Cardiology

OUTLINE
1. Embryologic Derivatives
Cardiology: 2.
●
Truncus Arteriosus
A. Physiologic
Embryology
● B. Persistent Truncus Arteriosus
● C. Transposition of Great Vessels
3. Atrial Septation
● A. Mechanism
● B. Patent Foramen Ovale
● C. Atrial Septal Defect
4. Aortic Arch Derivatives and Pharyngeal Arches
Cardiology: Embryology Bootcamp.com
https://commons.wikimedia.org/wiki/File:2037_Embryonic_Development_of_Heart.jpg
Heart begins beating

• Sinus venosus à Coronary sinus, posterior portion of right atrium
during Week 4
• Common cardinal veins à Superior vena cava
• Umbilical vein à Ligamentum teres hepatis
• Vitelline veins à Portal circulation and mesenteric veins
• Truncus arteriosus à Ascending aorta and pulmonary trunk
• Left and right dorsal aorta à Descending aorta
• Primitive ventricle à Trabeculated portion of right and left ventricle
• Primitive atria à Trabeculated portion of right and left atria
• Bulbus cordis à Smooth portion of the right and left ventricle
• Endocardial cushions à Valves and membranous portion of ventricular septum
https://commons.wikimedia.org/wiki/File:Truncus_arteriosus.jpg
https://commons.wikimedia.org/wiki/File:D-tga-575px.jpg
• Physiologic:
• Neural crest cell migration
• Aorta and pulmonary artery partitioned and undergo spiral formation à aorticopulmonary septum constructed
• Persistent Truncus Arteriosus:
• Partial (incomplete) aorticopulmonary septum formation
• Mixing of deoxygenated and oxygenated blood
• Classic Association: DiGeorge Syndrome
• Transposition of Great Vessels:
• Failed spiraling of aorticopulmonary septum à reversal of pulmonary artery and aorta
• Two parallel circuits
• Right ventricle à Aorta
• Left ventricle à Pulmonary artery
• Classic Association: Mothers with diabetes
• 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
Ventricular Septal Defects most commonly occur due to defects in

the membranous portion of the interventricular septum
https://commons.wikimedia.org/wiki/File:Gray473.png
• First Arch: Maxillary Artery

• Second Arch: Hyoid and Stapedial Arteries
• Third Arch: Common Carotid and Proximal Internal Carotid Arteries
• Left Fourth Arch: Aortic Arch
• Classic Pathology: Coarctation of the aorta
• Right Fourth Arch: Proximal Right Subclavian Artery
• Left Sixth Arch: Ductus Arteriosus and Proximal Pulmonary Arteries
• Classic Pathology: Patent ductus arteriosus
• Right Sixth Arch: Proximal Pulmonary Arteries
https://commons.wikimedia.org/wiki/File:Kiemenbogen.jpg
Pharyngeal Arches Pharyngeal Pharyngeal

Segment Vascular Supply Cranial Nerve Important Cartilage Classic Pouches Grooves
Muscles Pathology 1st: Eustachian tube, 1st: External auditory
tympanic cavity, meatus, auditory canal,
First- Maxillary Artery V2 and V3 -Muscles of Meckel’s Cartilage Treacher Collins
mastoid air cells outer tympanic
Mandibular mastication à Syndrome
membrane
Arch -Anterior belly of Mandible, maxilla
digastric Zygomatic bone Pierre Robin
-Tensor tympani, Malleus and incus Syndrome
tensor veli palatini
Second- Hyoid and Stapedial VII -Muscles of facial Reichert’s Cartilage Congenital 2nd: Epithelial lining of 2nd – 4th:
Hyoid Arch Arteries expression à Pharyngocutaneou palatine tonsils Obliterated in utero
-Posterior belly of Stapes, styloid s Fistula
digastric process
-Stylohyoid, Stylohyoid ligament
stapedius Lesser horn of
hyoid
Third Common Carotid and CN IX -Stylopharyngeus à Greater horn of 3rd: Dorsal à Inferior
Proximal Internal hyoid parathyroid glands
Carotid Arteries 3rd: Ventral à Thymus
Fourth Aortic Arch (L) CN X: Superior -Cricothyroid Superior thyroid Coarctation of

R Subclavian (R) Laryngeal Nerve -Palatopharyngeus cartilage Aorta 4th: Dorsal à Superior
-Levator veli parathyroid glands
palatini 4th: Ventral à
Parafollicular (C cells)
Sixth Ductus Arteriosus (L) CN X: Recurrent Intrinsic muscles of Inferior thyroid Patent Ductus of thyroid
L Pulmonary Artery (L) Laryngeal Branch larynx (except cartilage Arteriosus
R Pulmonary Artery Cricothyroid) Arytenoid,
(R) corniculate, and
cuneiform cartilage
≣ ⟽ ⟾
Item 1 of 1 Test Your Knowledge
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Question ID: 0030 Previous Next
https://commons.wikimedia.org/wiki/File:SVCCXR.PNG
A 57-year-old male with a past medical history of hypertension presents to his primary
care physician for hoarseness and dyspnea that has been progressively worsening over
the past two months. He has a chronic smoking history ”for as long as he can
remember”. He also states that he has been having double vision when leaning forward.
During physical examination, auscultation reveals mild end-expiratory wheezing
bilaterally over the lung fields. Heart sounds are normal with a regular rhythm. Radial
pulses are 2+ and symmetric bilaterally. No thyromegaly is present. Diffuse venous
distention is observed in the neck and chest wall. Edema is present diffusely throughout
the upper extremities. Fundoscopic examination reveals papilledema bilaterally. Chest
radiography is performed. A suspicious mass is identified and highlighted on the imaging
study below.
Which embryologic derivatives are most closely associated with the structured
compressed in this patient?
⚪ A. Truncus arteriosus
⚪ B. Cardinal veins
⚪ C. Endocardial cushions
⚪ D. Right sixth pharyngeal arch
⚪ E. Left fourth pharyngeal arch
OUTLINE
1. General Anatomical Overview
Cardiology: ●
●
2.
A. Cardiac Atria
B. Cardiac Ventricles
Cardiac Silhouette: Chest Radiography
Anatomy ●
●
3.
A. Cardiac Atria
B. Cardiac Ventricles
Axial Imaging: CT and MRI
● A. Ascending and Descending Aorta
● B. Pulmonary Trunk
● C. Cardiac Atria and Ventricles
4. Penetrating Cardiac Injury
5. Cardiac Conduction Anatomy
● A. Sinoatrial Node
● B. Atrioventricular Node
6. Radiofrequency Ablation Targets
● A. Atrial Fibrillation Foci
● B. Atrial Flutter Foci
7. Coronary Artery Anatomy
● A. Right Coronary Arteries
● B. Left Coronary Arteries
● C. Dominant Coronary Artery Circulation
8. Coronary Sinus
9. Cardiac Catheterization
● A. Swan-Ganz Catheter
● B. Coronary Angiography, Percutaneous Coronary Intervention
● C. Trans-Septal Left Atrial Catheterization
Cardiology: Anatomy Bootcamp.com
https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg
• Right Atrium:
• Right heart border
• Right Ventricle:
• Anterior and inferior heart border
• Left Atrium:
• Posterior border of heart (also minor component of left ventricle)
• Clinical Correlation: Enlargement leads to cardiovascular dysphagia
• Clinical Correlation: Transesophageal echocardiography
• Left Ventricle:
• Left heart border (also minor component of left atrial appendage)
https://commons.wikimedia.org/wiki/File:X-ray_of_cardiac_silhouettes.jpg
• Right Atrium:
• Right heart border
• Right Ventricle:
• Anterior and inferior heart border
• Left Atrium:
• Posterior border of heart (also minor component of left ventricle)
• Clinical Correlation: Enlargement leads to cardiovascular dysphagia
• Clinical Correlation: Transesophageal echocardiography
• Left Ventricle:
• Left heart border (also minor component of left atrial appendage)
https://commons.wikimedia.org/wiki/File:Cardiac_mri_slice_bionerd.jpg
• Ascending aorta
• Descending aorta
• Pulmonary trunk
• Atria and Ventricles
https://commons.wikimedia.org/wiki/File:SADDLE_PE.JPG
https://commons.wikimedia.org/wiki/File:Surface_projections_of_the_organs_of_the_trunk.png
• Mid-Left Sternal Border 3rd-4th Intercostal Space:

• Right ventricle susceptible to injury
• Left Sternal Border to Mid-Clavicular Line 5th Intercostal Space:
• Medial à Left ventricle and left lung susceptible to injury
• Lateral à Left lung primarily susceptible to injury
https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg
• Sinoatrial Node:
• Contains specialized pacemaker cells
• Location: Right atrium along roof (proximity
to opening of SVC)
• Atrioventricular Node:
• Delayed conduction between atria and
ventricle
• Location: Right atrium along interatrial
septum (proximity to tricuspid valve and
coronary sinus)
• Bundle of His
• Purkinje Fibers
• Atrial Fibrillation Foci:

• Left atrial myocardium
• Pulmonary vein ostia within left atrium
• Atrial Flutter Foci:
• Area between tricuspid valve and IVC
• 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
https://commons.wikimedia.org/wiki/File:PPM.png
• All coronary veins drain into the coronary sinus

• Location: Left posterior atrioventricular groove
• Drains directly into the right atrium
• Embryologic derivative: Sinus venosus
• Clinical Correlation: Biventricular pacemaker lead placement into LV
• Clinical Correlation: Dilated in pulmonary hypertension
https://commons.wikimedia.org/wiki/File:Pulmonary_artery_catheter_english.JPG
https://commons.wikimedia.org/wiki/File:Coronary_Angiography.png
• Swan-Ganz Catheter (Pulmonary Artery Catheter):

• Venous catheter
• Use: Measures right-sided pressures
• Pulmonary capillary wedge pressure: Surrogate marker for left
atrial pressure
• Coronary Angiography, Percutaneous Coronary
Intervention (PCI)
• Arterial catheter
• Use: Visualize atherosclerotic lesions and stenosis of coronary
vessels
• Trans-Septal Left Atrial Catheterization
• Venous catheter
• Use: Direct measurement of left atrial pressure and/or ablation of
pathogenic foci
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:ECG_Atrial_Fibrillation.jpg
A 25-year-old female presents to the emergency room with

dyspnea and palpitations. She states that she believes she may
be having a panic-attack. She reports that she was walking her
dog when suddenly she began to feel lightheaded and short of
breath. She denies any family history of heart disease. Telemetry
monitoring reveals an irregularly irregular heart rate of 134/min.
Blood pressure is 138/54, respiratory rate is 14/min, blood
glucose is 84 mg/dL. Fine tremors are observed in the distal
phalanges. Electrocardiogram is performed and shown. Initial labs
reveal a significantly decreased thyroid-stimulating hormone level.
Which of the following locations is likely a source of aberrant

electrical foci contributing to this patient’s symptoms?
⚪ A. Cavotricuspid isthmus of right atrium

⚪ B. Superior subendocardial right atrium
⚪ C. Membranous portion of interventricular septum
⚪ D. Left posterior atrioventricular groove
⚪ E. Pulmonary vein ostia of left atrium
⚪ F. Pulmonary artery root of right ventricle
OUTLINE
1. Aorta
Cardiology: ●
●
●
A. Vascular Structures and Branches
B. Ligamentum Arteriosum
C. Key Landmarks of the Aorta
Vascular System 2.
3.
●
Subclavian Steal Syndrome
Venous Drainage Obstruction
A. Superior Vena Cava Syndrome
● B. Brachiocephalic Vein Obstruction
● C. Subclavian and/or Axillary Vein Obstruction
4. Coronary Bypass Grafting
● A. Internal Thoracic Artery
● B. Great Saphenous Vein
4. Femoral Access
● A. NAVEL
● B. Femoral Arterial Access
● C. Femoral Venous Access
6. Inferior Vena Cava
● A. Key Landmarks of the Inferior Vena Cava
● B. Inferior Vena Cava Filter
Cardiology: Vascular System Bootcamp.com
https://commons.wikimedia.org/wiki/File:Aorta_branches.svg
• 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
• 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 into common iliac arteries (at navel)
https://commons.wikimedia.org/wiki/File:The_promixal_part_of_left_subclavian_is_blocked_on_left_side_so_no_flow_in_vertebra
l_and_to_left_arm-blood_from_right_vertebral_enters_left_vertebral_and_flows_back_to_supply_left_arm_2013-07-05_17-11.jpg
https://commons.wikimedia.org/wiki/File:Angiogram_of_Left_Subclavian_Steal_Syndrome.PNG
• 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
https://commons.wikimedia.org/wiki/File:2132_Thoracic_Abdominal_Veins.jpg
• 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 Azygos Vein
Right-sided vein
• Brachiocephalic Venous Obstruction Connects SVC and IVC
• Etiology: Pancoast tumor or thrombosis (venous catheter) Alternative pathway for blood to return to right atrium
• 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
https://upload.wikimedia.org/wikipedia/commons/c/c8/2136ab_Lower_Limb_Veins_Anterior_Posterior.jpg
• Internal Thoracic (Mammary) Artery

• Great Saphenous Vein
• Medial foot, medial malleolus, medial leg and thigh
• Joins femoral vein
• NAVEL (lateral to medial)

• Femoral Nerve
• Femoral Artery
• Femora Vein
• Empty
• Lymphatics
• Femoral Arterial Access
• At the site of femoral pulsation below inguinal ligament
• Coronary angiography, PCI
• Clinical Correlate: If access above inguinal ligament à ↑ risk of
retroperitoneal hemorrhage
• Femoral Venous Access
• Medial to the site of femoral pulsation below inguinal ligament
• Swan-Ganz catheter
• Trans-septal left atrial catheterization
https://radiopaedia.org/cases/normal-ct-abdomen?lang=us
https://commons.wikimedia.org/wiki/File:3D_Medical_Animation_Inferior_Vena_Filter.jpg
• Key Landmarks:
• T8: Traverses diaphragm
• L5: Formed by right and left iliac veins
• Inferior Vena Cava Filter
• Indication: Failure or contraindication to anticoagulation in the
setting of a lower extremity deep venous thrombosis
≣ ⟽ ⟾
A 67-year-old left-handed male is brought to the emergency room by paramedics for 9/10 acute onset chest pain
that began during a game a of ping-pong at his senior living facility. The patient states that he has been
noncompliant with his statin medication and has not been consistent in checking his blood pressure at home. He
reports having chest pain over the past week worsened with rapid left arm movement. His medical history is
significant for a myocardial infarction secondary to significant stenosis of the left anterior descending and circumflex
arteries and had previously undergone a coronary artery bypass grafting procedure. Physical exam reveals a cool
left extremity with a 1+ left radial pulse. The right upper extremity is normal in color with a systolic blood pressure
30 mmHg greater than the left. Cardiovascular surgery is emergently consulted, and a percutaneous
revascularization is performed.
Retrograde transport of blood through which of the following arteries most likely contributed to this patient’s
presentation?
⚪ A. Right vertebral artery

⚪ B. Left subclavian artery
⚪ C. Left internal carotid artery
⚪ D. Left axillary artery
⚪ E. Grafted internal thoracic artery
OUTLINE
1. Stroke Volume
Cardiology: ●
●
●
A. End-Diastolic Volume
B. End-Systolic Volume
C. Ejection Fraction
Cardiac 2.
●
●
Stroke Volume Variables
A. Preload
B. Afterload
Parameters of ●
3.
C. Contractility
Heart Rate
4. Frank-Starling Mechanism
Physiologic ●
●
A. Principle and Mechanism
B. Frank-Starling Curve
Function
6. Cardiac Output
● A. Fick-Principle
7. Mean Arterial Pressure
● A. Total Peripheral Resistance
● B. Pulse Pressure
8. Coronary Blood Flow and Autoregulation
Cardiology: Cardiac Parameters of Physiologic Function Bootcamp.com
• End-Diastolic Volume: ~ Preload

• End-Systolic Volume: ~ 1/Contractility
• Stroke Volume (SV) = End-diastolic volume (EDV) – End-systolic volume (ESV)
• Ejection Fraction (EF) = SV / EDV
• Preload:
• ↑ Venous return à ↑ EDV ~ ↑ Preload à ↑ Stroke volume, ↑ Contractility
• Afterload:
• ↑ TPR ~ ↑ Afterload à ↑ ESV à ↓ Stroke volume SV = EDV - ESV
• Preload compensates in healthy hearts
• Afterload has a more dominant effect in heart failure
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• Law of LaPlace: Wall stress = +(,, -.*/01#$$ = +(,, -.*/01#$$
• Contractility
• ↑ SNS activity à ↑ Contractility à ↓ ESV à ↑ Stroke volume
• Physiologic Mechanism: ↓ Vagal tone à SA Node à ↑ HR

• Coronary Perfusion:
• Left ventricular myocardial perfusion occurs primarily during diastole
• Tachycardia: CO = HR x SV
• Elevated heart rate
• ↑ HR à ↓ time of diastole à ↓ ventricular myocardial perfusion, ↓ diastolic filling time à ↓ CO
Maximal HR = 220 bpm – Age (in years)

• Principle:
• ↑ Preload à ↑ Contractility à ↑ SV
• Mechanism:
• ↑ Venous return SV = EDV - ESV
• ↑ 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)
• Cardiac Output = HR x SV
• Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference
• Total Peripheral Resistance (TPR) = Determined by state of arteriolar resistance

• Pulse Pressure (PP) = Systolic pressure – Diastolic pressure
• Mean Arterial Pressure (MAP) = CO x Total peripheral resistance (TPR)
• Mean Arterial Pressure (MAP) = 1/3 systolic pressure + 2/3 diastolic pressure
• Mean Arterial Pressure (MAP) = 1/3 PP + Diastolic Pressure
• Left Ventricular Coronary Blood Flow: ↑ Ventricular diastole

• Oxygen Extraction:
• Significant in myocardial tissues
• Coronary sinus à ↑↑↑ deoxygenation
• ↑ O2 demand à coronary vasodilation (nitric oxide, adenosine)
≣ ⟽ ⟾
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https://commons.wikimedia.org/wiki/File:Pulmonary_oedema.jpg
A 57-year-old male presents to the emergency department for a

dry cough and dyspnea. He states that over the past seven years
he has experienced mild shortness of breath with continued
physical exertion, however, over the past week he has suddenly
become short of breath at rest. He has a past medical history of
poorly controlled hypertension and hyperlipidemia. The patient
also admits to a 30-year smoking history. He is afebrile, blood
pressure is 102/64, heart rate is 102/min, oxygen saturation is
92% on room air. Auscultation of the heart reveals an S3 heart
sound and a faint systolic decrescendo murmur in the axillary
region. Lung auscultation is significant for diffuse crackles. There
is dullness to percussion over the lung fields. Chest radiography
is shown.
Which of the following is most consistent with this patient’s

presentation?
⚪ A. Elevated systolic aortic pressures

⚪ B. Elevated pulmonary capillary wedge pressure
⚪ C. Depressed left atrial pressure
⚪ D. Depressed pulmonary venous pressure
⚪ E. Unchanged left ventricular diastolic volume
OUTLINE
1. Cardiac Function Curves
Cardiology: 2. Venous Return Curves

3. Combined Cardiac Function and Venous Return Curves
● A. Steady State
Cardiac Function ● B. Specific Pathologic Processes
and Venous
Return Curve
Physiology
Cardiology: Cardiac Function and Venous Return Curve Physiology Bootcamp.com
• Cardiac Function Curve:

• X-axis: Right atrial pressure (independent variable)
• Y-axis: Cardiac output (dependent variable)
• Slope of curve: Defined by contractility, afterload, and heart rate
• Venous Return Curve:

• X-axis: Right atrial pressure (dependent variable)
• Y-axis: Cardiac output (independent variable)
• Slope of curve: Defined by total peripheral resistance
• X and Y intercept: Defined by venous compliance and total blood volume
• Intersection:
• Steady state operating target for right atrial pressure and cardiac output
• Variables:
• Slope of Cardiac Function Curve à Contractility, Heart rate, Afterload
• Slope of Venous Return Curveà TPR
• X-intercept of Venous Return Curve (Pm) à Total blood volume, Venous compliance
• Acute Hemorrhage: Disruption: ↓ blood volume

