Cardiovascular Anatomy & Physiology 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
Cardiovascular System Cardiovascular Structures 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) 3. 2.
4. 1. -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 Cells of the Cardiovascular System
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 Ach receptor Ca++ channel ATP
Ca beta receptors cAMP Ca Na Ca Na ATP Na channel
SR Na K K channel K digoxin ANS effects on heart and vessels Heart
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: 19-5 Interdependence 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: 19-7 Manifestations 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 threatenin Bolt-upright posture Dyspnea and anxiety Lungs are congested but systemic venous system is n Summary
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 0 LA/LV
gradient 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 180 120
Defects Acyanotic L to R shunt Atrial Septal Defect Ventricular Septal Defect Patent Ductus Arteriosus Cyanotic R to L shunt Transposition Tetralogy of Fallot 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. Dont 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. Vascular System Arterial Insufficiency Venous Insufficiency Risks for Vascular Insufficiency
Arterial smoking atherosclerosis inflammatory:Bu ergers trauma DIC emboli from LV vasospasm diabetes Venous stasis of bloodflow immobility
R heart failure prolonged standing obesity pregnancy trauma Pathophysiology of Insufficiency Heart Pump venous arterial
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
Thrombophlebitis Deep Vein (DVT) Extremity Edema General leg pain Fever High Risk of PE Treatment
Superficial local Inflammation warm tender red swollen Collateral veins minimize edema Assessment of Cardiac
Function Electrical Function Contractile Function Is Electrical Conduction Normal? R P T Q S ECG Assessment
Rate? Conduction Abnormality? Dysrhythmias Conduction blocks Ischemia/Infarction? LVH? Cardiovascular Pathophysiology Afterload The resistance that must be overcome to eject blood
from a cardiac chamber. Left ventricular afterload is correlative with the resistance in the systemic vasculature. Preload The volume of blood that remains in the cardiac chamber prior to systole. Classification of Hypertension Category SBP DBP Recommended Followup Normal
<130 <85 Recheck in 2 years High Normal 130-139 85-89 Recheck in 1 year Hypertension Stage 1 (mild)
Stage 2 (mod) 140-159 90-99 160-179 100-109 Confirm within 2 mo Eval or refer 1 mo 180-209 110-119 >210 >120 Eval or refer 1 week Eval or refer immediately Stage 3 (severe)
Type I - IV atherosclerotic plaques Types I-III Asymptomatic Arterial wall narrowing Types IV-VI Predispose to ischemic episodes Ischemic Heart Disease Etiology: Coronary Atherosclerosis
Risks: Clinical Syndromes: angina pectoris myocardial infarction chronic ischemic heart disease sudden cardiac death Pathogenesis of Atherosclerosis Lipid accumulates in vascular wall Macrophages infiltrate the wall and oxidize the lipids Cell injury and release of local growth factors (Angiotensin II)
Plaque formation on intimal wall Demand > Supply: Angina Perfusion pressure fixed stenosis oxygen content SUPPLY afterload contractility preload heart rate DEMAND How to increase supply?
