Cardiovascular System

Overview of Anatomy & Physiology Assessment of CV Function

Ezra Oktaliansyah

Department of Anesthesiology & Reanimation Medical Faculty Padjadjaran University / dr. Hasan Sadikin General Hospital Bandung

Function of the heart:

pump oxygenated (saturated) blood into the arterial system, which carries it to the cells pump deoxygenated (desaturated) blood back to the lungs via the veins for reoxygenation

 heart size depends on the size of the person approximately the size of the fist encased in a thin, fibrous sac called the pericardial sac or pericardium (2 layers) composed of three layers:

inner layer - endocardium middle layer - myocardium outer layer - epicardium

Cardiac chambers:
Right atrium - receives deoxygenated blood from the superior and inferior vena cava (venous return) Right ventricle - pumps blood against a low resistance in the pulmonary artery (PVR) on the way to the lungs where oxygenation takes place

 Left atrium - receives oxygenated blood from the lungs via 4 pulmonary veins Left ventricle - pumps blood to the systemic circulation via the aorta against a high resistance (SVR)

Cardiac valves:
ensure one way flow of blood two types:

atriovenricular valves
mitral (btw LA & LV) tricuspid (btw RA & RV)

closed during V. systole and therefore prevent backflow of blood to the atria during ventricular contraction (systole) open during ventricular relaxation (diastole) allowing for filling of the ventricles

semilunar valves
pulmonic valve (btw RV & pul. artery) aortic valve (btw LV & aorta)

closed during v. diastole and prevent backflow into the ventricles during relaxation (ventricular diastole) unlike the AV valves, they are open during contraction of the ventricles (ventricular systole) allowing for emptying of the ventricles

Cardiac cycle
Heart muscle contracts & relaxes rhythmically to assure proper circulation one cardiac cycle=1 heart beat two phases to the cardiac cycle:

systole diastole

Systole
ventricles contract blood ejected from the LVaorta and from the RVpulmonary artery

Diastole
ventricles relax pressure in the ventricle falls below that of the atria the AV valves open blood which has been pooling in the atria begins to flow into the ventricles

 as systole begins the AV valves (mitral & tricuspid) close, S1 (lubb) produced semilunar valves forced open, a silent event

 When ventricles are almost empty, pressure in the ventricles drops, allowing the semilunar valves (pulmonic and aortic) to close, S2 (dubb) produced at this time atrial pressure higher, mitral & tricuspid valves forced open, passively filling the ventricles up to a certain point (if rapid filling of dilated ventricle, S3 possible)

 to ensure that the blood remaining in the atria is ejected, the atria contract (atrial kick) if there is any resistance to filling by the ventricle, S4 possible

Electrical activity
An electrical conduction system is responsible for the sequence of muscle contractions that take place during the cardiac cycle in essence an electrical current stimulates each contraction under normal circumstances, this electrical impulse originates in the SA node

 this property of the SA node to initiate an impulse is known as automaticity automaticity can be disturbed in MI (d/t hypoxia), electrolyte imbalance, acid-base imbalance, drugs, etc. Non-automatic cell may become automatic and subsequently cause dysrhythmias, (e.g., PACs, PJCs, PVCs, escape rhythms, etc.)

Normal conduction pathway

SA node via internodal tracts to AV node to the Bundle of His the Bundle of His then divides into the Right Bundle Branch & the Left Bundle Branch each branch terminates to form the Purkinge fibers located in the ventricular myocardium, where the ventricles, when stimulated, contract

Two electrical events (recorded as waves on EKG):

depolarization - the spread of an electrical impulse through the heart muscle repolarization - the return of the heart muscle to a resting state the corresponding mechanical events are contraction and relaxation, respectively The ability of cardiac cells to respond to an electrical impulse is called excitability

 The sequence of depolarization and repolarization is called the cardiac action potential. It results when ions (charged particles such as Na, K, & Ca) shift across the cell membrane.

Conductivity
Refers to the ability of the heart muscle fibers to transmit electrical impulses along and across cell membranes can be enhanced or depressed by drugs, ischemia, trauma

Contractility
Refers to the heart muscle fibers ability to contract, or shorten, in response to an electrical impulse (irrespective of volume) can be impaired in MI, electrolye disturbances, drugs, hypoxemia decreased contractility results in a drop in the stroke volume and ultimately leads to a drop in cardiac output

Refractoriness
Refers to the hearts inability to respond to a new stimulus while still in a state depolarization from an earlier stimulus this prevents the possibility of tetanic contractions that would be fatal

Electrical activity & corresponding waves on EKG

P wave - corresponds to the spread of the impulse through the atria - atrial depolarization PR interval - conduction time through the atria (.12-.20 sec.) QRS complex - corresponds to spread of the impulse through the ventricles - ventricular depolarization

 QRS interval - conduction time through the ventricles (.04-.12sec.) ST segment & T wave - return of stimulated ventricular muscle to a resting state ventricular repolarization** QT interval - time it takes for the ventricles to depolarize & repolarize

Coronary circulation
Heart muscle itself requires a supply of oxygenated blood to meet its own metabolic needs supplied through the coronary arteries which branch off from the aorta just above the aortic valve, encircle the heart, and penetrate the myocardium returned to right side of the heart via the coronary veins

 Right Coronary Artery (RCA) Left Main Coronary Artery (LCA):

Left anterior descending (LAD) Circumflex artery

Collateral Circulation
The presence of more than one artery supplying a muscle (a capacity present at birth but not functional) develops when the blood flow through an artery progressively decreases and causes ischemia to the muscle extra blood vessels develop to meet metabolic needs of the muscle

