Hypertension Flashcards
What is Hypertension? • Elevated blood pressure (BP) • General Guide: – Diastolic > \_\_\_\_ mm Hg – Systolic > \_\_\_\_ mm Hg • Affects more than 25% of population – Increases with \_\_\_\_ – Twice as prevalent in \_\_\_\_
• Anything above 140/90 > seek treatment; but there are stages (I, II; prehypertension) • Anything above 120/80 needs to be monitored • There are ethnic variabilities ○ Genetic principles behind that!
90
140
age
AA
Classification of Hypertension
• Primary or Essential
– ____ (95%)
– Often ____
• Secondary (5%)
– ____, endocrine, neurologic, etc.
• Benign
– Stable at higher level
– Better ____
• Malignant
– Rises rapidly
– Poor ____
• Primary or essential ○ Don't know what causes; state of person combined with genetics and environment ○ Asymptomatic - why screenings are important • Secondary ○ Secondary to a preexisting condition § Renal - BP and kidney function are tightly linked ○ Pituitary, thyroid, etc. • Benign ○ High BP but around the same level; doesn't increase at dramatic rates ○ Responsive to treatment • Malignant ○ Erratic changes in BP § At very high levels § 200/120 BP § Risk for serious symptoms
idiopathic asymptomatic renal prognosis prognosis
Regulators of Hypertension
BP = ____ x ____
cardiac output
peripheral resistane
Cardiac Output
• Blood volume
– ____ homeostasis
• Cardiac factors – \_\_\_\_ – \_\_\_\_ ○ Neurologic ○Renal
Na+
heart rate
contractility
Peripheral Resistance
- Constrictors Vs Dilators
- Constriction increases BP
- Dilation decreases BP
– Autoregulation of resistance vessel
• Prevent ____
• Depends on how much you release, and how responsive your vasculature is to the factors • Autoregulation ○ Occurs in \_\_\_\_ to a fine degree ○ Vessels use the pressures in \_\_\_\_ systems to maintain the BP where they want it § Constrict and dilate at a rate \_\_\_\_ of other factors § Keeps brain functioning § Can also be bad - constant constricting of vessels > \_\_\_\_ of the vessels and will be less responsive
hyperperfusion brain closed independent thickening
• CO
○ ____
§ Targeted most readily
○ Cardiac factors
• PR ○ \_\_\_\_ pathway ○ Prostaglandins & kinins § These pathways keep peripheral resistance maintained ○ Autoregulation § Plays a \_\_\_\_ role ○ Neural factors § \_\_\_\_ § Major biologic underpinnings of mindfulness are these [???] □ Can control the systems by keeping yourselves in a \_\_\_\_ state
sodium renin/angiotensin local exercise mindfulness mindful
Role of kidney
• Affects both ____
• Renin/Angiotensin system
– ____
– ____ induces Na+ retention
• Antihypertensive source
– ____, Kallikrien/kinin, ____, NO
• Glomerular Filtration depends on ____
• ____ (i.e. ANF) inhibit Na+ reabsorption
• Vasoconstrictors and dilators is released by kidney • RAT ○ Leads to increased \_\_\_\_, and changes in CO § Affects both parts of equation • Antihypertensives ○ When kidney is dysfunctional, can increase BP and won't secrete antihypertensives § For long-term hypertensives this is bad! • Kidney function dependent on GMF ○ Glomeruli filter blood, excrete toxins and keep reagents; secrete sodium, keep water ○ Controls BP ○ If problem > affect RAT, AHS, and changes \_\_\_\_ (i.e. ANF)
CO and PR vasoconstriction aldosterone prostaglandins PAF BP natriuretic factors
PR
contractility
Role of Vessel Wall
• Peripheral Resistance
– ____
– Constriction
– ____
dilation
autoregulation
Potential Causes of Essential Hypertension
• Genetic
– ____/polygenic
– Continuous variation
– Rare single mutation (i.e. ____ syndrome)
– ____ in renin/angiotensin (accounts for racial differences)
– 107 hypertension related loci
• Environmental
– Stress, obesity, smoking, sedentary lifestyle
– High salt augments mechanism
GENETIC
• Multifactorial genes
○ 107 genes
§ Regulate systolic pressure, diastolic pressure, or pulse rate
○ Personalized and precision-based medicine
• Liddle syndrome
○ Causes change in ____ resorption
○ Single mutation
• Polymorphism in promoter for renin gene
○ Higher incidence in ethnic group
ENVIRONMENTAL
• Aging
• Things that put at risk for hypertension also put you at risk for atherosclerosis
multifactorial
Liddle
polymorphism
Na+
Proposed Mechanisms
- ____ Retention
- ____ and Vascular hypertrophy• Renal retention
○ Holds in salt, holds in water, which increases BP and increases CO > increases ____ [???]
