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Flashcards in CV week 4 Deck (165):

Secondary Prevention of CAD

actions taken after the development of disease to halt its progress and subsequent complications

-For pts with confirmed CAD or vascular equivalent (AAA, claudication, stroke)

Goal: prevent plaque rupture and progression


Pharmacologic reduction of CV risk with _____, ______ and ______

RAAS Inhibitors


Anti-platelet guidelines for CV risk reduction:

ASA alone? (2)
ASA + Clopidogrel? (1)
ASA or Clopidogrel alone? (2)

ASA alone:
-ALL CAD pts
-low dose for all pts on warfarin

Clopidogrel + ASA:
-all pts with ACS, PCI, or CABG for one year following event

ASA or Clopidogrel alone:
-all symptomatic (not asymptomatic) peripheral artery disease pts
-post-stroke pts (can do both ASA/Clopidogrel together also)


Class I and Class IIa
Beta-blocker guidelines for reducing CAD risk

Class I: B-blocker in all LVSD (EF less than 40%) and HF symptoms or MI/ACS in prior 3 years

Class IIa:
-B-Blockers in all with LVSD (EF less than 40%) even in absence of HF symptoms
-B-blocker in all with any history of MI/ACS


Goal of anti-platelet therapy in CAD secondary prevention:

prevent platelet adhesion to site of ruptured plaque, reduce platelet activation with use of _______, and prevent platelet aggregation with use of _______




Goal of B-blocker therapy in CAD secondary prevention

reduce HR, reduce contractility, reduce conduction velocity, reduce systemic BP → reduce myocardial oxygen demand


Goal of RAAS inhibition in CAD secondary prevention (4)

vasodilation, natriuresis, decreased SNS activity, reduce cardiac remodeling


Class I RAAS inhibition guidelines:

Aldosterone inhibtion

-all with LVSD (EF less than 40%), DM, HTN, or chronic kidney disease

-all with LVSD (EF less than 40%) and prior MI or HF symptoms who are ACE INTOLERANT

Aldosterone Inhibition:
-Post MI pts with LVSD (EF less than 40%) who are also taking BB, ACEI/ARB and have HF or DM
-AVOID in renal dysfunction or significant hyperkalemia


BP target goals

>60yrs --> 150/90
less than 60yrs --> 140/90


Typical strategies for controlling BP

1) Lifestyle (reduce saturated fat/sodium - DASH diet)

2) RAAS inhibitors (ACEis, ARBs)

3) Diuretics

4) Ca2+ channel blockers

5) B-blockers (not the best for HTN)

6) Direct vasodilators (only in certain pts)


Lipid management for CAD secondary prevention

-High dose statins more efficacious in reducing cardiac events
(Biggest side effect is myalgias)

-Non-statin lipid treatments have been shown to reduce lipid levels, but did NOT reduce cardiac events


Pharmacologic/Lifestyle strategies to reduce CAD risk (5)

1) BP control
2) Lipid management
3) Diabetes management
4) Depression screening and treatment
5) Smoking cessation


Lifestyle strategies for reducing CAD risk

1) Weight management
2) Physical Activity


Role of Monocytes in atherogenesis and disease progression (5)

innate immune system leukocyte

1) Monocytes adhere to endothelial cells expressing VCAM-1 and other adhesion molecules

2) Respond to chemokines (MCP-1) and migrate into intima

3) → Macrophage activation and ingestion of oxLDL → Foam cell

4) Secretion of IL-1, TNF, IFN-y and other proinflammatory mediators

5) Macrophage apoptosis promotes atherosclerosis progression


Role of T cells in atherogenesis and disease progression

Dendritic cell antigen presentation (connection between innate and adaptive immunity)→ T cell activation → clonal T cell expansion (Th1, Th17, Treg)


Th1 and atherogenesis

IFN-y secretion

-Mediates progression of atherosclerosis in conjunction with macrophage apoptosis

-Increases lesion formation and plaque vulnerability


Th17 and atherogenesis

promote plaque instability and angiogenesis (IL-17, IL-22, IL-21 secretion)


Treg and atherogenesis

→ IL-10, TGF-B

Decreased lesion formation and plaque vulnerability


Inflammatory cells and atherogenesis summary

-Immune response to injury initiates atherogenesis

-Innate immune cell interaction with endothelium drives initial plaque formation

-T cells promote further lesion expansion and plaque vulnerability


Drivers of Plaque Instability: (3)

Macrophage apoptosis and necrosis promotes necrotic core

MMPs degrade fibrous cap (Type I collagen)

Intra-plaque hemorrhage further weakens core



predicts excess risk of CV events (not yet used clinically)

