Cardiac Flashcards
1
Q
What is ischemic heart disease
A
characterized by an imbalance between metabolic oxygen demand and myocardial oxygen supply
- Metabolic oxygen DEMAND that EXCEEDS oxygen SUPPLY
- Most commonly caused by
-
Narrowing of coronaries →
- Atherosclerosis of the coronary arteries
-
Narrowing of coronaries →
- Can also be caused by:
- Severe hypertension or tachycardia
- extra demand on heart/O2 supply
- Coronary artery vasospasm (or plaques that lead to vasospasm)
- Supply reduced
- Severe hypotension (decreased supply to heart)
- Reduced supply
- Hypoxia
- Anemia
- Reducing O2 carrying capacity
- Severe AI or AS
- Aortic insufficiency (regurgitation)/Stenosis
- Severe hypertension or tachycardia
2
Q
Incidence of ischemic heart disease?
A
-
Incidence
- Present in 10 million American adults
- 1.5 million suffer from MI
- 1/3 mortality
- Major cause of perioperative morbidity and mortality
- Overall incidence in surgical pts: 30% of surgical patients
3
Q
Risk factors for ischemic heart disease?
A
MAJOR
- **increasing age
-
**male gender
- (men > 60 yo → assume they have some sort of atherosclerosis)
- Hypercholesteremia (increased LDL → more plaques)
- Diabetes
- Hypertension (increased demand)
- Cigarette Smoking
- Vascular disease → narrowing
- Positive family hx (genetic predisposition
Other:
- Obesity
- (probably have hyperlipidemia, hypercholesteremia)
- Cerebral Vascular Disease
- Peripheral vascular disease
- (for this and CVD, if they have atherosclerosis in one part of the body they probably have it in another part)
- Menopause
- Risk equalize with men
- Use of high estrogen contraceptives
- Sedentary lifestyle
- Psychosocial characteristics (high stress)
4
Q
What happens when ischemic chest pain present (flowchart)?
A
- Angina is one of the biggest sign of ischemic heart disease
- New or changed angina = Acute Coronary Syndrome
- Acute onset of S/D issue
- New or changed angina = Acute Coronary Syndrome
GET 12 lead EKG!!!
- No ST segment elevation and negative troponin/ CK-MB = unstable angina
- Signals an impending MI
- If no ST segment elevation and positive troponin/ CK-MB= NSTEMI (myocardial infarction)
- ST segment elevation and positive troponin/ CK-MB= STEMI (ST elevated myocardial infarction)
Gold Standard- Troponin/CK-MB test
- get a 12 lead and follow this algorithm and get a cardiology consult
- ST elevation not always present in MI
- **if they tell you that their chest pain has changed –> DO NOT do the case
5
Q
Pathogenesis of unstable plaques and thrombus formation?
A
MI→ formation of cardiac plaque that formed over time
- Body detects and grows collateral vessels over time → typically enough supplemental O2
- These are not the issue (acutely)
Atherosclerotic plaque
- Why is unstable angina not good?
- Because at any moment that person can have an MI – very high risk
- What is an unstable plaque?
- An atherosclerotic plaque with lipids inside and a thin fibrous cap
- The type of plaque is important
- Vulnerable plaques= rich lipid cores and thin fibrous caps
Athersclerotic plaque with lipid core and thin fibrous cap (typical culprit for MI)
- Causes shear force → anything causes blood to come through quicker or constriction (excited/stressed)
- Inflammation
- Apoptosis
- Macrophage- derived degradative enzymes
- (^) Responses to lipid rich core → thin fibrous cap gets sheared off and allows for rupture of plaque
- Increased inflammation with release of multiple cytokines, platelet activation and adherence → production of thrombin and vasoconstrictors (vasospasms)
- Thrombus formation over lesion plus vasoconstriction (release of thromboxane A2) of vessel → Acute decrease in coronary blood flow → lack of O2/blood arriving to myocardium →
- → UNSTABLE ANGINA OR MYOCARDIAL INFARCTION
6
Q
What does this picture show?
A
Angiography
- Plaque formation at baseline (A)
- Transient total occlusion (mental stress) (B)
- Give CCB or nitrate → allows for vasodilation of constricted vessel (C)
- Opens at the same diameter for blood to go through
*ACUTE OCCULUSION- complete occlusion distal/downstream to plaque upon exercise/stress
If meds don’t work → need stent or bypass placed
Why do you want to avoid phenylephrine in patients with a history of an MI? (pictures of the vessels)
- It can cause coronary artery vasospasm
- Also remember when surgery occurs you are causing stress
- If an occlusion occurs, administration of nitrates and nifedipine can reopen the artery to same diameter as baseline
7
Q
What is the role of stress in trigerrign cardiac clinical events?