• Cardiac Function Curve: No change
• Venous Return Curve: X-intercept shifts left
• Steady State: Shifted downward and to the left
• Intravenous Fluids: Disruption: ↑ blood volume
• Cardiac Function Curve: No change
• Venous Return Curve: X-intercept shifts right
• Steady State: Shifted upward and to the right
• Chronic Systolic Heart Failure: Disruption: ↓ contractility, Chronic à Compensation
• Cardiac Function Curve: ↓ slope
• Venous Return Curve: Slope decreases, X-intercept shifts right
• Steady State: Shifted downward and to the right
• Digoxin: Disruption: ↑ contractility
• Cardiac Function Curve: ↑ slope
• Venous Return Curve: Slope unchanged, X-intercept unchanged
• Steady State: Shifted upward and to the left
• Phenylephrine: Disruption: ↑ TPR (!1-agonist)
• Cardiac Function Curve: ↓ slope
• Venous Return Curve: ↓ slope , X-intercept unchanged (usually)
• Steady State: Shifted downward
• Hydralazine: Disruption: ↓ TPR
• Cardiac Function Curve: ↑ slope
• Venous Return Curve: ↑ slope , X-intercept unchanged (usually)
• Steady State: Shifted upward
Slope of Cardiac Function Curve à Contractility, Heart rate, Afterload

Slope of Venous Return Curveà TPR
X-intercept of Venous Return Curve (Pm) à Total blood volume, Venous compliance
≣ ⟽ ⟾
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A 67-year-old male with a chronic smoking history presents to the emergency

department by paramedics with hypotension refractory to intravenous fluids
following an episode of syncope at home. His daughter reports he suddenly loss
consciousness while watching television. Vitals are significant for a blood pressure
of 88/28 mmHg, heart rate of 124/min, and respiratory rate of 18/min. Imaging
reveals findings consistent with an aortocaval fistula. Surgery is emergently
performed.
Which of the following new steady states are most representative of the acute
pathophysiology observed in this patient prior to surgical intervention?
⚪ A. A.
Cardiac Output
Venous Return
⚪ B.
B.
⚪ C.
⚪ D. E. (E.) Prior to aortocaval fistula
⚪ E.
C. D.
Right Atrial Pressure
OUTLINE
1. Basic Principles
Cardiology: ●
●
A. Key Principles
B. Phases
2. Determinants
Pressure Volume ●
●
●
A. Preload
B. Contractility
C. Afterload
Loops 3. Valvular Disease

●
●
A. Aortic Regurgitation
B. Aortic Stenosis
● C. Mitral Regurgitation
● D. Mitral Stenosis
4. Advanced Pathophysiology
● A. Exercise
● B. Arteriovenous Fistula
● C. Systolic Heart Failure
● D. Diastolic Heart Failure
Cardiology: Pressure Volume Loops Bootcamp.com
• Key Principles:
• All valves are closed during isovolumetric phases (vertical lines)
• Width of the pressure volume loop ~ Stroke Volume
• Area of pressure volume loop ~ Ventricular Stroke Work
• Ventricular compliance makes up the base of the loop
• Phases:
• Isovolumetric contraction
• Left ventricular ejection
• Isovolumetric relaxation
• Ventricular filling
https://commons.wikimedia.org/wiki/File:Cardiac_cycle_(pressure_volume_loop).svg
• Preload:
• ↑ à EDV shifts right
• ↓ à EDV shifts left
• Contractility:
• ↑ à ESV shifts left
• ↓ à ESV shifts right
• Afterload:
• ↑ à ESV shifts right
• ↑ à ↑ LVP isovolumetric contraction
• ↓ à ESV shifts left
• ↓ à ↓ LVP isovolumetric contraction
• Hemorrhagic Shock:
• ↓ Total blood volumeà ↓ Preload
• Intravenous Fluids:
• ↑ Total blood volumeà ↑ Preload
• Nitroglycerin:
• Venodilator (primary)à ↓ Preload
• Vasodilator (secondary)à ↓ Afterload
• Sodium Nitroprusside:
• Vasodilator (primary)à ↓ Afterload, ↓ TPR (↓ DBP)
• Venodilator (primary) à ↓ Preload
https://en.wikipedia.org/wiki/Press
ure%E2%80%93volume_loop_ana
lysis_in_cardiology#/media/File:En
d_Systolic_Pressure_Volume_Rel
ationship.jpg
• Digoxin, Dobutamine:
• Inotropic agentà ↑ Contractility
• Slight increases in ventricular afterload are possible
• Phenylephrine:
• !1-agonist à ↑ Afterload, ↑ TPR (↑ DBP)
• Hydralazine:
• Vasodilatorà ↓ Afterload, ↓ TPR (↓ DBP)
• Aortic Regurgitation:
• Retrograde flow of oxygenated blood into LV à ↑ Preload
• Loss of isovolumetric phases
• Aortic Stenosis:
• Stenosis distal to left ventricle à ↑ Afterload
• Chronic: ↓ Ventricular compliance (Diastolic heart failure)
• Mitral Regurgitation:
• Retrograde flow of oxygenated blood into LA à ↑ Preload
• Loss of isovolumetric phases
• Mitral Stenosis:
• Stenosis proximal to left ventricle à ↓ Preload
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/
File:Mitral_stenosis.jpg
File:Mitral_regurgitation.jpg
File:Aortic_regurgitation.jpg
File:Aortic_stenosis.jpg
• Exercise:
• Venoconstriction, muscle and respiratory pumps à ↑ Preload
• Sympathetic stimulation to heart à ↑ Contractility
• Muscle vasodilation < ventricular afterload à ↑ Afterload (↓ DBP)
• Arteriovenous Fistula:
• Low resistance fistulaà ↓ Afterload
• High flow of blood through fistula à ↑ Venous return, ↑ Preload
• If fistula is large à hypotension à ↑ Contractility, heart rate à High-output cardiac failure
• Systolic Heart Failure
• Principal determinant: ↓ Contractility
• Chronic à ↓↓↓ Contractility, ↑ Preload, ↓ Afterload
• Diastolic Heart Failure
• Principal determinant: ↓ Ventricular compliance
• Chronic: ↓ Preload, variable changes in contractility and afterload
• Key point: Decrease in stroke volume and compliance
≣ ⟽ ⟾
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_diagram
A 57-year-old male with presents to an urgent care clinic with a numbness of his
right foot and shortness of breath. He states that he had three fall episodes over the
past month because “he can’t feel the floor”. He denies any dizziness and reports
that he has not been seen by a physician in over twenty years. Physical
examination reveals a left internuclear ophthalmoplegia. The pupils accommodate
but are not reactive to direct or indirect light stimulation. Locally destructive
ulcerative lesions are present diffusely throughout the face and upper back.
Cardiovascular examination demonstrates a high-pitched diastolic murmur most
prominent at the left fourth intercostal space along the left sternal border. Pulses are
notable for a rapid upstroke and downstroke. Reflexes are 1+ at L4 and C5
bilaterally. Sensory ataxia is also present.
A biopsy of the skin lesions is taken revealing a monocytic infiltrate. The patient is
referred for a lumbar puncture. Which of the following best demonstrates the time
along the left ventricular pressure-volume loop that this patient’s heart murmur will
be most prominent?
⚪ A. Distance between A to B
⚪ B. Distance between B to C
⚪ C. Distance between C to D
⚪ D. Distance between D to A
⚪ E. Point D
OUTLINE
1. Endothelial Regulated Vasodilation
Cardiology: ● A. Mechanism of Action

2. Excitation-Contraction Coupling
● A. Cardiac Myocyte
Vasodilation and ●
●
B. Vascular Smooth Muscle
C. Skeletal Muscle
3. G-Protein Coupled Receptor Vasoconstriction Pathway
Vasoconstriction ● A. Gq Pathway
4. Pharmacologic Targets
● A. !1 agonists
● B. Nonhydropyridine Calcium Channel Blockers
● C. Dihydropyridine Calcium Channel Blockers
● D. Phosphodiesterase-3 Inhibitors
● E. Additional Vasodilatory Drugs
Cardiology: Vasodilation and Vasoconstriction Bootcamp.com
• Endothelial Cell:
• Acetylcholine, bradykinin, and shear stress forces à ↑ cytosolic [Ca2+]
• Nitric oxide Synthase stimulated by ↑ [Ca2+]
• L-Arginine + O2 à Nitric oxide + Citrulline
• Nitric oxide diffuses freely among cells
• Vascular Smooth Muscle:
• Nitric oxide causes increased conversion of GTP à cGMP
• cGMP à activation of PKG à ↓ cytosolic [Ca2+]
• Relaxation of vascular smooth muscle
https://upload.wikimedia.org/wikipedia/commons/1/10/Cardiac_calcium_cycling_and_excitation-contraction_coupling.png
• Cardiac Myocytes
• Depolarization of cell membrane by action potential
• L-type calcium channel: influx of calcium ions from extracellular
• Calcium-induced calcium release: incoming calcium ions bind to
ryanodine receptor
• Ryanodine receptor: influx of calcium ions from SR
• Calcium ions bind to troponin-C
• Conformational change allows actin to interact with myosin head
• SERCA: Sequesters intracellular calcium into SR via ATP à
relaxation
• Smooth Muscle:
• Depolarization of cell membrane by action potential
• L-type calcium channel: influx of calcium ions from extracellular
• Calcium induced calcium release
• Calcium ions bind to calmodulin
• Conformation change in myosin light chain kinase (MLCK)
• Phosphorylates myosin light chain (MLC) à contraction
• Myosin light chain phosphatase dephosphorylates MLC à
relaxation
• Skeletal Muscle (Major Differences from Cardiac Myocytes):

• Pathway stimulated by acetylcholine (not automaticity)
• Mechanical coupling of LTCC with RyR
• Gq-GPCR Mechanism:
• Present on arterioles (↑ afterload) and veins (↑ preload)
• Gq protein à ↑ Phospholipase C (PLC)
• PIP2 à ↑ inositol triphosphate (IP3) + Diacylglycerol (DAG)
• IP3 à ↑ cytosolic [Ca2+] (from ER)
• DAG à Protein Kinase C (PKC) à ↑ cytosolic [Ca2+] (from extracellular space)
https://upload.wikimedia.org/wikipedia/commons/1/10/Cardiac_calcium_cycling_and_excitation-contraction_coupling.png
• !1-agonists
• Activation of Gq-GPCR pathway
• Primary effect: Vasoconstriction
• Drugs: Phenylephrine (selective), norepinephrine (nonselective)
• Nondihydropyridine Calcium Channel Blockers:
• Inhibition of L-type calcium channels
• Greater effect on calcium-induced calcium release
• Primary effect: ↓ Contractility, bradycardia, AV block
• Drugs: Verapamil, diltiazem
• Dihydropyridine Calcium Channel Blockers:
• Inhibition of L-type calcium channels
• Greater effect on calcium-induced calcium release
• Primary effect: Vasodilation
• Drugs: Nifedipine, nicardipine, felodipine, amlodipine (arterial > venous)
• Phosphodiesterase-3 (PDE-3) Inhibitor:
• PDE-3 à Inhibition of cAMP degradation (myocytes) and ↑ SR calcium uptake (vascular)
• Primary effect: ↑ Contractility, vasodilation
• Drugs: Milrinone, Cilostazol, Dipyridamole
• Additional Vasodilatory Drugs:
• Nitric oxide (venous > arterial)
• Hydralazine, minoxidil (arterial > venous)
• Nitroprusside (arterial = venous)
• Sildenafil (PDE-5 inhibitor) à (pulmonary and corpus cavernosum)
≣ ⟽ ⟾
A 77-year-old male is brought to the emergency department from his living facility
with lethargy. Vital signs reveal a blood pressure of 58/20 mmHg, heart rate 122
beats/min, respiratory rate 20 breaths/min, oxygen saturation 91% on room air, and
a temperature of 103.3F (39.6C). Initial labs reveal a lactate of 9.0 and white blood
cell count of 18,000/mm3. He is aggressively fluid resuscitated and started on slow
intravenous phenylephrine injection for blood pressure support. Which of the
following cellular changes are most likely to occur due to the direct effects of the
medication given?
⚪ A. Increased inhibition of adenylyl cyclase

⚪ B. Decreased intracellular concentrations of L-arginine
⚪ C. Decreased cyclic AMP degradation
⚪ D. Increased myosin light chain phosphatase activity
⚪ E. Decreased degradation of adenosine
⚪ F. Increased intracellular concentrations of inositol triphosphate
OUTLINE
1. Vessel Compliance
Cardiology: ● A. Key Principles

2. Blood Flow
● A. Poiseuille Equation
Pressure and ● B. Resistance

3. Sensory Receptors of the Vasculature
● A. Carotid Sinus and Aortic Arch Baroceptors
Flow Physiology ●
●
●
B. Carotid Sinus Massage
C. Carotid Sinus Hypersensitivity
D. Carotid and Aortic Body Chemoreceptors
Cardiology: Pressure and Flow Physiology Bootcamp.com
• Vessel Compliance:
• Compliance = ∆Volume / ∆Pressure
• Elastance = ∆Pressure / ∆Volume
• ↑ Compliance à Veins
• ↓ Compliance à Arterioles
• Poiseuille Equation:
!" #!$ 4
• Flow (Q) = rπ
8%&
• Q = Flow
• P = Pressure at point in blood vessel
• ! = viscosity of blood within blood vessel
• l = length of blood vessel
• r = radius of blood vessel
• Capillaries have greatest total cross-sectional area à lowest blood velocity
• Resistance:
%&
• R∝ !
'
• R = Resistance
• Arterioles are the primary regulator of total peripheral resistance
• Series: Total Resistance = RT = R1 + R2 + …Rn
• Parallel: Total Resistance = 1/%T = 1/%1 + 1/%2 + … 1/%n
• Carotid Sinus and Aortic Arch Baroceptors:

• ↑ stretch (↑ BP) à ↑ afferent ↑ efferent PNS firing à ↑ parasympathetic response à vasodilation, ↓ HR, ↓ contractility
• ↓ stretch (↓ BP) à ↓ afferent ↓ efferent PNS firing à ↓ parasympathetic response à vasoconstriction, ↑ HR, ↑ contractility
• Carotid Sinus Massage:
• ↑ afferent ↑ efferent PNS firing à ↑ parasympathetic response à vasodilation, ↓ HR, ↓ contractility
• Stable narrow complex tachycardia à Vagal maneuver
• Carotid Sinus Hypersensitivity:
• Develops severe hypotension and/or bradycardia after carotid sinus stimulation
• “Tight shirt collar”
• Presyncopal/syncopal event
• Carotid and Aortic Body Chemoreceptors:
• Effective at responding to chronic hypoxia (as opposed to central chemoreceptors)
• ↓ O2 (↑ CO2, ↓ pH) à ↑ sympathetic response à ↑ respiratory rate
≣ ⟽ ⟾
◽" Mark Difficulty: ✪ Bootcamp.com
A 78-year-old female with a past medical history of dyslipidemia, hypertension, and type 2 diabetes mellitus is evaluated at an acute
rehabilitation facility for dizziness during therapy. She denies any shortness of breath, vision changes, or chest pain. The patient has a
history of C3-C5 laminectomy for severe spinal stenosis. Vital signs are shown below. Auscultation of the heart reveals a regular rate
and rhythm with no murmurs or abnormal heart sounds. The lungs are clear to auscultation. Which of the following undiagnosed
conditions best describes a possible cause of this patient’s presentation?
Temperature: 97.8F (36.6C)
Blood pressure when lying supine: 144/88 mmHg

Heart rate when lying supine: 102/min
Respiratory rate when lying supine: 12/min
Blood pressure when standing: 110/56

Heart rate when standing: 112/min
Respiratory rate when standing: 14/min
⚪ A. Carotid sinus hypersensitivity

⚪ B. Autonomic neuropathy
⚪ C. Neurogenic shock
⚪ D. Constrictive pericarditis
⚪ E. Hypertrophic cardiomyopathy
OUTLINE
1. Auscultation 5. Classic Disorders
Cardiology: ●
●
●
A. Aortic Area
B. Pulmonic Area
C. Mitral Area
●
●
●
A. Aortic Stenosis
B. Aortic Regurgitation
C. Mitral Stenosis
Cardiac Cycle ●
●
D. Tricuspid Area
E. Erb’s Point
●
●
D. Mitral Regurgitation
E. Constrictive Pericarditis
2. Heart Sounds ● F. Cardiac Tamponade
● A. S1 ● G. Atrial Fibrillation
● B. S2 ● H. AV-dissociation
● C. Physiologic Splitting of S2
● D. Pathologic Splitting of S2
● E. S3
● F. S4
3. Cardiac Cycle
● A. Isovolumetric Contraction
● B. Ejection
● C. Isovolumetric Relaxation
● D. Ventricular Filling
● E. Atrial Systole
4. Jugular Venous Waveform
● A. A-wave
● B. C-wave
● C. X-descent
● D. V-wave
● E. Y-descent
Cardiology: Cardiac Cycle Bootcamp.com
https://en.wikipedia.org/wiki/Heart_sounds#/media/File:Gray1216_modern_locations.svg
• Aortic Area:
• 2nd R parasternal ICS
• Pulmonic Area:
• 2nd L parasternal ICS
• Tricuspid Area:
• 4th L parasternal ICS
• Mitral Area:
• 5th L mid-clavicular line ICS
• Erb’s Point
• 3rd L parasternal ICS
• S1:
• Produced by: Closure of tricuspid and mitral valves
• Best heard: Cardiac apex
Accentuation: Left lateral decubitus position in expiration
• S2:
• Produced by: Closure of the pulmonary (P2) and aortic valve (A2)
• Best heard: P2 à 2nd L parasternal ICS A2 à 2nd R parasternal ICS
• Physiologic S2 Splitting:
• Narrowing à Expiration
• Widening à Inspiration
• Pathologic S2 Splitting:
• Wide Fixed à Atrial septal defect
• Wide à Pulmonary stenosis, Right bundle branch block
• Paradoxical à Severe aortic stenosis, Left bundle branch block
• S3:
• Produced by: Rapid passive ventricular filling (↑ left ventricular volumes)
• Best heard: Cardiac apex (bell)
• Timing: Early diastole, after S2 (gallop)
• Physiologic: Young and fit, pregnancy
• Pathologic: Heart failure (systolic), mitral regurgitation, aortic regurgitation
• S4:
• Produced by: Atrial kick (↑ left ventricular pressures)
• Best heard: Cardiac apex (bell)
• Timing: Late diastole, before S1
• Physiologic: Elderly
• Pathologic: Heart failure (diastolic), chronic hypertension, aortic stenosis
https://commons.wikimedia.org/wiki/File:Wiggers_Diagram.svg
• Isovolumetric Contraction:
• Begins after closing of mitral valve (S1)
• Highest oxygen consumption
• QRS complex on ECG à ventricular depolarization
• Ejection:
• Begins after opening of the aortic valve
• Rapid Ejection: Rising LVP, ↓↓ LV volume
• Reduced Ejection: Decreasing LVP
https://commons.wikimedia.org/wiki/File:Wiggers_Diagram.svg
• Isovolumetric Relaxation:
• Begins after closing of aortic valve (S2)
• Dicrotic notch
• Coronary blood flow peaks
• Ventricular Filling:
• Begins after opening of the mitral valve
• Rapid Fillin
• S3: Rapid filling into volume overload LV
• Reduced Filling
• Atrial Systole:
• At conclusion of diastole
• S4: Atrial kick into “stiff” ventricle
https://commons.wikimedia.org/wiki/File:Wiggers_diagram_with_jugular_venous_waveform.png
• A-wave:
• Atrial systole (P wave)
• C-wave:
• Ventricular contraction
• Tricuspid valve protrudes into atrium
• X-descent:
• Atrial relaxation
• V-wave:
• Atrial filling à tricuspid valve “back-pressure”
• Y-descent:
• Ventricular filling
• Classic Disorders:
• Atrial fibrillation: Absent A-waves (absent P-waves on ECG)
• Tricuspid (or Mitral) regurgitation: ↑ V-wave > A-wave
• Tamponade: Blunting of Y-descent
• Constrictive pericarditis: Increased Y-descent
• Atrial contraction against closed tricuspid: “Cannon” A-waves
https://commons.wikimedia.org/wiki/File:Wiggers_diagram_with_jugular_venous_waveform.png
• Aortic Stenosis:
• LVP >> Aortic pressure
• Aortic Regurgitation:
• ↑ Aortic pressure during systole
• ↓ Aortic pressure at the end of diastole
• ↑ Pulse pressure (SBP - DBP)
• Loss of dicrotic notch
• Mitral Stenosis:
• LAP > LVP during diastole
• Mitral Regurgitation:
• Tall V-wave (similar to tricuspid regurgitation)
≣ ⟽ ⟾
https://upload.wikimedia.org/wikipedia/commons/7/75/Pulmonary_oedema.jpg
A 56-year-old male with a past medical history of alcohol use and withdrawal seizures is brought to the emergency
department from a homeless shelter with acute onset confusion, ataxia, and agitation. He is unable to recall the time of his
last drink. Blood pressure is 168/68, heart rate is 126/min, respiratory rate is 16/min. On physical examination he appears to
have diffuse muscular atrophy and peripheral edema in the distal lower extremities. The patient also appears tremulous and
has visible nystagmus on testing of the extraocular muscles. An electrocardiogram is performed showing sinus tachycardia
with no evidence of ST-segment elevation or depression. Chest radiography is shown below.
Which of the following additional examination findings would be most expected in this patient?
⚪ A. Wide-fixed splitting of S1 heart sounds

