Please enable JavaScript.

Coggle requires JavaScript to display documents.

CARDIOVASCULAR SYS. - Coggle Diagram

- - - - • Blood flow (=CO) is directly proportional to pressure gradient (=BP).
        • Blood flow (=CO) is inversely proportional to resistance (=TPR).
        • The new formula will look like this:
        
        rearranged to determine to explain the determinants of arterial blood pressure, which sets the background for the upcoming topics in this module.
  - - - Poiseuille's Law:
        
        the rate at which blood flows through a blood vessel (Q) is related with the difference in
        
        blood pressure at the two ends (P),
        
        the radius (r) and the length (L) of the artery, and
        
        the viscosity (n) of the blood.
    - - • pressure gradient (ΔP)
        • diameter of vessel (r)
    - - Vasodilation and vasoconstriction create a powerful control mechanisms in regulating blood flow to and within an organ, as well as for regulating blood pressure.
        
        Organs and tissues do not receive a fixed amount of blood flow all the time, with the exception of the brain.
        
        Blood flow to organs, or perfusion, needs to be adjusted according to its metabolic needs.
        
        Changes in vessel diameter, particularly in arterioles, enable organs to adjust their own blood flow to meet the metabolic needs of the tissue.
  - - - Blood pressure changes along the circulatory system.
        
        Blood flows from higher pressure to lower pressure in the body.
        
        This difference in pressure
        
        THE LARGER THE DIFFERENCE, THE FASTER THE BLOOD FLOW!
      - ΔP is the pressure difference between any two points along a given length of a blood vessel.
        
        The pressure difference in our circulation is the difference between aortic pressure and right atrium pressure
  - - - VASOCONSTRICTION
        
        resistance to blood flow increases and blood flow decreases. When vessel diameter increases (vasodilation), resistance decreases and increases flow.
        
        Therefore, the relationship between resistance and blood flow is an inverse relationship.
      - if an arteriole constricts/DILATE to 1⁄2 of its original diameter, the resistance to flow will increase/DECREASE 16 times, which means the blood flow will reduce 16x!
      - VASCULAR
        
        blood flow is the capillaries is the slowest due to the small diameter.
        
        This is beneficial because it allows for exchange of nutrients and gases between the capillaries and tissues.
        
        FACTORS
        
        • Angiotensin II
        
        • Anti-diuretic hormones / vasopressin
        
        • CO2
        
        • H+
        
        • Nitric oxide
        
        • Adenosine
      - VESSELS
        
        most resistance to blood flow are the arterioles. They are known as ‘resistance vessels’.
        • They have the greatest capacity for vasoconstriction, due to the tunica media being richly innervated with sympathetic nerves.
  - - - • Most arterioles and veins in the body are innervated by sympathetic adrenergic nerves.
        • NE preferentially binds α1 adrenoceptors à causes vasoconstriction.
        • These innervations are prominent in blood vessels in the skin, GIT, kidney. When stimulated, arterioles vasoconstrict.
        • Sympathetic effects on the brain and pulmonary capillaries are not significant. WHY THOUGH?
        
        The blood vessels supplying the skeletal muscles and the coronory arteries however, are unique; they contain b2 adrenoreceptors.
        • Epinephrine binds to b2 receptors and causes vasodilation.
        • During sympathetic stimulation, these blood vessels vasodilate instead of vasoconstrict.
        
        RESISTANCE
        
        sympathetic nerve is mainly responsible for vasoconstriction in the blood vessels.
        
        Blood vessels do not receive parasympathetic innervation, therefore vasodilation occurs when the sympathetic stimulation is removed or inhibited.
        
        There are other factors that can influence blood vessel diameter to a certain degree.
        
        These factors include hormones, various metabolites, and gases.
- - - - • Low BP or hypotension is defined as having SBP < 90 mmHg and DPB < 60 mmHg.
        • Low BP impedes blood flow and this can result in dizziness, blurry vision, and fainting.
        
        RESULT IN
        
        • severe dehydration
        
        • hemorrhage
        
        • postural change
      - Postural hypotension is referring to hypotension caused by an abrupt change to an upright posture,
        
        usually from a position of lying down (supine) or sitting.
        
        It is also known as orthostatic hypotension.
        
        It is characterised by a drop in SBP of > 20 mm Hg, or DBP of > 10 mm Hg within 3 minutes after standing.
        
        Reduction in SBP of <10 mmHg is considered normal.
        
        PH is common in older age, pregnancy and certain illness like fever.
      - Individuals with PH can present with reduction of baroreflex sensitivity.
        
        When BP drops, baroreceptor reflex is delayed. Immediate cardiovascular adaptation does not occur.
        • Blood continues to pool in the extremities -> venous return --> reduced CO.
        • Due to lack of sympathetic activation, reflex tachycardia is not present.
        
        BP is persistently low, reducing blood flow to the brain causing one to become dizzy and faints.
    - - SUPINE
        
        30% of blood volume is distributed evenly in the thorax, abdomen and legs because these compartments lie horizontally.
        • When one stands abruptly, gravity causes blood to pool in the lower extremities.
        • This leads to venous return, stroke volume, CO.
        • BP drops significantly.
        
        The carotid sinus is sensitive to a drop in BP in the head.
        
        In normal individuals, decreased BP triggers the baroreceptor reflex.
        • Sympathetic activation will immediately result in reflex tachycardia to maintain cardiac output.
        
        Increased in stroke volume and TPR will follow, leading to maintenance of BP.
        • BP is restored within 2-3 heart beats.
  - - - A pathophysiological disorder characterised by acute failure of the cardiovascular system to perfuse the tissues of the body adequately (low cardiac output).
        
        SYMPTOMS
        
        • Cold, clammy skin
        
        • Muscular weakness
        
        • Rapid and shallow breathing
        
        • Rapid and weak pulse
        
        • Reduced urine output
        
        • Confusion
      - HYPOVOLEMIC SHOCK
        
        all will result in low BP and hypoperfusion.
        
        hypovolemic shock, caused by severe blood loss. Also known as hemorrhagic shock.
        
