Cardiovascular Dysfunction Flashcards
Two major groups of Cardiovascular Dysfunction
Congenital Heart Disease and Acquire Heart Disorders
6 Tests for Cardiac Function
Electrocardiography echocardiography chest radiograph (x ray) cardiac catheterization excersize stress test cardiac magnetic resonance imaging (MRI)
4 uses of cardiac catherization
biopsy
hemodynamics
angiography
electrophysiology
Interventional Catheterization
A balloon catheter or other device is used to alter the cardiac anatomy to fix structural problems
complications of cardiac catheterization
hemorrhage from entry site low grade fever nausea/vomiting loss of pulse distal to catheterization site (results from clot, hematoma, or tear) transient dysrhythmias
preparation for cardiac catheterization in pediatric population
NPO 4-6 hrs before procedure entertainment for during procedure accurate weight/height developmentally appropriate explanation allergies potential sedation
postprocedural care for cardiac catheterization
check for: blood glucose level colour vital signs dressing fluid intake
two major cause of death in the first year of life
prematurity and CHD
most common congenital heart defect
ventricular septal defect - abnormal opening between the right and left ventricles
classified according to location: membranous or muscular
left to right shunt
an abnormality between the left and right ventricle cause blood to flow left to right as that is the path of least resistance (pressure and blood flow)
classification of defects
used to be cyanotic or acyanotic (changed bc children with acyanotic defects might develop cyanosis and those with cyanotic defects may appear pink and have more clinical signs of HF)
Now classified according to blood flow patterns: 4 patterns
increased pulmonary blood flow
decreased pulmonary blood flow
obstruction to blood flow out of heart
mixed blood flow (oxygenated and nonoxygenated blood mix)
right to left shunting
decreased pulmonary blood flow resulting from obstruction of pulmonary blood flow and an anatomical defect between right and left side of heart. The blockage increases the right side pressure causing it to exceed the left sided pressure and results in right to left shunting
Defects with increased pulmonary blood flow
atrial septal defect
ventricular septal defect
atrioventricular canal defect
patent ductus arteriosus
atrial septal defect
abnormal opening between the atria allowing blood from high pressure left to flow to low pressure right. 3 types of atrial defects. Pt asymptomatic but may develop HF. Treatment with path over hole, cardiac catheterization, cardiopulmonary bypass, and valve replacement
3 types of atrial septal defects
Ostium Primum (ASD1) - opening at lower end of septum; associated with mitral valve abnormalities Ostium Secundum (ASD2) - opening near center of septum sinus Venosus Defect - opening near junction of superior vena cava and right atrium; associated with partial anomalous pulmonary venous connection
ventricular septal defect
abnormal opening between the right and left ventricle. Classified as membranous or muscular. Common ventricle is when there is an absence of a septum. HF common. Pt at risk for bacterial endocarditis and pulmonary vascular obstructive disease. Tx; Placing a band around the main pulmonary artery to decrease pulmonary bloodflow, complete repair with sutures, cardiac catheterization, patch over large defects, cardiopulmonary bypass
Atrioventricular Canal Defect
Incomplete fusion of the endocardial cushions. Combined low ASD and high VSD. Allows blood to flow between all four heart chambers. Pt have moderate to severe HF, mild cyanosis, and increased risk of pulmonary vascular obstructive disease. Tx: pulmonary artery banding, surgical repair with patch
patent Ductus Arteriosus
failure of the fetal ductus arteriosus (artery connecting the aorta and pulmonary artery) to close within the first week of life. Pt asymptomatic or show signs of HF. Tx: IV admin of indomethacin (prostaglandin inhibitor) has shown effective in closing PDA - should be given via umbilical lines, thoracotomy for surgical division of patent vessel, thoracoscope inserted on left side of chest to clip ductus, coils to occlude PDA placed in pt in catheterization lab
Obstructive Defects
Coarctation of the aorta aortic stenosis valvular aortic stenosis pulmonic stenosis subvalvular aortic stenosis
coarctation of the aorta
localized narrowing near the insertion of the ductus arteriosus, which results in increased pressure proximal to the defect (head and upper extremities) and lower pressure distal to the obstruction (body and lower extremities). Pt has bounding pulse in upper extremities and weak pulse below. Cool lower extremities and low BP, signs of HF in infants. Tx: surgical repair, balloon angioplasty, stents
aortic stenosis
narrowing or stricture of the aortic valve, causing resistance to blood flow in the left ventricle, decreased cardiac output, left ventricular hypertrophy, and pulmonary vascular congestion. Prominent consequence of AS is the hypertrophy of the left ventricular wall. Valvular stenosis most common type of AS. infant S and S: faint pulse, hypotension, tachycardia, and poor feeding. Children S and S: excersize intolerance, chest pain, and dizziness
Valvular Aortic Stenosis
caused by malformed cusps that result in a bicuspid rather than a tricuspid valve or fusion of the cusps. Aortic valvotomy is performed under inflow occlusion or balloon dilation.