A
Acute mental stress –> Central and autonomic nervous system activity
-
Physiologic responses
- Increased catecholamines
- Increased HR
- Increased BP
- Decreased plasma volume
- Increased coronary constriction
- Increased platelet activity
-
Cardiac Effects
- Increased electrical instability
- (due to incr catecholamines, HR and BP)
- Increased demand (d/t incr catecholamines, HR and BP)
-
Decreased supply (d/t decr plasma volume and increased coronary constriction)
- S/D = really what leads to ischemia, plaque rupture, and ventricular F/T
- Increased electrical instability
-
Pathologic Result
- VF/VT (d/t electrical instability)
- Ischemia (d/t increased demand and decreased supply)
- Plaque rupture (d/t decreased supply and plaque rupture also leads to decreased supply)
-
Coronary thrombosis (d/t increased plt activity)
- Bottom 3 is what we see in ER → leads to MI
-
Cardiac Event
- Cardiac sudden death ( from VF/VT)
- Myocardial infarction (d/t ischemia, plaque rupture, coronary thrombosis)
-
Background factors Are (has cardiac effects)
- Atherosclerosis
- Prior MI
- Poor LV function
8
Q
What are some EKG changes that can be indicative of ischemia or infarction
A
- ST segment depression (chronic/previous MI)
- T wave inversion
- ST segment elevation (ACUTE MI/ischemia)
9
Q
What is stable angina?
A
- Baseline CAD, ischemic disease
-
No change in precipitating factors for at least 60 days (2 months)
- Frequency or duration of pain
- Associated with fixed narrowing (usually 75% or greater)
- O2 demand may be normal under basal conditions
-
Tx:
- Vasodilators (Nitrates or CCB)
- Relieved by rest, reducing demand
- Frequency or duration of pain
10
Q
What is unstable angina?
A
- Caused by less than normal activity
- Lasts for prolonged period
- Occurring more frequently
- Signals impending myocardial infarction
- Imminent danger of CV event
- Crescendo- starts slow and then becomes unbearable (worse and worse)
- Increased frequency, duration, etc
- New precipitating thing changes → unable to walk up steps acutely
- Can cause irreversible infarction
- Acute plaque changes
- Usually also partial thrombosis (shear forces that dislodged plaque)
- Tx: Medically manage, stent placement, cardiac bypass
11
Q
What is prinzmetal angina?
A
- At rest
- Coronary spasm- usually caused by this instead of atherosclerosis
- Occurrence:
- In a plaque area or normal vessel
- Associated with other vasospastic diseases (Raynaud’s Disease)
- Tx: medically manage, Nitrates, CCB
- *avoid phenylephrine (vasospasm)
- Maybe have nitro in the room
- Tx: medically manage, Nitrates, CCB
- Occurrence:
12
Q
What is myocardial infarction?
A
- Necrosis caused by ischemia
-
Within 20-30 minutes of ischemia
- Typically begin in the subendocardial regions (in between epi and endocardial layer)
- Full damage seen 3-6 hours after ischemia occurs
- Size depends on:
- Proximity of lesion
- Collateral circulation (if no collateral circ, damage can be very great because heart hasn’t time to develop collateral)
- CKMB/troponin usually increase right away and are even higher at 3-6 hours
- Numbers correspond to size of the infarct
13
Q
Complications of MI?
A
-
Papillary muscle dysfunction
- Causes valvular disease
-
External rupture of infarct
- day 4-7 most common – cardiac tamponade → followed by death
- Cardiac Tamponade- pericardium sac filled with blood and heart cant pump properly
- day 4-7 most common – cardiac tamponade → followed by death
- Mural thrombi – lead to stroke
-
Acute pericarditis (acute infection of the necrosed area): day 2-4 most common
- Pericardium filled with blood and leads to infection
- Ventricular aneurysm – fibrous outpouching of the ventricle- anteroapical region most common → cardiomyopathy
- Arrythmias
- LVF +/- pulmonary edema
- Cardiogenic shock (rare ~10%) → MODS
- Rupture of wall, septum, papillary muscle
-
Thromboembolism
- MI: mortality dependent on SIZE and LOCATION of thrombi/plaque
14
Q
What are various sensitivities of blood tests used to detect MIs?
