Week 4 Cardiovascular System Flashcards
Components of the CV Components
The heart = A pump that provides continuous linkage with the vascular components
The arterial system= A high-pressure distribution circuit
The capillaries = exchange vessels
The venous system = low pressure collection and return circuit
The blood = a body fluid that transports essential substances ad metabolic waste products
Anatomy of the heart Pericardium
Membrane surrounds & protects heart
Anatomy of the heart epicardium
External layer composed of fibroelastic & adipose tissue and contains blood vessels, lymphatics and nerves that supply the myocardium
Anatomy of the heart Myocardium
Middle layer composed of striated cardiac muscle tissue. Intercalated discs allow electrical impulses (AP) to spread cell-to- cell, resulting in a coordinated and efficient contraction / pump
Anatomy of the heart Endocardium
Innermost layer of endothelium overlying thin layer of connective tissue
Anatomy of the heart
-Two superior receiving chambers: Atria
-Two inferior pumping chambers: Ventricles
- Interventricular septum separates the right and left sides
- The atrioventricular valves (tricuspid and bicuspid/mitral valve) ensure one-way blood flow between the atria and ventricle
- Myocardial thickness varies according to the amount of stress placed upon it
Pulmonary circulation
Right side receives deoxygenated blood from the body (via vena cava) and pumps blood to the lungs
Systemic circulation
Left side receives oxygenated blood from the lungs (via pulmonary vein) and pumps blood into the aorta for distribution throughout the body
Coronary circulation
The myocardium has its own network of blood vessels called the coronary circulation
• The coronary arteries branch from the ascending aorta and encircle the heart
• Delivers oxygen and nutrients to the heart muscle and collects carbon dioxide and waste, and then moves into coronary veins
• Tissue damage caused by an interruption in blood flow known as infarct. Myocardial infarction (heart attack) caused by blockage in coronary circulation
The vascular system
Arteries (conduit vessels)
Arterioles (resistance vessels) control blood flow, feed capillaries
Capillaries (exchange vessels)
Venules
Veins (capacitance vessels)
STRUCTURE OF BLOOD VESSELS
Tunica intima (inner lining of vessel)
• Epithelial layer, consisting of endothelial cells lining the lumen of the vessel, and a connective tissue
Tunica media (middle layer)
• Smooth muscle and elastic connective tissue. Primary role is to regulate the diameter of the lumen.
Tunica adventitia (outer covering of vessel)
• Connective tissue mainly collagen fibers. Contains nerves and small blood vessels.
LAYERS OF THE ARTERY WALL
DETECTING ATHEROSCLEROSIS
CAPILLARIES – EXCHANGE VESSELS
Single layer of endothelial cells
• 500 – 2000 capillaries per mm2 of skeletal muscle tissue
• Large surface area + slow rate of blood flow = effective O2 & CO2 exchange
• Precapillary sphincter is a band of smooth muscle that adjusts blood flow into capillaries
• Local blood flow matched to metabolic
THE VENOUS SYSTEM – CAPACITANCE VESSELS
THE CONDUCTING SYSTEM & CARDIAC CYCLE
THE CONDUCTING SYSTEM
SA node spontaneously depolarize and repolarizes to provide innate stimuli for heart action
SA node
↓
Atria
↓
AV node
↓
AV bundle
↓
Purkinjie fibers
↓
Ventricles
ELECTROCARDIOGRAM (ECG)
Depolarization causes contraction
Repolarization causes relaxation of cardiac muscle fibers.
CARDIAC CYCLE
The cardiac cycle is a period from the beginning of one heart beat to the beginning of the next one. It can be divided into two basic phases: diastole and systole
Diastole
• Period of the cardiac cycle when the heart muscle relaxes, and blood fills the chambers
• At rest, the heart spends two-thirds of its time in diastole
Systole
• Period of the cardiac cycle when the heart muscle contracts and blood is pumped out of the chambers
• At rest, the heart spends one-third of its time in systole
PRESSURE ACROSS THE CARDIAC CYCLE
In Systole
Ventricles eject blood into the arterial system.