⚪ B. Wide-fixed splitting of S2 heart sounds
⚪ C. Prominent S3 heart sound
⚪ D. Prominent S4 heart sound
⚪ E. Paradoxical splitting of S2 heart sounds
OUTLINE
1. Regulation
Cardiology: ●
●
●
A. Renin
B. Angiotensin Converting Enzyme
C. Angiotensin II
Renin- ● D. Natriuretic Peptides

2. Direct Pharmacologic Targets
● A. Angiotensin Converting Enzyme Inhibitors
Angiotensin- ●
●
B. Angiotensin Receptor Blockers
C. Direct Renin Inhibitors
Aldosterone
● D. Neprilysin Inhibitors
● E. β1-antagonism
System
Cardiology: RAAS Bootcamp.com
https://en.wikipedia.org/wiki/Juxtaglomerular_apparatus#/media/File:Renal_corpuscle-en.svg
• Renin
• Location: Juxtaglomerular apparatus
• Stimulus: ↑↑ Renin: β1 stimulation, ↓ pressure in renal artery, ↓ Na to distal tubules (kidney)
• Function: Converts Angiotensinogen to Angiotensin I
• Angiotensin Converting Enzyme (ACE)
• Location: Lungs (primarily)
• Function: Angiotensin I converted to Angiotensin II (ATII) by ACE
https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg
• Actions Angiotensin II:

• ↑ Vasoconstriction (↑ TPR)
• ↑ Norepinephrine release and availability
• ↑ Na reabsorption, ↑ blood volume
• Stimulates aldosterone release from zona glomerulosa
• Stimulates vasopressin (ADH) release from posterior pituitary
• Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP)

• Location: Myocardium
• Stimulus: ↑ Atrial and ventricular pressures
• Function: ↑ Vasodilation, ↑ Diuresis, inhibition of aldosterone and renin release
• Attempts to compensate (temporarily) for ATII in heart failure
• Molecular Mechanism:
• ↑ cGMP à stimulates vasodilation and diuresis
• ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril)

• Inhibition of ACE à ↑ angiotensin I and renin, ↓ angiotensin II
• Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure)
• Adverse Effect: Dry cough, hyperkalemia, angioedema
• Angiotensin Receptor Blockers (ARBs) (Valsartan, Losartan, -sartan)
• Receptor blockade of angiotensin II type 1 receptor
• Direct Renin Inhibitors (Aliskiren)
• Inhibition of conversion of angiotensinogen to angiotensin I
• Use: Hypertension (not first line)
• Neprilysin Inhibitors (Sacubitril)
• Neprilysin inactivates ANP, BNP and AT-II
• Use: Heart failure when combined with angiotensin-II receptor inhibitor
• Selective β1-blockers (Metoprolol, Nebivolol, Esmolol, Atenolol)
• Antagonism of β1 receptors at juxtaglomerular apparatus
• Use: Coronary artery disease, cardiac arrhythmias (and many more)
• Adverse Effect: Bradycardia, bradyarrhythmia (AV nodal block)
≣ ⟽ ⟾
A 68-year-old female with a past medical history of

osteoarthritis and hyperthyroidism presents to the emergency
department with shortness of breath. She states that she has
been having palpitations for the past two hours. She reports
running out of her thyroid medication five weeks prior and
has not yet refilled her prescription. She is later diagnosed
with new onset atrial fibrillation with rapid ventricular
response. She is initiated on metoprolol for rate control.
Which of the following primary changes in chemical

mediators will likely occur due to the initiation of this
medication?
Renin Angiotensin I Angiotensin II Aldosterone
⚪ A. ↑ ↑ ↑ ↑
⚪ B. ↑ ↑ ↑ ↓
⚪ C. ↑ ↑ ↓ ↓
⚪ D. ↑ ↓ ↓ ↓
⚪ E. ↓ ↓ ↓ ↓
OUTLINE
1.
Cardiology: ●
●
●
A.
B.
C.
Exercise ●
●
●
D.
Physiology ●
●
●
2.
● A.
● B.
.
● A.
● B.
Cardiology: Exercise Physiology Bootcamp.com
• ↑ Preload
• Venoconstriction à ↑ Venous return à ↑ LVEDV
• Vasoconstriction of splanchnic vessels
• Vasodilation at skeletal muscle à ↓ SVR (↓ DBP) à ↓ Afterload
• ↑ Contractility
• ↓ Afterload
• Can be variable depending on dynamic vs static, muscle groups recruited, intensity, ect.
• ↑ Heart Rate
• ↑ Sympathetic tone (↓ Vagal tone)
• ↓ Coronary Perfusion
• ↓ Time spent in diastole at high heart rates
• ↑ Minute Ventilation
• ↑ O2 demand à ↑ RR, ↑TV à ↑ O2 consumption and CO2 production
• ↑ Temperature
• ↓ Arterial pH
• ↑ Lactic acidosis
Cardiology: Exercise Physiology Bootcamp.com
• Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference

• VO2 = Rate of oxygen consumption
• Oxygen Extraction Efficiency:
• PaO2 relatively normal
• PaCO2 relatively normal
• Venous O2 decreased
• Venous CO2 increased
Cardiology: Exercise Bootcamp.com
• General Rules:
• Max HR = 220 - Age
• Early exercise à HR and SV responsible for ↑ CO
• Intense exercise à HR primarily responsible for ↑ CO
• Athletic Cardiovascular Physiology:
• Max HR not affected by athletic ability
• Stroke volume primarily responsible for ↑↑ CO
• ↑ VO2 maximum
• ↑ RBC mass and plasma volume à ↑ O2 carrying capacity
• ↑ Efficiency of skeletal muscle oxygen extraction
• ↑ Vascularization of skeletal muscle
• ↓ resting heart rate
≣ ⟽ ⟾
A 26-year-old female professional cyclist is training for a 143-

km bicycle-road race. She is seen by her primary care
physician one week prior to the event for a check-up. Vital
signs are shown below. Her physical examination is
unremarkable.
Hemoglobin O2 Saturation (%)

Blood pressure: 110/62 mmHg
Heart rate: 52/min
Respiratory rate: 10/min
Oxygen saturation: 100% on room air
Which of the following is most consistent with the

hemoglobin-oxygen dissociation curve of the patient during
the upcoming cycling event, assuming the blue curve (A.) is
consistent with her baseline at rest?
⚪A
⚪ B.
⚪ C.
⚪ D.
⚪ E.
Arterial Partial Pressure of O2 (mmHg)
OUTLINE
1.
Cardiology: ●
●
●
A.
B.
C.
Cardiac ●
●
D.
E.
Conductive
2.
● A.
● B.
Physiology 3.
● A.
● B.
●
.
● A.
● B.
●
●
Cardiology: Cardiac Conductive Physiology Bootcamp.com
https://en.wikipedia.org/wiki/Purkinje_fibers#/media/File:ConductionsystemoftheheartwithouttheHeart-en.svg
Cardiac Conduction Velocity

Purkinje > Atrial myocytes > Ventricular myocytes > AV node
• Sinoatrial (SA) Node
• Site of electrical impulse generation
• Pacer rate of 60-100 per minute
• Supplied by RCA
• Atrioventricular (AV) Node
• Delays conduction from SA node
• Pacer rate of 45-55 per minute
• Supplied by PDA (usually RCA)
• Bundle of His
• Prevents retrograde electrical conduction
• Right Bundle à Right ventricle
• Left Bundle à Left ventricle (anterior and posterior)
• Purkinje Fibers
• Transmits conduction across ventricles
https://commons.wikimedia.org/wiki/File:2020_SA_Node_Tracing.jpg
• Pacemaker Cells
• Exhibit automaticity (spontaneous depolarization)
• Absence of Phase 1 and 2
• Phase 4 is a slow depolarization phase
• Phase 4: Pacemaker Potential

• Begins with: ↑ Permeability of inward Na+ (If) current à Slow, spontaneous depolarization
• Then: ↑ Permeability T-type and L-type Ca2+ current à Further depolarization
• Phase 0: Action Potential Depolarization
• Begins when threshold is reached
• Na+ current and T-type calcium current decreases
• Increased L-type Ca2+ current à Action potential depolarization
• Phase 3: Action Potential Repolarization
• Outward K+ current à Hyperpolarization
• Inward L-type Ca2+ current decreases (inactivation)
https://en.wikipedia.org/wiki/Ventricular_action_potential#/media/File:Action_potential_ventr_myocyte.gif
• Non-Pacemaker Cells
• Do not exhibit automaticity
• Phases 0-4 are present
• Phase 4 is a resting potential phase (approximates equilibrium potential of potassium)
• Phase 4: Resting Membrane Potential

• ↑ Permeability of outward K+ current
• Fast Na+ channels and L-type Ca2+ channels are closed
• Phase 0: Action Potential Depolarization
• Begins with depolarization from action potential at adjacent cell
• ↑ Permeability of inward fast Na+ current
• ↓ Permeability of outward K+ current
• Phase 1: Early Repolarization
• Transient ↑ permeability of outward K+ current
• Rapid closure of fast Na+ channels (inactivation)
• Phase 2: Plateau Phase
• L-type Ca2+ channels are open and balance K+ efflux
• Phase 3: Late Repolarization
• Various K+ channels open à ↑↑ permeability outward K+ current
• Inactivation of L-type Ca2+ channels
https://en.wikipedia.org/wiki/Long_QT_syndrome#/media/File:Long_QT_syndrome_type_1.jpg
https://www.wikidata.org/wiki/Q1625433#/media/File:Tosadesdepointes.jpg
• Sympathetic Stimulation Effects on Pacemaker Potentials

• β1 stimulation à ↑ cAMP à ↑ permeability of inward calcium current à ↑ HR
• Parasympathetic Stimulation Effects on Pacemaker Potentials
• M2 stimulation à ↓ cAMP à ↓ permeability of inward calcium current à ↓ HR
• Sodium Channelopathy:
• Impairment of inward fast Na+ current (Phase 0)
• Brugada Syndrome: AD, ECG: ST-elevation in V1-V3, pseudo-RBBB
• QT Interval Prolongation
• Delayed ventricular repolarization
• Impairment of voltage-gated potassium channels à delayed rectifier potassium current
• May lead to torsade de pointes (“twisting of the peaks”), ventricular tachycardia à sudden cardiac death
• Romano-Ward Syndrome: AD, no associated sensorineural hearing loss
• Jervell and Lange-Nielsen Syndrome: AR, associated congenital bilateral sensorineural hearing loss
• Drug Induced: *see table below*
Class Classic Drug Other Drugs/Effects
A Antiarrhythmics Quinidine Disopyramide, procainamide, sotalol, dofetilide

B Antibiotics Macrolides Fluoroquinolones
C Antipsychotics Haloperidol Ziprasidone
D Antidepressants Tricyclic Methadone
antidepressants
E Antiemetics/Electrolytes Ondansetron Hypocalcemia, hypokalemia, hypomagnesemia
F Antifungals Azoles
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:De-Acquired_longQT_(CardioNetworks_ECGpedia).jpg
A 14-year-old male with a past medical history of mild intermittent asthma presents to the
emergency department with a productive cough and mild shortness of breath that started
before going to school this morning. His mother reports that he has been nauseous this
morning and hasn’t eaten his breakfast. She also states that he has a family history of “bad
luck with the heart” on his father’s side. His father is deceased from unknown cause of sudden
cardiac death at age 38. The patient is up to date with vaccinations. Vitals are stable and he is
saturating 99% on room air. Mild end-expiratory wheezing is auscultated. Laboratory workup is
unrevealing. The patient is given a single dose of azithromycin and ondansetron. He is
monitored in the emergency room. The patient’s respiratory symptoms improve, and he is
prescribed a short-acting inhaled beta-agonist on discharge. Four hours later, the patient
returns to the emergency room with his mother for acute worsening of shortness of breath.
Electrocardiogram findings from lead II are shown below.
Which of the following most likely explains the cause of this patient’s return to the emergency
department?
⚪ A. Decreased inward calcium current in pacemaker cells

⚪ B. Decreased inward calcium current in cardiomyocytes
⚪ C. Decreased inward sodium current in cardiomyocytes
⚪ D. Decreased outward potassium current in cardiomyocytes
⚪ E. Increased outward potassium current in pacemaker cells
OUTLINE
1.
Cardiology: ●
●
●
A.
B.
C.
Antiarrhythmics ●
2.
D.
● A.
● B.
●
●
.
● A.
●
●
●
.
● A.
●
●
Cardiology: Antiarrhythmics Bootcamp.com
https://en.wikipedia.org/wiki/Antiarrhythmic_agent#/media/File:Cardiac_action_potential.png
Overview
• Class I
• Three subclasses: Class IA, IB, IC
• Blockade of fast Na+ channels
• Class II
• β-blockers
• Delayed atrial ➔ ventricular depolarization
• Class III
• Blockade of potassium channels
• Class IV
• Calcium channel blockers
• Delayed atrial ➔ ventricular depolarization
Cardiology: Antiarrhythmics https://commons.wikimedia.org/wiki/File:Action_potential_class_Ic.svg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Action_potential_class_Ia.svg https://commons.wikimedia.org/wiki/File:Action_potential_Class_Ib.svg
• Class IA
• Quinidine, Procainamide, Disopyramide
• Mechanism: Moderate blockade of fast Na+ channels (Non-pacemaker)
• ↑ Action potential duration, ↓ Diastole
• Widening of QRS, QT prolongation
• Quinidine à Cinchonism
• Drug-Induced Lupus à Procainamide
• Class IB
• Lidocaine, Mexiletine, Phenytoin
• Mechanism: Weak blockade of fast Na+ channels (Non-pacemaker)
• ↓ Action potential duration, ↑ Diastole
• QRS prolongation, shortened QT interval
• ↑↑ Efficacy on ischemic Purkinje and ventricular myocardial cells
• Class IC
• Flecainide, Propafenone
• Mechanism: Strong blockade of fast Na+ channels
•
•
• QRS prolongation, no significant change in QT (Exceptions exist)
• Flecainide à ↑ Action potential duration
• Contraindicated in ischemic heart disease (Proarrhythmic)
•
•
•
• Class II
• Metoprolol, Esmolol, Propranolol, Atenolol, Carvedilol
• Mechanism: Inhibition of cAMP à ↓ intracellular Ca2+
• Prolonged Phase 4 (Pacemaker)
• PR prolongation
• Class III
• Sotalol, Ibutilide, Dofetilide
• Mechanism: Inhibition of K+ channels (delayed rectifier potassium current)
• ↑ Action potential duration
• QT prolongation à torsades de pointes
• Sotalol prolongs PR interval; Ibutilide and Dofetilide do not
• Class IV
• Verapamil, Diltiazem
• Mechanism: Inhibition of L-type Ca2+ channels (Pacemaker)
• Prolonged Phase 0 and Phase 4 (Pacemaker)
• PR prolongation
• Adenosine
• Mechanism: Inhibition of L-type Ca2+ channels, ↑ K+ conductance
• Classic use: Paroxysmal supraventricular tachycardia
• Adverse effects: Sense of impending doom, flushing, chest pain
• Digoxin
• Mechanism: Inhibition of Na+/K+ ATPase à ↑ intracellular Ca2+
• Adverse effects: Blurry, yellow discoloration to vision
• Magnesium
• Mechanism: ↓ intracellular Ca2+
• Classic use: Torsades, digoxin toxicity
• Ivabradine
• Mechanism: Inhibition of Na+ slow (funny) channels
• Adverse effects: Visual luminous phenomenon (↑ visual
brightness)
≣ ⟽ ⟾
A 38-year-old male with a past medical history of hypertension, mild intermittent asthma, and a recent diagnosis of pre-excitation cardiac
conduction abnormalities, presents to his primary care physician for a fixed erythematous rash over the malar eminences with sparing of the
nasolabial folds. He reports that the rash started after a long afternoon at the beach. He denies any pruritis or drainage from the lesion. He also
reports feeling a dull, soreness in the deltoid region bilaterally. On physical exam multiple painless ulcers are noted along the oral mucosa.
After a thorough review of the patient’s medications, a laboratory workup is performed and shown below.
Leukocyte count: 10,800/mm3