• Vasoconstriction/vascular hypertrophy
○ Lifetime of ____
○ Vessels have wear and tear > become thicker > increases to ____, heart has to beat harder to get blood through
• Both comes from ____, evidence of both from patients
renal vasoconstriction PR autoregulation peripheral resistance pathology
Renal retention
- ____ is primary cause of HT
- Initiating event is increase ____ retention
- Increased H2O retention → increased ____
- Increased Cardiac output → autoregulation (vasocontriction) → ____
- Now Na+ can be excreted setting stable blood pressure at ____ level• More Na+ > increased H2O > increased CO > continues to increase, then PR is increased > now Na+ can be excreted, which will occur at new higher BP
○ Renal retention hypothesis
Na+ homeostasis Na+ CO PR higher
Some Evidence for Renal Retention
- Increase in Na+ intake increases ____
- Reducing Na+, reduces blood pressure
- Large increased Na+ loads → HT in normotensive individuals
- Genetically predisposed animals fed Na+ exhibit increased blood pressure• Normotensive people who eat more sodium > their BP will ____
○ People with high BP, reduce sodium > it goes down
• Animal studies match closely what is seen in people
○ Suggest it’s a good therapeutic target, but it’s insufficient
§ Doesn’t explain those who don’t eat salt and have ____; and vice-versa
BP
increase
hypertension
Vasocontriction/Vascular Hypertrophy
- Peripheral Resistance Primary cause
- Initiating events:
– Induce functional vasoconstriction
• ____ factors
• Vasocontricting agents
• Increased sensitivity of ____ to vasocontricting agents
– Induce structural changes in vessel wall
• ____ induces SMC proliferation
• SMC defect leading to chronic vasocontriction
• PR ○ Wear and tear; high BP increases with aging • Have constricting agents that are released as part of normal life ○ Neurogenic/vasoconstrictors > BV constrict • SMC may be more sensitive to constriction ○ May have \_\_\_\_ underpinnings • When those happens > structural changes > evidence seen pathologically: ○ \_\_\_\_ of vessel wall ○ Angiotensin II (secreted during hypertension): cause SMC to proliferate (may lead to \_\_\_\_ arteriosclerosis) ○ Some SMC may chronically vasoconstrict when they shouldn't
behavioral/neurogenic smooth muscle cells angiotensin II genetic thickening hyperplastic
Causes of Hypertension • Altered \_\_\_\_ Na+ retention • Levels of \_\_\_\_ substances (angiotensin II) • \_\_\_\_ of SMC to Pressor agents • Smooth Muscle Cell Growth
• Altered levels of substance that lead to vasoconstriction
renal
pressor
sensitivity
Actual mechanism
Elements of both altered ____ and ____ participate in idiopathic hypertension.
renal regulation
vasoconstriction/vascular hypertrophy
Malignant Hypertension
• Extremely high pressure (> ____) with steep rise
• Associated with more than 1 risk factor
– ____, age, ____, renal issues, essential hypertension
• Progress more ____ to pathologic consequences
– More ____ arteriolosclerosis
– Presence of ____
• New value is 190/100 • Unknown reason as to why BP spikes • Have more of the two types of \_\_\_\_ (hyaline and hyperplastic) • Will have inflammation of vessel wall that leads to death of that wall ○ Necrotizing arteriolitis ○ Death and collapse
220/120 race smoking quickly hyperplastic necrotizing arteriolitis arteriosclerosis
Clinical presentation: Malignant Hypertension
• Early symptoms include:
– ____, nausea, ____, visual impairments, ____ (spots before the eyes)
• Early signs
– ____, hematuria
• If untreated die of ____, cerebral damage, etc
• Symptoms do not imply malignant hypertension when first become apparent • Can also experience nosebleeds • Hematuria ○ May notice red urine; but \_\_\_\_ may mask it ○ Urine test • Proteinuria ○ Urine test ○ \_\_\_\_ (the only sign)