To empty, ventricular pressure must be high – equivalent to that in the arterial system
In Diastole
Ventricles fill with blood entering via the atria from the venous system. To fill, ventricular pressure must be low – equivalent to that in the venous system
FLOW ACROSS THE CARDIAC CYCLE
a) Atrial contraction forces a small amount of additional blood into the relaxed ventricles
b) Ventricular systole - first phase: Ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
c) Ventricular systole - second phase: As ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
d) Ventricular diastole – early: As ventricles relax, pressure drops, blood flows back against cusps of semilunar valves and forces them closed. Blood flows into the relaxed atria.
e) Ventricular diastole – Late: All chambers are relaxed. Ventricles fill passively
HEART SOUNDS ACROSS THE CARDIAC CYCLE
CARDIAC CYCLE VOLUMES
Venous Return (VR)
• The total blood volume returning to the heart by vena cava into the atria
Ventricular end diastolic volume (EDV)
• Total blood volume in each ventricle at the end of diastole
Ventricular end systolic volume (ESV)
• Total blood volume in each ventricle at the end of systole (ejection)
Stroke Volume (SV)
• The blood volume ejected per beat from each ventricle
SV
STROKE VOLUME (SV)
60% at rest in healthy active young adult
Ejection Fraction (%) = stoke volume/ end diastolic volume
End diastolic volume (EDV) 100ml b-1
End systolic volume (ESV) 40ml b-1
Stroke volume (sv) 60ml-b-1
CARDIAC OUTPUT
Cardiac output is the amount of blood pumped by each ventricle in 1 minute.
• Expressed in ml/min or L/min
Cardiac output = heart rate( HR) x stoke volume (SV)
Volumes at rest
Cardiac output (Q) 6.0 L/min
Heart rate (HR) 75bpm
Stoke volume 80ml
Q= HR X SV
Maximal exercise volumes
Q= 31.2 L. ^ 420%
HR= 195bpm ^160%
SV 160ml
HEMODYNAMICS
Blood flow = ΔP/R
Perfusion pressure (Δ P)
• Pressure difference drives blood flow
• Flows from regions of higher (Aorta) to lower (Vena Cava) pressure
Resistance (R)
• Resistance is the force that opposes blood flow
• Dependent on blood viscosity (ƞ), vessel length (L) & radius (r) -
Resistance = [ƞL/r4]
Small changes in vessel dimeter (through vasodilation / vasoconstriction) produce large alteration in resistance and therefore blood flow
BLOOD PRESSURE
Blood Pressure (BP) refers to the pulsatile force exerted by blood pushing against the walls of the arteries as the heart pumps blood
Systolic pressure (SBP)
• Highest pressure in artery during ventricular contraction
Diastolic pressure (DBP)
Lowest pressure in artery during ventricular relaxation
Mean arterial pressure (MAP)
• Average pressure (geometric mean) over entire cardiac cycle
• MAP = DBP + [0.333(SBP-DBP)]
Blood pressure values mm Hg
Normal = systolic less than 120 and diastolic less than 80
Elevated s= 120-129 and d less than 80
High blood pressure (hypertension) Stage 1 S (130-139) D 80-90
High blood pressure (hypertension) stage 2 s 140 or higher
D 90 or higher
Hypertensive Crisis higher than 180 an higher than 120
BLOOD PRESSURE / FLOW
BP and blood flow (BF) vary considerably in the systemic circulation
• Resting BP fluctuates between 120 (systolic) and 80 (diastolic) mmHg in the aorta and large arteries
• Big drop in BP across the resistance vessels due to ↑ CSA
• BF velocity slows down as capillaries branch out
• Capillary BP ~ 30 mmHg
• Venous BP < 10 mmHg
Blood pressure
Mean arterial BP = Flow x Resistance
Flow = Those that affect the
Cardiac Output
i.e. those that affect the heart
Stroke volume & heart rate
Resistance= Those that affect the systemic vascular resistance (total peripheral resistance, TPR)
i.e. those that affect the circulation
Vascular smooth muscle tone
REGULATION OF HEART ACTIVITY
INTRINSIC
Cardiac muscle has ‘spontaneous rhythmicity’, allows it to contract without external stimulation
EXTRINSIC
Neural (via ANS)
Hormones (via endocrine system)
AUTONOMIC EFFECTS ON THE HEART
Rate and strength of contraction can be altered by neural innervation & hormone secretion (chemical) stimulated through activation of Autonomic Nervous System (ANS)
• Epinephrine (Epi) = Adrenaline