        In hypovolemic shock, the blood volume is lost, leading to low CO and ultimately BP suffers.
        
        the body will attempt to restore arterial BP and blood volume through these short- and long-term mechanisms: baroreceptor reflex and RAAS.
        
        The main goal of the baroreceptor reflex is to maintain BP while the RAAS helps to restore blood volume.
        
        In this condition, the heart and the kidneys work together to maintain BP to ensure all tissues and organs are receiving enough blood flow despite blood loss.
        
        ‘compensated’ means that the cardiovascular system is able to adapt to the reduced blood volume by adjusting blood pressure.
        
        STAGES
        
        1.Compensated shock
        
        • Minor blood loss, dehydration
        • Cardiac output falls slightly due to reduced venous return.
        • SV LOW, CO LOW, BP LOW
        • BP restored almost instantly.
        
        SHORT TERM ADAPT'
        
        3 more items...
        
        • 30% blood loss, still compensated shock.
        
        Cardiac output falls due to reduced blood volume.
        • SV LOW, CO LOW, BP LOW
        
        Short- & long-term adaptations:
        
        4 more items...
        
        2.Progressive shock
        
        Blood loss is severe. BP is dangerously low.
        • Maximal activation of sympathetic ns and RAAS to preserve BP. Systemic vasoconstriction is enhanced via sympathetic ns and angiotensin II.
        • Blood is shunted from non-vital organs to the brain and heart muscles, which are critical for survival.
        • Progressive shock will get worse if no medical assistance is given.
        
        Prolonged vasoconstriction will cause reduced perfusion to all organs including vital organs.
        • Capillary permeability increases under hypoxic conditions, causing fluid to leak into interstitial spaces --> blood viscosity increase --> blockage of microcirculation --> perfusion reduced even further.
        
        Brain slowly undergo ischemia, thus causing death of brain tissue.
        
        Hypoperfusion also affects the medulla oblongata where the autonomic center and CV center are located.
        • Soon, the CV center fails --> sympathetic activity is lost --> TPR is lost --> all blood vessels undergo systemic vasodilation --> BP declines even further.
        
        3.Decompensated (irreversible) shock
        
        Without medical intervention, progressive shock leads to irreversible shock.
        
        Major organs failure due to tissue death.
        
        Irreversible shock is characterized progressive systemic vasodilation, very low BP, and heart failure.
        
        At this point, no medical intervention can save the victim.
  - - - Systolic BP may rise to 150 - 170 mmHg during exercise but diastolic generally remains unchanged.
        
        This increase in BP is due to increased cardiac output and increased peripheral resistance (vasoconstriction).
        
        BP generally remains increased during exercise, it will not be reduced by baroreceptor reflex.
        
        This is important because it ensures blood flow is maintained to working muscles.
        
        BP restores to normal after exercise ends due to sympathetic withdrawal.
- - - - SA & AV node
        
        • The heart is stimulated at only two locations: SAN and AVN.
        • THREE ions important in generating nodal action potential : Ca2+, Na, K+
        • Any imbalances in these electrolytes can affect the SAN rhythm.
    - - summary
        
        Action potential spreads along sarcolemma and down T-tubules.
        
        Ca²⁺ enters through L-type calcium channels (plateau phase).
        
        Ca²⁺ triggers more Ca²⁺ release from sarcoplasmic reticulum (Ca²⁺-induced Ca²⁺ release).
        
        Ca²⁺ binds to troponin, initiating cross-bridge cycling (contraction).
        
        After peak, Ca²⁺ is reabsorbed into SR and pumped out → relaxation.
        
        Refractory period ensures no additional contraction occurs until the muscle is fully relaxed.
      - CARDIAC CONDUCTION SYS
        
        Electrical impulses are then passed rapidly to adjacent cells through special channels called gap junctions.
        • This enables the heart to contract almost simultaneously.
  - - - ECG WAVES
        
        The ECG output forms a graph of multiple different waves, each corresponding to electrical activity at different angles of the heart.
        
        basic pattern = 3 waves (sequence of depol & repol of cardiac mm. of atria & ventricles)
        
        ECG TRACE: P, QRS, T
        
        P wave:
        • atrial depolarization
        • due to SAN firing
        • atria contracts after the start of P wave
        
        QRS complex:
        • ventricular depolarization
        • due to AVN firing
        • impulses move from AVN to the ventricles
        • ventricles contract after the peak of R wave
        
        T wave:
        • ventricular repolarization
        • ventricular relaxation
        • longer duration than depolarization
        ( ATRIAL REPOL WAVE CANNOT SEE, just ventricular can)
    - - V1 4th intercostal space to the right of the sternum
        V2 4th intercostal space to the left of the sternum
        V3 Midway between V2 and V4
        V4 5th intercostal space at the midclavicular line
        V5 Anterior axillary line at the same level as V4
        V6 Midaxillary line at the same level as V4 and V5
  - - - NORMAL & mean elec. axis = +60o
    - - PR- 0.12 - 0.2 sec
        
        QRS: 0.08 - 0.1 sec
        
        QT: 0.4 - 0.43 sec
        
        RR: 0.6 - 1.0 sec
        
        P wave: 0.08 - 0.1 sec
        
        heart rate: 75 beats/min
        
        RR interval
        
        the time from one heartbeat to another.
        • Heart rate (bpm) = 60 ÷ RR interval (sec)
  - - - Unidentifiable waves indicate ventricular fibrillation, a severe arrhythmia. [heart beats with an abnormal rhythm]
        
        The ventricles twitches in erratic manner, which prevents it from pumping blood effectively.
        