subvalvular aortic stenosis
stricture caused by a fibrous ring below a normal valve. Tx: incising a membrane if one exists or cutting the fibrous ring, a patch to enlarge the left ventricle outflow tract and annulus and replace the aortic valve
Supravalvular aortic stenosis
occurs infrequently
pulmonic stenosis
narrowing at the entrance of the pulmonary artery. Resistance to blood flow causes right ventricular hypertrophy and decreased pulmonary blood flow. Tx: infants - transventricular (closed) valvotomy is used. Children - pulmonary valvotomy with cardiopulmonary bypass. Nonsurgical - balloon angioplasty
pulmonary atresia
severe form of pulmonary stenosis in that there is total fusion of the commissures and no blood flow to the lungs
Decreased pulmonary Blood Flow
tetralogy of fallot
tricuspid atresia
Tetralogy of Fallot
classic form includes four defects: VSD, pulmonic stenosis, overriding aorta, and right ventricular hypertrophy. hemodynamic alterations vary widely depending on degree of PS and size of VSD and the flow resistance it creates. if the VSD is large, pressure in right and left ventricle equal so blood flow dependant on vascular resistance. Tx: palliative shunt, complete repair
Blue Spell or Tet Spells
Acute episodes of cyanosis and hypoxia. Called tet spells bc seen often in Tetralogy of Fallot
Tricuspid Atresia
Tricuspid valve fails to develop; no communication from the right atrium to the right ventricle. Blood flows through an ASD or patent foramen ovale to the left side of the heart and through a VSD to the right ventricle and out to the lungs. There is also complete mixing of oxygenated and unoxygenated blood in the left side of the heart. Tx: For the newborn whos pulmonary blood flow depends on a patent ductus arteriosus, continuous infusion of prostaglandin E until surgery, surgical tx is placement of a shunt, modified Fontan Procedure
Mixed Defects
Transposition of the great arteries OR Transposition of the great vessels
total anomalous pulmonary venous connection
truncus arteriosus
hypoplastic left heart syndrome
transposition of the great arteries/vessels
the pulmonary artery leaves the left ventricle and the aorta exits from the right ventricle, with no communication between the systemic and pulmonary circulations. Associated septal defects must be present to allow blood to enter the systemic or pulmonary circulation for mixing of blood. Most common defect associated with TGA is patent foramen ovale. Tx: IV of prostaglandin E to keep PDA or FO open, balloon atrial septostomy, arterial switch procedure, rastelli procedure
Rastelli Procedure
procedure of choice in TGA, VSD, and severe pulmonic stenosis
total anomalous pulmonary venous connection
rare defect characterized by failure of the pulmonary veins to join the left atrium, Instead, the pulmonary veins are abnormally connected to the systemic venous circuit via the right atrium or various veins draining toward the right atrium, such as the superior vena cava. The abnormal attached results in mixed blood returned to the right atrium and shunted from left to right through an ASD. TAPVS classified in 3 ways; supracardiac, cardiac, infradiaphragmatic. Tx: surgical approach varis with anatomical defect, in general the common pulmonary vein is anastomosed to the back of the left atrium, the ASD closed, and the anomalous pulmonary venous connection is ligated.