A
(Graph)Rate and extent of rise of cardiac troponin and myocardial creatine kinase (CK-MB) levels after a typical acute MI
-
Troponin level: rise QUICLKY and ACUTELY
- GOLD STANDARD→ can determine the presence and extent of injury (degree of myocardium damage)
-
Cardiac microinfarctions: can raise the troponin levels without increasing the CK-MB levels
- *Microinfarction: infarction of smaller areas and vessels
-
CK-MB level: elevated but not as good as troponin rate or rise and extent of rise
- More sensitive to larger vessels of heart
15
Q
What areas of the heart are infarcted with occlusion of RCA? LCA? LAD? LCX?
A
- Occlusions of the coronary arteries
- RCA= posterior, inferior MI (small portion of LV)
- LCA= massive anterolateral MI (big portion of LV)
- LAD= anteroseptal MI (portion of LV and RV)
- LCX= Lateral MI
All leads some LV dysfunction → large vessels
Don’t pump properly → poor systemic outcomes
16
Q
What is defnition of vascular hyertension? Incidence? Categories?
A
- Defined:
- Sustained diastolic of 90mmHg
-
Sustained systolic of 140mmHg
- Average of three different measurements at 3 different times
- Incidence
- 30% of general public (~1/3)
- Categories
- Normal < 120/80
- Prehypertension 120-139/80-89
- Stage 1 140-159/90-99
- Stage 2 >160/100
17
Q
Importance of controlling HTN?
A
- HTN is the most important risk factor in
- CAD
- CVA
- Cardiac Hypertrophy- LV tries to pump against HTN → grows larger, vessels constrict → CAD
- Renal Failure
- Aortic Dissection/Aneurysm
18
Q
What are some causes of HTN?
A
- 90-95% of HTN is idiopathic apparently primary (Essential HTN)- don’t know reason why it occurs
-
5-10% : mostly secondary d/t renal disease
- We know what the risk factors are for it (atherosclerosis, stress, pain, life style, smoking, renal, etc) but we don’t actually know what causes it except for organic things like pheochromocytoma
19
Q
What are some effects of HTN on the heart?
A
- Hypertension causes increased myocardial wall tension which can lead to:
-
Increased myocardial oxygen demand (need to feed a bigger muscle)
- Leads to coronary insufficiency
- Which can lead to heart failure
-
Left ventricular hypertrophy (which leads to increased o2 demand)
- Which leads to heart failure
- Infarction dysrhythmias can lead to coronary artery insufficiency and heart failure
-
Increased myocardial oxygen demand (need to feed a bigger muscle)
20
Q
What are types of HTN?
A
- Systolic and Diastolic
- Essential hypertension – 95%
- Secondary hypertension – 5%
- Renal
- Endocrine
- Cardiovascular
- Neurologic
21
Q
How is blood pressure normally regulated?
A
BP= Cardiac Output x Peripheral Resistance
-
Cardiac Output
- Determined by blood volume
- (stroke volume)
- Cardiac factors
- (how well is myocardium functioning → such as HR- frank starling curves)
- CO = SV x HR
- Determined by blood volume
-
Peripheral Resistance
- Humoral Factors (constrictors/dilators)
- Neural Factors (stress response, vagal response)
- Local (released locally, thromboxane vs NO produced)
22
Q
What is the pathogenesis of essential (primary ) HTN?
A
Risk factors
-
Genetic
- Polygenic and heterogenous
- Polymorphisms at several gene loci
-
Environmental
- *Stress
- Obesity
- Smoking
- Salt consumption
- Sedentary lifestyle
23
Q
Pathophys of HTN?
A
- Increased SNS activity in response to stress
- Overproduction of sodium retaining hormones
- Overproduction of vasoconstrictors
- Underproduction of vasodilators (NO, prostaglandins)
- Increase Na intake
- Inadequate intake of Ca and K
- DM – changes to vasculature that occur
- Obesity- plague formation and vasocontraction that occurs in disease
24
Q
Effect of sodium retention on BP?
A
- Salt/Water Retention: The final common pathway in the pathophysiology of essential hypertension
- PROBLEM: BV (going back to pic)
-
TX:
- Sodium restriction lowers BP
- Diuretics - act as effective antihypertensives by promoting sodium excretion/H2O
25
Q
What are some pathogenetic factors and clinical prsentation of HTN heart disease?