        Ventricular fibrillation will cause sudden cardiac death within minutes unless electrical resuscitation is performed immediately.
      - defibrillators
        
        In the event that the electrical activity of the heart is severely disrupted, cessation of electrical activity or fibrillation may occur.
        • The most common treatment is defibrillation, which applies electrical charges to the heart from an external electrical source in the attempt to establish a sinus rhythm.
        • A defibrillator effectively stops the heart to jump-start --> normal
- - - - GOAL: to ensure adequate blood flow to organs and tissue
        (perfusion)
        
        Maintaining blood pressure within normal limits is essential so blood flow will not be affected.
        
        Blood pressure that is too low --> organs receiving inadequate blood flow --> tissue hypoxia,
        
        while blood pressure above normal limits --> stroke and hypertension.
        
        Arterial pressure directly corresponds to cardiac output, and total peripheral resistance (TPR).
        
        Cardiac output is determined by the product of stroke volume and heart rate,
        
        while TPR is the collective resistance in our circulatory system, influenced by the sympathetic nervous system.
        
        Changes to cardiac output and TPR can change arterial pressure, or blood pressure (BP).
    - - BP can fluctuate from time to time in a single day due to stress, environmental conditions, illness, hydration status, etc.
        
        The cardiovascular system ensures that these fluctuations do not deviate far from the normal limits of 120/80 mmHg.
        
        To maintain BP, cardiac output and TPR need to be adjusted accordingly.
        
        The concept of regulating BP is very much similar to the concept of cardiac output regulation by stroke volume and heart rate.
        
        FACTORS
        
        CARDIAC OUTPUT
        
        SYSTEMIC VASCULAR RESISTANCE
  - - - negative feedback homeostatic mechanism;
        
        it involves a sensory receptor, that detects changes to our internal environment --> relays the signals to a control center (brain).
        
        The brain then interprets the signals and commands a particular organ (effector) to take action to correct any imbalances that occur.
        
        In BP regulation, the sensory receptors = baroreceptors that detect changes in the blood pressure;
        
        the control center = the cardiovascular center located in the medulla oblongata,
        
        the effector organ = the heart itself and blood vessels.
      - BARORECEPTOR
        
        detect changes in arterial pressure.
        
        are found in the walls of blood vessels:
        • aortic arch (aortic sinus)
        • carotid arteries (carotid sinus)
        
        Sensitive to stretching of the blood vessels that indicates changes in blood pressure:
        • low BP --> decreased stretch
        • high BP --> increased stretch
        
        The sensory signals are relayed to the CV center to be used to modify cardiac output and TPR
        
        REFLEX
        (correcting
        mechanism)
        
        fast-acting regulation of arterial BP that works to normalise BP in a matter of seconds.
        
        ADJUST: • heart rate
        • heart contractility
        •total peripheral resistance
        
        Low BP --> decreased stretch --> decreased firing of baroreceptors --> signals relayed to cardiovascular center --> stimulation of sympathetic nerve. (anxious)
        
        High BP --> increased stretch --> increased firing of baroreceptors --> signals relayed to CV centre--> stimulation of prasympathetic nerve (relax)
      - NERVE
        
        CARDIOVASCULAR CENTRE
        
        SYMPATHETIC
        
        innervate arterioles to control diameter
        
        to control HR and ventricular contractility (sympa)
        
        its STIMULATION CAUSE:
        • HIGH heart rate
        • HIGH contractility
        • HIGH TPR (vasoconstriction)
        
        also release CATECHOLAMINES
        
        catecholamines (NE & E) from the adrenal medulla which has the same functions as the neurotransmitters by the sympathetic nerve.
        
        PARASYMPATHETIC
        
        to control HR and ventricular contractility (sympa)
        
        its STIMULATION cause:
        
        LOW heart rate
        
        LOW contractility
        
        LOW TPR (vasodilation)
        
        The parasympathetic nerve does not innervate the blood vessels.
        
        Vasodilation is a result of sympathetic inhibition.
        
        REGULATE
        
        • Heart rate (chronotropy)
        
        • Contractility (inotrophy)
        
        • Blood vessel diameter (TPR)
    - - If baroreceptor reflex is not enough to restore BP over a longer period --> the kidneys will come in to help restore BP.
      - RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
        
        RAAS is a powerful, long-acting regulator of BP.
        
        The system can remain activated for weeks to maintain BP in the long-term.
        • The system relies on hormones that help to increase blood volume and TPR.
        • Increasing blood volume will increase CO --> maintaining BP.
        
        in decreased blood volume conditions (hypovolemia) caused mainly by:
        • blood loss [blood loss of 15 - 40% of blood volume will lead to reductions cardiac output]
        • severe dehydration.
        • To maintain blood volume and BP, the RAAS will be stimulated.
        
        COMP:
        
        RAAS respond to decreased BP and reduced Na+ levels in the distal convoluted tubules of the nephrons.
        
        Sensory receptors: baroreceptors, macula densa (Na+)
        
        Control center: cardiovascular center
        
        Effectors: kidneys (receive sympathetic innervation)
        
        LIST THE ACTION OF
        
        ALDOSTERONE (adrenal cortex)
        
        1 more item...
        
        ADH (post pitutary)
        
        1 more item...
        
        RENIN
        
        Upon stimulation of sympathetic nerve, enzyme renin is secreted by the juxtaglomerular cells in the kidneys.
        
        Renin enters the blood and comes in contact with angiotensinogen which is produced by the liver.
        
        The angiotensinogen is converted into angiotensin I by renin.
        
        Angiotensin I is then converted to angiotensin II by ACE enzyme produced by the lungs.
        
        ANGIOTENSIN II
        
        increases BP through these mechanisms:
        • potent vasoconstriction of arterioles throughout the body
        • increased sodium reabsorption within the kidney tubules which results in passive reabsorption of water leading to an increase in blood volume and thus cardiac output
        • stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland
        • stimulates the release of aldosterone from the adrenal cortex within the adrenal gland
  - - - HOW?
        