headaches vomitting scotomas proteinuria renal failure vitamins bubbly
Consequences of Hypertension
• ____
* Most important consequence that leads to MI * \_\_\_\_, lipid core, \_\_\_\_, dysfunctional endothelium, oxidized \_\_\_\_
atherogenesis
fibrous cap
macrophages
LDL
Consequences of Hypertension
- Atherogenesis
- Small Vessel Disease (arteriolosclerosis)
– Hyaline arteriolosclerosis
• Extravasation of ____ proteins • Increased ____ deposition
– Hyperplastic arteriolosclerosis • Reduplication of \_\_\_\_ • \_\_\_\_ proliferation • \_\_\_\_-skinning • More with \_\_\_\_ hypertension
• Small vessel disease ○ Hyaline § Extravasation of fibrin, albumin; forms on outside of vessel > smooth, \_\_\_\_ appearance (formation of a corona) § Less \_\_\_\_ - seen more in regular hypertension (some hyperplastic, but mostly hyaline) ○ Hyperplastic § More severe hypertension § In addition to plasma proteins > induce SMC to proliferate and put down another set of BM □ Multiple layers of \_\_\_\_ in these small vessels □ Looks like an onion (onion-skinning phenotype)
plasma ECM basement membrane smooth muscle cell onion malignant eosinophilic dangerous SMC
Consequences of Hypertension
• Vascular wall changes
– Aortic dissection
• Blood flowing into wall > ____ of vessel
• Combination of ____, and the ____ through the area > shearing of wall and blood going into it
– Cerebrovascular hemorrhage • Stroke (fresh) ○ Bursting of vessel > hemorrhage > if an \_\_\_\_ bursts (fast) and blood expands brain > fixed amount of space > pushed out \_\_\_\_ and crush cerebral tonsils • Fixed • \_\_\_\_ becomes much larger
occlusion
atherosclerosis
BP
arteriole
foramen magnum
hemispheres
Consequences of Hypertension
• Hypertensive Heart Disease
– Systemic (____) HHD
– Pulmonary (____) HHD
• Both depend on hypertension • Systemic (left sided heart disease) ○ High hypertension • Pulmonary (right sided heart disease) ○ Can be secondary to systemic
left sided
right sided
Systemic Hypertensive Heart Disease
Systemic Hypertensive Heart Disease
• Left Ventricular hypertrophy
– Absence of other ____
– ____ hypertrophy
- Left ____ dilation
- ____ (evidence) of hypertension – Even mild (ie 140/90 mmHg)
- Ventricle wall > ____cm in diameter
- Larger cells require more ____• BP is so high in ____ > now need to pump blood harder > left ventricle becomes thickened (now more than 2x the side of the RV)
• Without any other pathology (ischemia, etc.) > hypertension (thickened LV)
○ Walls become less ____ > do not pump blood as well > blood pools in ventricle > becomes dilated
• Blood cannot move forward > move back to lungs:
○ ____: difficulty breathing
○ Response to blood > alveolar macrophages try to clear blood in lungs > digest away RBC that enter alveoli > take in a lot of iron and heme > can break down heme somewhat > deformation of body pigments > ____ > ____ cells
• Larger cells requires more O2
○ Have hypertension, need to lower BP, but now you need more ____ to supply the heart that is working harder
cardiopathology concentric atrial history 2 O2
periphery elastic congestion hemosiderin HF cells O2
Consequences of Left Ventricle Hypertrophy
• Myocardial dysfunction (less elastic) • Ventricular and atrial \_\_\_\_ (accommodate increased blood in ventricle) • Congestive Heart Failure – \_\_\_\_ congestion – Reduced \_\_\_\_ perfusion • Water \_\_\_\_ • If severe, \_\_\_\_ • Sudden Death
• Atrial dilation > pulling back from the lungs • Pulmonary congestion > begins backing up in system > secondary RH failure ○ Because cannot get enough blood into system > kidney hypoperfused > release renin > activate \_\_\_\_ > retain H2O to raise the BP § Lifetime of high BP > now signaling to kidney that you need even higher BP in order for heart to work properly § A point to where it can revert to RSHF > \_\_\_\_ accumulating in your kidney * Thickness of the LV * \_\_\_\_ muscles are also hypertrophied
