WHO KILLED ALASKA? #15: "5½ STORIES Part Two" Transcript .pdf
Bootcamp.com Cardiology.pdf
1.
2.
3. OUTLINE
1. Embryologic Derivatives
2. Truncus Arteriosus
● A. Physiologic
● 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
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Cardiology: Embryology
• Sinus venosus à Coronary sinus, posterior portion of right atrium
• 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:2037_Embryonic_Development_of_Heart.jpg
Heart begins beating
during Week 4
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Cardiology: Embryology
• 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
https://commons.wikimedia.org/wiki/File:Truncus_arteriosus.jpg
https://commons.wikimedia.org/wiki/File:D-tga-575px.jpg
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Cardiology: Embryology
• 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
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Cardiology: Embryology
• 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:Gray473.png
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Cardiology: Embryology
Pharyngeal Arches
Segment Vascular Supply Cranial Nerve Important
Muscles
Cartilage Classic
Pathology
First-
Mandibular
Arch
Maxillary Artery V2 and V3 -Muscles of
mastication
-Anterior belly of
digastric
-Tensor tympani,
tensor veli palatini
Meckel’s Cartilage
à
Mandible, maxilla
Zygomatic bone
Malleus and incus
Treacher Collins
Syndrome
Pierre Robin
Syndrome
Second-
Hyoid Arch
Hyoid and Stapedial
Arteries
VII -Muscles of facial
expression
-Posterior belly of
digastric
-Stylohyoid,
stapedius
Reichert’s Cartilage
à
Stapes, styloid
process
Stylohyoid ligament
Lesser horn of
hyoid
Congenital
Pharyngocutaneou
s Fistula
Third Common Carotid and
Proximal Internal
Carotid Arteries
CN IX -Stylopharyngeus à Greater horn of
hyoid
Fourth Aortic Arch (L)
R Subclavian (R)
CN X: Superior
Laryngeal Nerve
-Cricothyroid
-Palatopharyngeus
-Levator veli
palatini
Superior thyroid
cartilage
Coarctation of
Aorta
Sixth Ductus Arteriosus (L)
L Pulmonary Artery (L)
R Pulmonary Artery
(R)
CN X: Recurrent
Laryngeal Branch
Intrinsic muscles of
larynx (except
Cricothyroid)
Inferior thyroid
cartilage
Arytenoid,
corniculate, and
cuneiform cartilage
Patent Ductus
Arteriosus
https://commons.wikimedia.org/wiki/File:Kiemenbogen.jpg
Pharyngeal
Pouches
Pharyngeal
Grooves
1st: Eustachian tube,
tympanic cavity,
mastoid air cells
1st: External auditory
meatus, auditory canal,
outer tympanic
membrane
2nd: Epithelial lining of
palatine tonsils
2nd – 4th:
Obliterated in utero
3rd: Dorsal à Inferior
parathyroid glands
3rd: Ventral à Thymus
4th: Dorsal à Superior
parathyroid glands
4th: Ventral à
Parafollicular (C cells)
of thyroid
9. ≣ Item 1 of 1
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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
https://commons.wikimedia.org/wiki/File:SVCCXR.PNG
10. OUTLINE
1. General Anatomical Overview
● A. Cardiac Atria
● B. Cardiac Ventricles
2. Cardiac Silhouette: Chest Radiography
● A. Cardiac Atria
● B. Cardiac Ventricles
3. 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
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Cardiology: Anatomy
• 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:Diagram_of_the_human_heart_(cropped).svg
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Cardiology: Anatomy
• 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
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Cardiology: Anatomy
• 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:Surface_projections_of_the_organs_of_the_trunk.png
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Cardiology: Anatomy
• 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
https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg
https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg
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Cardiology: Anatomy
• Atrial Fibrillation Foci:
• Left atrial myocardium
• Pulmonary vein ostia within left atrium
• Atrial Flutter Foci:
• Area between tricuspid valve and IVC
https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg
https://commons.wikimedia.org/wiki/File:Diagram_of_the_human_heart_(cropped).svg
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Cardiology: Anatomy
• Right Coronary Artery (RCA):
• Majority of right-side of heart
• Sinoatrial node
• Left Coronary Artery (LCA):
• Majority of left-side of heart
• Two major branches:
• Left Anterior Descending Artery (LAD)à Anterior 2/3
of interventricular septum, anterolateral papillary
muscle, anterior left ventricle
• Left Circumflex Artery (LCX) à Posterolateral LA and
LV, anterolateral papillary muscle
• Posterior Descending Artery (PDA):
• ~85% R-dominant, 8% L-dominant, 7% co-dominant
• Primarily inferior borders of heart
• Posterior 1/3 of interventricular septum
• Posteromedial papillary muscle
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Cardiology: Anatomy