A
- Top brown box → LVH (BLUE)
- BIGGEST MANIFESTATION OF HTN
- Boxes on side: contribute to the LVH
-
LVH:
-
Microangiopathy→ blood supply increase in response to increase in demand on heart → MI
- reduced coronary reserve
- Impaired Contractility
- As grows larger, not pump as efficient → impaired contractility (→ HF)
- Reduced LV filling
- Heart becomes stiff while growing larger
- During Diastole (when heart fills) becomes stiff after systole and wont fill properly
- Atrial Fibrillation/Ventricular dysrhythmia
- Heart enlarges, pushing against itself
- Ex: Push on→ Atria = a. fib or Purkinje fibers= vent. dysrhythmia
- → sudden death, cardiac emboli result
-
Microangiopathy→ blood supply increase in response to increase in demand on heart → MI
- Most important thing is – is HTN well controlled?
26
Q
Pathogenesis of secondary HTN?
A
(5% population)
- Oral contraceptives (high estrogen)
- Renal parenchymal disease
- Renin-secreting tumors
- Primary aldosteronism
- Cushings Syndrome
- Pheochromocytoma
- Endocrine disorders… discuss in endocrine
27
Q
Treatments for HTN?
A
-
Drug therapy (possibly a combination of 2 for stage 2 hypertension-usually a diuretic and something else)
- Diuretics- offload volume. (1st line)
- Ca channel blockers
- Ace inhibitors – helpful for renal prob (DM)
- Beta blockers- decreases workload of heart
- Angiotensin receptor blockers (similar to ACEI)
-
Non drug Therapy
- Lifestyle changes: weight reduction, smoking cessation, increased physical activity
- Sodium restriction, diets
- Reduction of ETOH
- Relaxation techniques
28
Q
What is peripheral vascular diseaes? What causes it? Prevalence?
A
Compromised blood flow to the extremities
-
Ankle-brachial index of less than 0.9
- Perfusion to upper and lower extremity not match (index < 0.9) = PVD
- Ratio of SBP in ankle vs SBP in brachial arteria?
- What causes it?
- Atherosclerosis- most often (PVD and CAD go hand in hand)
- Arterial embolism
- Vasculitis
- Prevalence
- 2 million Americans are symptomatic (have pain bc PVD)
- Associated with aging
- Exceeds 70% in people over the age of 75
- Increases with risk factors
- Way to avoid PVD= EXERCISE
33
Q
Pathophysiology of mitral stenosis?
A
-
Almost always due to fusion of the mitral valve leaflets at the commissures during the healing process of acute rheumatic fever
* Inflammatory process (rheumatic fever) → involvement of commissures and papillary muscles- Rheumatic Fever- risk for ALL valvular disorders
-
Almost always due to fusion of the mitral valve leaflets at the commissures during the healing process of acute rheumatic fever
-
2. When the mitral valve area/orifice < 1 cm2
- Normal: 4-6cm
- Stenotic: < 1-1.5cm (become symptomatic)
- → A mean left atrial pressure of about 25mmHG is necessary to maintain an adequate resting cardiac output (normal is 8-10mmHG)
- Atrial pressures need to get high to overcome stenotic valve= pressure problem!
-
3. Left atrial enlargement predisposes to atrial fibrillation
- Increased pressures in the LA required to move blood through tiny mitral opening which causes LA enlargement
- LV enlargement → changes morphology of SA node (predispose of a.fib)
- a. Stasis of blood in the distended LA predisposes to the formation of thrombi
- Mitral stenosis may be receiving chronic anticoagulant therapy. Thrombi can cause increase R/F MI or CVA.
- pooling of blood can also increase r/f infection
Symptoms:
- Dyspnea on exertion when CO is increased
- Severe MS →leads to CHF
mitral stenosis is heart on left of pic!!
34
Q
Effects of mitral stenosis on heart?
A
- Decrease of LA emptying–> Increase LA preload (pressure)
- Leads to back up in system (P. Edema) → → RV failure
- Decrease LA force of contraction as heart gets enlarged (frank starling not fx prop as getting larger) → decrease delivery of blood → decrease O2 supply → LV failure
- Eventual Tx: mitral valve stenosis–> mitral valve replacement
- Mitral stenosis also leads to “fish mouth” appearance on valve
37
Q
Aortic stenosis effects on heart?