        • Systolic pressure – when the 1st sound is heard
        • Diastolic pressure – the last sound heard before silence
      - KOROTKOFF SOUND
        
        created by turbulent blood flow through a compressed blood vessel. --> the sounds that are heard
        
        The sound disappears when blood vessel is no longer compressed and laminar flow resumes.
- - - - Superior: superior thoracic aperture
        
        Inferior: transverse thoracic plane
        
        Anterior: manubrium of sternum
        
        Posterior: bodies of upper 4 thoracic vertebrae
        
        Lateral: mediastinal pleura
    - - SUP
        
        CONTENT
        
        left end of sternohyoid, sternothyroid and longus colli
        
        Thymus
        
        Trachea & oesophagus
        
        Thoracic duct & lymphatic trunk / nodes
        
        Nerves - Phrenic, vagus & left recurrent laryngeal nerves
        
        GREAT VESSELS
        
        SUP VENA CAVA
        
        7cm long and 2 cm wide
        
        Returning deoxygenated blood to right atrium
        
        Formed by the joining of right and left brachiocephalic vein.
        
        ARCH OF AORTA
        
        Continuation of ascending aorta
        
        Runs slightly backward and to the left of the trachea
        
        Divided to three branches
        
        BRACHIOCEPHALIIS
        
        LEFT CCA
        
        LEFT SUBCLAVIAN
        
        NERVE
        
        PHRENIC NERVE
        
        Originate from anterior rami of C3 through C5
        
        Descends vertically and adjacent to IJV.
        
        Branches to right and left Phrenic Nerve
        
        Provide complete motor innervation to diaphragm and sensation to the central tendon aspect of diaphargm
        
        VAGUS NERVE
        
        Originate from brainstem
        
        Left Vagus Nerve enter mediastinum between left CCA and Subclavian Artery
        
        Right Vagus Nerve enter the chest anterior to the Right Subclavian Artery where it will give off Right Recurrent Laryngeal Nerve
      - INF
        
        ANT
        
        BOUNDARY
        
        Superior : Transverse thoracic plane
        
        Inferior : Diaphragm
        
        Anterior : Body of sternum
        
        Posterior : Pericardium (HEART)
        
        Lateral : Mediastinal pleura
        
        CONTENT
        
        No major structures
        
        Loose CT
        
        Sternopericardial ligament
        
        Inferior part of thymus
        
        Lymph nodes
        
        Mediastinal branches of internal thoracic artery
        
        MIDDLE
        
        BOUNDARY
        
        Superior : Transverse thoracic plane
        
        Inferior : Diaphragm
        
        Anterior and posterior : Pericardium
        Lateral : Mediastinal pleura
        
        CONTENT
        
        Heart and pericardium
        
        Tracheal bifurcation and main bronchi
        
        Vessels (roots of the great vessels):
        
        Ascending aorta
        
        Pulmonary trunk (with origins of pulmonary arteries)
        
        Superior vena cava & terminal azygos vein
        
        4.Pericardiacophrenic vv.
        
        Phrenic nerves, Cardiac plexus
        
        Lymph nodes
        
        POST
        
        BOUNDARY
        
        Superior : Transverse thoracic plane
        
        Inferior : Diaphragm
        
        Anterior : Pericardium and diaphragm
        
        Posterior : Body of T5-12 vertebrae
        
        Lateral : Mediastinal pleura
        
        CONTENT
        
        Esophagus
        
        Descending thoracic aorta
        
        Azygos hemiazygous vein
        
        Thoracic duct
        
        Lymphatic trunk
        
        Post mediastinal lymph nodes
        
        Vagus nerve, esophageal plexus and splanchnic nerve
        
        DESC. THORACIC AORTA
        
        O: Continuation of arch of aorta
        
        From the lower border of T4
        TERMINATION: Level of T12
        
        Continuous with abdominal aorta
        
        Ends at ‘aortic hiatus of diaphragm’
        
        LOC: POST mediastinum
        
        1 more item...
        
        AZYGOS SYS OF VEINS
        
        CONSIST OF
        
        3 more items...
        
        DRAINS BLD FROM
        
        1 more item...
  - - - Aneurysm in the arch of the aorta
      - Swallowing and breathing issue
    - - THYMOMA - cancerous tumors that start in thymus gland
      - Myasthenia gravis May have thymic gland abnormalities and thymic tumors, such as thymoma and follicular hyperplasia.
      - Hematoma
        
        Located directly posterior to the sternum
        
        Vulnerable to trauma to the anterior thorax
        
        Intrathoracic or thymic hematoma
    - - Cardiac Tamponade
        
        Compression of heart
        
        Due to occumulation of pericardial effusion
        
        Chambers of the heart unable to relax
        
        Decrease in cardiac output and shock
    - - Aortic Aneurysm
        
        balloon-like bulges that occur in the aorta has thick walls that stand up to normal blood pressure force of blood pushing against the weakened or injured wall
        
        Abdominal aortic aneurysm : most common
        
        Thoracic aortic aneurysm : occurs in chest area above the diaphragm and less common.
        
        can burst (rupture) or tear the wall of the artery (dissection) which can be life-threatening
- - - - expressed in L-min, is the amount of blood the heart pumps in one minute.
        
        Cardiac output is equal to the product of the stroke volume multiplied by the number heartbeat per minute.
        
        Using this formula, the average CO is 5.0 L-min, with a range of 4.0–8.0 L-min.
        
        Understand however, that these numbers refer to CO from each ventricle separately, not the total for the heart.
        
        STROKE VOLUME- The amount of blood pumped out by left ventricle in one beat
        CARDIAC OUPUT - The amount of blood pumped out by left ventricle in one minute
      - CARDIAC OUTPUT (ml?min = STROKE VOL (ml/beat) X HEART RATE (bpm
    - - DETERMINING
        
        stroke volume and heart rate.
        
        if heart rate increases, this will increase cardiac output. Same goes for stroke volume. It is a proportional relationship.
        
        heart rate is controlled by the autonomic nervous system: sympathetic and parasympathetic.
        