How to decrease demand? Pathogenesis of Ischemia Plaque Disruption or Breakdown Tissue Thromboplastin Exposed Platelet Aggregation and Clotting Cascade Activated Thrombus Formation Acute Ischemia Ischemic Syndromes Stable Angina Unstable Angina
MI Patho: Fixed stenosis Thrombus >75% + lysis Thrombus with occlusion Pain: predictable relieved by rest (3-5 min)
unpredictable not relieved rest unpredictable not relieved rest (>15-30) not elevated elevated Serum Enz: not elevated ECG Changes with Ischemia
Indicative Leads show: Ischemia: ST elevation or depression T-wave peaking, flattening, inversion Bigger than normal Q-waves ST elevation Q Sequela of Myocardial Infarction Decreased Myocardial Perfusion Partially ischemic cells
Totally ischemic cells Anaerobic metabolism and lack of ATP No ATP Ion leak across cell membrane ST changes Dysrhythmias Cell rupture and death Q-waves
Elevated Enzymes Figure: 18-9 Summary of events following MI Figure: 18-8 Time course of serum marker elevations after MI Serum markers released from damaged cardiac cells Cardiac isozymes MI indicators creatine kinase (CK-MB)
only present up to 72 hrs troponin I (present longer) troponin T (present longer) Compensatory Response to Decreased Stroke Volume Decreased Stroke Volume IMMEDIATE baroreceptor activation HOURS RAS activity WEEKS Increased LV wall tension
fluid retained SNS SV, CO preload SV, CO ventricular hypertrophy SV,
CO Differential Diagnosis of Chest Pain Cardiac ischemia Chest wall trauma, costochondritis Pleural pain - pneumonias Pneumothorax Gastrointestinal (GERD)
Treatment of Cardiac Ischemia Stable angina SL nitroglycerin Platelet inhibitor (e.g. ASA 325mg qod) beta blocker add long acting nitrate (remove at night) add calcium channel blocker (not verapamil) Treatment of Cardiac Ischemia
If ECG shows signs of current ischemia Continuous ECG monitoring, Labs Oxygen Give ASA Relieve pain with SL nitro, morphine Evaluate for thrombolytic therapy Decrease MVO2: bedrest, pain relief, etc Heart Failure Pathophysiological state Abnormality of cardiac function to supply blood to meet demand Pumps only from abnormally elevated diastolic filling pressure
Etiology Myocardial failure High demand on heart with near normal cardiac function Inadequate adaptation of cardiac myocytes to increased wall stress Causes circulatory failure but converse is not always true Adaptations Frank-Starling mechanism increased preload sustains cardiac performance Myocardial hypertrophy mass of contractile tissue increases Neurohumoral Activation Adrenergic cardiac nerves causes release of NE Positive inotropy Activation of RAA system salt and water retention (increased preload, increased energy expense) Release vasoconstrictive agents which increase afterload Increased cAMP causes increased calcium entry Positive inotropy, negative lusitropy Increased energy expenditure and reduced CO which further stimulates RAA system
Calcium overload may cause arrythmia and sudden death Cardiac AngII may cause negative lusitropy, positive inotropy, positive afterload, increased myocardial en expense Congestive Heart Failure Can result from most cardiac disorders. Most common causes of CHF is myocardial ischemia from coronary artery disease, hypertension and dilated cardiomyopathy Systolic dysfunction Reduced myocardial contractility Congestion is result of fluid backup in heart Common cause is myocardial cell death MI (neg inotropy) EF less than 50% Chronic overexcitation of b receptor SNS may be exacerbate condition B receptor blockers treatment
Heart failure Signs, symptoms CHF Reduced stroke volume Reduced cardiac output Reduced EF (typically < 40%; severe if EF<20%) Congestive Heart Failure Diastolic dysfunction Reduced myocardial relaxation Ventricle is not compliant and does not fill effectively Ventricle filling dependent on Ca2+ uptake (active phase of diastolic relaxation) Passive phase (myocardial stretch) impaired Common cause is myocardial cell death MI (neg inotropy) Heart failure Signs, symptoms CHF (congestion; edema) Reduced stroke volume Reduced cardiac output
Near normal EF > 50% Factors Affecting Cardiac Output Heart Rate (chronotropy) Contractility (inotropy) Preload Afterload How is Heart Rate Regulated?
