Exam 3 Week 3

left coronary artery (LCA)

- branches into two arteries 2 types: - left anterior descending artery -- supplies blood to left and right ventricles and the septum - circumflex -- left border of heart (left atrium and lateral wall of left ventricle and posterior surfaces of both)

Atherosclerosis

•a form of arteriosclerosis characterized by plaque development along the walls of the arteries •Mechanism: thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall •Process that occurs throughout the body •Complications: leading cause of coronary artery and cerebrovascular disease (stoke) Clinical manifestations •Depends on the organ affected •Symptoms and signs are the result of inadequate perfusion of tissues - ex. coronary vasculature leads to chest pain, SOB - ex. cerebralvascular may cause mental status or visual changes

Constrictive (restrictive) pericarditis

•Fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere - can be seen with malignancy, trauma, radiation exposure, rheumatologic •Clinical manifestations: exercise intolerance, dyspnea on exertion, fatigue, and anorexia

Mitral valve prolapse syndrome

•Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole - most common cause is myxomatous degeneration of the leaflets in which cusps are redundant, thickened, and scalloped - chordae tendineae may be elongated permitting valves to stretch upward - mitral regurgitation occurs if ballooning valve permits blood to leak into atrium •Clinical manifestations: asymptomatic

chemoreceptors relation to BP

•Are sensitive to oxygen, carbon dioxide, or pH - found in medulla oblongata, aortic and carotid arteries - send signal glossopharyngeal (vagus) nervous to medulla oblongata --- will activate sympathetic or parasympathetic nervous system based on signals received - hypoxemia shows an increase in CO2 and a decrease in pH which triggers an increase in HR, SV, and BP

myocardial relaxation

•Calcium, troponin, and tropomyosin also facilitate relaxation - after contraction free calcium is pumped out - as calcium concentration decreases troponin begins to release calcium molecules - tropomyosin molecules block active sites of actin which prevent cross bridges with myosin heads

myocardial contraction

•Change in the tension occurs at a given resting fiber length. •Contraction occurs when the sarcomere shortens, causing adjacent Z lines to move closer together. - Width of the A band (thick myosin filaments): unchanged - I band: becomes narrower - Overlap between the thick and thin filaments:increases •Cross-bridge cycling - Attachment of actin to myosin at the cross bridge -- Myosin head molecule undergoes a position change. -- Causes thin filaments to slide past thick filaments (contraction). •Calcium - Is stored in the tubule system and the sarcoplasmic reticulum - Enters the myocardial cell from the interstitial fluid after electrical excitation, which increases membrane permeability to calcium - Diffuses toward the myofibrils, where it binds with troponin •Excitation contraction coupling= the process by which an action potential triggers the cycle of events, leading to cross-bridge activity and contraction - Requires calcium - Calcium-troponin complex facilitates the contraction process.

what influences force of contraction?

•Changes in the stretching of the ventricular myocardium, caused by changes in ventricular volume (preload) •Alterations in nervous system input to the ventricles (inotropic agents- pos increase and neg decrease) •Adequacy of myocardial oxygen supply - less than 50% O2 decreases contraction

Laplace's law

•Contractile force within a chamber depends on the radius of the chamber and the thickness of its wall. - Smaller chambers and thicker chamber walls equal increased contraction force. - In ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force.

β3 receptors

•Decrease myocardial contractility (negative inotropic effect) •May provide a "safety mechanism" to prevent an overstimulation of the heart by the sympathetic nervous system

Cardiomypathies

•Effects of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling. •Many cases of cardiomyopathy are idiopathic. - groups of disease impaction myocardial layer

progression of atherosclerosis

•Endothelium injury •Inflammation of endothelium •Cytokines released •Cellular proliferation •Macrophage migration •Low-density lipoproteins (LDL) oxidation (foam cell formation) with oxidative stress •Fatty streak •Fibrous plaque •Complicated plaque (rupture and occlude vessels)

Patent ductus arteriosus (PDA)

•Failure of the ductus arteriosus to close (between pulmonary artery and aorta) - Normally closes within first few hours of birth. - PDA allows blood to shunt from the pulmonary artery to the aorta. Clinical manifestation •Continuous, machinery-type murmur •Bounding pulses, active precordium, thrill upon palpation, and signs and symptoms of pulmonary overcirculation.