        HEART RATE
        
        • Sympathetic and parasympathetic nerve fibers innervate the SA and AV nodes.
        • Sympathetic: increased HR (+ve chronotropy)
        • Parasympathetic: decreased HR (-ve chronotropy)
        
        TACHYCARDIA
        --> Sympathetic stimulation:
        
        © sympathetic neurons release norepinephrine
        
        © binds to adrenergic ß1 receptors on the SA & AV nodes
        
        © frequency of action potentials increases
        
        © increase in heart rate
        
        © ‘positive chronotropic’ effect
        
        BRADYCARDIA --> PARASYMPATHETIC
        
        © parasympathetic neurons release acetylcholine
        
        © binds to cholinergic muscarinic receptors on SA & AV nodes
        
        © frequency of action potentials decreases
        
        © ‘negative chronotropic’ effect
      - AFFECTING
        
        STROKE VOLUME
        
        dependent on several intrinsic factors.
        
        These factors are preload, contractility and afterload.
        -They can increase or decrease stroke volume, hereby affecting CO.
        
        PRELOAD
        
        the degree of ventricular stretch due to end diastolic volume (EDV) just before ventricular systole.
        • The greater the EDV, the more the muscle stretches, increasing preload (tension).
        • Increased preload --> HIGH contractility.
        • Thus, stroke volume HIGH
        
        three factors that can determine EDV.
        
        Whatever affects EDV, will in turn affect preload, then stroke volume and ultimately – cardiac output.
        • These factors are: venous return, increased diastolic time and skeletal muscle pump.
        
        CONTRACTILITY
        
        • Ventricular myocardium are innervated by sympathetic fibers.
        • Sympathetic stimulation HIGH contractility (positive inotropy).
        • This leads to HIGH stroke volume.
        • With sympathetic stimulation, more SV can be ejected with the same preload.
        
        SYMPATHETIC
        
        © sympathetic neurons release norepinephrine
        
        © binds to ß1 receptors on the ventricular myocardium
        
        © frequency of action potentials increases
        
        © increased in force of contraction
        
        © ‘positive inotropic’ effect
        
        AFTERLOAD
        
        • To eject blood, the ventricles must contract and generate enough pressure to open semilunar valves.
        • The pressure generated must overcome the aortic pressure, at least 80 mmHg.
        • Afterload : the aortic pressure that the left ventricle must overcome in order to pump blood into the aorta.
        
        • The higher the afterload, the more force of contraction the heart needs to generate. Thus, high afterload puts more stress on the heart.
        • In non-diseased hearts, afterload does not influence SV significantly, compared to the other two factors.
        • But in hypertension, afterload HIGH. This put added stress on the heart which later can make the heart become weakened.
      - INFLUENCING
        
        external and
        internal factors
        
        age, sex, physical activity, hormones and heart disease.
        
        AGE, SEX
        
        • CO in men is generally higher (~10%) compared to women.
        • More muscle mass in men.
        • CO declines with age.
        • Due to decline in heart rate and heart contractility.
        
        EXERCISE
        
        • Venous return to the heart HIGH due to skeletal muscle pump actions
        • EDV ñ, contractility HIGH (Starling’s law)
        • Sympathetic stimulation HIGH contractility
        • Sympathetic stimulation HIGH HR
        • Stroke volume HIGH
        • Cardiac output HIGH up to 20-25 L.min-1
        
        HEART DISEASE
        
        • Myocardium infarction (heart attack) can lead to weakening of the ventricles.
        • Contractility ↓, SV ↓
        
        HORMONES
        
        epinephrine, NE, glucagon, and thyroid hormones.
        
        Epinephrine and NE, secreted by the adrenal medulla, increase SAN depolarisation.
        
        Thyroxin and glucagon increase heart rate and contractility.
  - - - Atrial contraction
        
        Depolarization of atria by SA node.
        • Contraction of the atrial muscles.
        • P within the atrial chambers ↑↑.
        • Atrioventricular (AV) valves open.
        
        • Rapid flow of blood into the ventricles.
        • After atrial contraction is complete, repolarization occurs.
        • Atrial pressure begins to fall.
        
        REPEAT
        
        EVENT OCCURING IN HEART
        
        • Electrical changes
        
        • Pressure changes
        
        • Volume changes
        
        • Closure & opening of valves
        
        • Production of heart sounds
      - Isovolumetric contraction
        
        Depolarization of ventricles by AV node.
        • Ventricles begin to contract isometrically.
        • At this point, blood is not ejected yet.
        
        • Ventricular pressure (P) continues to rise until P ventricles > P atria.
        • Causes AV valves to close.
        • 1st heart sound (S1); “lub”
      - Rapid ejection
        
        • When the AV valves close, P ventricles keep rising.
        • Until P ventricles > P in aorta and pulmonary artery.
        • Causes semilunar valves to open.
        
        • Ventricles finally contract isotonically.
        • Ventricular ejection occurs!
        • AV valves remain close.
        • Simultaneously, blood flow into atria from the veins.
      - Isovolumetric relaxation
        
        • After ventricular contraction is over, repolarisation begins.
        • P ventricles drop rapidly.
        • Some blood in aorta will backflow toward the left ventricle.
        
        • Causes semilunar valves to to to close.
        • 2nd heart sound (S2); “dub”
        • All valves are now closed.
      - Rapid filling
        
        When ventricles are in diastole, the atria is filling with blood.
        • P ventricles continue to fall. But P atria begins to increase until P atria > P ventricles.
        • Causes to the AV valves to open.
        