• 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:Gray491.png
https://commons.wikimedia.org/wiki/File:PPM.png
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Cardiology: Anatomy
• 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:Pulmonary_artery_catheter_english.JPG
https://commons.wikimedia.org/wiki/File:Coronary_Angiography.png
20. ≣ Item 1 of 1
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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
https://commons.wikimedia.org/wiki/File:ECG_Atrial_Fibrillation.jpg
21. OUTLINE
1. Aorta
● A. Vascular Structures and Branches
● B. Ligamentum Arteriosum
● C. Key Landmarks of the Aorta
2. Subclavian Steal Syndrome
3. 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
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Cardiology: Vascular System
• 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:Aorta_branches.svg
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Cardiology: Vascular System
• 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: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
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Cardiology: Vascular System
• Superior Vena Cava Syndrome
• Etiology: Mass lesion (malignancy) or thrombosis (venous catheter)
• Edema à bilateral face, bilateral upper extremities
• Jugular venous distention
• Headache, ↑ intracranial pressure
• Brachiocephalic Venous Obstruction
• Etiology: Pancoast tumor or thrombosis (venous catheter)
• Edema à Unilateral face, unilateral upper extremity
• Subclavian and/or Axillary Venous Obstruction
• Edema à Unilateral upper extremity
• No facial involvement
• Inferior Vena Cava Compression
• Supine hypotensive syndrome (3rd trimester)
Edema à Bilateral lower extremities
Fetal hypoxia à improves with repositioning
https://commons.wikimedia.org/wiki/File:2132_Thoracic_Abdominal_Veins.jpg
Azygos Vein
Right-sided vein
Connects SVC and IVC
Alternative pathway for blood to return to right atrium
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Cardiology: Vascular System
• Internal Thoracic (Mammary) Artery
• Great Saphenous Vein
• Medial foot, medial malleolus, medial leg and thigh
• Joins femoral vein
https://upload.wikimedia.org/wikipedia/commons/c/c8/2136ab_Lower_Limb_Veins_Anterior_Posterior.jpg
https://commons.wikimedia.org/wiki/File:Gray522.png
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Cardiology: Vascular System
• 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://commons.wikimedia.org/wiki/File:Gray545.png
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Cardiology: Vascular System
• 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
https://commons.wikimedia.org/wiki/File:3D_Medical_Animation_Inferior_Vena_Filter.jpg
https://radiopaedia.org/cases/normal-ct-abdomen?lang=us
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Question ID: 0032
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⚪ A. Right vertebral artery
⚪ B. Left subclavian artery
⚪ C. Left internal carotid artery
⚪ D. Left axillary artery
⚪ E. Grafted internal thoracic artery
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?
29. OUTLINE
1. Stroke Volume
● A. End-Diastolic Volume
● B. End-Systolic Volume
● C. Ejection Fraction
2. Stroke Volume Variables
● A. Preload
● B. Afterload
● C. Contractility
3. Heart Rate
4. Frank-Starling Mechanism
● A. Principle and Mechanism
● B. Frank-Starling Curve
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
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Cardiology: Cardiac Parameters of Physiologic Function
• Preload:
• ↑ Venous return à ↑ EDV ~ ↑ Preload à ↑ Stroke volume, ↑ Contractility
• Afterload:
• ↑ TPR ~ ↑ Afterload à ↑ ESV à ↓ Stroke volume
• Preload compensates in healthy hearts
• Afterload has a more dominant effect in heart failure
• Law of LaPlace: Wall stress =
!"#$$%"# & '()*%$
+(,, -.*/01#$$
=
+(,, -#1$*21
+(,, -.*/01#$$
• Contractility
• ↑ SNS activity à ↑ Contractility à ↓ ESV à ↑ Stroke volume
SV = EDV - ESV
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Cardiology: Cardiac Parameters of Physiologic Function
• Physiologic Mechanism: ↓ Vagal tone à SA Node à ↑ HR
• Coronary Perfusion:
• Left ventricular myocardial perfusion occurs primarily during diastole
• Tachycardia:
• Elevated heart rate
• ↑ HR à ↓ time of diastole à ↓ ventricular myocardial perfusion, ↓ diastolic filling time à ↓ CO
CO = HR x SV
Maximal HR = 220 bpm – Age (in years)
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Cardiology: Cardiac Parameters of Physiologic Function
• Principle:
• ↑ Preload à ↑ Contractility à ↑ SV
• Mechanism:
• ↑ Venous return
• ↑ EDV ~ ↑ Preload
• ↑ Myocyte stretch prior to contraction
• ↑ Sarcomere length (↑ active tension and velocity of fiber shortening)
• Frank-Starling Curve:
• X-axis: LVEDP (preload, LVEDV, fiber length)
• Y-axis: Stroke Volume
• Slope of curve: Defined by afterload and contractility
• Point along curve: Defined by venous return (preload)
