Step 1 Cardio

Sinus Venosus

Cornary sinus

Common Cardinal Veins

Superior Vena Cava

Truncus Arteriosus

What is the physiologic process?

Ascending aorta & pulm trunk

Process:

Neural crest cells from hindbrain migrate to form division of truncus arteriosus into aorta & pulmnary artery (aorticopulmonary septum) ⟶ Spiraling

Primitive Ventricle

Trabeculated portion of Ventricles

Bulbus cordis

Smooth portion of L & R ventricle

Endocardial Cushions

Valves & membranous portion of ventricular septum

Persistent Truncus Arteriosus

What is it?

Association?

Aorticopulmonary septum incomplete ⟶ so oxygenated blood from LV & deoxygenated blood from RV mix

2nd most common heart defect in DiGeorge Syndrome (22 Chips)

• 22: 22q11.2 deletion

• C: Cardiac anomalies (1st Tetralogy of Fallot. Think 2+ 2 = 4)

• H: Hypocalcemia

• I: Immunodeficiency

• P: Platelet abnormalities

• S: Small nose & ears

Transposition of Great Vessels

Failed spiraling of aorticopulmonary septum à reversal of pulmonary artery and aorta

• Compatible with life only if Patent Ductus Arteriosus (PDA) present ⟶ So some oxygenated blood can mix in (machine like murmur)

• Give prostagladin to keep PDA open!

• Associated with gestational diabetes

*Think high blood sugar ⟶ cardiac risks ⟶ cardiac embryonic development affected

Atrial Septation Process

2 Potential Defects?

Step 1: Septum Primum Forms

• Forms inferiorly from superior primitive atrium

• Foramen primum: opening b/w septum primum + AV cushions

• Step 2: Foramen and Septum Secundum Form

• Foramen Secundum: Forms within septum primum

• Septum Secundum: Superior and inferior segment

• Step 3: Foramen Ovale Closes

• Foramen Ovale: Formed by area between septum primum and secundum

• ↓ pulmonary vascular resistance, ↑ LAP, ↓ RAP

Patent Foramen Ovale:

• Incomplete joining of septum primum and septum secundum

• Most patients are asymptomatic

• Cryptogenic cerebrovascular accident, paradoxical embolism

Atrial Septal Defect:

• Secundum-type is most common and tend to be isolated

• Primum-type generally associated with additional heart defects

• Cryptogenic cerebrovascular accident, paradoxical embolism

Wide fixed split S2 heart sound bc it takes longer for the pulmonic valve to close if there is more blood (coming from the Left Atrium) due to increased blood flow through the right side of the heart.

Atrial Septal Defect

How common are the 2 types? Are they associated with different things?

Association?

Heart Sound?

• Secundum-type is most common and tend to be isolated

• Primum-type generally associated with additional heart defects

• Cryptogenic cerebrovascular accident, paradoxical embolism

Wide fixed split S2 heart sound bc it takes longer for the pulmonic valve to close if there is more blood (coming from the Left Atrium) due to increased blood flow through the right side of the heart.

Ventricular Septal Defects

Ventricular Septal Defects most commonly occur due to defects in the membranous portion of the interventricular septum aka endocardial cushions

What comes from 1st Aortic Arch?

Maxillary Artery

What comes from fourth aortic arch? (L & R)

Left Fourth Arch: Aortic Arch

• Classic Pathology: Coarctation of the aorta

Right Fourth Arch: Proximal Right Subclavian Artery

What comes from sixth aortic arch? (L & R)

Left Sixth Arch: Ductus Arteriosus and Proximal Pulmonary Arteries

• Classic Pathology: Patent ductus arteriosus

Right Sixth Arch: Proximal Pulmonary Arteries

Aortic Coarctation
Potential Locations
Origina/Derivative
Associations
Presentations (w/ & w/o PDA)
Imaging
Management 

Locations: (1) juxtaductal narrowing (aortic isthmus) (2) Pre-ductal: infantile fform & most common (3) Post-ductal: Adult form

Origin: Derived from Left 4th arch

Associations:
(1) Turner Syndrome
(2) Williams Syndrome: Elfin face, hypersocialability, Hypercalcemia & supra valvular aortic stenosis *Think: William the social elf gave out too much CAndy & that's bad for the heart
(3) Berry aneurysm --> increased risk of rupture --> SAH

Presentation:

• w/o PDA:  

1. Harsh systolic murmur at multiple locations along left sternal border 

2. Differential cyanosis: Arms are good, but legs are not perfused 

3. Brachial-femoral delay: Brachial pulse strong, femoral weak

• w/ PDA: Generally asymptomatic 

#3 is PDA which allows for perfusion to lower body

Locations: (1) juxtaductal narrowing (aortic isthmus) (2) Pre-ductal: infantile fform & most common (3) Post-ductal: Adult form