A
LV outflow obstruction from stenotic valve leads to:
- Increase SBP (to get blood through valve)
- Increase LVET (LV exit time)- heart tries to compensate by forcing blood out in first portion of contraction (become reliant on atrial kick)
- Increase DBP (cant relax during diastole)
- Decrease Ao pressure (not enough blood coming through the aorta)- Increase in LV SBP and decrease Ao pressure creates gradient
- Increase myocardial O2 consumption and decrease diastolic time (when coronaries fill properly to get BF to heart itself)
- Decrease supply!!! → myocardial ischemia → LV failure
- Heart no longer efficient in pumping
- Increase myocardial O2 consumption and decrease diastolic time (when coronaries fill properly to get BF to heart itself)
39
Q
What is seen on central line with mitral regurgitation?
A
- Regurgitant flow is responsible for exaggerated V wave present on the recording of PAOP
- The size of the V wave correlates with the magnitude of the regurgitant flow
- This pic shows a normal wave (about 12) – an exaggerated wave will go to about 20-25 with regurgitation
- A wave- p wave (atrial contraction
- C wave- back pressure
-
V wave- SV (ventricular side)
- Regurgitation – when heart goes to pump blood, blood comes back into LA (exaggerated)
41
Q
Cardiac effects of aortic regurgitation?
A
- Decreased CO d/t regurgitation of part of the SV back into the LV during diastole
- Increased SV by increasing LVET ( increase time for LV ejection, this causes decrease in diastolic time of heart= decrase O2 available to heart)
- Decrease in effective stroke volume
- Causes combined pressure and volume overload on LV
(summary- increase demand/decrease supply)
42
Q
What does LV dysfunction result in? Types of hypertrophy?
A
-
LV dysfunction- results in progressive remodeling (myocytes themselves change) of the ventricular chamber
- Leads to:
- Dilation
- Low Ejection Fraction (EF)
- Leads to:
Can get either:
-
Eccentric Cardiac Hypertrophy: chamber size increase from increase volume → thinning membrane and dilation
- Chamber enlarged – muscle dilated
-
Concentric Hypertrophy- thickening of heart muscle because pressure problem. Muscle grows inward into chamber (chamber gets small)
- Chamber smaller- muscle hypertrophied
44
Q
What happens to the heart shape in dilated cardiomyopathy?
Hypertrophic?
Restrictive CMP?
A
-
Normal vs cardiomyopathy
-
B. In the dilated type of cardiomyopathy
- the heart has a globular shape and the largest circumference of the left ventricle is not at its base but midway between apex and base
- Eccentric Hypertrophy
- the heart has a globular shape and the largest circumference of the left ventricle is not at its base but midway between apex and base
-
C. In the hypertrophic type
- the wall of the left ventricle is greatly thickened; the left ventricular cavity is small but the left atrium might be dilated because of poor diastolic relaxation of the ventricle.
- This kind is not very common
- Concentric Hypertrophy
-
D. restrictive type (amyloid)
- the left ventricular cavity is normal size, but again the left atrium is dilated because of the reduced diastolic compliance of the ventricle.
- Usually due to mitral stenosis or regurg/stenosis together
-
B. In the dilated type of cardiomyopathy
Any time have B,C,D → heart cant relax properly during diastole (not good diastolic filling)
** Diastolic Filling pressures go up → changes in valves anatomically and LA dilation from backpressure
51
Q
What does dilated CMP do to heart structure? Myocardial tissue?
A
Dilated cardiomyopathy (DCM).
- A: Four-chamber dilatation and hypertrophy are evident. There is a small mural thrombus (arrow) at the apex of the left ventricle (on the right in this apical four-chamber view). There was no coronary artery disease.
- B: Histology of typical DCM demonstrating variable myocyte hypertrophy and interstitial fibrosis (collagen is highlighted as blue in this Masson trichrome stain)
57
Q
Treatments for hypertrophic CMP? Sx management? Echo findings?
A
- Beta blockers
- Blunt sympathetically mediated increases in subaortic stenosis
- Decrease tachyarrythmias
- Calcium channel blockers
- Improve diastolic relaxation
- Surgical management
- Myomectomy- surgically remove parts of enlarged ventricle
- Echo findings- usually diagnose with this
- Thickened IVS (base to apex)
- Poor septal motion
- Anterior displacement of the mitral valve
PIC: Concentric Hypertrophy: Enlarged heart muscle with small chamber size, muscle growing into chamber. During diastole → cant adequate fill
58
Q
Frank starling law of the heart? Effects during heart failure?