MI in relation to systolic HF

- MI causes decreased contractility -- causes decreased ejection fraction and increased left ventricular end diastolic volume ---- increased preload and renal failure leading to activation in RAS system and increased after load as a result - It also can damage the muscle, so that inotropy is impacted. Decreased force of contraction can lead to poor cardiac output and a decreased EF. (see slide 63)

What are the differences in blood flow of an adult heart v a fetal heart?

- fetal circulation differs from the adult pattern by the presence of alternate pathways known as fetal shunts: •Foramen ovale= the opening between the atria. •Ductus arteriosus= joins the pulmonary artery to the aorta. •Ductus venosus= connects the inferior vena cava to the umbilical vein. - fetal oxygenation occurs in the placenta through the umbilical vein instead of the lungs - Blood travels to the liver, where a portion enters the portal and hepatic circulation. -- Approximately one-half of the flow is diverted away from the liver through the ductus venosus and into the inferior vena cava. - Blood enters the right atrium from the inferior vena cava and is shunted through the foramen ovale and then into the left atrium, left ventricle, and aorta. - Less-saturated blood returns from the upper body, head, neck, and arms and travels from the superior vena cava into the right atrium. - A small portion of this blood flows into the right ventricle, out of the pulmonary artery, and enters the nonfunctioning lungs. - Most of the blood bypasses the lungs by flowing through the ductus arteriosus and into the descending aorta. - Blood from the descending aorta returns to the placenta through two umbilical arteries.

•Frank-Starling law of the heart

- length tension relationship •the volume of blood at the end of diastole impacts force of contraction in next systole cycle •look at relationship between Myocardial stretch determines the force of myocardial contraction. - More stretch = Increased force of contraction -- preload is index for how much volume is left in diastole ---- more volume creates more stretch

right coronary artery (RCA)

- travels behind the pulmonary artery and extends around the right side of the heart to the posterior surface (back) where it branches off to atrium and the ventricle 3 major branches: - conus artery -- supplies blood to upper right ventricle - right marginal branch -- supplies blood from right ventricle to apex of the heart - posterior descending branch -- branches off into both ventricles

S/S of Kawasaki and dx

Acute - fever - conjunctivitis - oral changes (strawberry tongue) - rash - lymphadenopathy - irritability Subacute - begins when fever ends and continues until clinical signs resolve - chills is most at risk for coronary artery aneurysm development - desquamation of the palms and soles occur - marked thrombocytosis d/t inflammation in the vasculature Convalescent - continued elevation of erythrocyte sedimentation rate and platelet count - arthritis may be present, continues until all laboratory values return to normal at 6-8 weeks after onset Diagnosis •Fever •Conjunctivitis •Oral changes (strawberry tongue) •Irritability •Rash •Lymphadenopathy

hormones related to BP

Arterial Pressure: Epinephrine and norepinephrine •Cause vasoconstriction Antidiuretic hormone •Increases blood volume by reabsorption of water from tubular fluid in the distal tubule and the collecting duct of the nephron Renin-angiotensin-aldosterone system •Aldosterone: stimulates reabsorption of sodium, chloride, and water to increase blood volume and stimulate thirst •Angiotensin II: vasoconstrictor Natriuretic peptides • released when heart muscle is stretched •Cause loss of sodium, chloride, and water through their effects on kidney function, decreasing blood volume • causes decrease in BP - can be measured by increased BNP for ex. elevated levels in pts with CHF Adrenomedullin •Powerful vasodilatory activity Nitric oxide, prostaglandins, endothelium-derived relaxing factor •Cause vasodilation Venous pressure •Main determinants - Volume of fluid in the veins - Compliance (distensibility) of the vessel walls •Mechanisms that affect venous pressure - Skeletal muscle pump --- when muscle contractions the veins are compressed decreasing venous capacity --- causes increased blood return to heart - Respiratory pump --- veins of abdomen are compressed during breathing and cause an increase in pressure moving the blood to the heart

hypertrophic cardiomyopathy

Hypertrophic obstructive cardiomyopathy - thickening of septal wall which cause an outflow obstruction to the left ventricular outflow tract - leads to altered contraction the heart r/t to altered proteins within myocytes - obstruction often occurs during exercise •Common inherited heart defect of a thick septal wall •Clinical manifestations: angina, syncope, palpitations, symptoms of MI, symptoms of left heart failure Hypertensive or valvular hypertrophic cardiomyopathy •Hypertrophy of the myocytes: attempts to compensate for increased myocardial workload - increased resistants to ventricular ejection - often seen in pts with HTN or stenotic valves •Clinical manifestations: asymptomatic or may complain of angina, syncope, dyspnea on exertion, and palpitations