SV = EDV - ESV
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Cardiology: Cardiac Parameters of Physiologic Function
• Cardiac Output = HR x SV
• Fick Principle à Cardiac Output = Rate of O2 consumption / Arteriovenous O2 difference
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Cardiology: Cardiac Parameters of Physiologic Function
• 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
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Cardiology: Cardiac Parameters of Physiologic Function
• 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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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
https://commons.wikimedia.org/wiki/File:Pulmonary_oedema.jpg
38. OUTLINE
1. Cardiac Function Curves
2. Venous Return Curves
3. Combined Cardiac Function and Venous Return Curves
● A. Steady State
● B. Specific Pathologic Processes
Cardiology:
Cardiac Function
and Venous
Return Curve
Physiology
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Cardiology: Cardiac Function and Venous Return Curve Physiology
• 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
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• 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
Cardiology: Cardiac Function and Venous Return Curve Physiology
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• 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
Cardiology: Cardiac Function and Venous Return Curve Physiology
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• 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
Cardiology: Cardiac Function and Venous Return Curve Physiology
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Question ID: 0034
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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.
⚪ B.
⚪ C.
⚪ D.
⚪ E.
Cardiac
Output
Venous
Return
Right Atrial Pressure
(E.) Prior to aortocaval fistula
A.
B.
C. D.
E.
44. OUTLINE
1. Basic Principles
● A. Key Principles
● B. Phases
2. Determinants
● A. Preload
● B. Contractility
● C. Afterload
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
45. Bootcamp.com
Cardiology: Pressure Volume Loops
• 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
46. Bootcamp.com
Cardiology: Pressure Volume Loops
• 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
https://commons.wikimedia.org/wiki/File:Cardiac_cycle_(pressure_volume_loop).svg
50. Bootcamp.com
Cardiology: Pressure Volume Loops
• 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:Aortic_stenosis.jpg
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/
File:Aortic_regurgitation.jpg
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/
File:Mitral_regurgitation.jpg
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_loop_analysis_in_cardiology#/media/
File:Mitral_stenosis.jpg
51. Bootcamp.com
Cardiology: Pressure Volume Loops
• 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
52. ≣ Item 1 of 1
Question ID: 0035
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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
https://en.wikipedia.org/wiki/Pressure%E2%80%93volume_diagram
53. OUTLINE
1. Endothelial Regulated Vasodilation
● A. Mechanism of Action
2. Excitation-Contraction Coupling
● A. Cardiac Myocyte
● B. Vascular Smooth Muscle
● C. Skeletal Muscle
3. G-Protein Coupled Receptor Vasoconstriction Pathway
● 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
54. Bootcamp.com
Cardiology: Vasodilation and Vasoconstriction
• 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
55. Bootcamp.com
• 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
https://upload.wikimedia.org/wikipedia/commons/1/10/Cardiac_calcium_cycling_and_excitation-contraction_coupling.png
Cardiology: Vasodilation and Vasoconstriction
56. Bootcamp.com
• 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)
Cardiology: Vasodilation and Vasoconstriction
58. ≣ Item 1 of 1
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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
59. OUTLINE
1. Vessel Compliance
● A. Key Principles
2. Blood Flow
● A. Poiseuille Equation
● B. Resistance
3. Sensory Receptors of the Vasculature
● A. Carotid Sinus and Aortic Arch Baroceptors
● B. Carotid Sinus Massage
● C. Carotid Sinus Hypersensitivity
● D. Carotid and Aortic Body Chemoreceptors
Cardiology:
Pressure and
Flow Physiology
61. Bootcamp.com
Cardiology: Pressure and Flow Physiology
• Poiseuille Equation:
• Flow (Q) =
!" #!$
8%&
r4π
• 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
62. Bootcamp.com
• 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
Cardiology: Pressure and Flow Physiology
63. ≣ Item 1 of 1
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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
64. OUTLINE
1. Auscultation
● A. Aortic Area
● B. Pulmonic Area
● C. Mitral Area
● D. Tricuspid Area
● E. Erb’s Point
2. Heart Sounds
● A. S1
● B. S2