Hemoglobin: 13.7 g/dL
Platelet count: 165,000/mm3
Sodium: 136 mEq/L
Potassium: 4.4 mEq/L
Chloride: 102 mEq/L
Which of the following changes to the Creatinine: 1.6 mg/dL
electrical conductivity is most likely occurring Antinuclear (ANA) antibody: Positive for elevation in ANA titer
in ventricular cardiomyocytes as a result of Anti-double-stranded DNA antibody: Negative
iatrogenic causes in this patient?
Antihistone antibody: Positive
Anti-smith antibody: Negative
Anti-Ro antibody: Negative
⚪ A. Increased potassium conductance
⚪ B. Decreased action potential duration
⚪ C. Increased action potential duration
⚪ D. Increased vagal nerve output to the atrioventricular node
⚪ E. Inhibition of L-type calcium channel conductance
OUTLINE
1. Atrial Fibrillation
Cardiology: ●
●
●
A. Pathophysiology
B. Presentation
C. Precipitating Factors
Atrial Arrhythmias ●
●
D. Complications
E. Rate Control
● F. Rhythm Control
● G. Catheter Ablation
● H. Anticoagulation
● I. Hemodynamics in Heart Failure
● J. Jugular Venous Pressure Tracing
● K. ECG Findings
2. Atrial Flutter
● A. Pathophysiology
● B. Presentation
● C. Precipitating Factors
● D. Management
● E. ECG Findings
3. Sick Sinus Syndrome
● B. Presentation
● C. Association
● D. Management
https://commons.wikimedia.org/wiki/File:Afib_ecg.jpg
Cardiology: Atrial Arrhythmias https://commons.wikimedia.org/wiki/File:Heart_conduct_sinus.gif Bootcamp.com
https://commons.wikimedia.org/wiki/File:Heart_conduct_atrialfib.gif
• Automatic foci in vicinity of pulmonary veins à structural fibrotic remodeling of atria à ↑ risk of occurrence
• Rapid uncoordinated atrial contractions à AV node intermittently refractory à Rapid ventricular response
• Presentation:
• Irregularly irregular rhythm, absence of P waves
• Palpitations
• Tachycardia
• Shortness of breath, dizziness, palpitations
• Precipitating Factors:
• Cardiovascular disease (Coronary artery disease, hypertension, heart failure)
• Hyperthyroidism
• Mitral stenosis
• ↑ Sympathetic tone (cocaine, amphetamines, EtOH)
• Complications:
• Embolic phenomena à left atrial appendage
• Pulmonary edema
• Ventricular tachycardia
Cardiology: Atrial Arrhythmias Bootcamp.com
• Rate Control:
• β-blockers and CCBs: Preferred first-line
• Digoxin: Second-line, useful in systolic dysfunction
• Rhythm Control:
• Class IC Antiarrhythmics (Flecainide, propafenone)
• Class III Antiarrhythmics (Ibutilide, sotalol)
• Amiodarone
• Catheter Ablation:
• Symptomatic paroxysmal atrial fibrillation à ablation at pulmonary vein ostia (left atrium)
• Persistent atrial fibrillation with RVR à ablation can be at other sites like AV node (right atrium)
• Amiodarone
• Anticoagulation
• Hemodynamics in Heart Failure
• Left atrial dilatation
• ↓ LV Preload à ↓ CO
• ↑ PCWP
• Pulmonary edema
• Jugular Venous Pressure Tracing
• Loss of a waves
https://commons.wikimedia.org/wiki/File:ECG_Atrial_Fibrillation.jpg
Absence of P waves
Irregularly irregular
(varying R-R intervals)
Narrow QRS complexes
• Re-entry circuit in right atrium (most common)
• Presentation:
• Sawtooth appearance of P waves
• Generally, regular rhythm (exceptions exist)
• 2:1 conduction is most common
• Tachycardia is common
• Shortness of breath, dizziness, palpitations
• Precipitating Factors:
• Similar to atrial fibrillation
• Management:
• Rhythm control, rate control
• Catheter ablation of re-entrant circuit (right atrium)
https://commons.wikimedia.org/wiki/File:Brady-tachy_syndrome_AV-junctional_rhythm.png
• Fibrosis and degeneration of the SA node (usually age-related)
• Iatrogenic (β-blockers, CCBs, Digoxin)
• Presentation:
• Bradycardia, delayed P waves, dropped P waves
• Junctional escape beats
• Syncope, fatigue, shortness of breath
• HR doesn’t increase as expected with exercise
• Tachycardia-Bradycardia Syndrome
• Association:
• Elderly
• Management:
• Iatrogenic: Stop offending medications as necessary
• Asymptomatic: Conservative
• Acute (Unstable) Symptomatic: Atropine à Temporary cardiac pacing
• Long Term (Stable) Symptomatic: Permeant Pacemaker placement, selective β-blockers
≣ ⟽ ⟾
Question ID: 0043 Previous Next https://commons.wikimedia.org/wiki/File:Atrial_Fibrillation_in_two_leads.jpg
A 46-year-old male with a past medical history of cocaine and alcohol use presents to the
emergency room for palpitations. He states that he went out on a “binge” prior to arrival. His
last drink was reported to have been five minutes prior to walking into the emergency
department. An ECG strip is shown below. Which of the following is most likely directly related
to the heart rate observed in this patient?
⚪ A. Accessory pathway bypassing the atrioventricular node

⚪ B. Pacing initiation triggered at the atrioventricular node
⚪ C. Complete conduction through the atrioventricular node
⚪ D. Intermittent conduction through the atrioventricular node
⚪ E. Negligible conduction through the atrioventricular node
OUTLINE
1. Supraventricular Tachycardia
Cardiology:
● B. Presentation
● C. ECG Findings
Ventricular
● D. Management
2. Wolff-Parkinson-White Syndrome
Arrhythmias and ●
●
●
B. ECG in Sinus WPW
C. ECG in AVRT WPW
D. Presentation
Pre-Excitation ●
●
E. Management
F. Complications
3. Torsades De Pointes
Syndromes ●
●
A. Pathophysiology
B. Causes
● C. ECG Findings
● D. Management
● E. Complications
4. Monomorphic Ventricular Tachycardia
● B. Causes
● C. ECG Findings
5. Ventricular Fibrillation
● B. Causes
● C. ECG Findings
Cardiology: Ventricular Arrhythmias Bootcamp.com
https://commons.wikimedia.org/wiki/File:SVT_Lead_II-2.JPG
SVT
• Re-entrant pathway within the AV node, accessory pathway, or SA node
• Most common = Atrioventricular nodal re-entrant tachycardia (AVNRT) AVRT AVNRT Atrial T.
• Second most common = Atrioventricular re-entrant tachycardia (AVRT)
• Presentation:
• Young patient, no significant cardiac history
• Abrupt onset, chest pain, dyspnea, palpitations
• ECG Findings:
• Narrow QRS (< 3 little boxes) tachycardia
• Heart rate usually >150 beats per minute
• P wave may be buried within the QRS complex
• Management (Stable):
• Vagal maneuvers (Carotid sinus massage)
• Adenosine
• CCBs, β-blockers
• Management (Unstable):
• Electrical cardioversion (Immediate)
• Catheter ablation of re-entry pathway (Definitive)
https://commons.wikimedia.org/wiki/File:SVT_Lead_II-2.JPG
• Sinus: Accessory pathway (Bundle of Kent) à bypass AV node (anterograde through bundle of Kent)
• Orthodromic AVRT: Re-entrant circuit (anterograde through AV node, retrograde through bundle of Kent)
• Antidromic AVRT: Re-entrant circuit (anterograde through bundle of Kent, retrograde through AV node)
• ECG in Sinus WPW:
• Shortened PR interval
• Early, “slurred” upstroke of QRS (delta wave)
• Wide QRS
• ECG in AVRT WPW:
• Narrow QRS
• P wave follows QRS (usually)
• Presentation:
• Sinus: Generally asymptomatic
• AVRT: Generally symptomatic
• Management (Stable):
• Procainamide à ideal for antidromic AVRT
• Adenosine, CCB à ideal for orthodromic AVRT
• Management (Unstable):
• Electrical cardioversion
• Catheter ablation (definitive)
• Complications:
• AV nodal blocking agents and vagal maneuvers à ventricular tachycardia or ventricular fibrillation (unrestricted transmission)
https://commons.wikimedia.org/wiki/File:Tosadesdepointes.jpg
• Prolonged action potential in cardiomyocytes à Prolonged QT interval à ↑ risk of TdP
• Causes:
• Congenital Long QT Syndrome (usually younger patient)
Class Classic Drug Other Drugs/Effects
A Antiarrhythmics Quinidine Disopyramide, procainamide, sotalol, dofetilide

B Antibiotics Macrolides Fluoroquinolones
C Antipsychotics Haloperidol Ziprasidone
D Antidepressants Tricyclic Methadone
antidepressants
E Antiemetics/Electrolytes Ondansetron Hypocalcemia, hypokalemia, hypomagnesemia
F Antifungals Azoles
• ECG Findings:
• Polymorphic ventricular tachycardia (“twisting of the peaks” pattern)
• Irregularly irregular rhythm
• Sinusoidal change in amplitude of QRS complexes
• Management:
• Intravenous magnesium
• Avoid QT-prolonging medications during acute TdP
• Complication:
• Ventricular fibrillation or sudden cardiac death
Cardiology: Ventricular Arrhythmias https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png
Bootcamp.com
https://commons.wikimedia.org/wiki/File:Lead_II_rhythm_ventricular_tachycardia_Vtach_VT_(cropped).JPG
Ventricular arrhythmias are

• Pathophysiology: common in the first 24-48
• Aberrant ventricular foci hours after MI
• Intraventricular re-entry circuit
• Causes:
• Ischemic and/or structural heart disease
• Complication of acute MI
• Electrolyte disturbances (hypokalemia, hypomagnesemia)
• Acidosis, hypoxemia
• ECG Findings:
• Wide QRS (≥3 little boxes) monomorphic tachycardia
• Typically, regular rhythm
• Poorly discernible P or T waves at high rates
• Heart rates of 100-300 beats per minute
• Uncoordinated ventricular depolarization
• Causes: Similar to Ventricular Tachycardia
• Association: Cardiac arrest
• ECG Findings:
• Wide QRS (≥3 little boxes) tachycardia
• Heart rates of 100-300 beats per minute
• Complication:
• Sudden cardiac death (rapid)
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png
A 28-year-old female with a past medical history of alcohol use presents to the emergency
department with palpitations and tremors. She denies any chest pain or nausea. The patient
states that she recently started using cocaine approximately two months prior. ECG reveals an
irregularly irregular rhythm with an erratic baseline, absent P-waves, and an approximate heart
rate of 140/min. An intravenous drug is administered. The patient reports becoming very
anxious after the drug is given. A cardiac monitoring rhythm strip taken after the patient
received the intravenous drug is also shown. The patient subsequently loses consciousness
and acute resuscitative measures are initiated.
Which of the following intravenous medications were most likely given to this patient?
⚪ A. Diltiazem
⚪ B. Procainamide
⚪ C. Quinidine
⚪ D. Amiodarone
⚪ E. Ibutilide
OUTLINE
1. Atrioventricular Blocks
Cardiology:
● A. First Degree
● B. Second Degree, Mobitz Type I (Wenckebach)
● C. Second Degree, Mobitz Type II
Conduction
● D. Third Degree
2. Bundle Branch Blocks
● A. Right Bundle Branch Blocks
Blocks ● B. Left Bundle Branch Blocks

3. Cardiac Conduction Blood Supply
● A. Right Coronary Artery
● B. Left Anterior Descending Artery
Cardiology: Conduction Blocks Bootcamp.com
https://en.wikipedia.org/wiki/Heart_block
Asymptomatic
High Yield Causes:
• First Degree:
• PR interval >5 little boxes (200ms) Ischemic heart disease
• Unchanged P-P intervals
• Regular rhythm Hyperkalemia
• Low risk block à Generally conservative management
• Second Degree, Mobitz Type I (Wenckebach): Lyme Disease
• Progressive lengthening of PR interval until QRS is dropped
• Regularly irregular rhythm
Endocarditis/ARF
• Low risk block à Generally conservative management
• Second Degree, Mobitz Type II:
• Intermittent non-conducted P-waves à dropped QRS Iatrogenic
• Unchanged P-P intervals Symptomatic
• Regularly irregular rhythm AV Nodal Blocking
• Medium-High risk block à Review medications, pacemaker Agents
• Third Degree: Calcium Channel
• Complete AV dissociation (between QRS and P waves) Blockers
• High risk block à Review medications, pacemaker
β-blockers
Adenosine
Digoxin
https://commons.wikimedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.svg
Cardiology: Atrioventricular Blocks https://commons.wikimedia.org/wiki/File:Right_bundle_branch_block_ECG_characteristics.svg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Cardiogram_indicating_right_bundle_branch_block.jpg
• Right Bundle Branch Block (RBBB):

• Classic causes: Pulmonary embolus, right heart strain, ischemic heart disease
• Pseudo-RBBB in Brugada (with ST-elevation in V1-V3)
• ”M” shape, “rabbit ears” (Focus on V1)
• Slurring of S-wave (Focus on V6)
• Left Bundle Branch Block (LBBB):
• Classic causes: AS, AR, Lyme disease, dilated cardiomyopathy, ischemic heart disease
• Lack of R waves (Focus on V1)
• Notched R waves (Focus on V6)
Cardiology: Atrioventricular Blocks Bootcamp.com
• Right Coronary Artery:

• SA node
• AV node (usually)
• Bundle of His (major)
• Proximal right bundle branch
• Left Anterior Descending Artery:
• Bundle of His (minor)
• Complete left bundle branch
• Distal right bundle branch
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:Complete_A-V_block_with_resulting_junctional_escape.png
A 14-year-old male presents to his pediatrician with his father for shortness of breath and fatigue. He has no significant past
medical history although his father has a history of asthma. His father denies any family history of heart disease or sudden
cardiac death. The patient states that he has felt “winded” with activity over the past week. According to his father, the
shortness of breath became particularly bothersome during football practice. The patient also reports a mild erythematous
rash on his forearm that had resolved within three days. The rash was first noticed two weeks earlier when on a hiking trip
with family. The patient denies any chest pain, nausea, and diarrhea. Vital signs are shown below. An ECG performed in-office
is also shown.
Heart rate: 30/min
Blood pressure: 74/44
Respiratory rate: 18/min
Oxygen saturation: 94% on room air
A drug with which mechanism of action

would most likely improve this patient’s
condition?
⚪ A. Inhaled short-acting β-agonist

⚪ B. Transient hyperpolarization of cardiac nodal cells
⚪ C. Inhibition of Na+/K+ ATPase in myocardial cells
⚪ D. Inhibition of cardiac L-type calcium channels
⚪ E. Irreversible inhibition of bacterial cell wall synthesis
OUTLINE
1. Heart Failure Overview
Cardiology:
● A. Heart Failure Variants of Disease
● B. Heart Failure Location (Left vs Right)
● C. Heart Failure Presentation
Heart Failure
2. Systolic Heart Failure
● A. Causes
● B. Pathophysiology
3. Diastolic Heart Failure
● A. Causes
4. High and Low Output Heart Failure
● A. Classic Causes
5. Pharmacologic Targets
● A. ACE Inhibitors, ARBs
● B. Mineralocorticoid Receptor Antagonists
● C. β-blockers
● D. Neprilysin Inhibitors
● E. Loop Diuretics
● F. Thiazine Diuretics
● G. Digoxin
Cardiology: Heart Failure Bootcamp.com
Heart Failure Variant Heart Failure Location
• Systolic:
• Heart failure with reduced ejection fraction (HFrEF) • Left:
• Principal determinant: ↓ Contractility à ↑↑↑ Volume • ↑ LAP (PCWP)
• Diastolic: • Pulmonary edema
• Heart failure with preserved ejection fraction (HFpEF) • Pleural effusion
• Principal determinant: ↑↑↑ Pressure à ↓ Compliance • Functional mitral valve regurgitation
• High-Output • Right:
• Low-Output • MCC à Left heart failure
• If not from left heart failure, unlikely pulmonary edema
• Hypoxic pulmonary vasoconstriction (Pulmonary HTN)
• Left parasternal lift
• Peripheral edema
• Hepatomegaly (Nutmeg liver)
• Ascites
• Functional tricuspid valve regurgitation
https://commons.wikimedia.org/wiki/File:Combinpedal.jpg
Cardiology: Heart Failure https://commons.wikimedia.org/wiki/File:Pulmonaryedema09.JPG
Bootcamp.com
https://commons.wikimedia.org/wiki/File:Normal_posteroanterior_(PA)_chest_radiograph_(X-ray).jpg
• Subjective:
• Dyspnea with activity (or at rest in severe stages)
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Objective
• Pulmonary crackles
• Reduced Lung Sounds
• Shifted PMI (LVH)
• Left parasternal lift (RVH)
• S3 heart sound
• S4 heart sound à classic for diastolic HF
• ↑↑↑ BNP
• Overview:
• Heart failure with reduced ejection fraction (HFrEF)
• Principal determinant: ↓ Contractility à ↑↑↑ Volume
• Causes:
• Ischemic heart disease
• Viral myocarditis
• Chronic Alcohol Use
• ↓ Contractility (↓ EF) à ↓ CO à ↑ LVEDP
• Eccentric hypertrophy: ↑ Contractile proteins added in series
• ↑ Compliance, ↓ CO, ↓ EF
• Overview:
• Heart failure with preserved ejection fraction (HFpEF)
• Principal determinant: ↑↑↑ Pressure à ↓ Compliance
• Causes:
• Prolonged hypertension
• Aortic stenosis
• Infiltrative disorders
• ↑ LVP à ↑ Contractility
• Concentric hypertrophy: ↑ Contractile proteins added in parallel
• ↓ Compliance, ↓ CO, normal EF
• Additional Clinical Features:
• S4 (due to stiff ventricle)
• Classic Causes:
• Thiamine deficiency
• Severe anemia
• Hyperthyroidism
• Arteriovenous fistula
• Classic Cause:
• Cardiogenic shock

• Inhibition of ACE à ↓ angiotensin II
• Adverse Effect: Dry cough, hyperkalemia, angioedema
• Mineralocorticoid receptor Antagonists (Spironolactone, Eplerenone)
• β-blockers (Metoprolol, Carvedilol)

• Neprilysin Inhibitors (Sacubitril):
• Neprilysin is a metalloproteinase that inactivates ANP, BNP, and AT-II
• ↑ ANP, ↑ BNP, ↑ AT-II
• Used with angiotensin-II receptor blocker
• Loop Diuretic (Furosemide):
• Inhibition of Na/K/Cl transporter in ascending limb of loop of Henle
• Primary use: Fluid retention and pulmonary edema
• Thiazide Diuretic (Metolazone):
• Inhibition of Na/Cl transporter in distal tubule
• Potentiation of loop diuretic effect
• Digoxin:
• Inhibition of Na+/K+-ATPase in myocytes
• ↑ Vagal activity to nodal cells
• ↑ intracellular calcium concentration in ventricular myocytes
• Toxicity: Disturbed color perception, GI symptoms, arrhythmias
• Precipitated by hypokalemia
≣ ⟽ ⟾
https://radiopaedia.org/articles/heart-failure-summary?lang=us
A 57-year-old obese female with a past medical history of type II diabetes mellitus, dyslipidemia, chronic hypertension, and
coronary artery bypass grafting performed 7 years earlier presents to the emergency department for shortness of breath. She
denies any tobacco use and states that she has a glass of wine on rare occasion. She states that she was having difficulty
sleeping through the night because she is running to the bathroom every few hours to void. She reports throwing away her
”water pills” last week due to frustration. Blood pressure is 164/88mmHg, heart rate 88/min, respiratory rate 14/min, saturating
94% on 2 liters of oxygen by nasal cannula. Physical exam reveals diffuse crackles bilaterally in the lung fields, an S3 heart
sound, and 2+ pitting edema in the bilateral lower extremities. Chest X-ray is shown below. ECG reveals a normal sinus
rhythm with mild left ventricular hypertrophy. Thyroid stimulating hormone levels are within normal limits. B-type natriuretic
peptide level is significantly elevated. Patient had an echocardiogram performed three months earlier revealing a left
ventricular ejection fraction of 30%.
Which of the following findings are most consistent with this patient’s acute
presentation?
⚪ A. Depressed pulmonary capillary wedge pressure

⚪ B. Depressed central venous pressure
⚪ C. Elevated cardiac index
⚪ D. Increased urinary potassium excretion
⚪ E. Significantly decreased serum levels of vitamin B1
OUTLINE
1. Cardiomyopathy Overview
Cardiology:
● A. Major Types of Cardiomyopathy
● B. Cardiac Myocyte Histology
2. Dilated Cardiomyopathy
Cardiomyopathy
● B. Systolic Heart Failure
● B. Other Classic Causes
3. Restrictive Cardiomyopathy
● B. Infiltrative Disease
● C. Diastolic Heart Failure
4. Hypertrophic Obstructive Cardiomyopathy
● B. Classic Causes
● C. Histopathology
● D. Management
5. Viral Myocarditis
6. Chagas Disease
7. Takotsubo Cardiomyopathy
8. Amyloid Cardiomyopathy
9. Aging of Cardiomyocytes
10. Other Causes of Cardiomyopathy
https://commons.wikimedia.org/wiki/File:Blausen_0470_HeartWall.png
Cardiology: Cardiomyopathy https://commons.wikimedia.org/wiki/File:414c_Cardiacmuscle.jpg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png
• Dilated Cardiomyopathy:
• Association with Systolic HF
• Restrictive Cardiomyopathy:
• Association with Diastolic HF
• Hypertrophic Obstructive Cardiomyopathy
• Normal contractility
• ↓ Ventricular cavity size
• Impaired diastolic function
• Septal hypertrophy
• Histology of Cardiomyocytes:
• Central appearing nuclei
• Striation's present
• Branching cardiomyocytes
Cardiology: Cardiomyopathy Bootcamp.com
• Pathophysiology Systolic Heart Failure:

• Eccentric hypertrophy
• ↑ Contractile proteins added in series
• ↑ LV mass, ↑ LV cavity, ↓ LV EF, Normal LV relaxation
• Highest Yield Causes:
• Systolic heart failure
• Viral myocarditis
• Chaga’s Disease
• Takotsubo
• Additional Causes:
• Familial (AD, truncating mutation of TTN gene)
• Pregnancy
• Anthracyclines (doxorubicin)
• Excess alcohol use
• Selenium deficiency
• Pathophysiology Diastolic Heart Failure:

• Concentric hypertrophy
• ↑ Contractile proteins added in parallel
• ↑ LV mass, ↓ LV cavity, Normal/↓ LV EF, ↓ LV relaxation
• Pathophysiology Restrictive Cardiomyopathy:
• Stiffened ventricular walls, not typically thickened (exceptions exist: Amyloidosis)
• Normal LV mass, Normal or ↓ LV cavity, Normal LV EF, ↓ LV relaxation
• Highest Yield Causes:
• Diastolic heart failure à Prolonged hypertension, Aortic stenosis
• Infiltrative disorders à Amyloidosis, hemochromatosis, sarcoidosis
• Radiation-induced
• Infiltrative Disease Considerations:
• Variable ventricular wall thickness (vs hypertensive secondary cause)
• Prominent y-descent
• Conduction abnormalities
Cardiology: Cardiomyopathy https://commons.wikimedia.org/wiki/File:HCM%EF%BC%BFHE.jpg Bootcamp.com
• Genetic mutations of cardiac sarcomere à
• β-myosin heavy chain and myosin-binding protein C
• Autosomal dominant (most cases)
• Dynamic LV outflow tract obstruction (↑ LV septal thickness)
• ↑ LV mass, ↓ LV cavity, Normal/↑ LV EF, ↓ LV relaxation
• Classic Case:
• Generally asymptomatic until strenuous exercise
• Sudden cardiac death, young patient
• Systolic crescendo-decrescendo murmur at LLSB +/- holosystolic murmur at
apex
• Valsalva à ↓ LV blood volume à Worsen obstruction à ↑ ejection murmur
• Passive leg raise à ↑ LV blood volume à Improve obstruction à ↓ ejection
murmur
• S4 heart sound
• Histopathology:
• Myofibrillary disarray and interstitial fibrosis
• Mitral Valve:
• Anterior mitral leaflet in closer proximity to aortic valve
• Distorted mitral valve à ejection against valve à functional mitral
regurgitation
• Management:
• Avoid dehydration and strenuous exercise
• β-blockers
• Direct viral-induced cytotoxic effect to myocardial cells
• Dilated cardiomyopathy (usually)
• Etiology:
• Coxsackievirus
• Adenovirus
• Influenza virus
• Classic Case:
• Young patient + viral prodrome
• Histopathology:
• Irregular banding patterns, less nuclei observed
• Inflammatory infiltration with lymphocytes
• Primary Cardiomyopathy Subtype:
• Dilated cardiomyopathy
Cardiology: Cardiomyopathy https://www.wikidoc.org/index.php/File:Heart_in_Chagas_disease_4.jpg Bootcamp.com
• Direct parasitic-induced cytotoxic effects
• Etiology:
• Trypanosoma cruzi (Reduviid family)
• Classic Case:
• Central and South America
• Histopathology:
• Protozoa peripheral to myocytes
• Inflammatory infiltration with lymphocytes
• Localized apical wall thinning and/or aneurysm
• ↑ risk of mural thrombus and/or emboli
• Other Features:
• Megaesophagus
• Megacolon
• Catecholamine surge à impaired kinetic activity of left ventricle
• Etiology:
• Emotional stress is classic
• Classic Case:
• Death of a loved one
• Postmenopausal female
• Ballooning of left ventricle
Cardiology: Cardiomyopathy https://www.flickr.com/photos/euthman/377559955/ licensed under CC BY-SA 2.0
Bootcamp.com
https://commons.wikimedia.org/wiki/File:Cardiac_amyloidosis_high_mag_he.jpg
• ↑ Extracellular deposition of amyloidogenic proteins
• Transthyretin (ATTR)
• Light chain (AL)
• Histopathology:
• Pink amorphous material surrounding cardiomyocytes
• Apple-green birefringence with polarized light and Congo red stain
• Restrictive cardiomyopathy (Ventricular wall thickening)
• Other Features of Amyloidosis:
• Nephrotic syndrome
• Hepatomegaly
https://commons.wikimedia.org/wiki/File:Cardiac_myocyte_showing_lipofuscin_pigment.jpg
• Gross Anatomical Changes:

• Sigmoidal shape of ventricular septum
• Histopathology:
• Myofibrillary disarray and interstitial fibrosis
• ↑ Lipofuscin pigment
• ↑ Connective tissue
• Hemochromatosis:
• ↑ Extracellular deposition of iron
• Prussian blue stain (stains iron blue-black)
• Peripartum/Postpartum:
• Dysfunctional angiogenic growth factors
• Third trimester peripartum female – postpartum female
• Anthracycline-Induced
• Anthracyclines: Daunorubicin, doxorubicin
• Binds with topoisomerase II à cleaves DNA in cancer cells
• ↑ with cumulative dose
• Prevent with dexrazoxane
• Trastuzumab-Cardiotoxicity
• Monoclonal antibody binding to human epidermal growth factor receptor-2 (HER2)
• Does not change with cumulative dose
• Tends to be reversible
≣ ⟽ ⟾
A 17-year-old male presents to the emergency room for 8/10 chest pain that began during a soccer practice a few hours
earlier. He states that he has experienced chest discomfort and shortness of breath in the past with sports activity and had
previously been diagnosed with asthma 3 years earlier. He states that he finds little improvement in his symptoms when using
his albuterol inhaler. He denies any other past medical or surgical history. He states that his father and first cousin are both
deceased from “heart problems” in their early thirties. He states that he vapes occasionally and denies any other substance
use. Blood pressure is 108/58 mmHg, heart rate is 76/min and regular, oxygen saturation is 99% on room air. The point of
maximal impulse appears to be modestly shifted laterally beyond the midclavicular line. A 2/6 crescendo-decrescendo systolic
murmur is auscultated at the lower left sternal border. The murmur is accentuated with standing. Pulmonary auscultation
reveals clear lung sounds bilaterally with no wheezing observed. ECG reveals a regular rhythm with left axis deviation and
deep Q waves in leads I, II, III, aVF and V5-V6 are observed. A transthoracic echocardiogram and cardiac MRI are performed.
The patient is subsequently prescribed a medication and restricted from further sports activity on discharge.
Which of the following mechanisms of action would most likely be consistent with the medication given?
⚪ A. Activation of β1-receptors in myocardial cells

⚪ B. Activation of guanylyl cyclase at venous and coronary vessels
⚪ C. Inhibition of Na+/K+ ATPase in myocardial cells
⚪ D. Inhibition of phosphodiesterase-5 enzymes in vascular smooth muscle
⚪ E. Inhibition of Na+/K+/Cl- co-transporters in the loop of Henle
⚪ F. Non-selective inhibition of β-receptors systemically
OUTLINE
1. Anatomical Considerations
● A. Aorta
Cardiology: ● B. Vessel Wall Layers

2. Aortic Dissection
Aortic Disease
● B. Etiology
● C. Presentation
● D. Stanford Classification
● E. Complications
● F. Imaging
● G. Management
3. Aortic Aneurysm
● A. Thoracic vs Abdominal
● C. Risk Factors
● D. Presentation
● E. Preventative Management
4. Cardiac Considerations of Marfan Syndrome
● B. Cystic Medial Degeneration
● C. Mitral Valve Prolapse
● D. Other Findings
5. Aortic Coarctation
● B. Associations
● C. Presentation
● D. Management
Cardiology: Aortic Disease https://commons.wikimedia.org/wiki/File:Gray506.svg Bootcamp.com
https://radiopaedia.org/cases/normal-cta-chest
Aortic Isthmus:
-Traumatic aortic rupture
• Aorta: -Coarctation
• Ascending: Proximal to brachiocephalic artery
• Arch of aorta: Between ascending and descending
• Descending: Distal to left subclavian artery
• Vessel Wall Layers:
• Luminal: Tunica intima
• Middle: Tunica media
• Peripheral: Tunica adventitia (externa)
Cardiology: Aortic Disease https://commons.wikimedia.org/wiki/File:Aortic_dissection_(1)_Victoria_blue-HE.jpg
Bootcamp.com
https://commons.wikimedia.org/wiki/File:Aortic_dissection_types.jpg
• Tear through intima and media à propagation of dissection through media
• Etiology:
• Acquired: Hypertension (#1), trauma, aortic vasculitis
• Connective Tissue Disease: Marfan syndrome, Ehlers-Danlos syndrome
• Structural Disease: Coarctation of aorta, Bicuspid aortic valve
• Presentation:
• Severe, acute “tearing” retrosternal chest +/- radiating back pain
• Asymmetric blood pressure and pulse discrepancies
• Stanford A:
• Location: Ascending aorta and/or descending aorta
• Classic origin: Sinotubular junction
• Surgical management (usually)
• Stanford B:
• Location: Descending aorta
• Classic origin: Left subclavian artery
• Medical management (usually)
• Complications:
• Aortic rupture
• Aortic regurgitation
• Cardiac tamponade
• Ischemia
https://commons.wikimedia.org/wiki/File:DissectionCT.png
Cardiology: Aortic Disease https://commons.wikimedia.org/wiki/File:Descending_(Type_B_Stanford)_Aortic_Dissection.PNG Bootcamp.com
https://commons.wikimedia.org/wiki/File:AoDiss_ChestXRay.jpg
• Imaging:
• CXR: Widened mediastinum
• CT Angiography (Gold standard): Intimal flap
• Transesophageal echocardiogram (TEE) for unstable or renal insufficiency
• Management:
• Stanford A à Surgery
• Stanford B à β-blocker then vasodilator
Cardiology: Aortic Disease https://commons.wikimedia.org/wiki/File:Thoracic_Aortic_Aneurysm.png
Bootcamp.com
https://commons.wikimedia.org/wiki/File:AneurysmT.PNG
Aortic Aneurysms Thoracic Abdominal

• Pathophysiology: Primary Risk Factor Hypertension Smoking
• Transmural inflammation à dilation of intima, media, and
adventitia
• General Risk Factors: Additional Important Tertiary syphilis Atherosclerosis
Bicuspid aortic valve
• Smoking Risk Factors
Connective tissue disease
• Atherosclerosis
• Old age
Classic Symptoms Chest pain Low back pain
• Connective tissue disease Mid (thoracic) back pain Abdominal bruit
• Tertiary Syphilis Hoarseness Pulsatile abdominal mass
• Classic Presentation: Dysphagia
• Generally asymptomatic until rupture
• Presentation in Rupture: Other CXR: Widened Abdominal U/S
• Acute onset, severe tearing/ripping abdominal/back pain mediastinum Infrarenal (classic location)
Ascending aorta (classic
• Severe chest/abdominal pain
location)
• Hypotension
• Preventative:
• Abdominal ultrasound screening in men aged 65-75 who
have ever smoked (USPSTF)
Cardiology: Aortic Disease https://www.researchgate.net/figure/Pathologic-finding-of-excised-aortic-tissue-A-cystic-medial-necrosis-which-is- Bootcamp.com
defined_fig4_221683474 https://creativecommons.org/licenses/by-nc/3.0/
• Defect in fibrillin-1
• Autosomal dominant
• Cystic Medial Degeneration of Aorta:
• Aortic aneurysmà Aortic root dilation (thoracic) à Aortic regurgitation and/or dissection
• Aortic dissection à most common cause of death
• Histopathology: Amorphous extracellular deposition into medial wall
• Mitral Valve Prolapse:
• Mid-systolic click at apex
• Other Findings:
• Tall stature, long extremities
• Joint hypermobility
• Ectopia lentis, upward lens dislocation
• Pectus deformity à carinatum, excavatum
• Kyphosis, scoliosis
• Arachnodactyly
Cardiology: Aortic Disease Bootcamp.com
https://commons.wikimedia.org/wiki/File:Rib_Notching.jpg
• Juxtaductal narrowing (aortic isthmus)
• Pre-ductal: Infantile form (most common)
• Post-ductal: Adult form
• Association:
• Turner syndrome
• Bicuspid aortic valve
• Williams syndrome
• Berry aneurysm à ↑ risk of rupture à SAH
• Clinical Findings + PDA:
• Generally asymptomatic
• Clinical Findings Without PDA:
• Harsh systolic murmur at multiple locations (LSB)
• Differential cyanosis
• Brachial-femoral delay
• Lower extremity claudication
• Imaging:
• CXR: Rib notching
• Management:
• Neonates à prostaglandin E1
• Operative repair
≣ ⟽ ⟾
https://radiopaedia.org/articles/aortic-dissection?lang=us
A 63-year-old male with an unknown past medical history presents to the emergency department with 10/10 “rip-roaring”
chest pain. The patient states that he was moving his couch when he suddenly experienced acute-onset of severe chest pain.
He denies similar pain in the past. He states that he had one episode of emesis prior to arrival and is feeling very nauseous.
He admits to a 35-pack-year smoking history. The patient is unable to provide more details due to the pain. Blood pressure is
204/122 mmHg, heart rate is 101/min and regular, respiratory rate is 18/min, and oxygen saturation is 98% on room air.
Electrocardiogram reveals sinus tachycardia and evidence of left ventricular hypertrophy with no signs of ST-segment
elevation. Relevant imaging is shown below. Based on these findings, the pathologic process observed most likely originated
closest to which of the following structures?
⚪ A. Left renal artery

⚪ B. Left subclavian artery
⚪ C. Right subclavian artery
⚪ D. Aortic isthmus
⚪ E. Sinotubular junction
OUTLINE
1. Overview
● A. Maneuvers
Cardiology: ● B. Murmur Grading

2. Aortic Stenosis
Valvular Disease
● B. Presentation
● C. Etiology
3. Aortic Regurgitation
● B. Presentation
● C. Etiology
4. Mitral Stenosis
● B. Presentation
● C. Etiology
5. Mitral Regurgitation
● B. Presentation
● C. Etiology
6. Mitral Valve Prolapse
● B. Presentation
● C. Etiology
7. Tricuspid Regurgitation
● B. Presentation
● C. Etiology
Cardiology: Valvular Disease Bootcamp.com
• ↑ Preload
• Passive leg raise
• Squatting
• Expiration: ↓ RV preload, ↑ LV preload à intensifies most left-sided murmurs, dulls most right-sided murmurs
• ↓ Preload
• Valsalva (straining phase)
• Standing (from squat or supine)
• Inspiration: ↑ RV preload, ↓ LV preload à intensifies most right-sided murmurs, dulls most left-sided murmurs
• ↑ Afterload:
• Hand Grip
• Squatting
• Systolic vs Diastolic
• Systolic may be physiologic
• Diastolic almost always pathologic
• Continuous murmur (ex. PDA)
• Grade
• I: Detected with very careful auscultation
• II: Detected quickly with auscultation
• III: Easily heard, with no thrill
• IV: Palpable thrill
• V: Detected with rim of stethoscope touching chest + palpable thrill
• VI: Audible with stethoscope off chest
https://commons.wikimedia.org/wiki/File:Amyloidosis,_dystrophic_calcification,_H%26E.jpg
• Left ventricular outflow obstruction à ↑ LVP à LV Concentric hypertrophy à DHF à S4 heart sound
• Presentation:
• Classic Triad: Exertional dyspnea, angina, syncope
• Pulsus parvus et tardus
• Single S2 (or soft S2)
• Murmur: Harsh crescendo-decrescendo systolic ejection murmur, radiates to carotids
• Murmur Auscultation: R 2nd ICS
• ↑ Murmur: ↑ Preload, ↓ Afterload, Expiration
• Age-related Aortic Valve Sclerosis:
• MCC overall
• Classically, elderly patients
• Earlier presentation if bicuspid aortic valve
• Bicuspid Aortic Valve:
• Fusion of two aortic leaflets in young patients
• ↑ risk of premature dystrophic calcification
• Acute: Regurgitant blood into LV à Poor compensation due to rapid physiologic changes
• Chronic: Regurgitant blood into LV à ↑ LVEDV à LV eccentric hypertrophy à SHF à S3 heart sound
• ↑ Pulse pressure
• Presentation:
• Exertional dyspnea
• Pulmonary edema
• “Water hammer” pulse
• Head bobbing
• Murmur: Early decrescendo diastolic murmur
• Murmur Auscultation: L 3rd-4th ICS along LSB (Erb’s Point)
• ↑ Murmur: ↑ Preload, ↑ Afterload, Expiration
• Age-related Aortic Valve Sclerosis:
• MCC overall
• Classically, elderly patients
• Bicuspid Aortic Valve:
• Fusion of two aortic leaflets in younger patients
• ↑ risk of dystrophic calcification to valve
• Aortic Dilatation:
• Secondary to: Aortic dissection, aneurysm, connective tissue disease, and/or tertiary syphilis
• Chronic poorly controlled hypertension à aortic dissection and thoracic aortic aneurysm
• Rheumatic Heart Disease
https://commons.wikimedia.org/wiki/File:Leg_with_erythema_marginatum_Wellcome_L0061869.jpg
• Left atrial outflow obstruction à ↓ LVEDV, left atrial dilation à ↓ CO
• Presentation:
• Pulmonary edema
• Hoarseness, dysphagia Acute Rheumatic Fever Presentation
• Loud S1
Acute/Subacute:
• Murmur: Opening snap, diastolic “rumbling” murmur, radiates to left axilla
Migratory arthritis
• Murmur Auscultation: L 5th ICS midclavicular line (apex) Pancarditis à mitral prolapse/regurgitation
• ↑ Murmur: ↑ Preload, ↓ Afterload, Expiration Sydenham chorea
• Murmur Interval: ↓ time between S2 and OS ~ ↑ disease severity Subcutaneous nodules
• Rheumatic Heart Disease: Erythema marginatum
• Most common cause overall
• Manifestations years after acute rheumatic fever Chronic:
• Complications: Mitral Stenosis
• Atrial fibrillation
• Acute: Regurgitant blood into LA à ↑ PCWP à Poor compensation due to rapid physiologic changes
• Chronic: Regurgitant blood into LA à ↑ LVEDV à LV eccentric hypertrophy à SHF à S3 heart sound
• Presentation:
• Pulmonary edema
• Hoarseness, dysphagia
• Soft S1
• Murmur: Holosystolic “blowing” murmur
• Murmur Auscultation: L 5th ICS midclavicular line (apex)
• ↑ Murmur: ↑ Preload, ↑ Afterload, Expiration
• Association:
• Papillary muscle rupture
• Mitral valve prolapse
• Infective endocarditis à Mitral valve (#1)
• Complication:
• Myxomatous degeneration of mitral valve à ↑ tension on chordae tendineae and papillary muscles
• Presentation:
• Murmur: Mid-systolic click, late systolic crescendo murmur
• Murmur Auscultation: L 5th ICS midclavicular line (apex)
• ↑ Murmur: ↓ Preload, Expiration
• Later click with ↑ afterload
• Association:
• Connective tissue disease (Marfan Syndrome)
• Infective endocarditis à Mitral valve (#1)
• Rheumatic heart disease
• Complication:
• Recurrence of infective endocarditis
• Acute: Regurgitant blood into RA à ↑ CVP à Poor compensation due to rapid physiologic changes
• Chronic: Regurgitant blood into RA à Right-sided heart failure
• Presentation:
• Distended jugular veins
t
• Hepatomegaly
• Ascites
• Murmur: Holosystolic murmur
• Murmur Auscultation: 4th ICS LLSB
• ↑ Murmur: ↑ Preload, ↑ Afterload, Inspiration
• Association:
• Infective endocarditis in IVDU à septic pulmonary emboli
• Carcinoid syndrome
Valvular Disease Murmur Auscultation Unique Feature Classic Cause Heart Failure ↑ Murmur Intensity
Location
Aortic Stenosis Holosystolic 2nd R ICS Radiation to Dystrophic Diastolic: Concentric ↑ Preload (Passive leg raise)
crescendo- carotids calcification hypertrophy (S4) ↓ Afterload
decrescendo
Aortic Regurgitation Diastolic decrescendo Erb’s point High pulse Multiple Systolic: Eccentric ↑ Preload (Passive leg raise)
murmur pressure hypertrophy (S3) ↑ Afterload (Hand grip)
Mitral Stenosis Diastolic decrescendo Cardiac apex Opening snap Rheumatic heart Low output ↑ Preload (Passive leg raise)
murmur disease ↓ Afterload
Mitral Regurgitation Holosystolic murmur Cardiac apex Radiate to axilla Mitral valve prolapse Systolic: Eccentric ↑ Preload (Passive leg raise)
hypertrophy (S3) ↑ Afterload (Hand grip)
Mitral Valve Prolapse Late-systolic Cardiac apex Mid-systolic click Multiple Mitral regurgitation à ↓ Preload (Valsalva)
crescendo murmur Systolic Later click with ↑ Afterload
Tricuspid Holosystolic murmur 4th L ICS ↑ with inspiration IVDU à Infective Right-sided ↑ with Inspiration
Regurgitation endocarditis ↑ Preload (Passive leg raise)
↑ Afterload (Hand grip)
Hypertrophic Systolic crescendo- Left lower sternal Young patient Inherited mutations Septal hypertrophy (S4) ↓ Preload (Valsalva)
Obstructive decrescendo murmur border in sarcomere ↓ Afterload
Cardiomyopathy
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:AP_portable_CXR_of_a_patient_in_acute_pulmonary_oedema.jpg
A 67-year-old male with a past medical history of obstructive sleep apnea, tobacco use, chronic hypertension, and
hyperlipidemia presented to the emergency department with acute onset of severe chest pain. Vital signs on arrival were
significant for a blood pressure of 94/58 mmHg, heart rate 102/min, respiratory rate 14/min, and oxygen saturation of 98% on
room air. Electrocardiogram revealed ST-segment depression and tall R-waves in leads V2, V3, and V4. Chest x-ray was
unremarkable. Percutaneous coronary intervention with stent placement was performed which disclosed severely obstructing
stenosis in the ostium of the posterior descending artery. On day 3 of admission, the patient develops acute dyspnea while
lying in bed with 3/10 non-specific chest pain. Blood pressure is 184/110 mmHg and a new 3/6 “blowing” holosystolic murmur
is auscultated at the cardiac apex radiating into the left axilla. Chest x-ray is shown below. A medication is administered, and
the patient’s murmur becomes softer and more difficult to auscultate.
Which of the following mechanisms of the unknown medication would be most likely responsible for decreasing the murmur
intensity in this patient?
⚪ A. Increased intracellular cGMP activity at arterioles and venules