β1 and β2

Overall β1 and β2 stimulation: - both cause increase in contraction and HR - Heart pumps more blood β1 - found in heart (atrial, ventricular myocardium) - stimulate contraction when activated β2 - β2 stimulation increases coronary blood flow - found in heart and vascular smooth muscle

Kawasaki disease

•Formerly known as mucocutaneous lymph node syndrome. •Is an acute, self-limiting systemic vasculitis that may result in cardiac sequelae. •Approximately 80% of cases occur in children under the age of 5. Cause •Unknown •Theories: An immunologic response to an infectious, toxic, or antigenic substance (including superantigen) Timeline and Process: - Stage I (0-12 days) -- capillaries, venues, arterioles, and heart become inflamed - Stage II (12-35 days) -- larger vessels become inflamed -- coronary aneurysms appear - Stage III (26-40 days) -- medium sized arteries begin the granulation process -- small vessel inflammation decreases - Stage IV (beyond day 41) -- scarring of the vessels -- thickening of the tunica intima -- calcification -- coronary artery stenosis

diastolic heart failure

•Heart failure with preserved ejection fraction •Decreased compliance of the left ventricle and abnormal diastolic relaxation (lusitropy) Clinical manifestations: dyspnea on exertion and fatigue - fewer systemic affects because heart is still able to get blood to tissues

dilated cardiomyopathy

•Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure - difficulty pushing blood out when it is so dilated •Causes: ischemic heart disease; valvular disease; diabetes; alcohol; drug toxicity; renal failure; hyperthyroidism, diabetes; deficiencies of niacin, vitamin D, and selenium; infection •Clinical manifestations: dyspnea, fatigue, pedal edema

Tricuspid atresia

•Imperforate tricuspid valve •No communication between the right atrium and the right ventricle - baby is reliant on a septal defect •Additional defects - Septal defect - Hypoplastic or absent right ventricle - Enlarged mitral valve and left ventricle - Pulmonic stenosis Clinical manifestations •Central cyanosis and growth failure •Exertional dyspnea, tachypnea, and hypoxemia Polycythemia, clubbing, hepatomegaly (r/t blood backing up from the R atria

Infective Endocarditis (IE)

•Inflammation of the endocardium from infectious agents - Most common: bacteria, especially streptococci, staphylococci, and enterococci - can be associated with IV drugs use, anytime there is a persistent blood infection •Pathogenesis - Endocardial damage - Bloodborne microorganism adherence - Formation of infective endocardial vegetations Clinical manifestations •Fever •New or changed cardiac murmur •Petechial lesions of the skin, conjunctiva, and oral mucosa •Osler nodes: painful erythematous nodules on the pads of the fingers and toes •Janeway lesions: nonpainful hemorrhagic lesions on the palms and soles •Weight loss, back pain, night sweats, heart failure, emboli (septic emboli)

Tricuspid regurgitation

•Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure - commonly associated with dilation and failure of the right ventricle secondary to pulmonary HTN - less commonly associate with rheumatic heart disease and infective endocarditis

Hypoplastic left heart syndrome

•Left-sided cardiac structures develop abnormally. - Obstruction to blood flow from the left ventricular outflow tract •Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed. •As the ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock.

structural and functional changes r/t to MI

•Myocardial stunning: is the temporary loss of contractile function that persists for hours to days after perfusion has been restored - if you do an ultrasound you will see akinesia in one of the walls •Hibernating myocardium: tissue that is persistently ischemic undergoes metabolic adaptation to prolong myocyte survival •Myocardial remodeling: process that occurs in the myocardium after an MI - leads to hypertrophy of cardiac cells, scarring, loss of contractile functions in areas distant to site of infarction - if flow is rapidly restored that reversal may occur

restrictive cardiomyopathy

•Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. •Clinical manifestations: right heart failure occurs with systemic venous congestion - fluid backs up so we see elevated carotids --- enlargement of liver, peripheral edema, etc

Pulmonary stenosis

•Narrowing of the pulmonary outflow tract •Abnormal thickening of the valve leaflets •Narrowing of the valve - as a result blood is not being pumped adequately through pulmonic valve and blood can back into RV •Pulmonary atresia: Severe form - congenital disorder where valve does not form as it should - blood that should be moving forward is moving back and you see RV hypertrophy and it becomes dilated and ability to contract Clinical manifestations •Often asymptomatic •Exertional dyspnea, murmur, fatigue, thrill, cyanosis, HF (R side- JVD, enlargement of spleen and liver)

what are the differences between a myocardial cell and skeletal muscle cell?