Cardiac Output
Volume of blood ejected by the heart/min. (~ 4-8L) Stroke volume X heart rate cardiac index - a calculation that helps to determine if CO is adequate in relation to body size

CI=CO/BSA (Dubois scale) in L/min/m2

Stroke volume
Determined by:

preload afterload contractile state of the myocardium

Preload
Myocardial fiber length of the ventricle at end diastole also known as amount of stretch Starlings law ( stretch force of contraction) * stretch determined by volume of blood in ventricle Preload = Venous Return

Afterload
The resistance against which the ventricle must eject its volume amount of pressure required by the LV to open the aortic valve during systole and to eject blood into the systemic circulation (SVR) afterload for right side of the heart (PVR) inversely related to stroke volume related to BP ( systemic/pulmonary)

Contractile (inotropic) state

Refers to the vigor of contraction generated by the myocardium regardless of its blood volume (preload) increased by SNS stimulation (epinephrine endogenously or exogenously) decreased by hypoxemia/acidosis

Regulation of CV system
involuntarily controlled by the ANS the ANS plays a role in regulating

heart rate (chronotropic effect) myocardial contractility (inotropic effect) conduction velocity at the AV node peripheral (systemic) vascular resistance
arteriole constriction and dilation

venous return
venule and vein constriction and dilation

 The two subdivisions of the ANS (sympathetic & parasympathetic) generally exert opposing influences and balance their activities to promote cardiovascular adaptation to internal and external demands

Parasympathetic nervous system

Mediated via the vagus nerve when stimulated, parasympathetic nerve endings release the neurotransmitter acetylcholine, which produces inhibitory effects decreases the rate of SA node firing, thus lowering HR lessens atrial conductivity

Sympathetic nervous system

Mediated by Beta receptors when stimulated, the nerve endings release the neurotransmitter norepinephrine and produce the following effects:

increase in heart rate increase in conduction speed through the AV node increased atrial and ventricular contractility peripheral vasoconstriction (? result)

Hormonal & other influences on CO

ADH renin-angiotensin-aldosterone mechanism exercise, anger, fear, pain, anxiety, excitement can augment the SNS effects drugs

2 adrenergic agonists - stimulate SNS (HR) blockers - Block SNS (HR) cardioselective blockers (block only 1 receptors)

Blood pressure
Expressed as systolic blood pressure/diastolic blood pressure SBP-peak pressure exerted against arteries when heart contracts (measure of contractile function) DBP-residual pressure during relaxation of the heart (er in atherosclerosis) BP=COxSVR

Important receptors
Changes in sympathetic and parasympathetic activity occur in response to messages sent from sensory receptors in various parts of the body for cardiovascular function, the important receptors are: arterial baroreceptors, stretchsensitive cardiopulmonary receptors of the atria and veins, and chemoreceptors

Baroreceptors
Stretch sensitive nerve endings affected by changes in art. BP located in the walls of the aortic arch and carotid sinuses stimulated by an in art. BP, a vagal response results in in heart rate and art. BP with BP, less stretch, fewer impulses, see sympathetic mediated in HR and vasoconstriction

Cardiopulmonary stretch receptors

located in vena cava & atria respond to length changes, reflective of circulatory volume status with in BP in vena cava and RA due to hypovolemia, stretch receptors send fewer impulses than usual to the CNS result is a sympathetic response to kidney to enhance Na and water retention & release of ADH (hypervolemia produces the opposite)

Chemoreceptors
Found in the aortic arch and carotid bodies sensitive to CO2 and arterial pH (acidemia) and secondarily sensitive to hypoxemia when such changes occur, they send impulses to the CNS to increase HR

Some factors affecting BP

cardiac output/blood volume systemic vascular resistance elasticity of blood vessels blood viscosity age weight emotion exercise

Assessment of CV function
History Physical Examination

inspection palpation percussion auscultation

Lab & Diagnostic Tests

Present History
Chief complaint & symptom analysis (PQRST)

chest pain dyspnea (DOE, othopnea, PND) cough (hemoptysis) palpitations skipped beats dizziness, fainting, syncope

fatigue/weakness weight gain peripheral skin changes (e.g., edema, PVD) leg pain

Past History
Hypertension Diabetes Rheumatic fever/Rheumatic heart disease Elevated homocysteine levels (homocysteine, an amino acid produced in the body, is considered to be a contributing risk factor and is associated with B12, folic acid, and B6 deficiencies)

Lifestyle
May constitute modifiable risk factors for heart disease

smoking elevated cholesterol levels/high fat diet (esp. saturated fats) sedentary activity/physical inactivity obesity stress

Physical Examination
Inspection

color presence of clubbing capillary refill edema vital signs peripheral pulses level of consciousness (LOC)

 Inspection contd

JVP urine output PMI xanthelasma arcus senilus ear lobe creases

 Percussion Palpation

thrill heave/lift abdomen liver (including the hepatojugular reflex)

 Auscultation

normal heart sounds (S1, S2) abnormal heart sounds

Gallops (S3, S4) pericardial friction rub murmurs

bruit lung sounds

Lab & Diagnostic Tests

Chest x-ray EKG & cardiac monitoring Stress test (ETT) Electrophysiological studies Cardiac catheterization Angiography

 Echocardiogram Intra-arterial pressure monitoring Hemodynamic monitoring (CVP, PA )

CBC (Hgb, Hct, WBC, Platelets) Serum lipids Cardiac enzymes Blood coagulation Serum electrolytes BUN & Cr Drug levels