Origin: Derived from Left 4th arch

Associations:
(1) Turner Syndrome
(2) Williams Syndrome: Elfin face, hypersocialability, Hypercalcemia & supra valvular aortic stenosis *Think: William the social elf gave out too much CAndy & that's bad for the heart
(3) Berry aneurysm --> increased risk of rupture --> SAH

Presentation:

• w/o PDA:  

1. Harsh systolic murmur at multiple locations along left sternal border 

2. Differential cyanosis: Arms are good, but legs are not perfused 

3. Brachial-femoral delay: Brachial pulse strong, femoral weak

• w/ PDA: Generally asymptomatic 

#3 is PDA which allows for perfusion to lower body

Imaging:
Rib notching on CXR (silation of vessel w/ blood looks like notch on rib)

Management:

• Neonates --> prostagladin E1 (to keep PDA open)

• Operative repair

Patent Ductus Arteriosus

If in a premature newborn and we want to close it, give prostaglandin inhibitors like indomethacin

Origin/derivative: Left 6th Arch (which is in charge of ductus arteriosus & proximal pulmonary arteries 

Murmur: Continuous machine-like murmur @ L infra clavicular. Palpable thrill. 

Radiofrequency Ablation Locations

A Fib?

A Flutter?

Afib —> in LA myocardium (near pulm vein ostium)

A Flutter —> In space between inferior vena cava and tricuspid valve

Coronary Artery Anatomy

Right Coronary Artery (RCA):

• Majority of right-side of heart

• Sinoatrial node

• Left Coronary Artery (LCA):

• Majority of left-side of heart

• Two major branches:

• Left Anterior Descending Artery (LAD)à Anterior 2/3

of interventricular septum, anterolateral papillary

muscle, anterior left ventricle

• Left Circumflex Artery (LCX) à Posterolateral LA and

LV, anterolateral papillary muscle

• Posterior Descending Artery (PDA):

• ~85% R-dominant, 8% L-dominant, 7% co-dominant

• Primarily inferior borders of heart

• Posterior 1/3 of interventricular septum

• Posteromedial papillary muscle

Ms Aorta had RCA & LCA
LCA had a LAD & a kid who liked to flex (L circumFLEx)

• LAD: (also called IVY - interventricular artery): Anterior left ventricle, anterior 2/3s interventricular septum & anterolateral papillary muscles aka muscle of the LV/mitral valve

• LCA: left atrium, posterior LV, anterolateral papillary muscles aka muscle of the LV/mitral valve

RCA focused on doing things “right” (aka entire right side of heart) and had PDA which showed too much PDA so that diva was relegated to back of the heart (inferior borders, inferior 1/3 of ventricular septum)

Coronary Sinus

All coronary veins drain into the coronary sinus

• Location: Left posterior atrioventricular groove

• Drains directly into the right atrium

• Embryologic derivative: Sinus venosus

Aorta

What are her branches?

Important landmarks?

• Descending aorta traverses' diaphragm via aortic hiatus

• Celiac trunk

• Superior mesenteric artery origin

• Inferior mesenteric artery origin

• Right and left renal arteries origin

• Gonadal arteries origin

• Bifurcation into common iliac arteries (at navel)

Vascular Structures:

• Coronary Arteries

• Brachiocephalic trunk

• Subclavian arteries

• Common carotid arteries

• Ligamentum Arteriosum:

• Remnant of ductus arteriosus

Key Landmarks:

• T12: Descending aorta traverses' diaphragm via aortic hiatus (vs IVC at T8)

• T12: Celiac trunk

• L1: Superior mesenteric artery origin

• L3: Inferior mesenteric artery origin

• L1-L2: Right and left renal arteries origin

• L2: Gonadal arteries origin

• L4: Bifurcation (bi-FOUR-cation) into common iliac arteries (at navel) (vs IVC where it is L5)

List vessels in order of most to least likely to have atherosclerosis

Circle of Willis

Carotid Arteries

Coronary Arteries (which one is most likely)

Popliteal

Abdominal Aorta

1. Abdominal aorta

2. Coronary arteries (LAD)

3. Popliteal Arteries

4. Carotid Arteries

5. Circle of Willis

Subclavian Steal Syndrome

Etiology: Atherosclerosis, Takayasu arteritis, previous thoracic (aortic) surgery

• Pathophysiology:

• Subclavian stenosis à contralateral vertebral artery steal phenomena

• Presentation:

• Ipsilateral limb ischemia

• Asymmetric BP between upper extremities

• Dizziness, diplopia, syncope

• Worsening of symptoms during activity of affected limb

• Imaging:

• Reduced contrast uptake in areas distal to stenosis and ipsilateral vertebral artery

Obstructive Venous Drainage

Presentation for each in terms of face and extremity swelling, etc. other sx

1. Superior Vena Cava Syndrome

2. Brachiocephalic

3. Subclavian

4. Inferior Vena Cava

Superior Vena Cava Syndrome

• Etiology: Mass lesion (malignancy) or thrombosis (venous catheter)

• Edema à bilateral face, bilateral upper extremities

• Jugular venous distention

• Headache, ↑ intracranial pressure

• Brachiocephalic Venous Obstruction

• Etiology: Pancoast tumor or thrombosis (venous catheter)

• Edema à Unilateral face, unilateral upper extremity

• Subclavian and/or Axillary Venous Obstruction

• Edema à Unilateral upper extremity

• No facial involvement

• Inferior Vena Cava Compression

• Supine hypotensive syndrome (3rd trimester)

Edema à Bilateral lower extremities

Fetal hypoxia à improves with repositioning

How do you get femoral access?
NAVEL

Which are encased in femoral sheath?