-Acute phase reactant produced by hepatocytes, macrophages, and smooth muscle cells

-Binds to: modified membranes, apoptotic cells, lipoproteins

-Activates classical complement pathway


Link between autoimmune disease and CV events

Treatment of autoimmune disease (psoriasis, RA) associated with a lower risk of CV events

Shows that targeting inflammation can help reduce CV evnts
-TNF-alpha, IL-6, IL-1 inhibition = possible treatment


Risk factors for peripheral artery disease (4)

Diabetes (4x risk)
Smoking (2-3x risk)
Lipids (2x risk)
HTN (2x risk)


Peripheral artery disease results in 6x increased risk of ______

CV death


Intermittent claudication

-cramp, calf fatigue with exercise, resolves with rest

-Blood flow normal at rest, limited with exercise


Ischemic LE rest pain

Pain in distal foot or heel, worsened by leg elevation and improved by dependency (hanging feet down off bed)

-Distal, painful ulcers on toes or heels

-Blood flow limited at rest and exercise


Physical exam signs of ischemic leg rest pain

Decreased or absent pulses

Bruits (abdominal, femoral)

Muscle atrophy

Severe PAD → pallor of feet with elevation, dependent rubor, ischemic ulcers, ischemic gangrene


Risk Factors for Abdominal Aortic Aneurysm (4)

Age, gender (male), smoking, family history


Normal aorta size vs. AAA size

Normal aorta: 3cm at root, 2.5-2cm for remaining

AAA: diameter > 3.0 cm (50% increase in size relative to proximal normal segment)

**5.0-5.9 cm diameter → 35% 5 year rupture rate


Arterial Aneurysm

pathological expansion of all three arterial layers


Arterial aneurysm mechanism of formation (4)

1) Weakened aortic wall (decreased elastin and collagen)
2) Inflammation (B and T lymphocytes, macrophages, cytokines, autoantigens)
3) Proteolytic Enzymes (increased MMP)
4) Biomechanical stresses (elastin distribution, turbulent blood flow, mural thrombus)


Clinical presentation of arterial aneurysms

-70% pts asymptomatic → sudden death

-30% have abdominal pain radiating to back → die

-Often incidental discovery from imaging for another problem

**Arteriography may miss aneurysm because it view LUMEN NOT ARTERIAL WALL


Risk factors for aortic dissection (9)

1) HTN
2) Drugs (cocaine)
3) Inherited connective tissue disorders (Marfan, Ehlers-Danlos Syndromes)
4) Bicuspid aortic valve
5) Coarctation
6) Pregnancy
7) Aortitis
8) Iatrogenic (surgery, arterial catheterization)
9) Trauma


Aortic dissection 2 possible mechanisms of formation?

vessel loses integrity due to disruption in vessel wall

1) Primary intimal tear
2) Rupture of vasa vasorum


Clinical manifestations of aortic dissection

Severe tearing pain

-Disruption of major arterial circulation (due to formation of false lumen blocking flow to particular area)
→ stroke (carotid), syncope (vertebral), MI (coronaries), intestinal ischemia (mesenteric vessels), renal failure (renal arteries)


Virchow's Triad

Abnormal flow (stasis)
Coagulation Factors


Fick equation

CO= VO2/a-v O2


What does the Fick equation tell us?

Relates respiratory VO2 (max oxygen consumption) with oxygen delivery (circulatory system), and oxygen extraction (skeletal muscle)


Fick equation during exercise

1. 5 fold increase in CO

2.3 fold increase in a-v O2

3.Oxygen consumption during exercise influence more by CO and blood flow than by oxygen extraction


What happens during exercise (3)

1) Increase in blood flow
- Increase Cardiac Output by :
a. Increase HR (Cannot increase HR alone, fast HR → shorter diastole)
b.Increase EF
At rest, normal LVEF is 60% → EF increases by 10-20% with exercise

2.Muscle Blood flow
- Redistribution of blood flow:
Inactive organs → active skeletal muscle

3) Maintain Blood Pressure

a. Driving force of blood flow
b. Maintain blood flow to vital organs (brain)


Heart rate response to exercise

HR increased with exercise → increase SV (peripheral vasodilation, increased venous return, venoconstriction)

i.HR increase directly related to exercise intensity

ii.Linear response of HR to workload up to near max exercise

iii.Max exercise HR highly reproducible and consistent (220-age)
- After age 15, max HR decreases by 1 bpm annually

iv.During lower levels of exercise, increase in HR up to 100bmp related to parasympathetic withdrawal
- Above that (moderate/heavy exercise), HR controlled by sympathetic activity


