rate of spontaneous depolarisation or duration of repolarisation, alters HR by changing time required for cells to reach threshold
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Factors affecting HR: Hormones
- Adrenaline, noradrenaline and thyroid hormones: increase HR (SA node)
- Adrenaline also affects contractile cells
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Factors affecting HR: Atrial reflex
- Adjustments to HR depending on venous return (amount of blood returning to heart through veins)
- Stretch on right atrium walls: triggers reflex to increase sympathelic activity, increases HR
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Factors affecting HR: Venous return
- Directly affects nodal cells - more rapid depolarisation increase HR
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Factors affecting stroke volume: EDV
- Filling time: duration of ventricular diastole
- Venous return: rate of blood flow during ventricular diastole
- Preload: degree of ventricular stretching; the greater the EDV, the greater the preload, affects ability of muscle cells to produce tension
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Factors affecting stroke volume: ESV
- Preload: the greater the preload, the smaller ESV
- Contractility: force produced during contraction, at a given preload, influenced by hormonal or sympathetic/parasympathetic activity
- Afterload: tension the ventricle produces to open the semilunar valve and eject blood, restricted arterial flow increases after load
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5 Major types of blood vessels
1) Arteries
2) Arterioles
3) Capillaries
4) Venules
5) Veins
Larger blood vessels served by own blood vessels located within their walls: vasa vasorum
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Vessel structure
- Arterial walls have 3 tunics
Tunica interna: endothelium, basement membrane, internal elastic lamina
Tunica media: thickest layer, elastic fibres, smooth muscle, external elastic lamina
Tunica externa: elastic and collagen fibres
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Arteries
- Elastic (conducting) arteries: largest diameter arteries, carry blood away from heart, tunica media contains large numbers of elastic fibres
- Function: store elastic energy (helps move blood during diastole)
- Muscular disturbing arteries: medium sized, tunica media contains high proportion of smooth muscle
- Function: distribute and regulate blood flow to muscles and internal organs, superficial muscular arteries form pressure points
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Arterioles
- Small, microscopic arteries - deliver blood to capillaries
- Function: very active in vasoconstriction and vasodilation, key regulators of systemic vascular resistance
- Metarterioles: emerge from arterioles - supply capillary beds, distal end has no smooth muscle: thoroughfare channel
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Capillaries
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Microscopic Vessels (microcirculation)
- walls consist of only endothelium and basement membrane
Function: exchange of nutrients and wastes via interstitial fluid
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True capillaries
- emerge from arterioles or metarterioles
- flow regulated by pre-capillary sphincter
- flow intermitters: caused by alternating contraction/relaxation of metarterioles and pre-capillary sphincters
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Types of Capillaries
1) Continuous capillaries: uninterrupted lining, most common
2) Fenestrated capillaries: many fenestrations/pores, found in e.g. kidney, choroid plexus of brain
3) Sinusoidal capillaries: large fenestrations and intercellular defts, incomplete basement membrane, found in e.g. liver, spleen, bone marrow
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Venules
- Small veins formed from merging of several capillaries
| - Venules merge to form veins
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Veins
- Composed of essentially same 3 tunics as arteries
- Many contains valves to prevent backflow of blood
- Function: hold ~60% of blood volume > capacitance vessels
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Hemodynamics
- Blood flow: volume of blood that flows through a tissue per unit time, determined by blood pressure and resistance
- Blood flow is proportional to the pressure gradient, inversely proportional to resistance
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Pressure VS. Resistance: Pressure
- Blood pressure (mmHg): arterial pressure (120mmHG at aorta > 35mmHg at start of capillaries)
- Capillary hydrostatic pressure (CPH) - pressure on capillary walls (35mmHg > 18mmHg)
- Venous pressure - venous system (low, ~18mmHg)
- Delta P = circulatory pressure (~100mmHg)
- For flow to occur circulatory pressure must be > Toal peripheral resistance (= resistance in entire CVS)
- TPR - determined by vascular resistance, blood viscosity, turbulence
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Pressure VS. Resistance: Vascular Resistance
- Opposition to blood flow due to friction between blood and vessel wall
- Depends on: vessel length (increased length increases resistance), vessel diameter (decreasing diameter increases resistance)
- Peripheral resistance highest in arterioles; actively controlled - vasoconstriction and vasodilation
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Blood viscosity and turbulence
- Blood viscosity: depends mostly on ratio of RBC to plasma (hematocrit), increases with polycythemia
- Turbulence: high flow rates, irregular surfaces and sudden changes in vessel diameter increase turbulence, turbulence slows blood flow
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Velocity of Blood flow
- Inversely related to cross-sectional area
- Velocity: decreases as blood flows from aorta to capillaries, increases as blood flows from capillaries to heart
- Velocity slowest in capillaries: allows increased time for exchange
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Blood pressure (BP)
- Pressure exerted on the walls of a blood vessel: reduces as move further away from heart