A
Frank Starling Curve:
Y axis: CO
X axis: end diastolic pressure (pump fx of heart-) How we measure SV
Increase EDP → increase SV → increase CO
HF:
As heart trying to generate pressure → cant get out even with increasing pressures. CO decreases as EDP increase. (not normal- should be letting CO increase)
Drugs:
- Nitrates
- Diuretics → decrease arterial side compensation (constriction→ dilate)
- Does not impact CO
- Potent vasodilator (phentolamine) with inotrope (Digitalis) → increasing contractility → more normal
- Nitroprusside & dopamine → closer to normal
59
Q
What are some common congenital heart defects?
A
- Patent ductus arteriosis
- Atrial septal defect
- Ventricular septal defect
- Tetrology of Fallot
- Coartation of the Aorta
- Pulmonary stenosis with right-to-left shunt
61
Q
What is an atrial septal defect?
A
ASD: FORAMEN OVALE not closing properly or completely (1st day of life)
- Allows for blood to flow from L atrium to right atrium
- Oxygenated blood goes back to the lungs and increases blood flow through the lungs
- Can lead to pulm HTN
- Bigger the defect, the bigger the problem
Mixed blood ends up going through the PA
Blood that enters systemically is still oxygenated blood
- Most common of the cardiac malformations diagnosed in adulthood
- Normally: Atrial Septum forms between 4-6 weeks of embryonic life
- *Pregnancy ETOH ingestion associated with ASD!
- Normally: Atrial Septum forms between 4-6 weeks of embryonic life
63
Q
What is a ventricular septal defect?
A
-
Most common heart defect at birth- more severe than ASD
- Normally: Develops between 4-8 weeks gestation
- Many close in childhood spontaneously
- Develops at the beginning of pregnancy (ETOH ingestion)
- Normally: Develops between 4-8 weeks gestation
-
VSD: Can cause severe L to R shunts, with pulm HTN and CHF as well as infective endocarditis
-
Surgery is needed for larger VSDs- optimize and then surgery
- Sometimes they’ll watch these kids and they can close spont
-
Surgery is needed for larger VSDs- optimize and then surgery
- VSDs become severe because pressure increase rapidly
- The bigger the hole, the bigger the problem, not enough blood to the body (blood is properly oxygenated, just not enough in systemic circulation)
- Kid is pink but lethargic from decrease in blood flow to body
- Increased pulmonary blood flow à pulm htn
- Often closes on its own
- Failure to thrive is symptom to note
67
Q
What is tetralogy of fallot?
A
example right to left shunt
- Most common cause of cyanotic congenital heart disease
- Risks: >40 yo moms, ETOH in pregnancy, DM, children with down syndrome
- Caused by abnormal division of the truncus arteriosus into a pulmonary trunk and aortic root
- Main defect: Anterior deviation of pulmonary outflow septum → narrowing of ventricular outflow tract → prevention of BF via aorta because pulmonary artery valve tends to be constricted
-
Has 4 components
- VSD- if they didn’t have this they wouldn’t survive
- Dextrapoased aortic root that overrides the VSD
- RV outflow obstruction
- RV hypertrophy
- VSD- needs to be there for child to survive
- Narrowing of pulmonary passageway
Misaligned aorta- has to be misaligned or wont get O2 to systemic system
70
Q
What is coarctation of the aorta?
A
-
Abnormal narrowing of aorta
- More common in males than females
- Can be preductal or post ductal- named due to where the narrowing occurs in relation to ductus arteriosus
- Post ductal (distal to the ductus arteriosus) is the more common type
-
Preductal COA
- Infantile
- Weak femoral pulses
- Cyanosis of lower extrems (mottled)
- CHF
- Need surgical correction to survive!
- Pink hands, blue feet= R to L shunt
-
Post ductal COA
- Older children/ young adults
- Collaterals have developed
-
Decreased perfusion to the kidneys
- Activation of RAS
- High pressures in upper extrem and low pressures in lower
- Intermittent claudication- exercise with leg pain
- High pressure above (head, arms), low pressure below (everything else)
- Blood has normal oxygenation, kid is pink
- Decreased or absent pedal pulses
- Problem: left ventricle hypertrophies à high BP in upper body, low BP in lower body
- Might be seen in older patients where nothing is bringing BP down
- Kidneys do long term control of blood pressure
- Renin- trying to increase BP to where it needs to be
- BP in ankle very low due to coarctation
- Upstream of coarctation extremely high
- Strong radial and carotid pulses