Stroke volume during exercise

SV increases during exercise up to workloads 40-60% max exercise, and then SV reaches a plateau with no further increases


Factors responsible for changes in stroke volume during exercise

1. Increased venous return:
- Venoconstriction (SNS activity on VSM)
- Muscle pump (venous return)
- Respiratory pump (negative thoracic pressure aids venous return)

2) Increased Ventricular Contractility:
- Increased SNS activity (direct innervation and elevation of NE/E)
- Frank Starling Effect - increased stretch of ventricular muscle fibers → enhanced contractility


Differences in athletes (like Josh)

Starling curve shifted left - greater increase in SV for any EDV value

1.Greater resting SV and some athletes even get continued SV increase throughout exercise → greater CO
- Increased EDV with enhanced Starling forces at lower levels of exercise and increased ventricular contractility at higher levels of exercise

2.Greater resting SV with lower resting HR → same CO during rest as untrained people ( 4.5-5 L/min)

3.Max CO is greater in trained athletes than untrained
- Max CO = 24-34 L/min (6-7 fold increase)

4.Chronic LV dysfunction: Starling curve shifted right, and flatter → less preload effect on SV


Untrained people (Charlie) during exercise

1. SV doubles with exercise, but starts at a lower level than athletes

2.Max CO = 18-22L/min (4-5 fold increase)


Cardiac output during exercise

i. Increase in CO proportional to metabolic rate and VO2 required to perform the exercise

ii.CARDINAL RULE: it requires 6 L/min in CO for each 1L/min increase in oxygen uptake beyond resting conditions

- Workload 50% VO2 max → increases in HR only → increase CO
EXCEPTION IS ELITE ATHLETES (increase SV throughout exercise)

iii.Max CO depends on body size (gender differences) and the degree of exercise conditioning


BP during exercise

Decrease in vascular resistance + increase in CO → BP maintained
- Increase in blood flow achieved by decrease in vascular resistance and NOT increase in BP
- Get some increase in systolic BP, little change in diastolic BP



= ⅓ systolic + ⅔ diastolic

1.MAP determines rate of blood flow through systemic circuit

2.Systolic pressure: pressure generated as blood is ejected from LV
a.The same as LV systolic pressure in absence of aortic valve obstruction

3.Diastolic pressure: pressure during ventricular relaxation
a.Reflects compliance of systemic vascular bed


Blood flow determined by: (3)

1. Autoregulation in exercising beds
2. Capillary recruitment
3. vasoconstriction of non exercising beds



1. Local release of substances at time of exercise→ Vasodilation in response to decreased PO2, increased PCO2, NO, [K+], acidosis, and adenosine

2.Intrinsic metabolic control

3.Regulation at arterioles and small artery level


Capillary recruitment

1. At rest only 5-10% capillaries in skeletal muscle open

2.During exercise → 100% of capillaries open → increase surface area for oxygen delivery and extraction


Vasoconstriction of non exercising muscle bed

1. Number of motor units recruited determine need for muscle blood flow and redirection of CO from non exercising vascular beds

2.SNS regulation increases vasoconstriction

3.Regulation by muscle ergoreceptors and CV control center (medulla)


Blood flow redistribution during exercise->

Increased muscle blood flow

i. At rest skeletal muscle blood flow = 15-20% total CO, increases to 80-85% during exercise

ii.Vasodilation to exercising muscle bed, vasoconstriction of non-exercising vascular beds (liver, kidneys, intestines)

iii.Blood flow to brain maintained during exercise


SNS activity and blood flow

key for maintaining blood flow to vital organs

i.Moderate to Heavy Exercise:

1.Sympatholysis → vasodilation and NOT constriction

2.MAP maintained by CO and vasoconstriction in non exercising vascular beds

ii.Very High Workloads:

1.Muscle vasodilation exceeds cardiac pump capacity

2.Sympathetic mediated vasoconstriction in exercising vascular beds to preserve MAP and blood flow to brain, etc.


Coronary vs. systemic circulation

Coronary: increases during exercise in proportion to increase in CO

1.At rest coronary venous O2 sat = 25% (mixed systemic venous O2 = 65%)

2.During Exercise coronary O2 sat = 10% (slight increase in extraction)

3.Coronary blood flow primary way to improve oxygenation of myocardium


Oxygen delivery =

blood flow x arterial O2 content

i.Blood flow = CO
ii.Arterial O2 content = [Hgb] x 1.34 x O2 saturation (%)


Arterial-venous O2 content difference

At Rest: arterial O2 content = 20 ml per 100 ml blood and venous O2 content = 15 ml per 100 ml blood
-> a-v O2 difference at rest = 5 ml O2 per 100 ml blood

At high intensity exercise: arterial = 20 ml, venous = 5 ml
-> a-v O2 difference at exercise = 15 ml O2 per 100 ml blood

****No change in arterial oxygen content, only change O2 extraction


Rate pressure product

RPP = HRmax x SBPmax

1.RPP (heart rate) where ischemia occur - determines the severity of coronary disease

2.Fixed stenosis → fixed RPP

3.Dynamic stenosis → variable RPP


Blastocyst is made up of what 2 layers?

