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Cardiovascular Anatomy & Physiology. Objectives. Function Anatomy Cells Cardiac Output Oxygen Transport Pathologies. Cardiovascular Function. Deliver oxygenated blood to tissues- where diffusion and filtration occur
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Objectives • Function • Anatomy • Cells • Cardiac Output • Oxygen Transport • Pathologies
Cardiovascular Function • Deliver oxygenated blood to tissues- where diffusion and filtration occur • Transport blood back to lungs- where oxygen and carbon dioxide exchange occur
Human Heart Surface anatomy of the human heart. The heart is demarcated by: -1. A point 9 cm to the left of the midsternal line (lower left or apex of the heart) -2. The seventh right sternocostal articulation (lower right side of heart) -3. The upper border of the third right costal cartilage 1 cm from the right sternal line (upper right side of heart) -4. The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line (upper left side of heart) 3. 4. 2. 1.
Cells of the Cardiovascular System • Cardiac cells • pacemaker cells • cardiac myocytes • Vascular cells • endothelial cells • smooth muscle cells
Cardiac Myocytes • Conduct AP cell-to-cell via gap junctions • Are packed with contractile elements • Have well developed sarcoplasmic reticulum which sequesters calcium • Are dependent on extracellular calcium for contraction
How does membrane depolarization lead to mechanical contraction? Action Potential Calcium influx from ECF Calcium release from SR Increased intracellular free calcium actin-myosin crossbridging myocardial cell shortening
Cardiac Muscle Cell Ca Ca++ channel Ach receptor ATP Ca beta receptors cAMP Ca Na Ca Na ATP K Na channel SR Na digoxin K K channel
ANS effects on heart and vessels Heart SNS PSNS • inotropy + - • chronotropy + - • dromotropy + - • lusitropy + - Vessels • pulmonary/coronary constrict dilate • most others constrict no effect
Cardiac Output THE most important variable in cardiac function! CO = HR x SV
Oxygen Transport pO2 lungs = 80-100 mm Hg pO2 tissues = 30-40 mm Hg SaO2 lungs = 95-100% SaO2 tissues = 60-80%
PaO2 Saturation 100 90 80 70 60 50 40 98% 96% 94% 92% 89% 83% 75%
Shift to left: affinity alkalemia hypothermia hypocarbia decreased 2,3DPG Shifts in Hb-O2 Affinity • Shift to right: affinity • acidemia • hyperthermia • hypercarbia • increased 2,3DPG
Carbon Dioxide Transport Physical Solution: (5%) PaCO2 X .06 Carbaminohemoglobin: (15%) HB N H COO- Bicarbonate ion (80%) CO2 + H2O H2CO3 H+ + HCO3-
Red Cell Production • iron • folate • vitamin B12 • erythropoietin • functional stem cells
Figure: 13-17The erythropoietin response to anemia, hypoxia, polycythemia
Cardiovascular Pathology • Anemia • Heart Failure • Valvular Defects • Cardiomyopathies • Congenital Defects • Vascular Insufficiency
General Signs and Symptoms of Anemia • Increased respiration • Increased heart rate • Fatigue • Decreased activity tolerance • Pallor • Murmur
Heart Failure • Def: Inability to effectively PUMP the amount of blood delivered to the heart • Left ventricular ejection fraction (EF) • Normal values: 60-80% • Important measure of heart failure • Etiologies: Many, but 2 main causes are hypertension and ischemia • MI • CIHD • Valve Disease • Congenital Defects • Cardiomyopathy
Figure: 19-5Interdependence of left and right heart function Clinical presentation of CHF Differs for left, right, or both ventricle failure Left Ventricular Failure (LVF)Right Ventricular Failure (RVF) Forward Failure Poor cardiac pumping = reduced CO Backward Failure Congestion of blood behind the heart
Figure: 19-7Manifestations of left heart failure Clinical presentation of LVF most common presentation for CHF Often leads to RVF (biventricular failure) Common causes Left ventricular infarction Cardiomyopathy Aortic and mitral valvular disease Systemic hypertension Forward effects – reduced CO leads to hypoxia Brain hypoxia – restlessness, mental fatigue, confusion, anxiety, impaired memory Cardinal symptom – dyspnea (early sign) Hypoxemia results from impaired gas exchange Cyanosis results from deOxyHgb (late sign) Arterial Blood Gas analysis Cyanotic Elevated Left arterial pressure Acute cardiogenic pulmonary edema – life threatening Bolt-upright posture Dyspnea and anxiety Lungs are congested but systemic venous system is not