        • In children, it represents the 3rd heart sound (S3). Not sound in adults.
        • Ventricular filling begins.
        • Cardiac cycle repeats.
    - - EDV: end diastolic volume
        
        Immediately before ejection, the volume of blood in ventricles
        
        high venous return
        
        long diastolic time
      - STROKE VOLUME
        
        Volume of blood ejected from each ventricle
        
        high EDV
        
        high vent. contractility
      - EJECTION FRACTION
        
        Not all blood in the ventricles is ejected during systole.
        • About 60% of EDV is ejected by a healthy heart.
        • Another 40% of blood remains in the ventricles.
      - ESV: end systolic volume
        
        Volume of blood that remain in ventricles
        after systole - 50ml
        When ventricles contract very strongly,
        ESV is reduced. ↑ SV leads to ↓ ESV.
    - - FORMATION
        
        © S1 – “lubb” caused by the closing of the AV valves
        
        © S2 – “dupp” caused by the closing of the semilunar valves
        
        © S3 – a faint sound associated with ventricular filling
        
        © S4 – a faint sound associated with atrial contraction
      - ABNORMAL
        
        HEART MURMUR
        
        A ‘hissing’ sound when blood flows backward
        through the valves (regurgitation).
        
        Due to defect in valves:
        
        © prolapse (does not close)
        
        © stenosis (narrowing)
        
        © sclerosis (hardening)
      - Auscultation – to listen to heart sounds via stethoscope.
    - - ©Atrial systole (contraction)
      - ©Atrial diastole (relaxation)
      - ©Ventricle systole
      - ©Ventricle diastole
- - - - the intrinsic ability of tissue to maintain constant blood flow despite changes in mean arterial pressure (MAP).
        
        This is important because certain organs need to have a constant blood flow like the brain and kidneys.
        -Thus, blood vessels in the brain and kidneys have excellent autoregulation capability .
        
        Blood vessels in skeletal muscle and splanchnic organs (GIT, reproductive) have moderate autoregulation capability while cutaneous (skin) blood vessels have minimal autoregulation.
        
        The ability to control own blood flow is due to the myogenic mechanism, which refers to the intrinsic ability of small arteries and arterioles
        --> alter their diameter automatically when there is a change in blood flow to the particular organ.
        
        If blood flow to an organ suddenly increased, the vessel responds by vasoconstriction.
        
        Sometimes, increased in arterial pressure will drive higher blood flow to a tissue and this may not necessarily mean a good thing.
        
        Thus, autoregulation is an efficient mechanism to control blood flow within a certain limits.
        
        In contrast, reduced blood flow to an organ causes vasodilation.
        
        Autoregulation ensures that no organ receives blood flow more than its requirement, and also each organ receives adequate blood flow according to their metabolic needs.
    - - ◉ Cerebral circulation
        
        Neurons have a high demand for energy but possess no energy or oxygen reserves.
        
        Because of this, neurons need a constant rate of blood supply.
        
        Reductions in blood supply will lead to neuronal death.
        
        Increase in blood flow can lead to excess pressure in the cranium (skull).
        
        Therefore, the brain is among the few organs in the body that has an excellent autoregulation mechanism.
        
        The brain has an extensive cerebral circulatory network.
        
        Arterial blood reaches the brain via carotid and vertebral arteries.
        
        CBF is typically 700 ml.min-1; and this remains constant all the time, unlike other organs.
        
        CBF remains constant within MAP of 50 – 150 mmHg via autoregulation.
        
        When systemic BP increases, blood flow to brain increase.
        
        This can lead to brain injury.
        
        Therefore, autoregulation helps to maintain constant CBF by vasoconstriction when blood flow suddenly increases.
        
        Similarly, when systemic BP decreases, blood flow to brain decreases.
        
        This can be fatal, so autoregulation helps to maintain CBF by vasodilation.
        
        This is particularly helpful in situations when blood volume is lost e.g. haemorrhage, so the brain gets to maintain its survival.
        
        BRAIN INJURY--> MECH FAIL
        
        HYPERPERFUSION
        
        increased intracranial pressure, edema.
        
        HYPOPERFUSION
        
        dizziness, altered mental status, irreversible infarction
        
        FACTOR
        
        CHEMICAL
        
        Hypoxia (PO2 <50 mmHg) --> vasodilation --> CBF HIGH
        
        Hypercapnia (↑PCO2) --> vasodilation --> CBF HIGH
      - ◉ Coronary circulation
        
        A specialized circulation (outside-in) that provides the myocardium with oxygen and nutrients to ensure normal function and viability of the heart.
        
        The arteries further divide and penetrate into the myocardium. The capillaries lie very close to myocardium.
        
        This and the high ratio of capillaries to myocardium ensure oxygen is delivered effectively to the heart.
        
        Myocardial cells are highly active cells as they contain more mitochondria compared to other cells, therefore they require adequate blood supply to match the demands.
        
        Coronary blood flow is typically 250 ml.min-1.
        
        DETERMINANT
        
        ◉ local metabolites
        
        ◎ Cardiac cells are very active tissues and by- products from the cellular metabolism act as vasodilators for the coronary vessels.
        ◎ When the metabolic activity of the myocardium increases, the amount of these substances will increase.
        
        Adenosine, CO2 are some these by- products. They promote vasodilation.
        ◎ Nitroglycerin (drug) is a powerful vasodilator in coronary circulation.
        
        ◉ diastolic time
        
        During systole, coronary blood vessels in the left ventricle are compressed by the contracting heart muscles.
        
        Therefore, blood flow in the left ventricle is usually at its lowest during systole.
        
        Blood low resumes during diastole when the heart relaxes.
        
        1 more item...
      - ◉ Fetal circulation
        
        The fetal circulation is a special circulation, because the pulmonary circulation (lungs) is not in use.
        
        It involves the placenta, umbilical cord (artery & vein) and blood vessels within the fetus.
        
        Fetus obtains O2 and nutrients from the mother via the placenta.
        
        Waste products are also exchanged via the placenta.
        
        o Oxygenated blood from placenta enters fetal circulation via umbilical vein.
        o Blood bypasses the liver via ductus venosus and merges with IVC, before enter RA.
        o Lungs are collapsed, pulmonary resistance in pulmonary artery is high, so blood from RA enters foramen ovale instead of PA.
        
        o Some blood may enter PA, but this blood will be directed into ductus arterious --> aorta.
        o From RA, blood enters LA via foramen ovale --> LV --> aorta --> systemic circulation.
        o Deoxygenated blood returns to placenta via umbilical arteries.
        
