Cardiovascular System: The Heart Chapter 18

Heart Anatomy w/Review Size of a fist In the mediastinum Obliquely situated ___?_____ to the diaphragm ___?_____ to the vertebral column ___?_____ to the sternum Lungs are ___?_____ and slightly obscure it Base is right and posterior, apex is point

Pericardium Serous membrane surrounding the heart Protects, anchors, and prevents overfilling Fibrous pericardium, collagen and elastic figure 8’s Link all parts together while providing additional support Limits AP spread 2 layers Parietal layer covers the _____?_____ Visceral layer (epicardium) covers the _____?___ Pericardial cavity between w/ serous fluid

Heart Wall Epicardium (visceral pericardium) Myocardium Endocardium www.faculty.ccri.edu Heart Wall Epicardium (visceral pericardium) Fatty layer Myocardium Cardiac muscle Endocardium Simple squamous epithelia Continuous with blood vessels Forms valves

Chambers of the Heart 2 superior atria 2 inferior ventricles Interatrial septum Coronary sulcus 2 inferior ventricles Interventricular septum Anterior and posterior ventricular sulcus REMEMBER: directions for specimen/model NOT self http://www.nku.edu/~dempseyd/HEART_1.htm

Atria of the Heart Receiving chambers Auricles to increase volume http://www.google.com/imgres?imgurl=http://www.washingtonhra.com/resources/Heart%2Banatomy.png&imgrefurl=http://www.washingtonhra.com/2.html&usg=__6-rsXPk2HfBZ4NNeV1B4Gs7DIgI=&h=500&w=342&sz=454&hl=en&start=0&zoom=1&tbnid=hUO3hlsVbY8FXM:&tbnh=143&tbnw=98&prev=/images%3Fq%3Datrium%2Banatomy%26um%3D1%26hl%3Den%26sa%3DN%26biw%3D834%26bih%3D667%26tbs%3Disch:1&um=1&itbs=1&iact=rc&dur=414&ei=K4pxTIzAFsP38AaI2o2ACw&oei=K4pxTIzAFsP38AaI2o2ACw&esq=1&page=1&ndsp=12&ved=1t:429,r:0,s:0&tx=48&ty=73 Receiving chambers Auricles to increase volume Pectinate muscles internal, anterior walls Fossa ovalis: remnant of fetal opening Right entry (O2 poor from systemic) Superior and inferior venae cavae Coronary sinus Left entry (O2 rich from pulmonary) Right and left pulmonary veins

Ventricles of the Heart http://www.google.com/imgres?imgurl=http://www.washingtonhra.com/resources/Heart%2Banatomy.png&imgrefurl=http://www.washingtonhra.com/2.html&usg=__6-rsXPk2HfBZ4NNeV1B4Gs7DIgI=&h=500&w=342&sz=454&hl=en&start=0&zoom=1&tbnid=hUO3hlsVbY8FXM:&tbnh=143&tbnw=98&prev=/images%3Fq%3Datrium%2Banatomy%26um%3D1%26hl%3Den%26sa%3DN%26biw%3D834%26bih%3D667%26tbs%3Disch:1&um=1&itbs=1&iact=rc&dur=414&ei=K4pxTIzAFsP38AaI2o2ACw&oei=K4pxTIzAFsP38AaI2o2ACw&esq=1&page=1&ndsp=12&ved=1t:429,r:0,s:0&tx=48&ty=73 Discharge chambers Trabeculae carneae, folds of muscle Papillary muscles Right (anterior) exit Pulmonary trunk Right and left pulmonary arteries Left (posterior) exit Aorta

Heart Valves Keep single directional blood flow Open/close due to pressure not contraction Atrioventricular valves (AV) Right is tricuspid Left is bicuspid or mitral Anchored to papillary muscles by chordae tendineae ‘heart strings’ Semilunar valves (SL) Aortic Pulmonary

Valve Function AV Returning blood to atria exerts pressure = valves open to ventricle Ventricles contract = increase pressure = valves close Chordae tendineae and papillary muscles prevent inward flip SL Ventricles contract = increase pressure = valves open Ventricles relax = blood flows back = close valves

Blood Flow Pathway Overview

Coronary Circulation Arterial supply in coronary sulcus Right coronary splits Marginal: lateral right myocardium Posterior interventricular: heart apex and posterior ventricular walls (join for right atria and ventricle) Left coronary splits Circumflex: left atria and posterior wall of left ventricle Anterior interventricular: interventricular septum and anterior ventricle walls (join for right atria and ventricle) Actually varies between individuals Venous supplies join in coronary sinus Great cardiac in anterior interventricular sulcus Middle cardiac in posterior interventricular sulcus Small cardiac w/marginal artery

Cardiac Muscle Anatomy Intercalated discs Gap junctions: passage/exchange of ions Desmosomes: stabilize and maintain structure Heart behaves as a single unit Other characteristics (review) Nuclei #? Control? Structure?

