Cardiovascular A

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Cardiovascular A P
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Cardiovascular AP
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The Pump

• The heart is a two sided pump used to move blood
  from one circuit to another
• Two circuits peripheral pulmonary
• Pulmonary circuit oxygenates blood.
• Peripheral circuit distributes the blood.

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Cardiac Circulation

• Myocardial muscle is perfused by the coronary
  arteries.
• Coronary arteries originate distal the Aortic
  Valve.
• Coronary filling is related to diastolic
  pressure.
• Coronary veins empty the deoxygenated blood into
  the right atrium.

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Vena Cava
Base
LAD
RCA
Apex
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Physiology

• Right heart is low pressure
• Low pressure allows pulmonary gas exchange
• Pulmonary circuit responsible for Central Venous
  Pressure
• (4) pulmonary veins flow into the pulmonary trunk
  which empties into the left atrium

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Physiology

• Left heart is high pressure
• Left atrium receives oxygenated blood for
  peripheral circulation
• Left ventricle larger more muscular
• Cardiac out-put related directly to left
  ventricular ejection fraction
• Left side seen on ECG due to size

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Aortic Arch
Pulmonary Veins
Pulmonary Artery
Left Atrium
Right Atrium
Left Ventricle
Right Ventricle
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Cardiac Cycle
QRS
P
T
depolarization electrical event
contraction physical event
ventricular repolarization
atrial contraction
ventricular contraction
atrial depolarization
ventricular depolarization
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Cardiac Cycle

• Pumping action is rhythmic
• Blood is pumped simultaneously from the atria to
  the ventricles
• Volume from the ventricles is equal to that from
  the atria
• Systole is contraction
• Diastole is relaxation (ventricular filling)

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Atrial Systole Diastole

• Atrial ventricular filling during diastole
• At the end of the diastolic cycle the atria
  contract giving a kick to ventricular filling
• Atria are reservoirs for the blood ejected from
  the ventricles

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Ventricular Systole Diastole

• Passive ventricular filling during diastole
  followed by atrial kick
• AV valves close due to pressure in the ventricles
• Ventricular contraction from apex to base
• Blood prevented from regurgitation into the
  ventricles by the aortic pulmonic valves

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Stroke Volume

• Amount of blood ejected from one ventricle during
  one contraction
• Dependant on pre-load (end-diastolic volume),
  afterload, myocardial contractility
• SV(PL (pre-load) CF (contractile force)) - AL
  (afterload)

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Preload

• Stroke volume 70 ml resting
• Preload is pressure of filling the chambers
• Increased preload increases stroke volume
• Increased preload used to perfuse body during
  stress

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Preload is atrial passive filling adding
atrial kick to ventricular filling
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Afterload is the pressure produced against the
aortic pulmonic valves by the TPVR pulmonary
resistance respectively.
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Frank-Starling Law

• Muscular out-put determined by stretch of muscle
  fibers
• Increased pre-load increases stretch therefore
  out-put
• Preload most important factor of cardiac out-put
• Limit to stretching of the myocardium
• Constant stretching yields myocardial hypertrophy
  (cardiomegaly)

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Afterload

• A result of TPVR
• Has little effect on CO except to cause
  regurgitation hypertrophy
• Decreased afterload increases SV decreases
  cardiac workload / oxygen demand

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Myocardial Contractility

• Myocardial oxygenation electrolytes have great
  affect on contractility
• Medications such as Beta Blockers (e.g.
  propranolol) hypoxia causes decreased
  contractility
• Potassium, Calcium, Sodium fluxes cause
  derangement to contractility

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Cardiac Output

• Equal to Stroke volume x heart rate
• The amount of blood pumped by each ventricle each
  minute
• PVR modifies CO through its effect on SV
• BP is a function of CO PVR
• A rise in either causes a rise in systolic
  pressure

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Left chamber is larger more muscular allowing
greater pump pressure. Cardiac out-put may be
decreased by dysfunctional valves allowing
regurgitation of blood back into the chambers.
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Nervous System Control

• Control by both the central peripheral nervous
  system
• Checks balances by sympathetic
  parasympathetic systems
• Controls contractility, conduction, heart rate

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Parasympathetic Control

• Main nerve is the Vagus (10th cranial nerve)
  mediated by ACh
• Causes a decrease in heart rate contractility
• Vagal stimulation by Valsalva, carotid sinus
  massage, NV, pain, distention of urinary
  bladder
• Greater effect of HR than SV

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Sympathetic Control

• Nerve ganglia originate in the thorax C-spine
• Post-ganglionic nerve mediator Norepinephrine
• Heart rate (chronotrophy) contractile force
  (inotrophy)
• Dilation of coronaries constriction of
  peripheral vasculature increases myocardial
  oxygen availability

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Sympathetic Control

• Alpha Beta receptors
• Few alpha cell receptors on the heart
• Primarily Beta receptors causing increased HR
  contractility
• Alpha effects in the peripheral vasculature
  causing increased TPVR thus increased BP
• Over stimulation of the HR leads to inadequate
  ventricular filling decreased SV

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Hormonal Regulation

• Increased levels of Epinephrine Norepinephrine
  are caused by increased demand
• Epinephrine inotrophe chronotrophe
• Norepinephrine inotrophe chronotrophe
• Alpha effects cause increased TPVR decreased
  renal output
• Beta effects cause increased HR, BP, bronchial
  dilation.

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Electrolytes

• Contraction stimulation controlled by
  electrolytes
• Magnesium ICF cation important for nervous
  transmission
• Calcium, Sodium, Potassium important at the
  cellular level for nerve transmission muscular
  contraction

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Stay tuned for electrophysiology of the
heart.
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