Trophoblast = outer cell mass
Embryoblast = inner cell mass


The Trophoblast gives rise to...

The Embryoblast gives rise to...

Trophoblast --> placenta and supporting tissues

Embryoblast --> the baby! aka Embryonic Disc


The Embryonic disc (Embryoblast) is made up of what to layers?

Epiblast (external layer)
Hypoblast (internal layer)


Epiblast cells migrate through the primitive streak to give rise to the 3rd layer of the embryonic disc called ______



Gastrula: 3 germ layers

1) Ectoderm (external)
2) Mesoderm (middle)
3) Endoderm (internal)


Precardiac cells orgininate from which germ layer?

Mesoderm - migrate cephalically


By day 19, the precardiac cells within the _______ area migrate _______ and begin to form _________

cardiogenic area

cephalically, so they are ventral to forebrain and foregut

begin to form 2 endocardial tubes


The two primitive endocardial tubes are formed of ______ and ______ and come together to form _________

endothelial cells
surrounded by splanchnic mesoderm

primitive heart tube


The primitive heart tube begins to beat by day ______!



Inner layer of heart tube (endothelial lining) → ?

Outer layer of heart tube (splanchnic mesoderm) → ?

Inner layer of heart tube (endothelial lining) → endocardium

Outer layer of heart tube (derived from mesoderm) → myocardium and epicardium


Pre loop 7 main structures

straight heart tube

From head to toe:
1) Aortic root
2) Truncus
3) Bulbus cordis
4) Primitive ventricle
5) AV sulcus
6) Primitive atria
7) Sinus venosus


Truncus --> ?

aortic/pulmonary valves and great vessels (ascending aorta, pulmonary trunk)


Bulbus cordis -->



Primitive ventricle -->



AV sulcus -->

interventricular septum

(connection between primitive atria and primitive ventricle)


Primitive atria -->



Sinus venosus -->

part of RA and coronary sinus


Conus -->

outflow tract (infundibula) of both ventricles


Cardiac looping

day 23-25

-Cardiac tube grows faster than rest of embryo, causing looping

-Normally, heart loops to right of embryo (D loop)

-Bulbus cordis (RV) drops down to right of embryo, with primitive ventricle (LV) to left

-Primitive atria loops up posteriorly

-Long axis of AV canal initially cephalic → caudal, but with looping becomes anterior → posterior (Atria behind ventricles)


Post loop

septation begins, great arteries form


The sinus venosus gets blood returned from the fetal body via what 3 sets of veins?

1) Umbilical vein (O2 blood from placenta)
-disappears after birth

2) Vitelline vein (from yolk sac)

3) Cardinal vein (drains embryo, deox blood from fetus)


R Umbilical vein → ?
L Umbilical vein → ?

R Umbilical vein → disappears
L Umbilical vein → ductus venosus (disappears after birth)


R Vitelline Vein → distal = ?, proximal = ?

L Vitelline Vein → ?

R Vitelline Vein → SMA (distal), suprahepatic portion of IVC (proximal), and hepatic sinusoids

L Vitelline Vein → hepatic sinusoids


R Cardinal Vein → ?

L Cardinal Vein → ?

R Cardinal Vein → SVC, brachiocephalic vein, innominate veins

L Cardinal Vein → Ligament of Marshall


The ascending aorta comes from ________, while the descending aorta comes from the __________

aortic sac

left dorsal aorta


There are _____ aortic arches



1st aortic arch --> ?

first to disappear
-contributes to maxilary and eternal carotid arteries


2nd aortic arch -->?

Dorsal portion --> stapedial artery


3rd aortic arch --> ?

carotid arteries


4th aortic arch --> ?

Right side --> R. braciocephalic artery, right subclavian artery

Left side --> transverse aortic arch


5th aortic arch --> ?



6th aortic arch --> ?

proximal portion of right --> proximal right pulmonary artery

proximal portion of left --> proximal left pulmonary artery

Distal portion of left --> ductus arteriosus


How are the great vessels formed from the conus, truncus, and aortic sac?