What Factors Affect Contractility? Anything that increases Ca++ availability in the heart muscle cell will increase Contractility. Anything that decreases Ca++ availability in the heart muscle cell will decrease Contractility. What would be the effect of: SNS PSNS
Digoxin Ca++ channel blocker B1 blocker Preload: Volume Work of the Heart S.V. preload The Frank-Starling Law of the Heart: Increased preload increases force of contraction Afterload: Pressure work of the Heart Increased Afterload occurs with
increased resistance to ejection of blood from the ventricle Increased Systemic Vascular Resistance Increased Diastolic Blood Pressure Aortic Stenosis Increased Afterload: Decreased stroke volume Constitution of normal blood Parameter Value
Hematocrit 45 7 (3852%) for males 42 5 (3747%) for females pH 7.357.45 base excess 3 to +3 PO2
1013 kPa (80100 mm Hg) PCO2 4.85.8 kPa (3545 mm Hg) HCO3 2127 mM Oxygen saturation Oxygenated: 9899% Deoxygenated: 75%
ANEMIAS ANEMIAS How can the different types of anemia be differentiated? Laboratory Diagnosis of Anemia Low Hematocrit Low Hemoglobin Low RBC count Red Cell Indices MCV (size) microcytic, normocytic
Polycythemia red cell mass normal increased check erythropoietin Relative polycythemia - hydrate high Secondary - assess lung and kidney function
low Vera - assess wbc, platelets Cardiovascular System Physiology Figure: 19-2 Compensatory mechanisms in heart failure These mechanisms attempt to improve cardiac output SNS activation early response to reduced CO Increased heart rate
Decreased CO reduces kidney perfusion Increased contractility Activates RAA system ultimately leading to increased fluid retentio Increased arterial vasoconstriction Decreased EF = Increased Preload = Reduced CO = Reduced GFR Increased renin release Increased Fluid Retention = Increased RAS activation = Increased Blood volume= Increased Chamber volume = Chronic SNS activation Increased Contraction (myocardial stretching) Increased afterload Increased workload = Reduced CO Higher Preload = Increased Contractility = Increased CO Left Heart Failure LVF
Backward effects Forward Failure Poor cardiac pumping = reduced CO Backward Failure Congestion of blood behind the Forwardheart effects EF Left Ventricular preload CO
Congestion & edema (dysfunction) Right ventricular afterload Right ventricular hypertrophy Forward Failure Poor cardiac pumping = reduced CO Right Heart Failure Backward Failure Congestion of blood behind the
heart RVF Forward effects Backward effects EF Output to LV Right Ventricular preload Left ventricular
CO Right atrial pressure Systemic Venous Congestion Fluid retention RAS activation Tissue perfusion
Figure: 19-9 Manifestations of right heart failure Clinical presentation of RVF Often results from LVF Common causes LVF Right MI Pulmonary disorders that increase pulmonary resistance increased right ventricular afterload reduce lung vascularization hypoxemia, emphysema, embolus RV compensates by increasing preload and hypertrophy Cardiomyopathy
Aortic and mitral valvular disease Systemic hypertension Forward effects reduces CO via action on LV Backward effects congestion of systemic venous system Impaired function of liver, portal system, spleen, kidneys, peripheral subcuatenous tissues, brain Edema apparent in lower extremities In biventricular heart failure both systemic venous and pulmonary systems are congested Principles of Heart Failure Treatment GOAL: Optimize Cardiac Output
and Minimize Cardiac Workload Management of Preload Management of Afterload Management of Contractility Drugs used in the management of Heart Failure (table 19-3) Phases of the Ventricular Action Potential Hyperpolarized (+) 1 2 K+ out
Ca++ in 0 Na+ in -70 mV Depolarized (-) 4 3 K+ out CO2 transport in Blood Also see Fig 13-16
1. 2. 3. Dissolved CO2 Carbaminoglobin Bicarbonate ion Chloride shift Cardiovascular System Cardiovascular Structures Structure diagram of the human heart from an anterior view. Blue components indicate de-oxygenated blood
pathways and red components indicate oxygenated pathways. Pacemaker Cells SA node, AV node, Purkinje fibers Spontaneously generate action potentials Vary rate in response to ANS Action potentials are associated
with opening of slow calcium ion channels Almost no contractile elements What is the basis of automaticity? Spontaneous Phase 4 depolarization threshold RMP Ca K out Na
pacemaker cells are leaky to sodium at rest -40 mV -60 mV ANS Influences on Ion Flux Sympathetic: to NE, E stimulates Beta receptors leading opening of Na/Ca channels. The cell depolarizes
faster. Parasympathetic: acetylcholine stimulates muscarinic receptors leading to opening of K channels. Potassium leak out offsets sodium influx. The cell depolarizes Autonomic NERVES
SNS (T1-L2) Ach N1 NE nicotinic a1, a2 b1, b2, b3 receptor PSNS (Cn IX, X) Ach N1
Ach nicotinic M1 to M5 muscarinic receptor alpha-MN Ach N2 (nicotinic) muscle
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