● 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
5. Classic Disorders
● A. Aortic Stenosis
● B. Aortic Regurgitation
● C. Mitral Stenosis
● D. Mitral Regurgitation
● E. Constrictive Pericarditis
● F. Cardiac Tamponade
● G. Atrial Fibrillation
● H. AV-dissociation
65. Bootcamp.com
Cardiology: Cardiac Cycle
• 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
https://en.wikipedia.org/wiki/Heart_sounds#/media/File:Gray1216_modern_locations.svg
66. Bootcamp.com
Cardiology: Cardiac Cycle
• 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
67. Bootcamp.com
Cardiology: Cardiac Cycle
• S3:
• Produced by: Rapid passive ventricular filling (↑ left ventricular volumes)
• Best heard: Cardiac apex (bell)
Accentuation: Left lateral decubitus position in expiration
• 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)
Accentuation: Left lateral decubitus position in expiration
• Timing: Late diastole, before S1
• Physiologic: Elderly
• Pathologic: Heart failure (diastolic), chronic hypertension, aortic stenosis
68. Bootcamp.com
Cardiology: Cardiac Cycle
• 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
69. Bootcamp.com
Cardiology: Cardiac Cycle
• 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.svg
71. Bootcamp.com
Cardiology: Cardiac Cycle
• 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://commons.wikimedia.org/wiki/File:Wiggers_diagram_with_jugular_venous_waveform.png
72. ≣ Item 1 of 1
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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
https://upload.wikimedia.org/wikipedia/commons/7/75/Pulmonary_oedema.jpg
73. OUTLINE
1. Regulation
● A. Renin
● B. Angiotensin Converting Enzyme
● C. Angiotensin II
● D. Natriuretic Peptides
2. Direct Pharmacologic Targets
● A. Angiotensin Converting Enzyme Inhibitors
● B. Angiotensin Receptor Blockers
● C. Direct Renin Inhibitors
● D. Neprilysin Inhibitors
● E. β1-antagonism
Cardiology:
Renin-
Angiotensin-
Aldosterone
System
74. Bootcamp.com
Cardiology: RAAS
• 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://en.wikipedia.org/wiki/Juxtaglomerular_apparatus#/media/File:Renal_corpuscle-en.svg
75. Bootcamp.com
Cardiology: RAAS
• 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
https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg
76. Bootcamp.com
Cardiology: RAAS
• 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
https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg
77. Bootcamp.com
Cardiology: RAAS
• 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
• Use: Hypertension, Nephroprotective effects (Diabetes), Cardioprotective effects (Heart failure)
• 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)
https://commons.wikimedia.org/wiki/File:Renin-angiotensin-aldosterone_system.svg
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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. ↓ ↓ ↓ ↓
79. OUTLINE
1.
● A.
● B.
● C.
● D.
●
●
●
●
●
2.
● A.
● B.
Cardiology:
Exercise
Physiology
.
● A.
● B.
80. Bootcamp.com
Cardiology: Exercise Physiology
• ↑ 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
81. Bootcamp.com
Cardiology: Exercise Physiology
• 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
82. Bootcamp.com
Cardiology: Exercise
• 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
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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.
Temperature: 97.2F (36.2C)
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.
Hemoglobin
O
2
Saturation
(%)
Arterial Partial Pressure of O2 (mmHg)
84. OUTLINE
1.
● A.
● B.
● C.
● D.
● E.
2.
● A.
● B.
3.
● A.
● B.
●
Cardiology:
Cardiac
Conductive
Physiology
.
● A.
● B.
●
●
85. Bootcamp.com
Cardiology: Cardiac Conductive Physiology
• 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://en.wikipedia.org/wiki/Purkinje_fibers#/media/File:ConductionsystemoftheheartwithouttheHeart-en.svg
Cardiac Conduction Velocity
Purkinje > Atrial myocytes > Ventricular myocytes > AV node
86. Bootcamp.com
Cardiology: Cardiac Conductive Physiology
• 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://commons.wikimedia.org/wiki/File:2020_SA_Node_Tracing.jpg
87. Bootcamp.com
Cardiology: Cardiac Conductive Physiology
• 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/Ventricular_action_potential#/media/File:Action_potential_ventr_myocyte.gif
88. Bootcamp.com
Cardiology: Cardiac Conductive Physiology
• 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
antidepressants
Methadone
E Antiemetics/Electrolytes Ondansetron Hypocalcemia, hypokalemia, hypomagnesemia
F Antifungals Azoles
https://www.wikidata.org/wiki/Q1625433#/media/File:Tosadesdepointes.jpg
https://en.wikipedia.org/wiki/Long_QT_syndrome#/media/File:Long_QT_syndrome_type_1.jpg
89. ≣ Item 1 of 1
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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
https://commons.wikimedia.org/wiki/File:De-Acquired_longQT_(CardioNetworks_ECGpedia).jpg
90. OUTLINE
1.