•Nearly identical to skeletal muscle cells - nucleus, mitochondria, plasma membrane, cytoplasm all similar -- most of cytoplasm consists of myofibrils arranged in units called sarcomeres --- skeletal cells are arranged in parallel units whereas myocardial cells are arranged in branching networks - skeletal cells have many nuclei whereas myocardial only have one •Intercalated disks - Specialized intercellular junctions - allow action potentials to travel faster cell to cell than skeletal muscle - myocardial cells need to maintain higher levels of energy synthesis than skeletal cells so they have more mitochondria to make ATP - myocardial cells have more t tubules which allows more access to ions (Na and K) in the extracellular environment to allow transmission of action potentials - myocardial cells work constantly which skeletal muscle cells cannot do

Eisenmenger syndrome

•Pulmonary vascular resistance increases that exceed or equal vascular resistance, resulting in a reversal of shunting Defects that cause hypoxemia and cyanosis: •Lesions that cause obstruction and shunting from the right side of the heart to the left side, as in the tetralogy of Fallot •Defects involving the mixing of saturated and unsaturated blood, as in the univentricular heart •Transposition of the great arteries Clinical manifestations •Mild hypoxemia - Cyanosis only occasionally when stressed •Severe hypoxemia - Feeding intolerance, poor weight gain, tachypnea, and dyspnea •Chronic hypoxemia - Small for their age, may display cognitive and motor skill delays. - Polycythemia, shortness of breath with exertion, easily fatigued, and exercise intolerance - Clubbing of the nail beds

Total anomalous pulmonary venous connection (TAPVC)

•Pulmonary veins connect to the right side of the heart, directly or indirectly, through one or more systemic veins that drain into the right atrium. •Nonobstructive vs. obstructive - nonobstructive the oxygenated blood is pumped in RA and would normally go from lungs into LA --- amount of blood being shunted depends on size of defect and compliance of RA --- enlargement of RA and RV which causes increased amounts of pulmonary venous return --- if defect is not restrictive and RV doesn't become thinner than most blood is shunted from RA to LA - obstructive the pulmonary venous HTN will revolve b/c blood is blocked and cannot enter RA --- results in pulmonary vascular pressures and RV pressures --- pulmonary edema can occur from hydrostatic capillary pressure and R HF can develop Clinical manifestation: Cyanosis - impaired growth - rapid detonation if not surgically corrected

Raynaud disease and Raynaud phenomenon

•Raynaud disease: primary vasospastic disorder •Raynaud phenomenon: secondary to other systemic diseases or conditions of unknown origin- accumulation of immune complexes •Episodic vasospasm (ischemia) in the arteries and arterioles of the fingers; less commonly in the toes Clinical manifestations: changes in skin color and sensation caused by ischemia - numbest, tingling, pain - differences in temperature

baroreceptors relation to BP

•Reduce blood pressure to normal by decreasing cardiac output and peripheral resistance •Can also increase blood pressure when needed - sensitive to changes in pressure and sit in carotid sinus and aortic arch - send signal glossopharyngeal (vagus) nervous to medulla oblongata --- will activate sympathetic or parasympathetic nervous system based on signals received - respond to changes in smooth muscle fiber length --- when activated (stretched) they decrease CO by lowering HR and SV and peripheral resistance, thus lowering BP

Atrioventricular canal (AVC) defect

•Results from nonfusion of the endocardial cushions. •Abnormalities demonstrated in the atrial and ventricular septa and AV valves •Complete, partial, and transitional AVC defects Clinical manifestations: Presents with a murmur; heart failure; respiratory tract infections.

chronotrophy and inotrophy

•Stimulation of both the β1 and β2: increases the heart rate (chronotropy) and force of the myocardial contraction (inotropy) - If the heart rate is affected, then the effect is called chronotropy. --- Negative chronotropy: decreases heart rate --- Positive chronotropy: increases heart rate - If the heart contraction is affected, then the effect is called inotropy. --- Negative inotropy: decreases force of contraction --- Positive inotropy: increases force of contraction

Tetralogy of Fallot (TOF)

•Syndrome represented by four defects - Large VSD (hole in septum) - Overriding aorta straddles the VSD - Pulmonary stenosis - Right ventricle hypertrophy Manifestations: •Cyanosis, hypoxia, and clubbing, feeding difficulty, dyspnea, restlessness, squatting •*Hypercyanotic spell or a "tet spell" that generally occurs with crying and exertion* - typically corrected with surgery during early infancy before one year of age