Classification of TAPVC
Supracardiac - attachment above the diaphragm, such as the SVC
Cardiac - direct attachment to the heart, such as the right atrium or coronary sinus
Infradiaphragmatic - attachment below the diaphragm, such as the inferior vena cava; most fatal form and associated with obstruction to pulmonary venous drainage and is surgical emergency
truncus arteriosus
failure of normal septation and division of the embryonic bulbar trunk into the pulmonary artery and the aorta, which results in development of a single vessel that overrides both ventricles. blood from both ventricles mixes in the common great artery, which leads to desaturation and hypoxemia. 3 types of truncus arteriosus. Tx: surgical repair involving closing the VSD so that the TA recieves the outflow from the left ventricle, excising the pulmonary arteries from the aorta and attaching them to the right ventricle by homograft. Conduit replacement needed as the child grows as they will not grow with the child
3 types of truncus arteriosus
type I - a single pulmonary trunk arises near the base of the truncus and divides into the left and right pulmonary arteries
type II - the left and right pulmonary arteries arise separately but in close proximity and at the same level from the back of the truncus
type III - the pulmonary arteries arise independently from the sides of the truncus
Hypoplastic Left Heart Syndrome
underdevelopment of the left side of the heart resulting in a hypoplastic left ventricle and aortic atresia. most blood from the left atrium flows across the patent foramen ovale to the right atrium, to the right ventricle and out of the pulmonary artery. Tx: newborn stabilized with nechanical ventilation and inotropic support preoperatively. IV prostaglandin E to maintain PDA. Multistage surgical approach, heart transplant
Calculate maintenance fluid during dehydration
421 rule (4 x first 10kg, 2 x next 10kg, 1 x rest kg)
cardiac output
HR x SV
the amount of blood the heart pumps in a minute
heart failure
inability of the heart to pump an adequate amount of blood to the systemic circulation to meet metabolic needs. separated into right or left sided failure. S and S: impaired myocardial fraction, pulmonary congestion, systemic venous congestion. Diagnosis made on clinical symptoms (tachypnea, tachycardia, retractions, fluid retention, etc), chest x ray, ECG
left sided heart failure
left ventricle unable to pump blood into systemic circulation, resulting in increased pressure in the left atrium and pulmonary veins. Lungs congested with blood, elevated pulmonary pressures and edema
right sided heart failure
right ventricle unable to pump blood effectively into pulmonary artery, resulting in increased pressure in right atrium and systemic venous circulation. systemic venous hypertension causes hepatosplenomegaly and edema
treatment for heart failure
goals: improved cardiac function (increased contractility and decreased afterload), remove accumulated fluid and sodium (decrease preload), decrease cardiac demands, improve tissue oxygenation and decrease oxygen consumption.
HF: improve cardiac function
admin of digitalis glycosides in one digitalizing dosage oral or IV over 24 hours and maintenance dosage given twice a day orally to maintain blood levels. ACE inhibitors to block conversion of angiotensin I into II so that vasodilation instead of vasoconstriction occurs. beta blockers used to decrease HR, BP and vasodilation. Cardiac resynchronization therapy being explored in peds pop.
HF: remove accumulated fluid and sodium
diuretics, possible fluid restriction, possible sodium restriction
HF: decrease cardiac demands
metabolic needs minimized by providing neutral thermal environment to prevent cold stress, treating infections, reduce efforts for breathing (semi fowler position), meds to sedate irritable child, and providing rest and reducing environmental stimuli
HF: improve tissue oxygenation
supplemental cool, humidified oxygen
HF: nursing care
support child and family assist in measures to promote fluid loss maintain nutritional status decrease cardiac demands reduce respiratory distress monitor afterload reduction assist in measures to improve cardiac function
hypoxemia
arterial oxygen tension (or pressure, Pao2) that is less than normal and can be identified by a decreased arterial saturation or a decreased Pao2. Heart defects that cause hypoxemia (and cyanosis) result from desaturated venous blood entering the systemic circulation without passing the lungs
hypoxia
reduction in tissue oxygenation that is caused by low oxygen saturations and Pao2 and results in impaired cellular processes
cyanosis
blue discolouration in the mucous membranes, skin, and nail beds of the child with reduced oxygen sat. results from the presence of deoxygenated Hemoglobin. Apparent when arterial oxygen sat is 80-85% and findings are subjective
Hypoxemia: clinical manifestation
chronic hypoxemia results in polycythemia and clubbing. Polycythemia is an increased number of red blood cells to increase the oxygen carrying capacity of the blood. Anemia may results as iron is not readily available for the formation of hemoglobin. Polycythemia increases blood viscosity and crowds out clotting factors. Clubbing is a thickening and flattening of the tips of the fingers and toes
Hypoxemia: Diagnostics