● A.
● B.
● C.
● D.
2.
● A.
● B.
●
●
Cardiology:
Antiarrhythmics
● A.
●
●
.
.
● A.
●
●
●
91. Bootcamp.com
Cardiology: Antiarrhythmics
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
https://en.wikipedia.org/wiki/Antiarrhythmic_agent#/media/File:Cardiac_action_potential.png
92. Bootcamp.com
Cardiology: Antiarrhythmics
• 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)
•
•
•
https://commons.wikimedia.org/wiki/File:Action_potential_Class_Ib.svg
https://commons.wikimedia.org/wiki/File:Action_potential_class_Ia.svg
https://commons.wikimedia.org/wiki/File:Action_potential_class_Ic.svg
93. Bootcamp.com
Cardiology: Antiarrhythmics
• Class II
• Metoprolol, Esmolol, Propranolol, Atenolol, Carvedilol
• Mechanism: Inhibition of cAMP à ↓ intracellular Ca2+
• Prolonged Phase 4 (Pacemaker)
• PR prolongation
94. Bootcamp.com
Cardiology: Antiarrhythmics
• 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
95. Bootcamp.com
Cardiology: Antiarrhythmics
• Class IV
• Verapamil, Diltiazem
• Mechanism: Inhibition of L-type Ca2+ channels (Pacemaker)
• Prolonged Phase 0 and Phase 4 (Pacemaker)
• PR prolongation
99. ≣ Item 1 of 1
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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
Creatinine: 1.6 mg/dL
Antinuclear (ANA) antibody: Positive for elevation in ANA titer
Anti-double-stranded DNA antibody: Negative
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
Which of the following changes to the
electrical conductivity is most likely occurring
in ventricular cardiomyocytes as a result of
iatrogenic causes in this patient?
100. OUTLINE
1. Atrial Fibrillation
● A. Pathophysiology
● B. Presentation
● C. Precipitating Factors
● 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
● A. Pathophysiology
● B. Presentation
● C. Association
● D. Management
Cardiology:
Atrial Arrhythmias
101. Bootcamp.com
Cardiology: Atrial Arrhythmias
• Pathophysiology:
• 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
https://commons.wikimedia.org/wiki/File:Heart_conduct_atrialfib.gif
https://commons.wikimedia.org/wiki/File:Heart_conduct_sinus.gif
https://commons.wikimedia.org/wiki/File:Afib_ecg.jpg
102. 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:Diagram_of_the_human_heart_(cropped).svg
Cardiology: Atrial Arrhythmias
104. Bootcamp.com
• Pathophysiology:
• 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:Diagram_of_the_human_heart_(cropped).svg
Cardiology: Atrial Arrhythmias
105. Bootcamp.com
• Pathophysiology:
• 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
Cardiology: Atrial Arrhythmias
https://commons.wikimedia.org/wiki/File:Brady-tachy_syndrome_AV-junctional_rhythm.png
106. ≣ Item 1 of 1
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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
https://commons.wikimedia.org/wiki/File:Atrial_Fibrillation_in_two_leads.jpg
107. OUTLINE
1. Supraventricular Tachycardia
● A. Pathophysiology
● B. Presentation
● C. ECG Findings
● D. Management
2. Wolff-Parkinson-White Syndrome
● A. Pathophysiology
● B. ECG in Sinus WPW
● C. ECG in AVRT WPW
● D. Presentation
● E. Management
● F. Complications
3. Torsades De Pointes
● A. Pathophysiology
● B. Causes
● C. ECG Findings
● D. Management
● E. Complications
4. Monomorphic Ventricular Tachycardia
● A. Pathophysiology
● B. Causes
● C. ECG Findings
5. Ventricular Fibrillation
● A. Pathophysiology
● B. Causes
● C. ECG Findings
Cardiology:
Ventricular
Arrhythmias and
Pre-Excitation
Syndromes
108. Bootcamp.com
Cardiology: Ventricular Arrhythmias
• Pathophysiology:
• Re-entrant pathway within the AV node, accessory pathway, or SA node
• Most common = Atrioventricular nodal re-entrant tachycardia (AVNRT)
• 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
SVT
AVRT AVNRT Atrial T.