Septation of conus (merge with ventricular septum caudally)

Septation of truncus (form part of pulmonary and aortic valves)

Aorticopulmonary septum is becomes spiral shaped as conus, truncus, and aortic sac septum merge


Describe the relationship between tha aorta and pulmonary artery at:

Valve level
Great artery level

At infundibulum: pulm is anterior and to right of aortic

At valve level: pulm valve is anterior and to left of aortic

At great artery level: pulm artery is posterior and to left of aorta


Fetal Circulation:

Oxygenated blood comes in from placenta via _________ and then...

Umbilical Vein

-½ of blood goes through ductus venosus directly into IVC

-½ of blood goes into portal vein to liver and then into IVC


Fetal Circulation:

Oxygenated blood from umbilical vein mixes with _____________ and enters ______ through _______

draining deoxygenated blood from fetus

enters RA through IVC


Fetal Circulation:

Once the mixed oxygenated blood is in the RA, 1/3 of the blood goes _______ and 2/3 of the blood goes ________

1/3 --> across patent foramen ovale into LA (one way flap that allow R to L flow in atrial chambers)

2/3 --> RV --> pulmonary artery


Fetal Circulation:

blood that crossed the foramen ovale into LA then goes from the LA --> ______ and then to 3 possible places.

LV (where it mixes with poorly oxygenated blood from pulmonary veins)

1) Coronary arteries (myocardium)

2) Carotid and subclavian arteries (head and neck)
-System setup such that most highly oxygenated blood feeds head, neck and myocardium

3) Descending aorta (fetal body)


Fetal Circulation:

Blood in the RV enters the pulmonary artery and then goes ________ or ________

12% of blood goes to lungs

88% of blood → ductus arteriosus crossing into descending aorta → fetus body circulation


Ductus Venosus

connection between umbilical vein (oxygenated blood from placenta) and IVC


Ductus Arteriosus

connection between pulmonary artery and descending aorta


Closure of ductus arteriousus

becomes ________?

Ligamentum arteriosum

-Functional closure 10-15 hours after birth
-Anatomic closure 2nd-3rd week of life
-By age one >98% have closed DA


Foramen ovale

formed during atrial septum formation - septum secundum only partially fuses with endocardial cushion

-Acts like a flap valve allowing R → L flow between atria (fetal RA pressure higher than LA pressure)

-Closes when baby takes first breaths and pressure shifts so LA > RA


Atrial septum

Septum primum = ridge of tissue on roof of primitive atrium grows down and fuses with endocardial cushion

-Doesn’t close completely (osteum primum) - eventually closes

-Osteum secundum forms due to cell apoptosis in ostium primum

-Septum secundum = second ridge of tissue that grows downward, partially fusing with endocardial cushion = foramen ovale


Ventricular septation

Post loop stage: day 28-42

-Ridges of septum grow towards base of heart as ventricular outpouchings develop

-4 endocardial cushions appear concurrently (inferior, superior, left, and right)

=Creates right and left atrioventricular canal, and become parts of the tricuspid and mitral valves

-Septum primum, endocardial cushions, and primitive interventricular septum become continuous


Why does the ductus arteriosus stay open?

Prostaglandins (arachidonic acid metabolism, potent vasoactive agent)


Increased incidence of patent ductus arteriosus with what 3 conditions

>9,000 ft elevation

maternal rubella infection

premature infants


A patent ductus arteriosus is a persistant _______

distal portion of left 6th aortic arch


Clinical presentation of PDA

-Increased pulmonary blood flow, and decreased systemic blood flow
-Feeding intolerance
-Respiratory problems (pulm edema)
-Renal insufficiency

Older infant or young children → hoarse cry, pneumonias, failure to thrive, increased work breathing and diaphoresis with activity/feeding


What can be seen with a large PDA (6)

1) Wide pulse pressure

2) Bounding pulses

3) Increased work of breathing

4) Hyperactive precordium

5) Continuous machine-like murmur along LU sternal border (aorta P > pulmonary P always)

6) Accentuated P2 if associated pulm HTN


What's the murmur heard in PDA

Continuous machine-like murmur along LU sternal border

-hearing blood crossing DA because aorta P always > pulmonary P (Systole and diastole)


Treatment of PDA:
Symptomatic vs. asymptomatic neonate

Asymptomatic neonate → conservative management

Symptomatic neonate →
1) IV COX inhibitors (NSAIDS) - Indocin, Ibuprofen Lysine
70% effective in closing PDA in preterm neonates
-Block conversion of arachidonic acid to PG

2) If NSAIDS fail → surgical ligation via lateral thoracotomy


Treatment of PDA:

Symptomatic older child vs. asymptomatic older child

Symptomatic older child → percutaneous occlusion

Asymptomatic older child → controversial
Murmur → percutaneous closure
Silent → don’t intervene


Secundum ASD can be caused by...(2)

1) too large central hole (ostium secundum) in septum primum

2) inadequate development of septum secundum


Magnitude of shunt across an ASD based on (2)

-Size of defect

-Relative inflow resistances of left and right ventricles


Large defect in ASD if...

diameter equal or greater than that of mitral valve


ASD begins as a L--> R shunt because ________ and ______

Will remain as a L-->R shunt if _________ and ______

If ASD is large then...