hyperoxia test: infant/child placed in a 100% oxygen environment and blood parameters monitored. A Pao2 of 100mmHg or higher suggest lung disease and Pao2 less than 100mmhg suggest cardiac disease. also used are accurate history, chest radiograph, and echocardiogram (ECG)
Hypoxemia: Therapeutic Management
Admin of IV prostaglandin E to keep PDA until diagnosis is confirmed - need PDA open to maintain pulmonary blood flow until intervention. Cyanotic infant should be kept hydrated to keep the hematocrit and blood viscosity within normal limits to reduce risk of CVA (cerebrovascular accident - stroke). Agresssive pulmonary hygiene, chest physical therapy, admin of antibiotic, and use of oxygen to improve arterial saturation are important interventions
Hypoxemia: nursing Care
Appearance is blue lips, blue nails, clubbing, and small thin stature. Children are excited for surgery as it will “make them pink”. dehydration prevented to reduce risk of CVA. Fluid status monitored frequently, accurate intake and output and daily weight measures. Maintenance fluid therapy, supplemental fluids, gavage feeding and IV hydration for children unable to adequately meet needs orally. Infection prevention measures, especially for respiratory infections as they will increase hypoxemia. Special note: intracardiac shunting from right to left allows air into the venous system and can cause air embolism, thus all tubing should be checked for air bubbles and promptly removed
Treating Hypercyanotic (blue or tet) spells
place infant in knee-chest position
use calm and comforting approach
administer 100% oxygen by blow by
give morphine subcutaneously or through existing IV line
begin IV fluid replacement and volume expansion if needed
repeat morphine admin
postoperative complications after cardiac surgery
heart failure - tx: digoxin, diuretic
low cardiac output - tx: IV inotropes
dysrhythmias - tx: drug treatment, possible pacing, cardioversion
tamponade (blood or fluid in the pericardial space constricting the heart) - tx: removal of fluid by pericardiocentesis
atelectasis - tx: chest physical therapy, coughing, deep breathing, ambulation
pulmonary edema - tx: diuretics
pleural effusions - tx: diuretics, possible chest tube drainage
pneumothorax - tx: chest tube drainage
seizure - tx: assessment, antiepileptic drug
CVA, cerebral edema, neurological defect - tx: assessment and treatment
infection - tx: antibiotics
anemia - tx: iron supplement, transfusion
postoperative bleeding - tx: clotting factors, blood products: may need repeat surgery to locate and stop bleeding
postpericardiotomy syndrome - tx: antipyretics, diuretics, anti-inflammatory meds
bacterial (infective) endocarditis
bacterial endocarditis (or subacute bacterial endocarditis) is the infection of the inner lining of the heart (endocardium), generally involving the valves. Can occur without underlying hear disease, but tends to be sequela of bacterium in the child with congenital or acquired anomalies of the heart or great vessels
Bacterial Endocarditis: diagnosis
clinical manifestation, ECG changes (long PR interval), radiographic evidence of cardiomegaly, anemia, elevated erythrocyte sedimentation rate, leukocytosis, microscopic hematuria. Vegetation on the valve and abnormal valve function can often be visualized by echocardiography. Definitive diagnosis rests on growth and identification of the causative agent in the blood
Bacterial Endocarditis: therapeutic Management
admin of high dose of antibiotics IV for 2-8 wks. blood cultures taken periodically to determine response to meds. Prevention is admin of prophylactic antibiotic therapy 1 hr before procedure known to increase risk of infection. Dental work in those with cardiac diagnosis increases risk of infection
Bacterial Endocarditis: Nursing Care Goals
preparation of the child for IV infusion, usually with intermittent infusion device, and several venipuncture for blood cultures
observation for adverse effects of antibiotics, especially inflammation of venipuncture site
observation for complications, including embolism and HF
education regarding the importance of follow up visit for cardiac evaluation, echocardiographic monitoring, and blood cultures
Rheumatic Fever
poorly understood inflammatory disease that occurs after infection with group A-hemolytic streptococcal pharyngitis (GABHS). occurs most often in late age school children or adolescents. self limiting, involving the joints, brain, skin, serous surface, and heart. Cardiac valve damage (rheumatic heart disease) is the most significant complication (mitral valve most often affected)
Rheumatic Fever Diagnosis
presence of two major manifestations or one major and two minor manifestations with supportive evidence of recent streptococcal infection, indicates high probability of RF
Rheumatic Fever: therapeutic Management
goals of medical management: eradication of hemolytic streptococci, prevention of permanent cardiac damage, palliation of the other symptoms, prevention of recurrent RF. Penicillin med of choice either oral or IM (erythromycin sub for penicillin resistance kids)
Rheumatic Fever: Nursing Care
Monthly injections can be subbed for daily oral med if adherence to treatment plan is poor. Complication of Chorea (movement disorder of involuntary, irregular, unpredictable muscle movements) is possible and may occur weeks to months after illness. Chorea is transitional and all manifestations eventually disappear