dilation pulmonary kidney retention azotemia
RAT
hyperemia
papillary
• Using ____
○ Macrophages filled with hemosiderin in the ____
PAS
alveoli
Pulmonary Hypertension
• Secondary to increased ____ in pulmonary vasculature
– i.e. Atheromas in pulmonary vasculature, ____, bronchiectasis, ____, emphysema, ____
• Right ventricular hypertrophy if ____
• ____, Spleen and Liver congestion
• ____(legs/ankles)
• ____ (pure right sided heart failure)
• Right sided heart failure ○ Secondary to high BP in the lung • Not caused by hypertension, but specifically in the lung ○ Lung BP is quite lower than \_\_\_\_; but still has range where it has to be maintained • Normal left ventricles > right ventricles will hypertrophy ○ Not as impressive as LV; but it will almost be as large as \_\_\_\_ § Not normal • Blood pools in periphery > hyperemia in kidney spleen and liver ○ And peripheral edema > classic feature of \_\_\_\_ > more of an indication of \_\_\_\_ because of peripheral accumulation • Cor pulmonale ○ Anything pure RSHF ○ Blood isn't being pumped into lungs at high rate, chronic, \_\_\_\_ accumulation § Chronic pulmonale ○ Anything that leads to acute blockage of blood into lungs § \_\_\_\_ of leg trauma moving into heart and blockage of flow before lungs □ \_\_\_\_ cor pulmonae
resistance cystic fibrosis pulmonary thromboemboli COPD chronic kidney peripheral edema cor pulmonale
systemic
LV
CHF
RHF
peripheral
embolus
acute
Chronic Cor Pulmonale
• ____ dilation and hypertrophy
• Right ventricle is almost as thick of left ventricle ○ LV is normal • \_\_\_\_ is dilated bcause blood is pooling backwards into system
right ventricle
right atria
• Something that may cause pulmonary hypertension
• If you have ____ in legs > leg veins are ____ > travel through heart and enter lungs and dissolve; but when they don’t > can embed and recanalize, eventually one can embolize > reduce ability of blood to flow through the lungs
○ Reduces lumen size
thrombi
large
Arteriolosclerosis
• Will see because will have hypertension in pulmonary system
○ Can also occur in the ____
○ ____ (onion-skinning)
lung
hyperplastic
Liver Hyperemia
• ____ liver
• Backing up of blood
• Hyperemia in ____
Centri-lobular Congestion
• Central lobular congestion
• Normal ____; congestion around the ____
nutmeg
portal tracts
hepatocytes
veins
Consequences of Hypertension
• Other Organs
– Eyes
– Kidneys
Retinopathy
• Fundoscopy
○ Left is normal retina
§ Nice edges on optic nerve; arterioles are even and smooth, can see the lumen in some of them
○ Right is hypertensive retina
§ Image below the one on the right
§ Pale areas > ____ spots > micro-infarcts > damage to underlying tissue
§ ____ > hemorrhages > the BV is a lot thicker
§ Arteriole-venous thickening
□ ____ then thick, and so on
□ Not even arterioles
§ Blurring of the optic disk > ____ > impair vision
□ ____
cotton-mole flame spots thin papilloedema scotomas
Kidneys
• Benign Nephrosclerosis – \_\_\_\_ due to narrowed vessels – \_\_\_\_Thickening – \_\_\_\_ Arteriolosclerosis – Rarely \_\_\_\_ (mild \_\_\_\_)
• Benign and malignant NS • BN ○ Hyalinzed arteriosclerosis > arterioles \_\_\_\_ > hypoperfusion > ischemic areas ○ Thickening of the \_\_\_\_ • Kidneys look \_\_\_\_ ○ Areas of microinfarctation ○ Otherwise, kidney is fairly normal
focal ischemia medial hyaline symptomatic proteinuria smaller media leathery
Kidneys
• Malignant Nephrosclerosis – \_\_\_\_ Arteriolosclerosis – \_\_\_\_ arteriolosclerosis – \_\_\_\_ – Ischemia – Kidney damage • (i.e. long standing \_\_\_\_ hypertension, arteritis, \_\_\_\_) • Activation of renin:angiotensin – Initially \_\_\_\_ and hematuria, but progresses to \_\_\_\_ failure