109. Bootcamp.com
Cardiology: Ventricular Arrhythmias
• Pathophysiology:
• 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:SVT_Lead_II-2.JPG
110. Bootcamp.com
Cardiology: Ventricular Arrhythmias
• Pathophysiology:
• Prolonged action potential in cardiomyocytes à Prolonged QT interval à ↑ risk of TdP
• Causes:
• Congenital Long QT Syndrome (usually younger patient)
• 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
Class Classic Drug Other Drugs/Effects
A Antiarrhythmics Quinidine Disopyramide, procainamide, sotalol, dofetilide
B Antibiotics Macrolides Fluoroquinolones
C Antipsychotics Haloperidol Ziprasidone
D Antidepressants Tricyclic
antidepressants
Methadone
E Antiemetics/Electrolytes Ondansetron Hypocalcemia, hypokalemia, hypomagnesemia
F Antifungals Azoles
https://commons.wikimedia.org/wiki/File:Tosadesdepointes.jpg
111. Bootcamp.com
Cardiology: Ventricular Arrhythmias
• Pathophysiology:
• Aberrant ventricular foci
• 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
• Pathophysiology:
• 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:Lead_II_rhythm_ventricular_tachycardia_Vtach_VT_(cropped).JPG
https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png
Ventricular arrhythmias are
common in the first 24-48
hours after MI
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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
https://commons.wikimedia.org/wiki/File:Ventricular_fibrillation.png
113. OUTLINE
1. Atrioventricular Blocks
● A. First Degree
● B. Second Degree, Mobitz Type I (Wenckebach)
● C. Second Degree, Mobitz Type II
● D. Third Degree
2. Bundle Branch Blocks
● A. Right Bundle Branch Blocks
● B. Left Bundle Branch Blocks
3. Cardiac Conduction Blood Supply
● A. Right Coronary Artery
● B. Left Anterior Descending Artery
Cardiology:
Conduction
Blocks
114. Bootcamp.com
Cardiology: Conduction Blocks
• First Degree:
• PR interval >5 little boxes (200ms)
• Unchanged P-P intervals
• Regular rhythm
• Low risk block à Generally conservative management
• Second Degree, Mobitz Type I (Wenckebach):
• Progressive lengthening of PR interval until QRS is dropped
• Regularly irregular rhythm
• Low risk block à Generally conservative management
• Second Degree, Mobitz Type II:
• Intermittent non-conducted P-waves à dropped QRS
• Unchanged P-P intervals
• Regularly irregular rhythm
• Medium-High risk block à Review medications, pacemaker
• Third Degree:
• Complete AV dissociation (between QRS and P waves)
• High risk block à Review medications, pacemaker
High Yield Causes:
Ischemic heart disease
Hyperkalemia
Lyme Disease
Endocarditis/ARF
Iatrogenic
AV Nodal Blocking
Agents
Calcium Channel
Blockers
β-blockers
Adenosine
Digoxin
Asymptomatic
Symptomatic
https://en.wikipedia.org/wiki/Heart_block
115. Bootcamp.com
Cardiology: Atrioventricular Blocks
• 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)
https://commons.wikimedia.org/wiki/File:ConductionsystemoftheheartwithouttheHeart-en.svg
https://commons.wikimedia.org/wiki/File:Cardiogram_indicating_right_bundle_branch_block.jpg
https://commons.wikimedia.org/wiki/File:Right_bundle_branch_block_ECG_characteristics.svg
https://commons.wikimedia.org/wiki/File:Left_bundle_branch_block_ECG_characteristics.svg
116. Bootcamp.com
Cardiology: Atrioventricular Blocks
• 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
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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.
⚪ 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
https://commons.wikimedia.org/wiki/File:Complete_A-V_block_with_resulting_junctional_escape.png
Temperature: 99.7F (37.6C)
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?