Summary • Anemia • Heart Failure • Valvular Defects • Cardiomyopathy • Congenital Defects • Vascular Insufficiency
Valvular Disorders • Abnormalities of Valve function: • Stenosis & Regurgitation • Etiology • congenital • rheumatic • degenerative calcification • infective • Diagnostic Evaluation: Echo-doppler
Common Valve Disorders • Mitral Stenosis • Mitral Regurgitation • Aortic Stenosis • Aortic Regurgitation Mitral valve lies between the left atrium and left ventricle. Stenosis – obstruction to blood flow thru cardiac valves that are not opening completely Regurgitation – retrograde blood flow through a cardiac valve when the valve is closed
Differential Diagnosis of Murmur • Mitral Stenosis • Increased Left Arterial Pressure • Loud S1 opening snap at apex • Murmur rare, if present, short diastolic • atrial fibrillation is common
Mitral Stenosis 120 90 60 30 LA/LV gradient 0
Differential Diagnosis of Murmur • Mitral Regurgitation • Systolic Murmur • Radiates to left axilla • Pansystolic, blowing • Prominent S3
Mitral Regurgitation 120 90 60 large regurgitant V-wave 30 0
Differential Diagnosis of Murmur • Aortic Stenosis • Mid systolic • Crescendo-decrescendo • Radiates to neck • S4 prominent • Angina, syncope common
Aortic Stenosis 180 LV/Aortic pressure gradient 120 90 40 0
Differential Diagnosis of Murmur • Aortic Regurgitation • Diastolic murmur • Bounding Pulse “waterhammer” • Wide pulse pressure
Aortic Regurgitation 180 aortic pressure with Aortic Regurgitation 120 90 normal aortic pressure 40 0
Cardiomyopathy • Dilated • enlarged heart chambers • poor contractility • Hypertrophic • outflow obstruction • ischemia • Restrictive • impaired diastolic filling
Acyanotic L to R shunt Atrial Septal Defect Ventricular Septal Defect Patent Ductus Arteriosus Cyanotic R to L shunt Transposition Tetralogy of Fallot Congenital Heart Defects
Shock • Defining Characteristic: Oxygen Delivery to one or more tissues is below basal requirements leading to hypoxic and immunologic injury. • Types of Shock: • Hypovolemic • Cardiogenic • Distributive (e.g. anaphylactic, septic, neurogenic) • Manifestations: Signs and symptoms of tissue ischemia and death.
Diagnosis of Shock • Tachycardia • Hypotension (orthostatic) • Peripheral hypoperfusion (slow capillary refill, cool, mottled) • Oliguria or anuria • Metabolic acidosis • In septic shock: fever, chills
General Treatment Measures • Supine position • Oxygen • Analgesics • Labs: CBC, ABG, Renal panel, Type & X, UA • Cardiac Monitoring • CVP Monitoring (at least) • Volume replacement (colloid vs crystalloid vs blood) • Vasoactive Drugs
Septic Shock • Usually caused by gram negative bacteria. Monoclonal antibody to endotoxin may be used. • Don’t be fooled by high cardiac output, still have insufficient blood volume to fill the tank. • Oxygen consumption is often low due to abnormal distribution and shunt. Look for increased consumption with treatment. • Mortality is high: 40-80%
Vascular System Arterial Insufficiency Venous Insufficiency
Arterial smoking atherosclerosis inflammatory:Buergers trauma DIC emboli from LV vasospasm diabetes mellitus Venous stasis of bloodflow immobility R heart failure prolonged standing obesity pregnancy trauma hypercoagulable high platelets high hematocrit Risks for Vascular Insufficiency
Heart Pump venous arterial ischemia edema capillary Pathophysiology of Insufficiency
Arterial Insufficiency Flow Downstream ischemia chronic acute Pain Pallor Pulselessness Paresis Paralysis Poikilothermy Intermittent claudication Atrophy (skin, hair) Thickening of nails
Venous Insufficiency Obstruction of Venous Drainage capillary hydrostatic pressure edema, stasis pain risk of pulmonary embolus stasis ulcers and skin changes
Deep Vein (DVT) Extremity Edema General leg pain Fever High Risk of PE Treatment immobilize anticoagulate treat risk factors Superficial local Inflammation warm tender red swollen Collateral veins minimize edema Low Risk of PE Thrombophlebitis
Assessment of Cardiac Function Electrical Function Contractile Function
R P T Q S Is Electrical Conduction Normal?