LA pressure > RA pressure and LV a “stiffer” chamber

Remains L → R if:
1) RV thinner and has higher compliance than LV (typical)
2) Systemic vascular resistance > pulmonary vascular resistance = dependent shunt (flow dependent on resistance and pressure)

BUT if ASD is large, LA and RA pressures begin to equalize


Does ASD present in infancy? why?

Rarely presents in infancy (LV and RV have similar pressures after birth = minimal atrial shunt, and thus minimal symptoms)

As pulmonary vascular resistance falls and RV wall thins (more compliant), then L → R shunting increases


Physical exam findings of ASD (5)

Small defect with no/minimal shunt or neonate → normal exam

Large defect: may present in infancy (may also be asymptomatic)
1) Increased respiratory rate
2) Sweating with feeds
3) Liver 2-3cm below R costal margin
4) Systolic ejection murmur at UL sternal border +/- diastolic rumble at LL sternal border
5) Second heart sound (S2) widely split


murmur(s) and heart sounds in ASD and what explains them

1) Systolic ejection murmur at UL sternal border (Secondary to excessive blood flow across pulmonary valve)

2) +/- diastolic rumble at LL sternal border (excessive blood flow in diastole across tricuspid valve)

**Murmur NOT caused by flow across defect (pressure differential is too small)**

3) Second heart sound (S2) widely split
-RV volume overload in ASD → delayed RV emptying and wide fixed splitting of S2


ASD findings for:


CXR: heart may or may not be enlarged, main pulmonary artery enlarged, pulmonary vascular markings prominent


Possible long term complications of hemodynamicalls significant ASD left untreated (3)

1) Pulmonary vascular disease (high pulmonary blood flow --> increased PVR)

2) Atrial arrhythmias (secondary to atrial enlargement over time)

3) Onset of heart failure (due to pulmonary vascular disease)


Treatment of ASD:

Older children, adolescents, adults

Infants: medical therapy (diuretics)

Older children, adolescents, adults → CLOSE THE HOLE
-Percutaneous device closure


Ventricular septal defects represent ___ of all congenital heart defects and most ____ close



4 types of VSDs

1. Perimembranous VSD (most common, 75% of VSDs)

2.Muscular VSDs (any part of muscular septum)

3.Atrioventricular Septal Defect (AV canal)

4.Subarterial VSD (outlet VSD)


Large VSDs

Large defects: measuring same diameter as aortic orifice

Often “unrestrictive” - causing equalization of right and left ventricular pressure


Magnitude of VSD shunt depends on (3)

a. Size of defect

b.Systemic and pulmonary vascular resistance

c.If other heart lesions are causing obstruction of shunt


In a VSD, if the PVR is lower than SVR:

L→ R shunt

a.Increases blood flow returning to LA and thus increase LV EDV, muscle fiber length, and thus increases LV contractility → increased LV output


Clinical manifestations of VSD

1. Asymptomatic until PVR falls after birth (fall in PVR delayed at altitude)

2.Large VSD → respiratory distress, diaphoresis with feeding, failure to thrive

3.Small VSD → tachypnea, diaphoresis (mild or absent)


PE findings of large VSD

a. Active precordium

b.Accentuated S2 heart sound

c.Harsh, holosystolic murmur loudest at LL sternal border

- Caused by flow across defect (LV and RV significant pressure differential)

d.Diastolic murmur (due to increased flow across mitral valve)


PE findings of small VSD

a. Precordial activity normal

b.Normal S2 heart sound

c.Early systolic murmur (LOUDER) - due to closing/restrictive VSD or low PVR

- Smaller means louder!

d.No diastolic murmur


VSD murmur that goes away...... Good right?