118. OUTLINE
1. Heart Failure Overview
● A. Heart Failure Variants of Disease
● B. Heart Failure Location (Left vs Right)
● C. Heart Failure Presentation
2. Systolic Heart Failure
● A. Causes
● B. Pathophysiology
3. Diastolic Heart Failure
● A. Causes
● B. Pathophysiology
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
119. Bootcamp.com
Cardiology: Heart Failure
• Systolic:
• Heart failure with reduced ejection fraction (HFrEF)
• Principal determinant: ↓ Contractility à ↑↑↑ Volume
• Diastolic:
• Heart failure with preserved ejection fraction (HFpEF)
• Principal determinant: ↑↑↑ Pressure à ↓ Compliance
• High-Output
• Low-Output
https://en.wikipedia.org/wiki/Heart_block
Heart Failure Variant Heart Failure Location
• Left:
• ↑ LAP (PCWP)
• Pulmonary edema
• Pleural effusion
• Functional mitral valve regurgitation
• Right:
• MCC à Left heart failure
• If not from left heart failure, unlikely pulmonary edema
• Hypoxic pulmonary vasoconstriction (Pulmonary HTN)
• Left parasternal lift
• Jugular venous distention
• Peripheral edema
• Hepatomegaly (Nutmeg liver)
• Ascites
• Functional tricuspid valve regurgitation
120. Bootcamp.com
Cardiology: Heart Failure
• Subjective:
• Dyspnea with activity (or at rest in severe stages)
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Objective
• Jugular venous distention
• Pulmonary crackles
• Reduced Lung Sounds
• Shifted PMI (LVH)
• Left parasternal lift (RVH)
• S3 heart sound
• S4 heart sound à classic for diastolic HF
• ↑↑↑ BNP
https://commons.wikimedia.org/wiki/File:Normal_posteroanterior_(PA)_chest_radiograph_(X-ray).jpg
https://commons.wikimedia.org/wiki/File:Pulmonaryedema09.JPG
https://commons.wikimedia.org/wiki/File:Combinpedal.jpg
121. Bootcamp.com
Cardiology: Heart Failure
• Overview:
• Heart failure with reduced ejection fraction (HFrEF)
• Principal determinant: ↓ Contractility à ↑↑↑ Volume
• Causes:
• Ischemic heart disease
• Viral myocarditis
• Chronic Alcohol Use
• Pathophysiology:
• ↓ Contractility (↓ EF) à ↓ CO à ↑ LVEDP
• Eccentric hypertrophy: ↑ Contractile proteins added in series
• ↑ Compliance, ↓ CO, ↓ EF
https://en.wikipedia.org/wiki/Heart_block
122. Bootcamp.com
Cardiology: Heart Failure
• Overview:
• Heart failure with preserved ejection fraction (HFpEF)
• Principal determinant: ↑↑↑ Pressure à ↓ Compliance
• Causes:
• Prolonged hypertension
• Aortic stenosis
• Infiltrative disorders
• Pathophysiology:
• ↑ LVP à ↑ Contractility
• Concentric hypertrophy: ↑ Contractile proteins added in parallel
• ↓ Compliance, ↓ CO, normal EF
• Additional Clinical Features:
• S4 (due to stiff ventricle)
https://en.wikipedia.org/wiki/Heart_block
124. Bootcamp.com
Cardiology: Heart Failure
• ACE Inhibitors (Lisinopril, Captopril, Enalapril, -pril)
• Inhibition of ACE à ↓ angiotensin II
• Adverse Effect: Dry cough, hyperkalemia, angioedema
• Angiotensin Receptor Blockers (ARBs) (Valsartan, Losartan, -sartan)
• Receptor blockade of angiotensin II type 1 receptor
• 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://en.wikipedia.org/wiki/Heart_block
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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%.
⚪ 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
Which of the following findings are most consistent with this patient’s acute
presentation?
https://radiopaedia.org/articles/heart-failure-summary?lang=us
126. OUTLINE
1. Cardiomyopathy Overview
● A. Major Types of Cardiomyopathy
● B. Cardiac Myocyte Histology
2. Dilated Cardiomyopathy
● A. Pathophysiology
● B. Systolic Heart Failure
● B. Other Classic Causes
3. Restrictive Cardiomyopathy
● A. Pathophysiology
● B. Infiltrative Disease
● C. Diastolic Heart Failure
4. Hypertrophic Obstructive Cardiomyopathy
● A. Pathophysiology
● 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
Cardiology:
Cardiomyopathy
127. Bootcamp.com
Cardiology: Cardiomyopathy
• 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
https://commons.wikimedia.org/wiki/File:414c_Cardiacmuscle.jpg
https://commons.wikimedia.org/wiki/File:Blausen_0470_HeartWall.png
https://commons.wikimedia.org/wiki/File:Tipet_e_kardiomiopative.png
132. Bootcamp.com
Cardiology: Cardiomyopathy
• Pathophysiology:
• 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