Hyperlipidemia/Hypercholesterolemia
hyperlipidemia - general term for excessive lipids
hypercholesterolemia - refers to excess cholesterol in the blood
high lipid and cholesterol play an important role in producing atherosclerosis (fatty plaque on the arteries), which can eventually lead to coronary artery disease (primary cause of mortality and morbidity in the adult pop)
dyslipidemia
abnormalities in lipid metabolism, including low levels of high density lipoprotein
high density lipoproteins (HDL)
low concentration of triglycerides, relatively low cholesterol, high levels of protein. transport free cholesterol to the liver for excretion in the bile
High levels of HDL are though to protect against cardiovascular disease
Low density lipoproteins (LDL)
low concentration of triglycerides, high levels of cholesterol, moderate levels of protein. major carrier of cholesterol to the cells. use cholesterol for synthesis of membranes and steroid production. elevated LDL risk factor for cardiovascular disease
cardiac dysrhythmias
abnormal heart rhythms, can occur in children with structurally normal hearts, as features of some congenital heart defects, and in patients after surgical repair of congenital heart defects. they are also seen in patients with cardiomyopathy and cardiac tumours and can occur secondary to metabolic and electrolyte imbalances. classified by either tachycardia or bradycardia and origin in atria or ventricles. 3 types of dysrhythmias: bradydysrhythmias, tachydsyrhythmias, conduction disturbances
bradydysrhythmias
abnormally slow heart rate. sinus bradycardia in children can be influence of the autonomic nervous system, as with hypervagal tone, or in response to hypoxia and hypotension. also known to develop after complex surgical repairs involving atrial suture lines. Complete AV (atrioventricular) block - also referred to as complete heart block - most often related to edema around the conduction system and resolve without treatment. Some children may need pacemakers to take over or assist in the hearts conduction function.
tachydysrhythmias
sinus tachycardia (abnormally fast heart rate) secondary to fever, anxiety, pain, dehydration, hypovolemia, hypoxia, shock, pulmonary edema, medication or any other etiological factor requiring increased cardiac output should be ruled out before diagnosis of pathological increased heart rate. Supraventricular tachycardia (SVT) is the most common tachydsyrhythmias found in children and refers to rapid regular HR of 200-300 bpm. tx: vagal maneuvers (such as applying ice to the face), massaging the carotid artery (on one side of the neck only), or having an older child perform valsalva manoeuvre (exhaling against a closed glottis, blowing on a thumb as if it were a trumpet for 30-6o sec) have terminated SVT. If these manoeuvres dont work adenosine is given by rapid IV push with saline bolus. if it is still compromised cardioversion (delivering electrical shock to heart) is performed on sedated pt.
pulmonary hypertension
pulmonary artery hypertension describes a group of rare disorders that result in an elevation of pulmonary artery pressure above 25mmHg at rest (after neonatal period). characterized by vascular narrowing leading to an increase in pulmonary vascular resistance. generally result in remodeling of the pulmonary circulation, characterized by occlusion of the lumen in medium and small pulmonary arteries because of cellular proliferation.
cardiomyopathy
abnormalities of the myocardium in which the cardiac muscles ability to contract is impaired. 3 types of cardiomyopathy; dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy.
dilated cardiomyopathy
ventricular dilation and greatly decreased contractility, resulting in symptoms of HF. most common type in children, cause unknown
hypertrophic cardiomyopathy
increase in heart muscle mass without an increase in cavity size, usually occurring in the left ventricle and associated with abnormal diastolic filling. most common genetically transmitted cardiovascular disease (autosomal dominant).
restrictive cardiomyopathy
rare in children. restriction to ventricular filling caused by endocardial or myocardial disease or both. characterized by diastolic dysfunction and absence of ventricular dilation or hypertrophy
systemic hypertension
consistent elevation of BP beyond values considered to be the upper limits of normal. two major categories are essential hypertension (no identifiable cause) or secondary hypertension (subsequent to an identified cause). Stage 1 hypertension - pt with BP reading between 95-99 percentile. Stage 2 hypertension - pt with BP reading over 99 percentile plus 5mmHg. additional group include children with prehypertension (high normal BP) fall between 90-95 percentile. most common cause of hypertension is secondary to renal disease
general instructions for antihypertensive medication
rise slowly from a horizontal position and avoid sudden position changes
take meds as prescribed
maintains adequate hydration
notify healthcare provider if adverse effects occur, but do not discontinue meds
avoid alcohol and stay of prescribed diet
Kawasaki Disease (mucocutaneous lymph node syndrome)
acute systemic vasculitis of known cause. self limited.