Fuck no
Can indicate large VSD caused equalization of RV/LV pressure or elevation in PVR


Diagnosis of VSD (3)

ECHO (gold standard): location and number of defects, magnitude of shunt, identify associated lesions (e.g. aortic insufficiency)

ECG: normal in small defects
Large defect → RAD and RV/LV hypertrophy (combined hypertrophy)

CXR: increased lung vascularity, enlarged pulmonary arteries, cardiomegaly


Treatment of VSD

Treat symptoms: diuretics, digoxin, afterload reduction (ACEI)

a.Heart failure symptoms - tachypnea, diaphoresis

b.Pulmonary edema

2.Surgery Indications: Try to let defects close on their own!

a.Development of pulmonary vascular changes

b.Persistent symptoms or poor growth despite medical therapy

c.Development of secondary complications (aortic insufficiency, double-chambered RV)


VSD associated with which complications

1. Most small defects close spontaneously, and large defects decrease in size - but large defects untreated can be devastating

2.Eisenmenger’s Syndrome:

a.L→ R shunt → increased pulmonary blood flow → muscularization of pulmonary arterioles → pulmonary HTN → increased RV pressure → SHUNT REVERSAL (R → L)

b.→ Cyanosis and clubbing → Heart/Lung transplant or death


Most common cyanotic defect>

Tetralogy of Fallot


Four defects associated with tetralogy of fallot

1. RV outflow tract obstruction

2. RVH

3 Dextroposition of aorta (aorta overrides the VSD)

4. VSD


What the fuck is monology of fallot?

anterior and superior deviation of infundibular portion of ventricular septum → obstruction of subpulmonary outflow tract

1.One embryologic thing that goes ary and causes all these problems


VSD in tetralogy of fallot

VSD large in most cases → RV and LV pressures equal


Magnitude of pulmonary blood flow in tetralogy of fallot determined by

1. Source of pulmonary blood flow
- Normal RV output to pulmonary arteries
- Ductus Arteriosus flow - primary PBF source if outflow obstruction is severe
- Size of DA primary determinant of magnitude of PBF

2) Severity of RV outflow obstruction
- Narrowing of infundibular region and stenosis of pulmonary valve
- Determines direction of shunt:
R → L if RV outflow resistance higher (very bad obstruction) than SVR → Cyanosis (Blue Tetrology)
L→ R if RV outflow resistance less than SVR → no cyanosis (Pink Tetrology)

3) Balance of RV and LV pressures

4) Ductus arteriosus


How do you treat a tet spell (4)

increase PBF

a.Knee to chest position → increase SVR

b.Phenylephrine (alpha agonist)→ increase SVR

c.Morphine (sedation)

d.Volume expansion with IV fluids


How do you prevent tet spells

B-blockers (decreases infundibular obstruction)


Clinical presentation of tetralogy of fallot

1. Widely variable based on:
a.Size of VSD
b.Severity of RV outflow obstruction
c.SVR (what direction is blood going)

2.Almost always present in infancy (blue baby, loud murmur-blood trying to get through pulmonary artery outflow tract)

3.Cyanosis gets worse as ductus arteriosus closes
a.Can use prostaglandins to keep DA open when dependent on it for PBF


Physical exam of tetralogy of fallot (5)

1. Tachycardic, cyanotic (blue tet)

2.Diaphoretic and tachypneic (pink tet)

3.Precordial impulse displaced to LL sternal border (RV dominance)

4.Short systolic murmur of pulmonary stenosis



Treatment of tetralogy of fallot

1. Outpatient if adequate O2 sat once ductus is closed

a.+/- propranolol for tet spell prevention

b.Elective surgical repair at 2-4 months

2.Ductal dependent PBF → maintain PG infusion

a.Early surgical repair or palliation


Associated complications tetralogy of fallot

1. Death when DA closes if RVOT obstruction severe and ductal dependent

2.Can survive into young adulthood

a.Cyanotic saturations (75-95%)
b.Clubbing of fingers
c.Poorly developed dental enamel, soft teeth
d.Bleeding tendencies
e.Limited exercise tolerance (squat, trying to increase SVR and improve PBF)


Cerebral abcesses

known complication of unrepaired congenital heart diseases:
- unusual before 1.5-2 years
- persistant unexplained fevers
- behavioral changes


Coarctation of the aorta

Narrowing of aortic lumen → poor descending aorta perfusion

1.Decreased blood flow to bowel → infants can have necrotizing enterocolitis

2.Decreased blood flow to leg muscles → children complain of leg pain with exercise

3.Decreased blood flow to kidneys → increased RAAS activation
-> Rebound hypertension after coarctation repair


Coarctation of the aorta

Narrowing of aortic lumen → poor descending aorta perfusion

1.Decreased blood flow to bowel → infants can have necrotizing enterocolitis

2.Decreased blood flow to leg muscles → children complain of leg pain with exercise

3.Decreased blood flow to kidneys → increased RAAS activation
-> Rebound hypertension after coarctation repair