• Primary Cardiomyopathy Subtype:
• Localized apical wall thinning and/or aneurysm
• ↑ risk of mural thrombus and/or emboli
• Dilated cardiomyopathy
• Other Features:
• Megaesophagus
• Megacolon
https://en.wikipedia.org/wiki/Heart_block
https://www.wikidoc.org/index.php/File:Heart_in_Chagas_disease_4.jpg
133. Bootcamp.com
Cardiology: Cardiomyopathy
• Pathophysiology:
• Catecholamine surge à impaired kinetic activity of left ventricle
• Etiology:
• Emotional stress is classic
• Classic Case:
• Death of a loved one
• Postmenopausal female
• Primary Cardiomyopathy Subtype:
• Ballooning of left ventricle
• Dilated cardiomyopathy
https://en.wikipedia.org/wiki/Heart_block
134. Bootcamp.com
Cardiology: Cardiomyopathy
• Pathophysiology:
• ↑ 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
• Primary Cardiomyopathy Subtype:
• Restrictive cardiomyopathy (Ventricular wall thickening)
• Other Features of Amyloidosis:
• Nephrotic syndrome
• Hepatomegaly
https://commons.wikimedia.org/wiki/File:Cardiac_amyloidosis_high_mag_he.jpg
https://www.flickr.com/photos/euthman/377559955/ licensed under CC BY-SA 2.0
136. Bootcamp.com
Cardiology: Cardiomyopathy
• 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
137. ≣ Item 1 of 1
Question ID: 0047
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Test Your Knowledge
Difficulty: ✪✪✪ Bootcamp.com
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
138. OUTLINE
1. Anatomical Considerations
● A. Aorta
● B. Vessel Wall Layers
2. Aortic Dissection
● A. Pathophysiology
● B. Etiology
● C. Presentation
● D. Stanford Classification
● E. Complications
● F. Imaging
● G. Management
3. Aortic Aneurysm
● A. Thoracic vs Abdominal
● B. Pathophysiology
● C. Risk Factors
● D. Presentation
● E. Preventative Management
4. Cardiac Considerations of Marfan Syndrome
● A. Pathophysiology
● B. Cystic Medial Degeneration
● C. Mitral Valve Prolapse
● D. Other Findings
5. Aortic Coarctation
● A. Pathophysiology
● B. Associations
● C. Presentation
● D. Management
Cardiology:
Aortic Disease
139. Bootcamp.com
Cardiology: Aortic Disease
• Aorta:
• 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)
https://radiopaedia.org/cases/normal-cta-chest
https://commons.wikimedia.org/wiki/File:Gray506.svg
Aortic Isthmus:
-Traumatic aortic rupture
-Coarctation
140. Bootcamp.com
Cardiology: Aortic Disease
• Pathophysiology:
• 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:Aortic_dissection_types.jpg
https://commons.wikimedia.org/wiki/File:Aortic_dissection_(1)_Victoria_blue-HE.jpg
141. Bootcamp.com
Cardiology: Aortic Disease
• 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
https://commons.wikimedia.org/wiki/File:AoDiss_ChestXRay.jpg
https://commons.wikimedia.org/wiki/File:Descending_(Type_B_Stanford)_Aortic_Dissection.PNG
https://commons.wikimedia.org/wiki/File:DissectionCT.png
142. Bootcamp.com
Cardiology: Aortic Disease
• Pathophysiology:
• Transmural inflammation à dilation of intima, media, and
adventitia
• General Risk Factors:
• Smoking
• Atherosclerosis
• Old age
• Connective tissue disease
• Tertiary Syphilis
• Classic Presentation:
• Generally asymptomatic until rupture
• Presentation in Rupture:
• Acute onset, severe tearing/ripping abdominal/back pain
• Severe chest/abdominal pain
• Hypotension
• Preventative:
• Abdominal ultrasound screening in men aged 65-75 who
have ever smoked (USPSTF)
Aortic Aneurysms Thoracic Abdominal
Primary Risk Factor Hypertension Smoking
Additional Important
Risk Factors
Tertiary syphilis
Bicuspid aortic valve
Connective tissue disease
Atherosclerosis
Classic Symptoms Chest pain
Mid (thoracic) back pain
Hoarseness
Dysphagia
Low back pain
Abdominal bruit
Pulsatile abdominal mass
Other CXR: Widened
mediastinum
Ascending aorta (classic
location)
Abdominal U/S
Infrarenal (classic location)
https://commons.wikimedia.org/wiki/File:AneurysmT.PNG
https://commons.wikimedia.org/wiki/File:Thoracic_Aortic_Aneurysm.png
143. Bootcamp.com
Cardiology: Aortic Disease
• Pathophysiology:
• 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
https://www.researchgate.net/figure/Pathologic-finding-of-excised-aortic-tissue-A-cystic-medial-necrosis-which-is-
defined_fig4_221683474 https://creativecommons.org/licenses/by-nc/3.0/