kawasaki disease: diagnosis
child must have fever for more than 5 days along with four of five clinical criteria
- changes in the extremities’: acute phase, edema and erythema of the palms and soles, and in the subacute phase, periungual desquamation (peeling) of the hands and feet
- bilateral conjunctival injection (inflammation) without exudation
- changes in the oral mucous membrane, such as erythema of the lips, oropharyngeal reddening, or “strawberry tongue”
- polymorphous rash
- cervical lymphadenopathy (one lymph node larger than 1.5 cm)
note: can be diagnosed with fewer clinical criteria if coronary artery changes are notes
kawasaki disease: pathophysiology
cardiovascular: extensive inflammation of the arterioles, venules, and capillaries occurs. segmental damage to the medium size muscular arteries, mainly the coronary arteries, can occur, causing formation of coronary artery aneurysm in some cases. death usually due to myocardial ischemia from coronary thrombosis, or, over time severe scar formation and stenosis in coronary aneurysms
kawasaki disease: phases and treatment
3 phases; acute, subacute, and convalescent
acute - abrupt onset of fever unresponsive to antibiotics and antipyretics. then development of remaining clinical symptoms, child usually irritable
subacute: resolution of fever and lasts until all clinical signs of KD have disappeared. greatest for coronary artery aneurysm
convalescent: all clinical signs have resolved, but lab values have not returned to normal (complete when values return to normal; generally 6-8 wks after onset)
tx: high dose IV gamma globulin, aspirin (for fever and then low dose for antiplatelet)
shock (circulatory failure)
complex clinical syndrome characterized by inadequate tissue perfusion to meet the metabolic demands of the body, resulting in cellular dysfunction and eventual organ failure. different causes by physiological consequences are also hypotension, tissue hypoxia, and metabolic acidosis
types of shock
hypovolemic - reduction in the size of vascular compartment, falling blood pressure, poor capillary filling, low central venous pressure
distributive - reduction in peripheral vascular resistance, profound inadequacies in tissue perfusion, increased venous capacity and pooling, acute reduction in return blood flow to the heart, diminished cardiac output
cardiogenic - decreased cardiac output
3 stages of shock
compensated shock - vital organ function is maintained by intrinsic compensatory mechanism; blood flow is usually normal or increased but generally uneven or maldistributed in the microcirculation
decompensated shock - efficiency of the cardiovascular system gradually diminishes until perfusion in the microcirculation becomes marginal despite compensatory adjustments. outcomes of circulatory failure that progress beyond the limits of compensation are tissue hypoxia, metabolic acidosis, and eventual dysfunction of all organ systems
irreversible, or terminal, shock - damage to vital organs, such as the heart or brain, is of such magnitude that the entire organism will be disrupted regardless of intervention. death occurs even if cardiovascular measures return to normal with therapy
Differentiating signs in all stages are BP, LOC, and degree of tachycardia and perfusion of extremities
treatment of shock
3 major interventions; ventilation, fluid administration, improvement of the pumping action of the heart (vasopressor support)
first priority is to establish a patent airway and admin oxygen, followed by circulatory stabilization, finally adequate IV access with multilumen central line for fluids and meds
anaphylaxis
acute clinical syndrome resulting from interaction of an allergen and a patient who is hypersensitive to that allergen. the earlier the onset, the more severe the rx. can cause bronchiolar constriction, which is narrowing of the airway, and can be fatal. Laryngeal edema with severe acute upper airway obstruction is life threatening. shock occurs as a result of vasodilation, which causes capillary permeability and loss of intravascular fluid into the interstitial space. Sudden hypotension and impaired cardiac output seen
atopy
genetic tendency to develop allergic disease, especially if immediate family has allergy
septic shock
caused by an infectious organism. normally infection triggers inflammatory response un local area, resulting in vasodilation, increase capillary permeability, and eventually elimination of the infectious agent. Widespread activation and system release of inflammatory mediators results in sepsis. Sepsis shock is defined as sepsis with organ dysfunction and hypotension
3 stages of septic shock
early stage: fever, chills, vasodilation w/ increased cardiac output (results in warm flushed skin)
second stage - normodynamic, cool, or hyperdynamic decompensated stage: last few hours, skin is cool but pulse and BP normal. UO diminishes, mental state becomes depressed
hypodynamic, or cold, stage: cardiovascular function deteriorates, even with therapy. hypothermia, cold extremities, severely lethargic or comatose, weak pulse, hypotension and oliguria or anuria. multiorgan failure common