Nerve, Artery, Vein, Empty Space, Lymphatics

Feel for pulsation, then go medial

all but nerve are encased in femoral sheath

When does coronary perfusion occur?

Where in the heart is the most susceptible to ischemic injury?

Coronary perfusion occurs during diastole, primarily when the heart muscle is relaxed. The subendocardium is the most susceptible to ischemic injury due to its position and high demand for oxygen.

Hydralyzine

Arterial vasodilation

Phenylephrine

Arterial vasoconstriction (a2 agonist)

Sodium Nitroprusside

50/50 venous & arterial dilation

Epinephrine, digoxin & dobutamine

All increase contractility

Frank-Starling Mechanism

Principle:

• ↑ Preload à ↑ Contractility à ↑ SV

• Mechanism:

• ↑ Venous return

• ↑ EDV ~ ↑ Preload

• ↑ Myocyte stretch prior to contraction

• ↑ Sarcomere length (↑ active tension and velocity of fiber shortening)

• Frank-Starling Curve:

• X-axis: LVEDP (preload, LVEDV, fiber length)

• Y -axis: Stroke Volume

• Slope of curve: Defined by afterload and contractility

• Point along curve: Defined by venous return (preload)

Two equations for Cardiac Output

MOST IMPORTANT

CO = HR x SV

Fick Principle

CO = VO2 / (CaO2 - CvO2)

Mean Arterial Pressure

Average pressure in a complete cardiac cycle

Pulse Pressure

PP = Systolic Pressure - Diastolic Pressure

Cardiac Curve w/ Venous Return Curve

Describe x & y axis

What does the x intercept represent? What changes it?

What changes the slopes?

Pressure Volume Loop

What does each corner & line mean?

What factors change them?

Pressure Volume Curve for Valvular Disease

What does each one look like?

• Aortic Regurgitation

• Aortic Stenosis

• Mitral Regurgitation

• Mitral Stenosis

List Endothelial Regulated Dilation Pathway

In the endothelium (which is lined by smooth muscle)

(1) Sheer stress (from blood passing through) or Acetylcholine or Bradykinin —> makes NO from arginine

(2) NO is released & diffuses to smooth muscles

(3) NO leads to conversion of GTP to cGMP

(4) cGMP activates PKG —> decreases cytosolic Ca2+ —> smooth muscle relaxation

Excitation-Coupling constriction Mechanisms for:

• Cardiac Myocytes

• Smooth Muscle

• Skeletal Muscle

Cardiac Myocytes

SA node —> Ca2+ come in through L type Calcium channel

1. Action potential leads to Ca2+ influx. 2. Ca2+ triggers further Ca2+ release from the sarcoplasmic reticulum. 3. Ca2+ binds to troponin, exposing binding sites on actin. 4. Myosin heads attach to actin, causing contraction.

Smooth Muscle

Same thing as cardiac except we also have the GqPCR pathway —> cleaves PIP2 into IP3 and DAG —> IP2 goes to SR —> releases calcium

intracellular calcium levels, where Ca2+ binds to calmodulin, activating myosin light chain kinase (MLCK) that phosphorylates myosin heads. This promotes myosin-actin interaction, leading to contraction.

To relax: Intracellular Ca2+ levels must decrease, MLCK is inactivated, and myosin light chain phosphatase (MLCP) dephosphorylates myosin.

Skeletal Muscle

Same thing as cardiac myocytes except pathway stimulated by Acetylcholine (no automaticity from SA node)

Mechanical coupling of LType Calcium Channel with RyR (which is why Ca2+ channel blockers do not have a major effect on skeletal muscle)

Nifedipine & Amlodipine

• Class:

• Mechanism:

• Primary site of effect:

• Class: Dihydropyrindine Ca Channel Blockers

• Mechanism: Inhibits L type calcium channel —> vasodilation

• Primary site of effect: Mostly vascular smooth muscle cells (arteries)

Diltiazem & Verapamil

• Class: Non- Dihydropyrindine Ca Channel Blockers

• Mechanism: Inhibits L type calcium channel —> vasodilation

• Primary site of effect: Primarily cardiac myocytes, some vascular smooth muscle cells (arteries)

Vasoconsctriction & Vasodilation Targets Meds (Video 4)

Blood Flow

• Poiseuille Equation

• Resistance