Cardiac Muscle Contraction Neural stimulation not needed = autorhythmicity Can influence pace Whole organ (not just motor units) contracts Signals carried through gap junctions Longer absolute refractory period Regulates contraction rate Prevents sustained contraction (tetanus) Lots of mitochondria Greater dependence on O2 Presence of fuel source more important than type

Autorhythmic Cells Initiate action potentials in the heart Due to pacemaker potential or unstable resting period Basic steps of an AP (review) Changes Continuous depolarization to threshold (no flat line) Ca 2+ channels open and Ca2+ rushes in AP NOT triggered by Na+ Found in specific locations Sinoatrial and atrioventricular nodes Right and left bundle branches Ventricular walls (Pukinje fibers)

Beating to It’s Own Drum Sinoatrial (SA) node or ‘pacemaker’ Depolarization rate is fastest Impulse ~75 times/min Atrioventricular (AV) node delays impulse Bundle of His electrically connects chambers Bundle branches to apex Pukinje fibers to contractile fibers in ventricles

Extrinsic Heart Control Cardiac centers in medulla Cardioacceleratroy center Sympathetic NS Pre- from T1-T5 up Post- through cardiac plexus to SA and AV nodes & arteries Cardioinhibitory center Parasympathetic NS Pre- from vagus to heart Post- to SA and AV nodes

Electrocardiogram (ECG or EKG) Records all electrical autorhythmic cell activity Distinguishable waves P wave: SA node depolarizes atria Atria contracts Drop from AV node delay QRS complex: ventricle depolarization Ventricle contracts Masks atrial repolarization T wave: ventricle repolarization

Heart Sounds ‘Lub’ when AV valves close ‘Dup’ when SL valves close Ventricular systole (contraction) begins Bicuspid (mitral) before tricuspid ‘Dup’ when SL valves close Ventricular diastole (relaxation) begins Aortic before pulmonary Listen to 4 regions for differences

Cardiac Cycle Ventricular filling Ventricular systole (contraction) Relaxed chambers creates low pressure  allows passive blood flow in Atria contract, ‘topping off’ ventricles = end diastolic volume (EDV) Ventricular systole (contraction) Ventricles contract increasing pressure (isovolumetric contraction phase) AV valves close and SL valves open End systolic volume (ESV) remains Early diastole Ventricles relax decreasing pressure (isovolumetric relaxation phase) SL valves close

Cardiac Output (CO) Amount of blood pumped by each ventricle CO (ml/min) = HR (beats/min) x SV (ml/beat) Stroke volume (SV) is amount of blood per ventricular contraction Variable and increases with demand Max CO – rest CO = cardiac reserve Athletes have higher

Regulating Stroke Volume SV = EDV – ESV EDV is amount of blood in ventricle during diastole ESV is amount of blood in ventricle after systole Affecting factors EDV by preload: degree of cardiac stretch pre-contraction in ventricles Slow HR increases volume of return Exercise increases speed of return ESV by contractility: contractile force of cardiac cells SNS innervation, Ca2+ entry, and hormones increase More blood leaves = decrease in ESV Ca2+ blockers, increased extracellular K+ , and acidosis decrease ESV by afterload: pressure needed to eject blood High BP  more difficult to eject blood = increased ESV

Regulating Heart Rate ANS Chemical controls Other factors SNS stimulates with stress, excitement, or exercise PNS stimulates with ACh and opposes SNS Majority of autonomic stimuli; slows heart rate Chemical controls Hormones: epinephrine, norepinephrine, and thyroxine increase Ions Other factors Temperature Age and exercise

Homeostatic Imbalances Pericarditis: inflammation of pericardium roughens serous membrane Cardiac tamponade: heart is compressed by fluid in pericardial cavity Angina pectoris: deficient blood flow to myocardium Myocardial infarction: prolonged coronary blockage; heart attack Incompetent valves: valves fail to close allowing blood backflow Stenosis: valves are stiff or obscure opening; heart must work harder Ischemia: depriving tissue of oxygen Arrhythmia: uncoordinated atrial/ventricular contractions Fibrillation: rapid, out of phase contraction Heart block: AV node damage; ventricles contract on own Heart murmurs: blood swooshing; valves fail to close Tachycardia: abnormally fast HR; stress, drugs, or temp cause Bradycardia: abnormally slow HR; drugs, endurance training, or PNS