Acute Rheumatic Fever and Rheumatic Heart Disease

•a diffuse, inflammatory disease caused by a delayed immune response to infection by the group A beta-hemolytic streptococci - Is a febrile illness --- Fever, lymphadenopathy, arthralgia, nausea, vomiting, epistaxis •If left untreated, rheumatic fever causes rheumatic heart disease. (It may have a genetic component.) •Abnormal immune response to the M proteins that cross react with normal tissues •Fibrinoid necrotic deposits: Aschoff bodies Clinical manifestations •Carditis: murmur •Polyarthritis: large joints mainly affected •Subcutaneous nodules •Chorea: sudden, aimless, irregular, involuntary movements •Erythema marginatum: truncal rash

Thromboangiitis obliterans (Buerger disease)

•an inflammatory disease of the peripheral arteries (digital, tibial, plantar, ulnar, and palmer arteries) •Occurs mainly in smokers •Obliterates the small- and medium-sized arteries •Pain and tenderness develop in the affected part. •Sluggish blood flow, rubor (flushed skin), and cyanosis result.

Transposition of the great arteries

•aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. - Results in two separate, parallel circuits. -- Unoxygenated blood continuously circulates through the systemic circulation. -- Oxygenated blood continuously circulates through the pulmonary circulation. •Extrauterine survival requires communication between the two circuits. Clinical manifestations: - Cyanosis may be mild shortly after birth and worsen during the first day.

orthostatic (postural) hypotension

•decrease in the systolic on standing by 20 mmHg or more and by 10 mmHg or more in diastolic blood pressures, respectively •Lack of normal blood pressure compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation •Primary - chronic condition seen in older adults with neurological conditions such as PD, MS - can predispose to falls •Secondary - dehydration or new BP medicines and overmedicated - prolonged immobility, hyponatremia, etc Clinical manifestation: - lightheadedness - dizziness - syncope

systolic heart failure

•inability of the heart to generate adequate cardiac output to perfuse tissues - reduced ejection fraction - characterized by combination of neuro, humeral, and metabolic process: •Catecholamines- to compensate fo a decrease in CO by increasing HR and peripheral vascular resistance -- creates extra work for heart leading to myocyte apoptosis and myocardial remodeling •RAAS: angiotensin II and aldosterone - compensate for decrease ejection fraction - more work •Arginine vasopressin (antidiuretic hormone) - vasoconstriction and fluid retention- more work •Natriuretic peptides - BNP r/t to increase pressure - triggers kidneys to excrete fluid and sodium •Inflammatory cytokines: endothelial hormones, tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) - cause changes in myocardial hypertrophy and remodeling •Myocyte calcium transport - changes in ion channels which decrease contractility and worsening of HF •Insulin resistance and diabetes - abnormal fatty acid metabolism and generation of ATP contributing to decreased myocardial contractility and remodeling Clinical manifestations •Dyspnea, orthopnea, cough of frothy sputum •Fatigue •Decreased urine output and edema

aneurysm

•local dilation or outpouching of a vessel wall or cardiac chamber True aneurysms •Involvement of all three layers of the arterial wall which causing weaken and dilatation - Fusiform aneurysms - Circumferential aneurysms False aneurysms •Leak between a vascular graft and a natural artery - hematoma will form and remain in extravascular space but communicate with intravascular space - may cause clot or leakage Manifestations •Heart: include dysrhythmias, heart failure, and embolism of clots to the brain or other vital organs •Aorta: asymptomatic until it ruptures, then it becomes painful •Thoracic: dysphagia (difficulty in swallowing) and dyspnea (breathlessness) are caused by the pressure •Abdomen: flow to an extremity is impaired, causing ischemia. Complication •Aortic dissection= a devastating complication that involves the aorta (ascending, arch, or descending); can disrupt the flow through the arterial branches •Is a surgical emergency

Aortic stenosis

•narrowing of the aortic outflow tract (10% of defects) caused by malformation or fusion of the cusps. •Causes an increased workload on the left ventricle because blood cannot pass easily through the stenosed aorta Clinical manifestations •Often asymptomatic •Signs of exercise intolerance in preadolescence •Syncopal episodes, epigastric pain, and exertional chest pain in more severe forms •Murmur