• Both hyaline and hyperplastic arteriosclerosis • Complete destruction of the vessel: necrotizing arteriolitis ○ \_\_\_\_ necrosis • Damage to vessel > ischemia and kidney damage ○ Kidney will interpret as hypoperfusion > activate RAT > risk for malignant hypertension (rising BP)
hyaline hyperplastic necrotizing arteriolitis benign coagulopathy proteinuria renal
fibrinoid
Kidneys
• Tiny microhemorrhages > the vessels are becoming no longer intact ○ \_\_\_\_ presentation § Attacked by a swarm of flees
fleebin
Fibrinoid necrosis
• ____ of vessel
• Cannot see the ____ anymore, completely obliterated
destruction
vessel wall
Renal dysfunction
• Ischemia induced activation of ____
– Na+
– Vasocontriction
- No longer secrete ____
- Inability to secrete ____
- ____, hematuria, proteinuria• ____ neproschlerosi > renal dysfunction
○ Activate RAT
§ Na+ retention
§ Vasoconstriction
○ BP being raised, and removal of breaks (anti’s)
○ Azotemia
§ ____-based compounds remaining in your blood
§ High level of ____ (nitrogen-urea based compounds)
renin-angiotensin antihypertensives Na+ azotemia malignant nitrogen BUN
Consequences of Hypertension (ALL OF THEM)
• ____
• ____
– Hyaline arteriolosclerosis
– Hyperplastic arteriolosclerosis
• ____
– Aortic dissection
– Cerebrovascular hemorrhage
• ____
– Systemic (left sided) HHD
– Pulmonary (right sided) HHD
• ____
– Eyes
– Kidneys
atherogenesis small vessel disease (arteriolosclerosis) vascular wall changes hypertensive heart disease other organs
Valvular diseases
• Consequences: – Stenosis • Failure to \_\_\_\_, obstruction of forward flow – Insufficiency • Failure to close, \_\_\_\_
• Affects \_\_\_\_ valve most often • May occur singly or \_\_\_\_ • Produce murmurs • Outcome – Degree of impairment – Speed of development, – Compensatory mechanisms
• Stenosis ○ Do not open - blood doesn't go forward • Regurgitation ○ Blood falling \_\_\_\_ ○ Does put heart at risk of \_\_\_\_, when you do procedure that may lead to bacteremia? • Whether to prophylactically treat patients with antibiotics prior to dental procedures ○ No prophylaxis with antibiotics • More than one valve can become affected • Speed of development ○ If born and adjustment as developing § Can be okay ○ Damaged to valve if heart isn't ready to deal with § More dangerous
open regurgitation mitral simultaneously back infection
Degenerative valve disease • Calcific Aortic Stenosis – \_\_\_\_ valves – Associated with \_\_\_\_, atherosclerosis – Affects \_\_\_\_ valve – \_\_\_\_ hypertrophy – Patients develop \_\_\_\_, CHF, syncope
• Calicified valves ○ Can occur on the \_\_\_\_, at place of annulus, along on the leaflet (anywhere in between) ○ Will affect valve function; heart will have to compensate > beat harder ○ Common consequence > \_\_\_\_ of compartment behind § Mitral > ventricle will be hypertrophy [???] • CHF ○ Secondary to the valve itself ○ Same mechanism as in ventricular hypertrophy, insufficiency to push blood to the system
calcified aging aortic left ventircular angina cusps hypertrophy
- (A) Calcium deposits on leaflet > the valve has difficulty ____ > blood flows back
- (B) Two fused leaflets ____ > oopening based on the calcification > congenital > predisposed to calcium > difficult closing
- © on ____
- (D) calcium extending into ____; extends down below the valve itself
- All lead to regurgitiation effects in the valve
closing
congenitally
annulus
myocardium
Degenerative Valve
• Myxomatous Mitral Valve – Affects 3-5% of adults – Genetic linkage to \_\_\_\_ disorders – 7X more likely in \_\_\_\_ – Floppy \_\_\_\_ valve leaflets – Most are \_\_\_\_ – \_\_\_\_ click by auscultation – 3% go on to develop \_\_\_\_ – Risk for \_\_\_\_?