⚪ B. Increased intracellular phospholipase C activity at arterioles and venules
⚪ C. Increased intracellular cAMP activity at cardiac myocytes
⚪ D. Decreased intracellular cAMP activity at arterioles and venules
⚪ E. Decreased intracellular Na+/K+-ATPase activity at cardiac myocytes
OUTLINE
1. Overview 5. Patent Ductus Arteriosus

● A. Acyanotic ● A. Pathogenesis
Cardiology: ●
●
B. Cyanotic
C. Symptomatic Patient
●
●
B. Pathophysiology
C. Presentation
Acyanotic
● D. General Diagnostics ● D. Diagnostics
2. Ventricular Septal Defect ● E. Management
● A. Pathogenesis ● F. Association
Congenital Heart
● B. Pathophysiology 6. Eisenmenger Syndrome
● C. Presentation ● A. Pathophysiology
● D. Diagnostics ● B. Presentation
Defects
● E. Association
3. Atrial Septal Defect
● A. Pathogenesis
● C. Presentation
● D. Diagnostics
● E. Association
4. Patent Foramen Ovale
● A. Pathogenesis
● C. Presentation
● D. Diagnostics
Cardiology: Acyanotic Congenital Heart Defects Bootcamp.com
• Acyanotic
• Left à Right shunting
• Tends to be later presentation overall
• 3 D’s: ASD, VSD, PDA
• Cyanotic
• Right à Left shunting
• Early presentation (shortly after birth)
• Cyanotic Presentation: Blue skin discoloration, mucosal cyanosis, failure to thrive, dyspnea
• 5 T’s: Tetralogy of Fallot, TAPVR, Truncus Arteriosus, Tricuspid Valve Atresia, Transposition of Great Vessels
• General Presentation of Symptomatic Patient:
• Tachypnea
• Failure to thrive
• Cyanosis à Cyanotic CHD, Eisenmenger syndrome
• Recurrent bronchopulmonary infections à Acyanotic
• Diagnostics:
• Echocardiography à Confirmatory test
• Bubble study à Useful in detecting RàL shunts
https://commons.wikimedia.org/wiki/File:Vsd_simple-lg.jpg
• Pathogenesis:
• Defect in membranous part of ventricular septum (most common)
• Left à Right shunting through defect in interventricular septum
• RV volume overload à
• Presentation:
• Harsh holosystolic murmur, LLSB
• ↓ Murmur à ↑ Severity/Size
• Usually at 2-3 months in severe disease (vs most cyanotic)
• Diagnostics:
• Association:
• Down syndrome
• Maternal diabetes
https://commons.wikimedia.org/wiki/File:Asd-web.jpg
• Pathogenesis:
• Defect in inter-atrial septum, ostium secundum defect (most common)
• Left à Right shunting through defect of atrial septum
• Valsalva à ↑ RAP with subsequent Right à Left shunting
• Presentation:
• Classically, adolescent or adult
• Wide fixed split S2
• Paradoxical embolism à Cryptogenic stroke
• Diagnostics:
• Association:
• Down syndrome
• Fetal alcohol syndrome
• Holt-Oram syndrome
https://commons.wikimedia.org/wiki/File:Foramen_ovale.png
• Pathogenesis:
• Impaired fusion of septum primum and septum secundum
• Left à Right shunting through defect of atrial septum
• Valsalva à ↑ RAP with subsequent Right à Left shunting
• Presentation:
• Usually, asymptomatic
• Paradoxical embolism à Cryptogenic stroke
• Diagnostics:
https://commons.wikimedia.org/wiki/File:Patent_ductus_arteriosus.svg
• Pathogenesis:
• Impaired closure of ductus arteriosus
• Derived from sixth, left aortic arch
• Left à Right shunting from aorta to pulmonary vessels
• Prostaglandins and low oxygen tension à maintain PDA
• Presentation:
• Continuous “machine-like” murmur, left infraclavicular region
• Usually, asymptomatic if mild case
• Severe cases more likely to be symptomatic
• Wide pulse pressure (similar to AR)
• Diagnostics:
• Management:
• Premature symptomatic infant à Indomethacin à Close PDA
• Cyanotic congenital heart defect à Prostaglandin E1 (Alprostadil) à Maintain PDA
• Association:
• Prematurity
• Rubella (first trimester)
• Fetal alcohol syndrome
• Fetal hydantoin syndrome
• Shunt reversal
• Pulmonary vessel sclerosis
• Chronic L to R shunting à pulmonary hypertension à RVH à RVP > LVP à R to L shunting
• Presentation:
• Cyanosis
• Fingernail clubbing
• Heart failure
• Differential cyanosis and clubbing with PDA
≣ ⟽ ⟾
A 9-month-old female with known Trisomy 21 presents with her mother with a chief complaint of progressively worsening
difficulty breathing and a new nonproductive cough that started approximately one month earlier. Her mother reports the
symptoms are most noticeable when breastfeeding. Physical examination reveals a respiratory rate of 52/min with otherwise
stable vital signs, upslanting palpebral fissures, low set ears, perioral cyanosis, and mild nasal flaring. Bronchial breath
sounds and a heart murmur are auscultated. Chest X-ray reveals diffuse patches of opacification and cardiomegaly. An
echocardiogram is performed and followed by a cardiac catheterization procedure.
Oxygen saturation by cardiovascular location is listed below. Which of the following most likely describes the cause of this
patient’s presentation?
Superior vena cava: SpO2 68%
Inferior vena cava: SpO2 70%
Right atrium: SpO2 69%
Right ventricle: SpO2 69%
Left atrium: SpO2 98%
Left ventricle: SpO2 87%
Pulmonary artery : SpO2 69%
Pulmonary vein: 98%
⚪ A. Long-term exogenous prostaglandin exposure

⚪ B. Atrial septal tissue deficiency
⚪ C. Impaired fusion of septum primum and secundum
⚪ D. Reversal of atrial shunt
⚪ E. Reversal of ventricular shunt
OUTLINE
1. Overview 5. Tricuspid Atresia

● A. Acyanotic
Cardiology:
● A. Pathogenesis
● B. Cyanotic ● B. Pathophysiology
● C. Symptomatic Patient ● C. Presentation
Cyanotic
● D. General Diagnostics ● D. Diagnostics
2. Tetralogy of Fallot ● E. Management
● A. Pathogenesis ● F. Association
Congenital Heart
● B. Pathophysiology 6. TAPVR
● C. Presentation ● A. Pathogenesis
● D. Diagnostics ● B. Pathophysiology
Defects
● E. Management ● C. Presentation
● F. Associations ● D. Diagnostics
3. Transposition of Great Vessels ● E. Management
● A. Pathogenesis ● F. Associations
● C. Presentation
● D. Diagnostics
● E. Management
● F. Association
4. Persistent Truncus Arteriosus
● A. Pathogenesis
● C. Presentation
● D. Diagnostics
● E. Association
• Acyanotic
• Left à Right shunting
• Tends to be later presentation overall
• 3 D’s: ASD, VSD, PDA
• Cyanotic
• Right à Left shunting
• Early presentation (shortly after birth)
• Cyanotic Presentation: Blue skin discoloration, mucosal cyanosis, failure to thrive, dyspnea
• 5 T’s: Tetralogy of Fallot, TAPVR, Truncus Arteriosus, Tricuspid Valve Atresia, Transposition of Great Vessels
• General Presentation of Symptomatic Patient:
• Tachypnea
• Failure to thrive
• Cyanosis à Cyanotic CHD, Eisenmenger syndrome
• Recurrent bronchopulmonary infections à Acyanotic
• Diagnostics:
• Bubble study à Useful in detecting RàL shunts
Cardiology: Cyanotic Congenital Heart Defects https://commons.wikimedia.org/wiki/File:Heart_tetralogy_fallot.svg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Boot-shaped_heart.jpg
• Pathogenesis:
• Deviation of infundibular septum
• A. Pulmonic Stenosis (RVOTO)
• B. Overriding aorta
• C. Ventricular septal defect (VSD)
• D. RV hypertrophy
• Severity of RVOTO determines blood flow
• Mild RVOTO: L à R
• Severe RVOTO: R à L
• Presentation (tachypnea, cyanosis):
• Tet spells
• Harsh systolic ejection murmur, LUSB
• Diagnostics:
• CXR: Boot-shaped heart
• Management:
Hyperoxia Test:
• Severe: PGE1 à Surgery
100% O2 administered
• Knee to chest
~10 minutes
• Oxygen
Measure PaO2
• Associations:
• DiGeorge syndrome
• Down syndrome Pulmonary Dz: Congenital Heart Dz:
• Fetal alcohol syndrome ↑↑↑ PaO2 -/↑ PaO2
Cardiology: Cyanotic Congenital Heart Defects https://commons.wikimedia.org/wiki/File:D-tga-575px.jpg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Transposition-of-great-vessels.jpg
• Pathogenesis:
• Failed spiraling of aorticopulmonary septum à reversal of pulmonary artery and aorta
• Two parallel circuits
• RVà Aorta
• LV à Pulmonary artery
• Diagnostics:
• CXR: “Egg-on-a-string”
• Management:
• PGE1 à Surgery
• Balloon septoplasty
• Association:
• Maternal diabetes
Cardiology: Cyanotic Congenital Heart Defects Bootcamp.com
https://commons.wikimedia.org/wiki/File:Truncus_arteriosus.jpg
• Pathogenesis:
• Partial (incomplete) aorticopulmonary septum formation
• Failure of neural crest cell migration
• Mixing of oxygenated and deoxygenated blood at the ventricles
• Ventricular septal defect
• Harsh systolic ejection murmur, LLSB
• Diagnostics:
• Management:
• Surgery
• Association:
• DiGeorge syndrome
https://commons.wikimedia.org/wiki/File:Tricuspid_atresia.svg
• Pathogenesis:
• Absent tricuspid valve
• ↓↓↓ Blood to RVà RV hypoplasia, RA dilation
• Atrial septal defect
• Diagnostics:
• CXR: Cardiomegaly
• Management:
• PGE1 à Surgery
• Association:
• Ebstein Anomaly (Lithium exposure)
*Tetragenic exposure from lithium during early stages of pregnancy

is associated with the development of Ebstein Anomaly in the fetus*
Cardiology: Cyanotic Congenital Heart Defects https://commons.wikimedia.org/wiki/File:Tapv-575px.jpg Bootcamp.com
https://radiopaedia.org/articles/snowman-sign-total-anomalous-pulmonary-venous-return-1?lang=us
• Pathogenesis:
• Anomalous pulmonary veins
• Pulmonary veins à Right heart circulation (rather than LA)
• ↑ Pulmonary pressures
• Atrial septal defect
• Diagnostics:
• CXR: Snowman sign
• Management:
• Surgery
# Disease Principle Problem Distinguishing Unique CXR Associations

Features Findings
Persistent Truncus Arteriosus Incomplete Typically, with minimal ---- DiGeorge Syndrome
1 aorticopulmonary cyanosis initially
septum formation à
single vessel
Transposition of Great Vessels Failed spiraling of Severe cyanosis at birth Egg-on-a-string Maternal diabetes
2 aorticopulmonary Two parallel circuits,
septum à aorta and requires ASD, PFO,
pulmonary artery VSD, and/or PDA for
switched locations survival
Tricuspid Atresia No functional tricuspid Severe cyanosis at birth ↓ Pulmonary markings Ebstein Anomaly
3 valve, hypoplastic RV Requires ASD, PFO, (Lithium)
VSD, and/or PDA
Tetralogy of Fallot Deviation of infundibular Tet spells Boot-shaped heart DiGeorge syndrome
4 septum, pulmonic Down syndrome
stenosis, overriding Maternal alcohol use
aorta, RVH, VSD
Total Anomalous Pulmonary Venous Return Pulmonary veins drain Pulmonary hypertension Snowman sign ----
5 into right heart
circulation
≣ ⟽ ⟾
Question ID: 0051 Previous Next https://commons.wikimedia.org/wiki/File:E204_(CardioNetworks_ECGpedia).jpg
A 24-year-old male with a past medical history of bipolar type I disorder who presents to the emergency department with a 3-
week history of palpitations and dyspnea. He states that his symptoms occur sporadically with no clear trigger and last up to
30 minutes at a time. He denies any tobacco or illicit drug use and states that he has a glass of wine every weekend. Vital
signs include a temperature of 98.4F (36.9C), blood pressure of 110/88, heart rate of 66/min, and a respiratory rate of 12/min.
Physical examination reveals a 2/6 holosystolic murmur at the left sternal border. The murmur is accentuated with deep
inspiration. Electrocardiogram is shown below. Transthoracic echocardiography is performed. Which of the following imaging
findings would most likely be consistent with this patient’s initial presentation?
⚪ A. Right ventricular outflow tract obstruction

⚪ B. Right ventricular atrialization
⚪ C. Right ventricular structural attachment to aorta
⚪ D. Malpositioning of pulmonic veins
⚪ E. Single outflow vessel from right and left ventricles
OUTLINE
1. Arterial Disease 5. Chest Pain DDx

● A. Atherosclerosis
Cardiology:
6. Anti-anginal Therapy
● B. Mönckeberg Arteriosclerosis ● A. Nitrates
● C. Arteriosclerosis ● B. β-blockers
● C. Calcium Channel Blockers
Stable Angina and
2. Atherosclerosis
● A. Pathogenesis ● D. Ranolazine
● B. Location
Atherosclerosis
● C. Risk Factors
● D. Complications
3. Plaque Stability
● A. Stable
● B. Unstable
4. Coronary Artery Disease
● A. Angina Terminology
● B. Variant Disease
5. Stable Angina
● A. Pathogenesis
● C. Presentation
● D. Diagnostics
● E. Medical Management
6. Vasospastic Angina
● B. Presentation
● C. Diagnostics
● D. Associations
● E. Management
https://commons.wikimedia.org/wiki/File:Moenckeberg.jpg
Cardiology: Stable Angina and Atherosclerosis https://commons.wikimedia.org/wiki/File:Blausen_0055_ArteryWallStructure.png

https://commons.wikimedia.org/wiki/File:%22Onion-skin%22_renal_arteriole.jpg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Renal_arterial_hyalinosis_-_pas_-_very_high_mag.jpg
• Atherosclerosis
• Cholesterol plaque accumulation within vessel walls
• Intima classically involved
• Mönckeberg Arteriosclerosis
• Dystrophic calcification within vessel walls
• Media classically involved
• Lumen unaffected
• Arteriolosclerosis:
• Response to ↑ pressure
• Hyaline à pink amorphous deposits in arterial wall
• Hyperplastic à “Onion-skin” appearance
Cardiology: Stable Angina and Atherosclerosis https://commons.wikimedia.org/wiki/File:CT_image_of_atherosclerosis_of_the_abdominal_aorta.svg
Bootcamp.com
https://commons.wikimedia.org/wiki/File:Late_complications_of_atherosclerosis.PNG
• Pathogenesis:
• Endothelial stress à Dysfunction à Subendothelium exposure à Platelet binding à PDGF and cytokine release
• Monocyte's adhesion à Macrophages activated in vessel intima
• Smooth muscle cells recruited to intima via PDGF, FGF, endothelin-1, interleukin-1
• Macrophage and smooth muscle cell digestion of lipids (LDL) à Foam cells à Fatty streak
• Smooth muscle cell proliferation, deposition of extracellular matrix à Fibrous cap formation
• Fibrous atheroma (plaque) à Complex atheroma (calcification)
• Location:
• Abdominal aorta > Coronary artery > Popliteal artery > Carotid artery > Circle of Willis
• Risk Factors:
• Smoking
• Diabetes mellitus
• Hypertension
• Dyslipidemia (↑ LDL)
• Age
• Complications:
• Obstructive plaque à At risk for local vascular occlusion
• Plaque rupture à Thrombus at risk of vascular occlusion
• Aneurysm and rupture
Cardiology: Stable Angina and Atherosclerosis Bootcamp.com
• Stable Atherosclerotic Plaque:

• Progressive ↓ coronary blood flow
• ↑ growth factor release (ex. VEGF)
• Collateral circulation
• Unstable Atherosclerotic Plaque:
• Chronic inflammation à Macrophage activation à
• Metalloproteinases break down extracellular matrix proteins à Thin-cap fibroatheromas
• ↑ Risk of rupture à Rupture à Thrombus formed over plaque à Acute coronary syndrome
• Typical Angina: Requires all 3 criteria below are met