        Patent Foramen Ovale
        
        Failure of the foramen ovale to close
        
        The term “ patent ” means open. Quite common but asymptomatic and therefore undiagnosed in adults.
        
        Patent Ductus Arteriosus
        
        Failure of the ductus arteriosus to close after birth is referred to as patent ductus arteriosus.
        
        PDA is common in premature neonates with respiratory problems who are often ‘cyanotic’.
        
        PLACENTA
        
        The placenta is a unique, vascular organ that receives blood supplies from both the maternal and the fetal systems and thus has two separate circulatory systems for blood:
        
        (1) the maternal-placental circulation, and
        
        (2) the fetal-placental circulation.
        
        The maternal blood flows into the placenta where exchange of oxygen and nutrients occur.
        
        Deoxygenated blood and wastes drain into the uterine veins and back to the maternal circulation.
        
        The umbilical vein carries oxygenated and nutrient-rich blood from the placenta to the fetal systemic circulation.
        
        UMBILICAL CORD
        
        Connects the fetus with the placenta via:
        ◉ 2 umbilical arteries
        ◉ 1 umbilical vein
    - - Blood flow to the organs (regions) of the body is regulated efficiently to ensure adequate delivery of oxygen according to the tissue needs.
        
        Since metabolic requirements are different for each organs, therefore demand for blood flow also varies.
        
        Tissues and organs are able to regulate, to varying degrees, their own blood supply in order to meet their metabolic and functional needs.
        
        This is achieved without influence from the autonomic nervous system (neural) or hormones.
  - - - • Runs parallel to the circulatory system.
        • Functions:
        -> Reabsorb excess ISF
        -> Transport immune cells
        -> Transport fats to bloodstream
        • Responsible for returning fluids into the circulatory system.`
        
        If excess fluid cannot be effectively drained into the lymphatic system, interstitial fluid builds up, leading to swelling of tissues with fluid, a condition known as EDEMA
    - - CAUSE
        
        The build up of fluid in the interstitial spaces is a result of an imbalance between the forces driving filtration and reabsorption.
        
        Too much of hydrostatic pressure or too low of osmotic pressure will lead to accumulation of fluid in the interstitial spaces.
        
        Decreased blood oncotic pressure
        
        • Reduced plasma proteins (albumin) due to liver disease, malnutrition.
        • Loss of plasma proteins due to hemorrhage, burns, kidney disease..
        • Filtration > reabsorption
        
        Increased blood hydrostatic pressure
        
        Increased blood volume due to congestive heart failure, pregnancy, kidney failure
        • Filtration > reabsorption
        
        Lymphatic obstruction:
        
        • Lack of fluid drainage leading to accumulation of fluid in affected area
        • Tumor in lymphatic system, lymphatic filariasis.
    - - • Arterioles
      - • Capillaries
        
        • Very thin endothelial cells surrounded by basement membrane − no smooth muscle cells.
        • Known as exchange vessels: site for exchange for fluid, electrolytes, gases, nutrient molecules, etc.
        • Greatest total surface area, slowest velocity of blood flow --> enhances exchange.
        
        EXCHANGE
        
        If you are a one-cell organism, the exchange process is easy --> diffusion! BUT HUMAN'S NOT LIKE THAT
        
        Involves movement of fluid and solute between blood capillary and surrounding tissues via :
        
        DIFFUSION:
        solute movement
        
        Movement of solutes across capillaries (e.g. glucose, oxygen) from blood into the tissues and from the tissue (e.g. CO2) into the blood.
        
        This movement occur from a region of HIGH concentration to LOW concentration.
        
        BULK FLOW:
        fluid movement
        
        Large movement of fluid and lipid-insoluble solutes across capillaries.
        
        This movement is bi-directional and depends on the net filtration pressure derived from the Starling forces acting upon the capillaries.
        
        Filtration ( BLOOD -> ISF) is movement of fluid from an area of higher pressure in the capillaries to an area of lower pressure in the tissues.
        
        Reabsorption (ISF -> BLOOD) is the movement of fluid from an area of higher pressure in the tissues into an area of lower pressure in the capillaries.
        
        2 more items...
        
        Filtration and reabsorption are determined by two major pressures (also known as Starling forces) interacting to drive each of these movements:
        
        2 more items...
      - • Venules
        
        • Drains blood from capillaries.
        • Thin wall, less smooth muscles.
        • Also called capacitance vessels because they contain 60% of the body's blood volume.
        • Blood drains from venules into larger veins and back to the heart.
      - • Terminal lymphatics
        
        The remaining 15% of the fluid that is not reabsorbed by the capillaries will enter the terminal lymphathic vessels.
        
        and circulate in the lymphatic system.
        
        LYMP. VESSELS
        
        • Terminal lymphatics --> vessels --> nodes --> ducts.
        • One-direction flow: upward towards the neck.
        • Presence of one-way valves in the lymph vessels.
        • Lymph passes through lymph nodes which filter debris and pathogens.
        • Drains into left & right subclavian veins.
        
        LYMPHATIC DUCTS
        
        RIGHT
        
        1 more item...
        
        LEFT
        
        2 more items...
- - - - generate BP
        
        When the heart beats, it creates a pressure that pushes blood to flow through the blood vessels.
        
        Blood pressure is the result of two forces: systolic pressure (contraction) and diastolic pressure (relaxation). 5 Functions of the Heart
        
        Pumps and Routes Blood
        
        When the heart contracts, blood is delivered into the systemic (whole body) and pulmonary (lung) circuits at the same time.
      - Ensures One-Way Blood Flow
        The valves allows for blood flow in one direction only and prevent the backward flow of blood into atria and ventricles.
    - - PULMONARY- blood to and from the lungs
        
        Blood leaves the right ventricles --> pulmonary arteries --> alveoli for gas exchange --> pulmonary vein --> left atrium
      - SYSTEMIC- blood to and from the
        rest of the body
        
        Oxygenated blood leaves the left ventricle --> ascending aorta --> carotid arteries and descending aorta --> whole body
      - CORONARY- Blood to the heart itself
        
        Like all other tissues in the body, the heart muscle needs oxygen-rich blood to function. The blood is supplied by the coronary arteries, that branch off from the aorta.
    - - AUTORHYTMIC
        
        About 1% of cardiac cells have this ability. They are called pacemaker cells.
        • Generate their own action potentials (impulse) without the need for external stimuli
        • These impulses result in electrical activity throughout the heart.
        