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Systomic Pressure (120mmHg)
- peak pressure measured during ventricular systole
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Diastolic Pressure (80mmHg)
- minimum pressure at end of ventricular diastole
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Pulse pressure (40mmHg)
- difference between systolic and diastolic pressures
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Mean arterial Pressure
MAP = DBP +1/3PP
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Venous return
- Volume of blood returning to heart from systemic veins
- Maintain by:
Pressure gradient established by heart
Skeletal muscle pump
Respiratory pump
Valves
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Capillary pressure and capillary exchange
- Substances enter and leave capillaries by three methods
1) diffusion (most important)
2) transcytosis (vesicular transport)
3) bulk flow (filtration and absorption)
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Capillary exchange
- important for regulation of relative volumes of blood and interstitial fluid
- driven by balance between hydrostatic and osmotic pressures (net filtration pressure)
volume of blood filtered = 24L/day
volume of fluid reabsorbed = 20.4L/day
- difference of 3.6L/day flows through tissues and reabsorbed through lymphatic system
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Cardiovascular regulation
- Homeostatic mechanisms regulate CV activity to ensure adequate tissue perfusion
- Primary homeostatic variable is Mean Arterial Pressure (MAP): achieved by regulating CO (HR, SV) and total peripheral resistance (TPR) - via negative feedback mechanisms
MAP = CO x TPR
- Regulated via 3 mechanisms
1) autoregulation
2) neural mechanisms
3) hormonal mechanisms
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Autoregulation
- Local factors alter pattern of blood flow through capillaries via local vasodilators or local vasoconstrictors
- Act on precapillary sphincters to control blood flow through a single capillary bed
Local vasodilators e.g.
- decreased tissue O2 or increased CO2
- lactic or other acid from tissue cells
- chemicals released during inflammation e.g. histamines
- nitric oxide from endothelial cells
- elevated local temperature
Local vasoconstrictors e.g.
- prostaglandins from activated platelets
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Neural Mechanisms
- Neural control via cardiac centres and vasomotor centres in medulla oblongata
- Heart rate, contractility (SV) [CO]
- Blood vessel diameter (resistance)
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Cardiovascular Centre
- Cardiovascular centre receives input from: higher brain regions, proprioceptors, baroreceptors, chemoreceptors
- CV centre sends outputs via
1) Sympathetic impulses:
cardioaccelerator nerves - increase heart rate, increase contractility
vasomotor nerves - vasoconstriction in most tissue, vasodilation in skeletal muscle and brain
2) Parasympathetic impulses
vagus nerves decrease heart rate
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Baroreceptor Reflex
- Baroreceptors located in carotid sinus and aorta: monitor degree of stretch, when BP falls, the baroreceptors are stretched less - send impulse to CV centre, increased CO via HR and SV and vasoconstriction via sympathetic stimulus
- BP increases
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Hormones and Cardiovascular Regulation
- Endocrine system provides both short-term and long-term regulation of CV system
1) E and NE from adrenal medulla: increase CO and peripheral vasocontriction
2) Antidiuretic Hormone (ADH) from posterior pituitary: increases peripheral vasoconstriction - increases BP
3) Angiotensin II: causes vasoconstriction - increases BP
4) Erythropoietin from kidneys: stimulates increased RBC production in bone marrow
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Cardiovascular responses to exercise
1) extensive vasodilation: in skeletal muscle and skin > decreases peripheral resistance, but, vasoconstriction in in gut, kidney and other tissue
2) Venous return increase: skeletal muscle and respiratory pumps
3) Cardiac output increases, via: increases venous return, atrial reflex, increases sympathetic activity > increases HR + contractility > increases SV
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CV Parameters affected by training: Heart Size
- Left ventricle changes the most in response to endurance training
- Internal dimensions of the left ventricle increase: mostly due to an increase in ventricular filling
- Wall thickness of left ventricle increases: potential contraction of the left ventricle more foreful
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CV Parameters affected by training: Stroke Volume
- Endurance training increases SV at rest and during submaximal and maximal exercise
- EDV increases, caused by an increase in blood plasma and greater diastolic filling time, contributing to increased SV
- The increased side of the heart allows the left venticle to stretch more and fill with more blood
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CV Parameters affected by training: Heart Rate
- Heart becomes more efficient through training
- At sub-maximal exercise levels HR may decrease by 20 to 40bpm after 6 months of moderate training
- No change of HR max (may slightly decrease)
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CV Parameters affected by training: Cardiac output
- CO increases dramatically at maximal exertion due to the increase in maximal SV
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CV Parameters affected by training: Blood flow
- increased capillarisation of trained muscles (higher capillary-to-fibre ratio): greater opening of existing capillaries in trained muscle
- more effective blood redistribution: blood goes where it is needed - to and within active muscle
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CV Parameters affected by training: Blood volume
- Blood volume increases due to: an increase in plasma volume (2 weeks), an increase in RBC volume (2-3 weeks)
- Blood viscosity decreases: improving circulation and O2 delivery