• Congenital disorder • Floppy mitral valve ○ Looks like a parachute ○ A little extra tissue that's extended [???] • Asymptomatic ○ But can hear with stethoscope • Would treat with prophylaxis? ○ Right now: \_\_\_\_
• Ballooning up of the mitral valve • Hypertrophy of the LV and the papillary muscles ○ No other \_\_\_\_
connective tissue women mitral asymptomatic mid systolic CHF infective endocarditis no
pathologies
Rheumatic Heart Disease
• Sequelae of ____ Infection
• Inflammation of myocardial tissues
– Myocardium –____
– Pericarditis (____ exudate)
– ____ necrosis of the valves, ____ formation
• Stenosis and regurgitation
– ____ treatment of Strep reduces sequelae
• Fibrinoid necrosis of valves ○ Growths on valves > cannot connect > valve regurgitiation • Can be prevented by treating strep infections with antibiotics > reduces sequelae ○ Can cause other secondary effects
strep aschoff bodies fibrinous fibrinoid verrucae antibiotic
• Valve doesn’t close
• Aschoff bodies
○ Form in accumulations of ____ aggregates within normal myocardia
inflamed
Infective Endocarditis
• Serious Infection requiring prompt diagnosis and intervention
• Composed of ____, thrombus and organisms
• Acute
– ____, bulky and destructive vegetations
• ____, inflammatory cells and ____
• Subacute
– Low ____ infection overlying previously damaged valves
• Inflammation due to infection • Bland vegetations that aren't infectious, but can also have infectious ○ Active bacteria growing > treatment • Unlike calcifications > these vegetations are \_\_\_\_ and grow on top ○ Largely made up of fibrin, inflam cells • Subacute ○ Infection laying on top of previous-exisitng damage ○ Will not know until \_\_\_\_ symptoms (dysfunction of valve, or if it becomes acute)
necrotic debris
friable
fibrin
microorganisms
virulent
loose
severe
Congenital diseases
• Non-cyanotic – Left to right shunts • \_\_\_\_ defects • \_\_\_\_ defects • \_\_\_\_
– May become cyanotic if pulmonary hypertension develops leading to ____ syndrome
• reversing shunt flow from right to left.
• Forcing ____ blood into the system
• Lead to \_\_\_\_ hypertrophy (depending on valve affected), and whether or not to treat with antibiotics
CONGENITAL DISEASES
• Aren’t genetically defined - have to do with an aberration during development
○ Allow child to be born and live; no ____
• Non-cyanotic
○ Whether this defect allows oxy blood to go into system (inefficient circulation - non-cyanotic)
○ [???]
○ Can become cyanotic > eisenmeger syndrome
§ ____ develops in system > reversal of flow; blood leading from blood shunting from left to right atria > can switch and go the other direction; unoxygenated blood going out into the periphery
• Cyanotic
○ Unoxy blood shunted into oxy blood flow > unoxy blood entering the system
atrial septal ventricular septal patent ductus arteriosis eisenmenger unoxygenated ventricular
still-births
hypertension
• Atrial septal defect
○ Communication btween ____; oxy being shunted to right
• Vent septal defect
○ Oxy blood back and ____
• PDA defect
○ Aorta in communication with pulmonary vessel > oxy blood into the ____ system
• All are left-to-right shunt
LA to RA
reoxygenated
pulmonary
Congenital malformations
• Cyanotic
– Tetralogy of Fallot • \_\_\_\_ septal defect • Right ventricular outflow obstruction (\_\_\_\_) • Overriding the VSD by the \_\_\_\_ • \_\_\_\_ hypertrophy
– ____ of the great arteries
– Both require surgical correction, are associated with ____, osteoarthropathy, and ____
• Tetralogy of Fallot ○ Combination of congenital defects > cyanotic fomraiton § Induced Eisenweger ○ Two ventricles talking to each other ○ Obstruction of flow out of \_\_\_\_ ○ Aorta coming near the VSD > \_\_\_\_ blood into the aorta ○ RVH ○ VSD normally has blood going other direction, obstructing outflow, and aorta in right location > uxoxy blood is going into RV instead of other direction • Transpoisiton of great arteries ○ Aorta and pulmonary \_\_\_\_ switch • Paradoxical emobolism ○ Normally emboli are in venous system; don't end up arteries ○ In this case, because you get crosstalk bt oxy and unoxy > emboli occur in \_\_\_\_ system
ventricular subpulmonic stenosis aorta right ventricular transposition polycythemia paradoxical embolism RV unoxy trunk arterial
• (A) > blocking flow to ____ system; backflow that makes difficult to go pulmonary
○ Aorta is close to septal defect > unoxy blood entering into the system
• (B) tranpsoition of vessels
○ ____ off RV
○ ____ of LV
○ Can also have the VSD > good coming here, blood oxy switching
§ Can be compensatory
• Both need to be corrected with surgery
pulmonary
aorta
pulm trunk
Obstructive Lesions
• Aortic Coarctation – Narrowing of Aorta • Seen in \_\_\_\_, \_\_\_\_ syndrome – 2x more likely in \_\_\_\_ – Most common \_\_\_\_ abnormality – Clinical manifestations depend upon • \_\_\_\_ of narrowing • Presence or absence of \_\_\_\_
• AC ○ Aorta itself becomes narrowed > more difficult for blood to flow through > LV hypertrophy ○ Most common congenital abrnoamlity in the heart
down syndrome turner's males congenital severity PDA