Coarctation of the aorta is associated with

turner syndrome and bicuspid aortic valve


Clinical presentation of coarctation: Newborn, infancy, childhood, and adult

1. Asymptomatic as newborn (patent ductus allows adequate post-coarctation flow)

a.When ductus closes (1-2 weeks) → tachypnea, diaphoresis, poor feeding, and can have shock with cardiac failure

2.Infancy → lack of femoral pulse

3.Childhood → systemic HTN, intermittent LE claudication, headaches

4.Adult → systemic HYN


Physical exam of coarctation (5)

1. Tachycardic

2.BP differential between upper and lower extremities (100/70 in arm, 50/30 in legs)

3.Pulmonary rales, hepatomegaly

4.Accentuated S2 + S3 heard

5.Soft systolic murmur + systolic click over apex (if associated bicuspid aortic valve)


Diagnosis of coarctation

1. ECG:

a.Infants → RAD, RVH

b.Children → modest increase in LV forces

c.Adults → ST depression, T wave flattening, inversion (strain pattern)

2.CXR: signs of cardiac failure (cardiomegaly, prominent pulmonary arterial markings, pulmonary edema, rib notching)

a.3 sign in older children and adults: aortic knob, coarctation, post stenotic dilation

3.ECHO: site and severity of obstructions, head/neck vessel anatomy, presence of ductus, associated intracardiac anomalies


Diagnosis of coarctation

1. ECG:

a.Infants → RAD, RVH

b.Children → modest increase in LV forces

c.Adults → ST depression, T wave flattening, inversion (strain pattern)

2.CXR: signs of cardiac failure (cardiomegaly, prominent pulmonary arterial markings, pulmonary edema, rib notching)

a.3 sign in older children and adults: aortic knob, coarctation, post stenotic dilation

3.ECHO: site and severity of obstructions, head/neck vessel anatomy, presence of ductus, associated intracardiac anomalies


Treatment of coarctation

1. Infants → maintain on PGs until surgery

a.End-to-end anastomosis surgical repair

b.Risk of re-coarctation and aneurysm long term

2.Young children → balloon angioplasty vs. surgery

3.Adults → surgery vs. stent placement


Associated complications of coarctation

1. Development of collaterals in setting of marked obstruction (reduced BP gradient and increased femoral pulses can result)

2.Causes of death in untreated cases:
a.Heart failure (28%)
b.Aortic rupture or dissection (21%)
c.Infective endocarditis (18%)
d.Cerebral hemorrhage (12%)


Dilated cardiomyopathy is due to an impairment of _________ and an ejection fraction of...

Contractility (systolic dysfunction)

LVEF less than 40%


Hypertrophic cardiomyopathy is due to an impairment of _________ and an ejection fraction of...

compliance (diastolic dysfunction)

LVEF = 50-80%


Restrictive cardiomyopathy is due to an impairment of _________ and an ejection fraction of...

compliance (diastolic dysfunction)

LVEF = 45-90%


Non-ischemic causes of dilated cardiomyopathy (5)

Toxic (ethanol)
Metabolic (hemochromatosis)
Inflammatory (sarcoidosis, myocarditis)
Traumatic (peripartum)
Degenerative (dystrophy)

30-40% genetic causes


Non-ischemic causes of hypertrophic cardiomyopathy

1) Degenerative (dystrophy)
2) Metabolic (glycogen storage disease)
3) Infants of diabetic mothers

100% genetic causes!


Non-ischemic causes of restrictive cardiomyopathy

1) metabolic-ischemic (amyloidosis)
2) Traumatic (radiation)
3) Inflammatory (sarcoidosis)


Genetic mutations in dilated cardiomyopathy (3)

1) mutations in cytoskeleton (sarcoglycan, dystrophin, desmin)

2) Mutations in nuclear envelope (lamin A/C)

3) Mutations in mitochondria


Genetic mutations in hypertrophic cardiomyopathy (3)

Myosin-Binding Protein C ** (70-80% of cases!)

Troponin T

B-myosin heavy chain


In the setting of multiple myeloma, what cardiac complication is common?

Restrictive cardiomyopathy

-Immunoglobulin light chain (**AL) synthesized in plasma cells


Proposed biological mechanism relating Depression and CVD

Defective serotonin signaling → dysfunction of amygdala →

1) Autonomic dysfunction
2) Hypercortisolemia

→ Elevated catecholamines, elevated inflammatory markers, endothelial dysfunction, platelet activation


Treatment of depression can... (4)

Decrease platelet activation markers
Improve HR variability
Reduce inflammatory markers
Normalize brain serotonin turnover