• Retrosternal chest pain
• Worsened with exertion or emotional stress
• Improved with rest or nitroglycerin
• Atypical Angina: 2 out of 3 criteria are met
• Nonanginal: Less than 2 out of 3 criteria are met
Coronary Artery
Disease
Acute
Angina Coronary
• Stable Angina: Atherosclerotic lesion, >70% stenosis Syndrome
• Vasospastic Angina: Hyperactive vascular smooth muscle
• Unstable Angina: Atherosclerotic lesion, partially obstructive thrombus
• NSTEMI: Atherosclerotic lesion, partially obstructive thrombus Unstable
Stable Angina NSTEMI
• STEMI: Atherosclerotic lesion, completely obstructive thrombus Angina
Vasospastic
STEMI
Angina
• Pathogenesis:
• Fixed stenosis of coronary vessel (>70%) without tissue infarction
Pathophysiology:
• Atherosclerotic disease (usually) à ↓ Coronary perfusion
• Temporary oxygen supply-demand mismatch with activity
• Presentation:
• Reproducible symptoms with activity
• ↑ Symptoms with ↑ myocardial oxygen demand à Exercise, dobutamine
• ↓ Symptoms with ↓ myocardial oxygen demand à Rest, nitroglycerin
• Classic chest pain: Retrosternal, radiating, non-pleuritic, non-reproducible to palpation
• Other: Chest pressure, tightness, squeezing
• Diagnostics:
Stress testing
• Exercise à ↑ Myocardial O2 demands
• Pharmacologic à Dobutamine, Dipyridamole, Adenosine à ↑ Myocardial O2 demands
• ECG used to evaluate for acute ST changes
• Echocardiography or myocardial perfusion scan can also be utilized
Cardiac angiography
ECG à No significant ST-changes
Cardiac enzymes à Not significantly elevated
• Medical Management:
• Antianginal therapy à Nitrates à Symptomatic relief
• Antiplatelet therapy à Aspirin or Clopidogrel à ↓ Risk of occlusive thrombus formation
• Statin therapy à Atorvastatin à ↓ Risk of acute coronary events
• Antihypertensive therapy (if applicable) à ACE inhibitor, ARB
• Transient, spontaneous coronary vasospasms
• Presentation:
• Recurrent chest pain/discomfort, resolving with minutes
• Classically occurring at night (↑ vagal tone)
• Not affected by exertion
• Younger patient, usually lacking risk factors for CAD (exception smoking)
• Diagnostics:
• ECG: ST-segment elevation with an episode
• -- Symptoms à Rest
• ↓ Symptoms à Nitroglycerin
• Associations:
• Tobacco use
• Cocaine
• Amphetamines
• Triptans, Ergot alkaloids
• Alcohol
• Management:
• Acute à Nitroglycerin
• Preventative à Avoid precipitating factors (ex. smoking), calcium channel blockers
• Nitrates
• Nitroglycerin (Sublingual à rapid effect)
• Isosorbide Dinitrate
• ↑ cGMP à peripheral and coronary vasodilation à ↓ preload, ↑ myocardial perfusion
• Right Ventricular MI: Avoid agents that ↓ preload
• Nitrate Tolerance: Maintain nitrate free intervals
• Adverse Effects: Hypotension, flushing, headaches
• Avoid with concomitant use of PDE-5 inhibitors (ex. Sildenafil)
• β-blockers
• Metoprolol
• ↓ cAMP à ↓ intracellular Ca2+
• β-Blocker Withdrawal Syndrome: ↑ HR, contractility à Angina, following discontinuation of β-blocker therapy
• Avoid in the setting of AV block
• Nondihydropyridine Calcium Channel Blockers
• Verapamil, Diltiazem
• ↓ Binding to calcium channels à ↓ intracellular Ca2+
• Avoid in setting of AV block
• Ranolazine
• Inhibition of late inward sodium channels à ↓ Ca2+ influx à ↓ intracellular Ca2+
• Adverse Effects: QT prolongation
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:Histopathology_of_progressive_atherosclerotic_lesions.jpg
A 69-year-old obese male with an unknown past medical history is rushed to the emergency department by friends after being
found unconscious in the bathroom. The patient and his friends were playing a poker game, drinking alcohol, smoking
cigarettes, and eating pizza. The patient left the room to use the bathroom and had not returned for approximately 45 minutes.
He was found face down on the floor, unconscious and unresponsive. The patient regained consciousness intermittently en
route to the emergency department with EMS during CPR. The patient was hemodynamically unstable on arrive despite
inotropic agents. Within minutes of arrival, he went into an episode of cardiac arrest and subsequently expired. Autopsy
performed revealed a complete thrombotic occlusion of the left main coronary artery. Several atheroma's were identified
throughout the coronary vasculature. A histological section is analyzed. A fibrous cap (FC) atheroma with a well-formed
necrotic core (NC) is observed and shown below. Which of the following cell types are most directly responsible for the
formation of FC?
⚪ A. Foam cells
⚪ B. Monocytes
⚪ C. Macrophages
⚪ D. Smooth muscle cells
⚪ E. Endothelial cells
OUTLINE
1. Overview 6. Management
● A. Unstable Angina ● A. Statin
Cardiology: ●
●
B. NSTEMI
C. STEMI
●
●
B. Antiplatelet
C. Glycoprotein IIb/IIIa Inhibitor
2. Myocardial Infarction ● D. Anticoagulation
Myocardial ●
●
A. Pathogenesis
B. Pathophysiology
●
●
E. Thrombolytics
F. Percutaneous Coronary Intervention
Infarction
● C. Left Ventricular Dysfunction
● D. Right Ventricular Dysfunction
● E. Myocardial Stunning
● F. Myocardial Hibernation
● G. Reperfusion Injury
3. Post-MI Timeline
● A. Acute Phase
● B. Inflammatory Phase
● C. Proliferative Phase
● D. Remodeling Phase
4. ECG Localization in STEMI
● A. Infarct Age
● B. ST-Elevations
● C. Lead Localization
5. Cardiac Biomarkers
● A. Troponin
● B. CK-MB
Cardiology: Myocardial Infarction Bootcamp.com
https://commons.wikimedia.org/wiki/File:Heart_attack-NIH.gif
• Unstable Angina:
• Atheromatous plaque rupture à Incomplete occlusion à No appreciable infarction
• ECG: T wave and ST-segment abnormalities are possible, no ST-elevation
• Cardiac biomarkers are not significantly elevated
• NSTEMI:
• Atheromatous plaque rupture à Incomplete occlusion à Subendocardial infarction
• ECG: T wave and ST-segment abnormalities are possible, no ST-elevation
• Cardiac biomarkers are significantly elevated
• STEMI:
• Atheromatous plaque rupture à Complete occlusion à Transmural infarction
• ECG: Peaked T-waves à ST-elevation (minutes) à deep Q-waves (hours)
• New LBBB can be suggestive of STEMI
• Cardiac biomarkers may be significantly elevated
• Pathogenesis:
• Complete occlusion (usually) of coronary vessel (LAD most common)
• Atheromatous plaque rupture is classic à Acute thrombus occludes vessel lumen
• Pathophysiology
• ↓ Aerobic metabolism à ↑ Anaerobic metabolism à ↑ Lactate, ↓ ATP (Reversible if rapid reperfusion)
• ↓ Contractility due to ischemic insult à Heart failure, cardiogenic shock
• Left Ventricular Dysfunction:
• Anterolateral MI à Leads I, aVL, V1-V6
• Supply: Left main, LCX and/or LAD
• ↓ Contractility à ↓ Cardiac outputà Cardiogenic shock
• Left-sided heart failure à ↑ PCWP à PHTN à Pulmonary edema à ↑ CVP
• Right Ventricular Dysfunction
• Inferior wall MI à Leads II, III, aVF
• Supply: Posterior descending artery (RCA in right-dominant circulation)
• Right-sided heart failure à Preload-dependency, ↑ CVP in setting of normal or ↓ PCWP
• Avoid ↓ preload if possible (venodilators, diuresis)
• Electrical conductivity defects
• Myocardial Stunning:
• Reperfusion to myocardium à Delay in return of complete normal function
• Myocardial Hibernation:
• Chronic ischemic myocardium à Left ventricular adaptation à Ischemic cardiomyopathy, LV systolic dysfunction
• Reperfusion Injury:
• Reperfusion to myocardium à Oxidative and inflammatory damage to myocardium
https://commons.wikimedia.org/wiki/File:Histopathology_of_myofiber_waviness_in_myocardial_infarction.jpg
https://commons.wikimedia.org/wiki/File:Glanzstreifen.jpg
https://commons.wikimedia.org/wiki/File:Histopathology_of_myocardial_infarction_with_karyorrhexis_and_few_lymphocytes.jpg
• Acute Phase (First 24 hours): https://commons.wikimedia.org/wiki/File:Histopathol

ogy_of_fibroblast_proliferation_and_early_collagen
• Gross exam: No abnormal changes up to about 12 hours _deposition_in_myocardial_infarction.jpg
• Histopathology: ↑ Neutrophils, bordering wavy fibers, cytoplasm hypereosinophilia, pyknotic nuclei
• Inflammatory Phase (Hours-Days): https://commons.wikimedia.org/wiki/File:Histopatho
logy_of_dense_fibrous_scar_replacing_myocyte_l
• ↑ Inflammatory response oss_in_myocardial_infarction.jpg
• Macrophages and neutrophils à Phagocytose necrotic tissue, release cytokines à Stimulate tissue proliferation
• Histopathology: Coagulative necrosis, loss of nuclei, neutrophil and macrophages present
• Proliferative Phase (Days-Weeks):
• ↓ Inflammatory response (TGF-β)
• Fibroblasts à Collagen deposited (Type I and III) à ↓ Electrical conductivity through areas of fibrosis
• Histopathology: Granulation tissue, collagen deposition
• Remodeling Phase (Weeks-Months):
• ↓ Inflammatory response (TGF-β)
• Matrix metalloproteinases à Collagen crosslinking à Scar tissue
• Histopathology: Scar tissue, ↑ Collagen, ↓ Cellularity
Cardiology: Myocardial Infarction https://commons.wikimedia.org/wiki/File:Heart_pseudoaneurysm_a4c.jpg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Heart_lv_aneurysm_4c.jpg
• Acute Phase (First 24 hours):

• Ventricular arrhythmia à Sudden cardiac death
• Papillary muscle rupture (posteromedial papillary muscle à posterior descending artery occlusion) à Acute mitral regurgitation
• Interventricular septal rupture à Ventricular septal defect
• Inflammatory Phase (Hours-Days):
• Peri-infarction pericarditis à Inflammatory response near infarct à Diffuse STE, pleuritic chest pain
• Interventricular septal rupture
• Proliferative Phase (Days-Weeks):
• Left ventricular pseudoaneurysm (right coronary artery occlusion is classic) à Mural thrombus
• Left ventricular free wall rupture à Cardiac tamponade
• Remodeling Phase (Weeks-Months):
• Left ventricular aneurysm à Persistent STE and TWI, ↑ Risk of free wall rupture and mural thrombus
• Dressler syndrome à Antibodies against myocardium à Diffuse STE, pleuritic chest pain
• Reinfarction risk ↑ over time
Cardiology: Myocardial Infarction https://commons.wikimedia.org/wiki/File:EKG_leads.png Bootcamp.com
https://commons.wikimedia.org/wiki/File:Blausen_0256_CoronaryArteries_02.png
https://commons.wikimedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.svg
• Infarct Age:
• Hyperacute à Peaked T-waves
• Acute à ST-elevations, new LBBB
• Chronic (Previous MI) à Deep Q-waves, T-wave inversions
• ST elevations:
• Peaked T-waves (initial)
• ST-elevation in 2 contiguous leads
• Reciprocal ST-depression
Location Leads Affected Artery
Lateral I, aVL, V5-V6 Left lateral circumflex
Anterior V1-V4 Left anterior

descending
Anterolateral I, aVL, V1-V6 Left main
Inferior II, III, aVF Right coronary
Posterior ST depression and tall R Posterior descending

waves in V1-V3 artery
ST elevation in V7-V9
https://commons.wikimedia.org/wiki/File:EKG_leads.png
Location Leads Affected Artery
Lateral I, aVL, V5-V6 Left lateral circumflex
Anterior V1-V4 Left anterior

descending
Anterolateral I, aVL, V1-V6 Left main
Inferior II, III, aVF Right coronary
https://commons.wikimedia.org/wiki/File:ECG_001.jpg
Posterior ST depression and tall R Posterior descending

waves in V1-V3 artery
ST elevation in V7-V9
https://commons.wikimedia.org/wiki/File:AMI_bloodtests_engl.png
• Troponin
• Peak: 12-48 hours
• Return to normal: 5-14 days
• CK-MB
• Peak: 24 hours
• Return to normal: 48-72 hours
• Potential marker for re-infarction
https://commons.wikimedia.org/wiki/File:HWI_PTCA.jpg
• Statin:
• Atorvastatin, Rosuvastatin: HMG-CoA reductase inhibitor à ↓ LDL, stabilize plaque, ↓ inflammation
• Antiplatelet:
• Aspirin: Inhibition of cyclooxygenase à Irreversible inhibition of platelet aggregation
• Clopidogrel: P2Y12 inhibitor à Irreversible inhibition of platelet aggregation
• Glycoprotein IIb/IIIa Inhibitor::
• Abciximab, Eptifibatide, Tirofiban: Inhibition of fibrinogen binding to platelets
• Can be utilized in preparation for PCI
• Anticoagulation:
• Heparin: ↑ activity of antithrombin III à ↓ thrombin and factor Xa
• Thrombolytics (Fibrinolytics):
• Alteplase, tenecteplase (tPA) à ↑ Plasmin à Fibrin thrombus breakdown
• ↑ Risk of bleeding
• Percutaneous Coronary Intervention (PCI):
• Preferred for revascularization in STEMI
• Femoral or radial artery access site
• Balloon dilation over atheromatous plaque +/- stent placement
• Door-to-balloon time 90 minutes or less
• PCI not typically performed when >120 minutes from first medical contact
≣ ⟽ ⟾
Question ID: 0052 Previous Next https://commons.wikimedia.org/wiki/File:Mushroom-cloud-a-giant-left-ventricular-
pseudoaneurysm-after-a-myocardial-infarction-due-to-1476-7120-7-36-S2.ogv
A 63-year-old male with a past medical history of hyperlipidemia and type II diabetes mellitus presents to the emergency
department with progressively worsening retrosternal chest discomfort and dyspnea for the past week. He states that he
frequently wakes up in the middle of the night due to the pain. The patient was recently admitted for percutaneous coronary
intervention for a complete obstruction of the right coronary artery approximately 1 week earlier. On physical examination
blood pressure is 156/88 mmHg, heart rate is 84 beats/min, respiratory rate is 12/min, and oxygen saturation is 97% on room
air. Electrocardiogram reveals deep Q waves in leads II, III, and aVF. Chest X-ray reveals cardiomegaly with clear lung fields.
Echocardiography is shown below. Doppler flow reveals the presence of bidirectional turbulent flow into an ominous
“mushroom cloud”. Which of the following best describes the cause of this patient’s presentation?
⚪ A. Localized thinning and dyskinesia of myocardium

⚪ B. Contained left ventricular free wall rupture
⚪ C. Open left ventricular free wall rupture into pericardium
⚪ D. Interventricular septal wall rupture
⚪ E. Posteromedial papillary muscle rupture
OUTLINE
1. Peripheral Venous Disease

● A. Lower Extremity Veins
Cardiology: ●
●
B. Chronic Venous Insufficiency
C. Deep Vein Thrombosis
Peripheral Venous
● D. Migratory Superficial Thrombophlebitis
2. Peripheral Artery Disease
● A. Lower Extremity Arteries
and Arterial
● B. Peripheral Arterial Disease
● C. Leriche Syndrome
● D. Ankle-Brachial Index
Disease 3. Lower Extremity Ulcer Comparison

●
●
A. Venous Ulcer
B. Arterial Ulcer
● C. Neuropathic Ulcer
Cardiology: Peripheral Venous and Arterial Disease Bootcamp.com
https://commons.wikimedia.org/wiki/File:Leg_Before_1.jpg
• Lower Extremity Veins Affected in PVD

• Superficial: Great saphenous, small saphenous veins
• Deep: Anterior, Posterior tibial + Fibular veins à Popliteal vein à Femoral vein à External iliac vein
• Chronic Venous Insufficiency:
• Incompetent venous valves à Blood remains in veins à ↑ Venous hydrostatic pressure
• Tortuous dilated superficial veins (Varicose veins)
• Presentation: Lower extremity pain, skin pigmentation of medial malleolus, varicose veins
• Improves with ↓ venous hydrostatic pressure (raising leg)
• Improves with ambulation
• Venous Duplex U/S: Venous reflux
• Symptomatic Management: Compression stocks, leg elevation
• Definitive Management: Vein ablation
• Complications: Venous ulcer à Proximal to ankle, +/- infection
• Complications: Stasis dermatitis, chronic edema
• Deep Vein Thrombosis
• Virchow’s Triad: Venous stasis, damage, hypercoagulability
• Unilateral (classically)
• Homan’s sign
• Erythematous swelling
• D-dimer: Negative test à Rules out (SN-OUT)
• Positive D-dimer does not diagnose a DVT!
• Venous Duplex U/S: Incompressible, luminal mass, ↓ flow
• Management: Anticoagulation, IVC filter
• Complication: Pulmonary embolus
• Migratory Superficial Thrombophlebitis
• Trousseau syndrome
• Classically associated with malignancy
• Hypercoagulability à Superficial venous thrombus
• Recurring at multiple sites
https://commons.wikimedia.org/wiki/File:2136ab_Lower_Limb_Veins_Anterior_Posterior.jpg
https://commons.wikimedia.org/wiki/File:Chronicvenousinsufficiency.jpg
https://commons.wikimedia.org/wiki/File:GangreneFoot.JPG
• Lower Extremity Arteries Affected in PAD

• Femoral artery à Popliteal artery à Anterior, Posterior tibial and Fibular arteries
• Peripheral Arterial Disease:
• Atherosclerosis à ↓ Arterial perfusionà ↑ Venous hydrostatic pressure
• Smoking is primary risk factor
• Presentation: Intermittent claudication (calf is classic) à Worse with exertion, improves with rest
• Weakened pulses (femoral, posterior tibial, dorsalis pedis)
• Absent hair growth, cyanosis peripheral to lesion
• Improves with ↑ arterial hydrostatic pressure (lowering leg)
• Worsened with ambulation and leg elevation (elevation pallor)
• Duplex U/S: Venous reflux
• Management: ↓ Modifiable risk factors (smoking), graded exercise therapy, cilostazol
• Definitive Management: Vein ablation
• Complications: Arterial ulcer à Pressure points, lateral malleolus is classic
• Complications: Distal gangrene
• Leriche Syndrome:
• Triad: Bilateral hip/thigh claudication, erectile dysfunction, diminished femoral pulses
• Ankle-Brachial Index:
• Systolic Ankle BP / Systolic Brachial BP (some stipulations)
• < 0.9 suggests PAD
https://commons.wikimedia.org/wiki/File:Blausen_0607_LegArteries.png
Type Location Exacerbating Pain Improving Pain Other
Proximal to ankle At rest, gravity dependent Activity, leg raise Varicose veins
Venous Peripheral edema
Pressure points Activity, leg raise At rest, gravity dependent ABI < 0.9
Arterial
↓ DP and PT pulses
Cyanosis, absent hair peripheral

to lesion
Plantar surface of foot Absent pain Absent pain Diabetic peripheral neuropathy
Neuropathic
Diminished S1 reflex
≣ ⟽ ⟾
A 65-year-old female with a past medical history of morbid obesity, chronic systolic heart failure, and poorly controlled hypertension who presents
to her primary care provider for a “sore above her foot”. The patient states that she noticed a small wound above her left ankle two months earlier
that has been progressively growing in size. She also reports noticing some yellow-gray color fluid draining from the wound this morning. The
patient mentions that she prefers to keep moving since the pain is worse when resting. The patient has a 1cm superficial irregularly-shaped ulcer
located on the medial lower leg approximately 10cm above the medial malleolus. The wound is actively draining purulent exudate. Peripherally,
the patient has evidence of brown discoloration leading up to the pretibial surface of the leg. Both lower extremities demonstrate 2+ pitting edema
up to the knee. The patient is tender to light palpation in the area surrounding the lesion. Which of the following best describes the mechanistic
etiology of this patient’s ulcer?
⚪ A. Sensory neuropathy
⚪ B. Decreased arterial luminal diameter
⚪ C. Peri-local mechanical stress
⚪ D. Infection of glandular tissue
⚪ E. Elevated venous hydrostatic pressure
OUTLINE
1. Overview 6. Antihypertensives
● A. ACE Inhibitors
Cardiology:
2. Essential Hypertension
● A. Pathophysiology ● B. Angiotensin Receptor Blockers
● B. Risk Factors ● C. Calcium Channel Blockers
● D. Thiazide Diuretics
Hypertension
● C. Screening
● E. β-blockers
3. Hypertension Variants
● F. Nitrates
● A. White Coat Hypertension
● G. Hydralazine, Minoxidil
● B. Isolated Systolic Hypertension
● C. Hypertensive Urgency
● D. Hypertensive Emergency
4. Hypertensive End-Organ Disease
● A. Cardiovascular
● B. Neurovascular
● C. Renovascular
5. Secondary Hypertension
● A. Aortic Coarctation
● B. Cushing Syndrome
● C. Hyperaldosteronism
● D. Renal Artery Stenosis
● E. Obstructive Sleep Apnea
● F. Pheochromocytoma
● G. Hyperthyroidism
Cardiology: Hypertension Bootcamp.com
• Definition:
• JNC 8: SBP ≥ 140 mmHg and/or DBP ≥ 90mmHg
• Essential Hypertension:
• Majority of cases
• Idiopathic
• Secondary Hypertension
• Underlying etiology à treat cause, treat HTN
• Uncommon
• MAP = CO x TPR = (SV x HR) x TPR
• SV ~ Preload à ↑ Serum Na+
• HR à Anxiety/stress
• TPR à Atherosclerosis
• Risk Factors:
• Older age, ethnicity
• Obesity
• Diabetes Mellitus
• Tobacco use
• High sodium diet
• Screening:
• >40 years old or ↑ risk à Screen annually (USPSTF)
• White Coat Hypertension:

• ↑ BP in clinical setting
• Normal BP at home
• Isolated Systolic Hypertension
• Elderly patient
• Normal DBP
• ↑ Arterial stiffness, ↓ arterial compliance
• Hypertensive Urgency
• ≥180/120 mmHg (no evidence of end-organ damage)
• Hypertensive Emergency
• ≥ 180/120 mmHg + evidence of end-organ damage
• Rx: Labetalol
• Rx: Nitrates (Angina)
• Rx: Fenoldopam (AKI)
Cardiology: Hypertension https://commons.wikimedia.org/wiki/File:Papilledema.jpg Bootcamp.com
https://commons.wikimedia.org/wiki/File:Hypertensiveretinopathy.jpg
• Cardiovascular:
• Concentric LVH à Diastolic heart failure (↑ β-myosin heavy chain)
• Coronary artery disease
• Aortic dissection
• Neurovascular:
• Lacunar CVA (classic)
• Retinopathy
• Diabetes Mellitus
• Tobacco use
• High sodium diet
• Renovascular:
• Chronic kidney disease
• Hyperplastic arteriosclerosis à “onion skin” appearance
• Aortic Coarctation:
• Asymmetric BP between arms and legs
• Brachial-femoral pulse delay
• Cushing Syndrome:
• Iatrogenic common cause
• Central obesity, proximal muscle weakness, hirsutism, abdominal striae, “moon facies”
• Hyperaldosteronism
• Metabolic alkalosis, hypokalemia +/- hypernatremia
• Renal Artery Stenosis
• Young patient à Fibromuscular dysplasia
• Older patient à Atherosclerosis
• Unilateral à Hypoperfusion à Atrophy of affected kidney (Contralateral renal hypertensive nephrosclerosis)
• Obstructive Sleep Apnea:
• Snoring, intermittent period of apnea reported by patient partner
• Daytime sleepiness
• Rx: CPAP qhs
• Pheochromocytoma:
• Episodes of ↑ sympathetic response
• Serum metanephrines à 24h urinary metanephrines
• Rx: Irreversible non-selective ⍺-block à β-blocker à Surgery
• Hyperthyroidism:
• ↓ TSH, ↑ free T4
• Pretibial myxedema, heat intolerance, ↑ pulse pressure, exophthalmos, goiter
https://commons.wikimedia.org/wiki/File:%22Onion-skin%22_renal_arteriole.jpg

• Inhibition of ACE à ↑ angiotensin I and renin, ↓ angiotensin II
• Adverse Effect: Dry cough, hyperkalemia, angioedema, teratogenic
• Adverse Effect: Hyperkalemia, teratogenic
• Dihydropyridine Calcium Channel Blockers (Amlodipine, Nifedipine)
• Adverse Effect: Peripheral edema
• Thiazide Diuretic (Hydrochlorothiazide, Chlorthalidone)
• Adverse Effect: Hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia, hyponatremia
• β-blockers
• Labetalol: Blockade of β1, β2, ⍺1 à Hypertensive emergency
• Metoprolol: Blockade of β1 receptorsà Added for heart failure, coronary artery disease, atrial fibrillation
• Adverse Effect: Bradycardia
• Nitrates (Sodium nitroprusside)
• ↑ cGMP à ↓ Intracellular Ca2+ à Venous and arterial vasodilation (Nitroglycerin primarily venous)
• Adverse Effect: Reflex tachycardia, Monday’s Disease, cyanide toxicity (chronic use), avoid with PDE-5 inhibitors
• Hydralazine, Minoxidil
• Arterial vasodilation
• Hydralazine used in pregnancy
• Adverse Effect: Reflex tachycardia, peripheral edema, DIL (Hydralazine)
≣ ⟽ ⟾
A 41-year-old male with a past medical history of intermittent asthma as an adolescent presents to his primary care physician stating that he has
worsening of his panic attacks over the past two months. He reports episodes of diffuse sweating and palpitations that last approximately 10
minutes on average with some instances lasting up to one hour. The patient reports increased frequency of symptoms when he is active or
exercising. He also states that he has had unrelenting headaches when the episodes are at their worst. The patient is currently not taking any
medications and denies any alcohol or recreational drug use. Vital signs reveal a temperature of 98F (36.7C), blood pressure of 154/92 mmHg,
heart rate of 112/min, and a respiratory rate of 18/min. Physical examination reveals tachycardia with a regular rhythm and is otherwise relatively
unremarkable. An electrocardiogram reveals sinus tachycardia. A detailed workup is performed revealing a large left-sided adrenal mass. A
decision is made to proceed with laparoscopic tumor resection. Prior to the procedure, two antihypertensive medications were given. Which of the
following was most likely the first of these medications administered to the patient?
⚪ A. Nephron inhibitor of Na/K/Cl cotransporters

⚪ B. Nephron inhibitor of Na/Cl cotransporters
⚪ C. Nonselective ⍺-blocker
⚪ D. Nonselective β-blocker
⚪ E. Cardioselective β-blocker
OUTLINE
1. Acute Pericarditis
● A. Pathogenesis
Cardiology: ●
●
B. Etiology
C. Presentation
Pericardial
● D. Diagnostics
● E. Management
● F. Complications
Disease
2. Constrictive Pericarditis
● A. Pathogenesis
● B. Etiology
● C. Presentation
● D. Diagnostics
● E. Management
3. Pericardial Effusion
● A. Pathogenesis
● B. Etiology
● C. Diagnostics
● D. Management
4. Cardiac Tamponade
● A. Pathogenesis
● B. Etiology
● C. Presentation
● D. Diagnostics
● E. Management
● F. Complication
Cardiology: Pericardial Disease Bootcamp.com
https://commons.wikimedia.org/wiki/File:PericarditisECG.JPG
• Pathogenesis:
• Pericardial inflammation
• Etiology:
• Viral à Coxsackie B virus (classic)
• Bacterial
• Myocardial infarction à Peri-infarction pericarditis, Dressler syndrome
• Post-operatively, Blunt or penetrating trauma
• Uremia
• Radiation
• Autoimmune
• Presentation:
• Pleuritic, sharp, retrosternal chest pain
• Improves with leaning forward
• Worsens with lying down
• +/- Fever
• Friction rub
• Diagnostics:
• ECG: Diffuse ST-elevations, PR-depressions
• CXR: Non-specific, enlarged silhouette
• Echocardiography: Non-specific, +/- pericardial effusion
• Management:
• Treat underlying etiology
• Conservative
• NSAIDs symptomatic control and preventative
• Complications:
• Constrictive pericarditis
• Pericardial effusion à Tamponade
https://intjem.biomedcentral.com/articles/10.1186/1865-1380-5-37/figures/1
• Pathogenesis:
• Fibrous pericardium à Restricted right ventricular filling
• Etiology:
• Chronic Pericarditis
• Radiation
• Tuberculosis
• Presentation:
• Jugular venous distension
• Kussmaul sign
• Hepatomegaly
• Pericardial knock
• Pulsus paradoxus
• Diagnostics:
• ECG: Non-specific, low voltage
• CXR: Thickening of pericardium, calcifications
• Echocardiography: Thickening of pericardium
• Management:
• Variable depending on severity
• Pericardiectomy
https://commons.wikimedia.org/wiki/File:Electrical_Alternans.JPG https://commons.wikimedia.org/wiki/File:PericardialeffusionUS.PNG
• Pathogenesis:
• Fluid accumulation within pericardial space
• Etiology:
• Acute pericarditis
• Malignancy
• Presentation:
• Incidental finding (common)
• Orthopnea
• Chest pain
• Diagnostics:
• CXR: Water-bottle sign (if massive)
• ECG: Electrical alternans, low voltage
• Echocardiography: Pericardial fluid
• Management:
• Conservative vs Pericardiocentesis
https://commons.wikimedia.org/wiki/File:Pericarditis_can_progress_to_pericardial_effusion_and_eventually_cardiac_tamponade.jpg https://commons.wikimedia.org/wiki/File:Massivepericarialeffusion.png
• Pathogenesis:
• Rapid ↑ in pericardial effusion à ↑↑↑ Pericardial pressure à Chamber compression
• Etiology:
• Aortic dissection
• Ventricular free wall rupture (Complication of MI)
• Post-operative, trauma
• Worsening of pericardial effusion
• Presentation:
• Beck’s Triad: Hypotension, ↑ JVP, Muffled heart sounds
• Pulsus paradoxus
• Tachycardia
• Diagnostics:
• Echocardiography: Collapsing cardiac chambers
• Similar EDP throughout cardiac chambers
• Management:
• Pericardiocentesis (generally)
• Pericardial window (hemopericardium)
• Complication:
• Obstructive shock à Cardiac arrest à PEA
≣ ⟽ ⟾
https://commons.wikimedia.org/wiki/File:33-01-Pericarditis_calcarea_pa.png
A 67-year-old female presents to the emergency department with shortness of breath. She states that her symptoms have
progressively been worsening and are most notable when climbing stairs in her home. She has a 50-pack year smoking
history and a history of non-metastatic esophageal carcinoma. The patient has completed a course of chemoradiation therapy
6 months earlier. She denies any family history of heart disease. Vital signs reveal a temperature of 98.7F (37.1C), blood
pressure of 94/58 mmHg, heart rate 102/min, and a respiratory rate of 14/min. Jugular venous distension and hepatomegaly
are observed. Lung sounds are vesicular in nature. Systolic blood pressure measured in deep inspiration is 76 mmHg. Chest
X-ray is shown. Which of the following findings would be most consistent with the jugular venous tracing observed in this
patient?
⚪ A. Prominent x and y descent

⚪ B. Prominent v waves
⚪ C. Cannon a waves
⚪ D. Absent a waves
⚪ E. Absent y descent
OUTLINE
1. Overview
● A. General Principles
Cardiology: ● B. Management
2. Hypovolemic Shock
Shock ●
●
●
B. Etiology
C. Hemorrhagic Shock
E. Management
3. Cardiogenic Shock
● B. Etiology
● C. Presentation
4. Obstructive Shock
● B. Etiology
● C. Presentation
5. Septic Shock
● B. Etiology
● C. Presentation
6. Anaphylactic Shock
● B. Etiology
● C. Presentation
7. Neurogenic Shock
● B. Etiology
● C. Presentation
Cardiology: Shock Bootcamp.com
• General:
• ↓ Organ perfusion à ↑ Lactic acidosis à ↑ AG-metabolic acidosis
• ↑ Ventilation à ↓ PaCO2 à Compensatory respiratory alkalosis
• Management:
• Variable for each disease process
• Treat underlying pathology if possible
• IVF +/- blood products (when applicable)
• Adrenergic agonists (vasopressors) à Phenylephrine, norepinephrine
Shock Disturbance Compensation CVP PCWP Stroke Volume Heart Rate TPR
(forward)
Hypovolemic ↓ Circulating
volume
↑ HR, ↑ TPR ↓ ↓ ↓ ↑ ↑
Cardiogenic ↓ LV function ↑ HR, ↑ TPR
↑ ↑ ↓ ↑ ↑
Obstructive
↓ Forward flow ↑ HR, ↑ TPR ↑ ↑/↓ ↓ ↑ ↑
Septic Systemic
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
Anaphylactic Systemic
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
Neurogenic Systemic
vasodilation
Minimal ↓ ↓ ---/↓ ---/↓ ↓
• Disturbance: ↓ Circulating volume à ↓ LVEDV à ↓ SV à ↓ CO
• Compensation: ↑ HR, ↑ TPR
• Etiology:
• Hemorrhage à Traumatic injury, UGIB
• Severe dehydration à Diarrhea, burn, iatrogenic
• Hemorrhagic Shock Classification:
• Tachycardia (early), hypotension (later)
• ↑ HR, ↓ MAP, ↑ RR, ↓ UOP
• Presentation:
• Cold, clammy skin
• Low volume status à ↓ skin turgor, dry oral mucosa, ↓ JVP, pre-renal azotemia (BUN/Cr > 20:1)
• Management:
• Blood pressure support
• Hemorrhagic: Eliminate sources of bleeding, blood products, crystalloid solutions
(forward)
volume
↑ HR, ↑ TPR ↓ ↓ ↓ ↑ ↑
• Disturbance: LV failure à ↓ Contractility, ↓ SV à ↓ CO
• Etiology:
• Cardiovascular disease à MI (MCC), HF, arrhythmias
• Trauma
• Iatrogenic
• Presentation:
• Chest pain, dyspnea, palpitations
• High volume status (Low ECV) à ↑ JVP
• Management:
• Inotropic agent when applicable
• MI à Revascularization, thrombolytic
• Arrhythmia à Antiarrhythmic
(forward)

↑ ↑ ↓ ↑ ↑
• Disturbance: Obstruction to forward flow à ↓ CO
• Etiology:
• Pulmonary disease: Tension pneumothorax, PHTN, PE
• Pericardial disease: Cardiac tamponade, constrictive pericarditis
• Myocardial disease: Restrictive cardiomyopathy
• Aortic disease: Aortic dissection, aortic stenosis
• Presentation:
• High volume status (Low ECV) à ↑ JVP
• Correlate with specific etiology presentation
(forward)
Obstructive
• Disturbance: Systemic vasodilation à ↓ TPR
• Initial Compensation: ↑ HR, ↑ SV à ↑ CO
• Late Stage: ↓ Circulating volume à à ↓ LVEDV à ↓ SV à ↓ CO
• Etiology:
• Sepsis, inflammatory response
• Presentation:
• Warm, dry skin (early) à Cold, clammy skin (late)
• ↑ Mixed venous O2 saturation
• Correlate with specific etiology presentation
• Management:
• Antibiotics
(forward)
Septic Systemic
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
• Disturbance: Mast cell degranulation à ↑ Histamine à ↓ TPR
• Initial Compensation: ↑ HR, ↑ SV à ↑ CO
• Late Stage: ↓ Circulating volume à à ↓ LVEDV à ↓ SV à ↓ CO
• Etiology:
• Type I hypersensitivity
• Presentation:
• Management:
• Epinephrine
(forward)
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
• Disturbance: ↓ SNS à ↓ TPR
• No compensation in HR or contractility
• Etiology:
• Autonomic dysregulation
• Presentation:
• Hypotension in setting of bradycardia
• Differential:
• β-blocker overdose à Glucagon
• Management:
• Atropine
(forward)
Neurogenic Systemic
vasodilation
Minimal ↓ ↓ ---/↓ ---/↓ ↓
(forward)
volume
↑ HR, ↑ TPR ↓ ↓ ↓ ↑ ↑
↑ ↑ ↓ ↑ ↑
Obstructive
Septic Systemic
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
vasodilation
↑ HR, ↑ SV ↓ ↓ ↑ ↑ ↓
Neurogenic Systemic
vasodilation
Minimal ↓ ↓ ---/↓ ---/↓ ↓
≣ ⟽ ⟾
A 57-year-old male is sent to the emergency department from his cardiologist’s office for severe chest pain and diaphoresis.
He is a former smoker and has a history of poorly controlled type II diabetes mellitus, dyslipidemia, and symptomatic
peripheral artery disease. ECG reveals ST-segment elevation in the anterolateral leads. The patient undergoes
revascularization without complication. The patient is subsequently discharged and returns one week later with dyspnea and
pre-syncope. Blood pressure is 84/58mmHg, heart rate 110/min, respiratory rate is 20/min. Heart sounds are difficult to
auscultate. Hepatomegaly and modest jugular venous distention are appreciated. Low voltage R waves are observed on ECG
with alternating amplitudes. Chest X-ray is shown below.
Which of the following pathophysiologic changes most correlate with this patient’s current presentation?
Central Venous Pulmonary Cardiac Output Total Peripheral

Pressure Capillary Wedge Resistance
Pressure
⚪A ↓ ↓ ↑ ↓
⚪B ↓ ↓ ↓ ↓
⚪C ↓ ↓ ↓ ↑
⚪D ↑ ↑ ↓ ↑
⚪E ↑ ↓ ↓ ↑

Cardiology

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Cardiology

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OUTLINE

Heart begins beating

• Step 1: Septum Primum Forms

Ventricular Septal Defects most commonly occur due to defects in

• First Arch: Maxillary Artery

Pharyngeal Arches Pharyngeal Pharyngeal

Fourth Aortic Arch (L) CN X: Superior -Cricothyroid Superior thyroid Coarctation of

1. General Anatomical Overview

• Mid-Left Sternal Border 3rd-4th Intercostal Space:

• Atrial Fibrillation Foci:

• Right Coronary Artery (RCA):

• All coronary veins drain into the coronary sinus

• Swan-Ganz Catheter (Pulmonary Artery Catheter):

A 25-year-old female presents to the emergency room with

Which of the following locations is likely a source of aberrant

⚪ A. Cavotricuspid isthmus of right atrium

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

• Superior Vena Cava Syndrome

• Internal Thoracic (Mammary) Artery

• NAVEL (lateral to medial)

⚪ A. Right vertebral artery

• End-Diastolic Volume: ~ Preload

• Physiologic Mechanism: ↓ Vagal tone à SA Node à ↑ HR

Maximal HR = 220 bpm – Age (in years)

• Total Peripheral Resistance (TPR) = Determined by state of arteriolar resistance

• Left Ventricular Coronary Blood Flow: ↑ Ventricular diastole

A 57-year-old male presents to the emergency department for a

Which of the following is most consistent with this patient’s

⚪ A. Elevated systolic aortic pressures

1. Cardiac Function Curves

Cardiology: 2. Venous Return Curves

Cardiac Function ● B. Specific Pathologic Processes

• Cardiac Function Curve:

• Venous Return Curve:

• Acute Hemorrhage: Disruption: ↓ blood volume

Slope of Cardiac Function Curve à Contractility, Heart rate, Afterload

A 67-year-old male with a chronic smoking history presents to the emergency

Loops 3. Valvular Disease

1. Endothelial Regulated Vasodilation

Cardiology: ● A. Mechanism of Action

• Skeletal Muscle (Major Differences from Cardiac Myocytes):

⚪ A. Increased inhibition of adenylyl cyclase

Cardiology: ● A. Key Principles

Pressure and ● B. Resistance

• Carotid Sinus and Aortic Arch Baroceptors:

Temperature: 97.8F (36.6C)

Blood pressure when lying supine: 144/88 mmHg

Blood pressure when standing: 110/56

⚪ A. Carotid sinus hypersensitivity

1. Auscultation 5. Classic Disorders

⚪ A. Wide-fixed splitting of S1 heart sounds

Renin- ● D. Natriuretic Peptides

• Actions Angiotensin II:

• Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP)

• ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril)

A 68-year-old female with a past medical history of

Which of the following primary changes in chemical

Renin Angiotensin I Angiotensin II Aldosterone

• Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference

A 26-year-old female professional cyclist is training for a 143-

Temperature: 97.2F (36.2C)

Hemoglobin O2 Saturation (%)

Which of the following is most consistent with the