        “automatic + rhythmic”
      - CONTRACTILITY
        
        The ability to contract almost simultaneously in response to receiving impulse.
        • Contraction is performed by cardiac contractile cells. 99% of cardiac cells are of this type.
        • Found in atrial and ventricular muscles.
      - CONDUCTIVITY
        
        The ability to spread impulse rapidly and in synchronised manner throughout the heart.
        • Due to the presence of gap junctions.
        • The impulse are spread through a specialised pathway called the cardiac conducting system.
        
        cardiac conducting system.
        
        Sinoatrial (SA) Node – "The pacemaker"
        
        Location: Right atrium, near the superior vena cava
        
        Function: Spontaneously generates action potentials (~60–100 bpm)
        
        Spreads impulse across atria → atrial contraction
        
        Atrioventricular (AV) Node
        
        Location: Interatrial septum, near tricuspid valve Function:
        
        Delays the impulse (~0.1 sec) → Allows atria to fully contract before ventricles do
        
        Bundle of His (AV Bundle)
        
        Location: Interventricular septum
        
        Function: Conducts signal from AV node to ventricles
        
        Right and Left Bundle Branches
        
        Carry impulse down interventricular septum to apex of the heart
        
        Purkinje Fibers
        
        Spread impulse upward through ventricular myocardium
        
        Trigger ventricular contraction from apex upward, pushing blood into arteries
        
        FLOW= SA node → Atria → AV node → Bundle of His (AV BUNDLE)→ Bundle branches → Purkinje fibers → Ventricles
        
        FXN= to generate and transmit electrical impulse.
      - MUSCLE
        
        CARDIAC
        
        cardiac muscles require both Na+ and Ca2+ for contraction.
        
        The initiation of action potential is derived from the entry of Na+ across the cell membrane.
        
        The inward influx of Ca2+ helps to sustain the depolarisation period (plateau) in cardiac cells.
        
        This plateau phase is critical, since this allows only a single contraction occur following an electrical event.
        
        Without long refractory periods, premature contractions (spasm) would occur in the heart and would not be compatible with life.
    - - SA NODE
        
        The pacemaker of the heart.
        • Generates spontaneous impulses about 80 beats per minute.
        • Location: immediately below and slightly lateral to the opening of the superior vena cava (right atrium).
        
        The impulse generated in the SA node spreads through out the atrial muscle via two routes:
        
        internodal pathways (Bachman, Wenckebach & Thoral)
        
        ordinary atrial muscle fibers Bachmann
        • The internodal pathways conduct impulses at a faster rate than the ordinary atrial muscle fibers.
        • It takes 0.03 sec to reach the AV node.
      - AV NODE
        
        Receives impulses from SA node.
        • Location: in the posterior wall of the right atrium immediately behind the AV valve.
        • When the impulse reaches the AV node there is a delay before the AV node fires.
        • This gives the atria time to squeeze blood into the ventricles before the AV fires.
        
        AV BUNDLE
        
        Impulse leaves the AV node and travels through the Bundle of His in the interventricular septum
        • Splits into right and left bundles.
        • Each branch spreads downward toward the apex of the ventricles.
        • Further divides into smaller thin fibers; Purkinje fibers.
        
        PURKINJE F.
        
        transmit impulse to the ventricular cells to produce contraction.
        • Large muscle fibers (specialized cardiac cells) - possess maximum conduction velocity.
        • Ensures that ventricles are excited simultaneously and contract as a unit.
      - The conducting system is designed to depolarise the atria first and make them contract as a unit, and then to depolarise the ventricles and cause them to contract as a unit...
      - The contraction of the ventricles starts at the apex and travels towards the base where the blood is finally ejected from the ventricles.
        
        The time from impulse generation at the SAN to the completion of ventricular contraction is ~ 825 msec!
        
        IF DAMAGED - normal rhythm of the heart will be disturbed.
        • If SA node or internodal pathways are damaged or blocked, the AV node will act as pacemaker.
        
        “junctional rhythm”; 40-60 bpm
        
        impulses come from a locus of tissue surrounding AVN
        --> The atria still contracts due to retrograde conduction.
    - - SYMP
        
        postganglionic neurons release norepinephrine which bind to adrenergic ß1 receptors on the SAN & AVN
        
        frequency of action potentials increases
        
        ‘positive chronotropic’ effect
      - PARASYMP
        
        postganglionic neurons release acetylcholine which bind to cholinergic muscarinic receptors on SAN & AVN
        
        frequency of action potentials decreases
        
        ‘negative chronotropic’ effect
        
        normal resting HR in adults: 60 – 70 beats min-1. instead of 100.
        
        If the vagus nerve to the heart is cut, resting HR will jump to 100 bpm.
      - MO
        
        Cardioacceleratory center:
        © cardiac nerve (symp.)
        © innervate the SAN, AVN, ventricles
        © increase HR, contractility
        
        Cardioinhibitory center:
        © vagus nerve (parasymp.)
        © innervate the SAN, AVN
        © slows HR
      - HEART RATE
        
        • Tachycardia: resting adult HR above 100
        
        exercise, stress, anxiety, drugs, body temp.
        • Bradycardia: resting adult HR < 60
        
        sleep, high fitness
    - - SEMILUNAR
        
        AORTIC
        
        PULMONARY
      - ATROVENTRICULAR
        
        BICUSPID (mitral)
        
        TRICUSPID