• Norepinephrine (NE) = Noradrenaline
Exercise anticipation from higher centres activates sympathetic neurones in the hypothalamus
Vagus nerve fibres slow heart rate and conduction velocity through action of ACh at Sa and av node
Efferent sympathetic fibres increase heart rate and myocardial contractility and dilate coronary arteries
Sympathetic nervous stimulation of adrenal medulla causes epinephrine release
Released epinephrine delivered via blood accelerates SA node discharge, filters coronary vessels and increases myocardial metabolism
Central command
Feed-forward control: Neural impulses from motor cortex irradiate to autonomic neurons, leading to parasympathetic withdrawal & sympathetic activation
Skeletal muscle Mechanoreceptors / Metaboreceptors
Receptors in the muscle gather info concerning the mechanical (muscle length/tension etc) and metabolic (amount of metabolite accumulated) condition of the muscle
Chemoreceptors
Central [medulla] and peripheral [aortic arch & carotid body] receptors activated by ↑ H+ and PCO2 = ↓ blood pH
Baroreceptors
Receptors in the walls of aortic arch & carotid body monitor arterial blood pressure
Cardiac accelerator nerve
Increased rate of depolarization in SA node (and AV node) increases HR. Increased contractility of atria and ventricles increases stroke volume
Vagus nerves
Decreased rate of depolarization in SA node (and AV node) decreases HR
Activation of the parasympathetic nervous system (PNS)
• Stimulates the release of acetylcholine (neurotransmitter) from the Vagus nerves
• Binds to muscarinic receptors on cardiac cells
• Causes hyperpolarization of cells in SA and AV node = ↓ HR
• At rest, PNS activity predominates; heart under ‘vagal tone’
• An increase of vagal tone slows HR (Bradycardia)
• A decrease of vagal tone increases HR (Tachycardia)
• As exercise begins, there is a ↓ in PNS activity
Activation of the sympathetic nervous system (SNS)
• Stimulates the release of catecholamines:
o Noradrenaline (neurotransmitter) is released from sympathetic fibers / cardiac accelerator nerves o Adrenaline (hormone) is released from the adrenal gland
• Which activates adrenoceptors (β-receptors) on the cardiac cells
• Causing ↑ HR and ↑ force of ventricles contraction
• The SNS predominates during stress, when HR > 100BPM
REGULATION OF STROKE VOLUME (SV)
Filling pressure (preload): Starlings law of the heart
Filling’ influenced by End diastolic ventricular stretch
Arterial pressure opposing ejection (afterload)
Contractility:
Sympathetic nerves circulating agents
↑ contractility = ↑ Ejection Fraction
Total peripheral resistance (TPR)
Emptying’ influenced by ventricular contractility & aortic artery pressure
↓ arterial BP during diastole = ↓ Afterload = Semilunar valves open sooner when BP in aorta & pulmonary artery is lower
↑ ventricular stretch prior to contraction = ↑ sarcomere length of cardiac myocyte = ↑ strength of contraction = ↑ EF
REGULATION OF BLOOD PRESSURE & FLOW
LOCAL= Ability of local blood vessels to dilate / constrict altering regional BF depending on metabolic needs of the tissue
SYSTEMIC
SHORT TERM: Redistribution of systemic BF is controlled by neural mechanisms & hormones
LONG TERM: Changes in blood volume and blood pressure regulated by hormones
SYSTEMIC REGULATION OF BP / FLOW
Sympathetic vasoconstriction is prominent in blood vessels of the skin, pancreas, GI tract, kidneys and helps to redirect blood flow to vital organs during the ‘fight or flight’ response
Skeletal muscle Mechanoreceptors / Metaboreceptors= Monitor joint movements
Chemoreceptors= Monitor blood acidity
Baroreceptors Monitor blood pressur
Adrenaline released from the adrenal medulla triggers vasoconstriction of most blood vessels (e.g. skin / GI tract) but dilation in others (e.g. muscle)
Postganglionic sympathetic fibers release noradrenaline which binds to α-receptors to cause vasoconstriction of arterioles.
Sympathetic stimulation will increase blood pressure by:
- Increasing the strength (and rate) of the heart beat
- Constricting arterioles (vasoconstriction) and so increase vascular resistance
- Release adrenaline and increase the strength of the heart beat