Coarctation of the aorta

•narrowing of the lumen of the aorta that impedes blood flow (8% to 10% of defects) •Almost always found in the juxtaductal position, but it can occur anywhere between the origin of the aortic arch and the bifurcation of the aorta in the lower abdomen. Clinical manifestations: Newborns usually exhibit L HF. - Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock. Clinical manifestations: Older children •Hypertension in the upper extremities •Decreased or absent pulses in the lower extremities •Cool mottled skin •Leg cramps during exercise

superior vena cava (SVC) syndrome

•progressive occlusion of the SVC that leads to venous distention in the upper extremities and head •Etiologies: non-small cell lung cancer, small cell lung cancer, lymphoma, cystic fibrosis, some infections Manifestations •Edema •Venous distention of face, neck, trunk, upper extremities •Cyanosis •Dyspnea •Dysphagia •Hoarseness •Stridor •Cough •Chest pain •CNS changes •Respiratory distress

unstable angina

•reversible myocardial ischemia and a harbinger of impending infarction •Transient episodes of thrombotic vessel occlusion and vasoconstriction occur at the site of plaque damage with a return of perfusion before significant myocardial necrosis occurs. - signifies atherosclerotic plaque has ruptured s/s - new onset occurring at rest or increasing in severity or frequency - dyspnea - diaphoresis - anxiety

ejection fraction

•the amount of blood ejected per beat •Normal is 66% for women and 58% for men. •Calculated by dividing the stroke volume by the end-diastolic volume •An indicator of ventricular function - increased by factors that increase contractility

Truncus arteriosus

•the failure of the embryonic artery to divide into the pulmonary artery and aorta. •Trunk straddles an always present VSD. •Types I through IV - I: Most common; the main pulmonary artery arises from the truncus. - II: Pulmonary arteries arise from the posterior aspect of the truncus. - III: Pulmonary arteries arise from the lateral aspect of the truncus. - IV: Pseudotruncus; is a severe form of tetralogy of Fallot with the bronchial arteries arising from the descending aorta to supply the lungs. Clinical manifestations •Cyanosis; mild-to-moderate cyanosis that worsens with activity •Murmur • eventually sighs of HF

high output heart failure

•the inability of the heart to supply the body with blood borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility Common causes •Anemia - decreases oxygen carrying capacity leading anaerobic metabolism causing lactic acid - HR and SV increase in response but with severe anemia blood does not have enough O2 for tissues •septicemia - vasodilation and fever - in severe cases heart cannot compensate •hyperthyroidism - during thyroid storm metabolic acidosis may occur - cardiac output may not be enough to compensate for high levels of thyroxine •beriberi - thiamine deficiency causes decrease cellular metabolism in heart cells leading to insufficient contractile strength - vasodilation also occurs

afterload

•the resistance (pressure) to ejection during systole •Aortic systolic pressure is a good index of afterload for the left ventricle. •Decreased afterload: heart contracts more rapidly •Increased afterload: slows contractions and increases work load •Systemic vascular resistance (SVR) or total peripheral resistance (TPR)- pressure heart is being forced to pump against

preload

•the volume inside the ventricle at the end of diastole (rest phase when filling) • Also called ventricular end-diastolic volume (VEDV) and ventricular end-diastolic pressure (VEDP) •Determined by two primary factors - Amount of venous return to the ventricle - Blood left in the ventricle after systole or end-systolic volume •When preload exceeds physiologic range, further muscle stretching causes a decline in cardiac output.

cardiac output

•the volume of blood flowing through either the systemic or the pulmonary circuit expressed in liters per minute (L/minutes) •Calculated by multiplying the heart rate in beats per minute by the stroke volume •Normal adult cardiac output at rest is 5 L/minutes.

varicose veins

•veins in which blood has pooled leading to distortion, leakage, increased intravascular hydrostatic pressure, and inflammation of veins •Etiologies: incompetent valves, venous obstruction, muscle pump dysfunction, or combination of these. Risks - sedentary life or excessive standing - women - pregnancy - weight gain - age - leg trauma - family hx •Mechanism: Altered ratio of prostacyclin (usually inhibits platelet activation and vasodilator) to thromboxane A2 with higher potential for clotting, increased fibroblast growth factor, and increased transforming growth factor B in vein walls - contributes to clotting and obstruction of the veins from engorgement of vessels •Manifestations: Visible distention of veins, itching, burning or throbbing pain around the lower extremity veins - can regress to chronic venous insufficiency if left untreated -- persistent ambulatory lower extremity venous hypertension