M2 Cardiology Key Facts - Week 1 Flashcards
Impact of Gs of Cardiac Myocytes (3)
All via PKA
1) Increase Phospholamban = Increases SERCA = Increase Ca in the SR for Release
2) Increase L-Type Ca Channels - More Ca coming In
3) Uncouples Troponin I/C to induce relaxation and prep for next contraction
Heart Sounds - Increase S1 - Causes (3)
1) Short PR (Rapid Atrial Contraction)
2) Mild Mitral Stenosis
3) High CO (Short Diastole)
Heart Sounds - Decreased S1 - Causes (4)
1) Long PR (1st Degree AV Block)
2) Mitral Regurg.
3) Significant Mitral Stenosis
4) Stiff Left Ventricle (LVH Hypertrophy)
Heart Sounds - Physiological P2 Splitting - When + Causes (1)
Description - Increased Delay of P2 (E.g. A2 then P2 both heard) on inspiration
Increased Venous Return from Cause - Inspiration delays RV systole (more blood to pump) + Pulmonic Closure
Heart Sounds - Widened P2 Splitting - Description + Causes (2)
Description - Increased P2 Delay on Inspiration
Causes - Delayed Right Depolarization/Emptying - RBBB + Pulmonic Stenosis
Heart Sounds - Fixed P2 Splitting - Description + Causes (1)
Description - Split on Expiration and Inspiration match
Causes - ASD = R/L Pressures balanced by ASD flow no matter venous return
Heart Sounds - Paradoxical P2 Splitting - Description + Causes (2)
Description - P2 Heard First on Expiration and S2 Together on Inspiration
Cause - Delayed Left Depolarization/Emptying - LBBB + Advanced Aortic Stenosis
Heart Sounds - Early Systolic Click - Description + Causes (3)
Description - Ejection Click right after S1 due to audible opening of the Semilunar
Causes - Aortic/Pulmonic Stenosis + Dilated Aortic Root
Heart Sounds - Mid Systolic Click - Description + Causes (1)
Description - Click in mid-systole
Squatting (Increase Venous Return) - Makes the Murmur Occur Later
+ Decreases the Murmur - Valsava Increase Murmur
Causes - Mitral Valve Prolapse
Heart Sounds - Opening Snap - Description + Causes (2)
Description - Diastolic Murmur heard after P2 regardless of inspiration/expiration
Causes - Mitral/Tricuspid Stenosis
Heart Sounds - S3 - Description + Causes (2)
Description - Heard Right after P2 - Lub Dub Dub
Causes - Normal in children - significant heart failure in adults
Heart Sounds - S4 - Description + Causes (2)
Description - Late Diastole sound right before new S1 - Tub Lub Dub
Cause - Atrium contracting into a stiff LV - E.g. Hypertrophy
5 Major Clicks/Snaps/Extra Sounds + Diseases
1) Early Systolic/Ejection - Aortic/Pulmonic Stenosis + Aoritc Root Dilation
2) Mid-Systolic - Mitral Prolapse
3) Opening Snap (Diastolic) - Mitral/Tricuspid Stenosis
4) S3 - Early Systole - CHF
5) S4 - Late Systole - LVH
Mitral Stenosis Murmur Notes (Extra from Lecture 2) - 4
1) Hockey Stick Look
2) LA Dilation causes Afib
3) Opening Snap (Diastole) with increased S1 (Atrial Contraction at the end of diastole pushes hard on the stenosis)
4) Short Snap Interval = More Severe Stenosis
Define Phase of Each Wave JVD/RA Wave Initial Upslope Initial Downslope Notch on Initial Downslope Second Upslope Second Downslope
Initial Upslope - A Wave - Backflow from Atrial Contraction
Initial Downslope - X Wave - Decline after a wave + atrial relaxation
Notch on Initial Downslope - C Wave - Tricuspid closure deflection
Second Upslope - V Wave - Atrial Filling with closed Tricuspid
Second Downslope - Y Wave - Tricuspid opens and blood flows into RV
Major Changes in JVD/RA Waves + Causes (4)
Increased A Wave - Strong Atrial Contraction - RVH or Tricuspid Stenosis
Increased P Wave - Abnormally large amount of venous return in diastole = Tricuspid Regurgitation
Blunt Y Wave - Decreased Filling = Cardiac Tamponade
Exaggeration of the Y Wave - Constrictive Pericarditis
Murmur Pitch Meaning (Lecture 2) - High vs. Low
High - Tight Opening + High Pressure Difference
Low - Loose Opening + Low Pressure Difference
Maneuvers to Increase Murmurs (5) + Impacted Murmur
1) Valsalva + 2) Standing - Decreased Venous Return + High Thoracic Pressure - Increase Left Flow Murmurs
3) Inspiration - Increased Venous Return + Low Thoracic Pressure - Increase Right Flow Murmurs
4) Squatting - Increase Venous Return - Increase LV Volume - Increase Aortic Stenosis + Delay Mitral Valve Prolapse
5) Clenching Fist - Increase Resistance/Afterload - Increases BP - Increases Backflow Murmurs (AR/MR/VSD)
Hypertrophic Cardiomyopathy Murmur vs. Aortic Stenosis Murmur - Maneuvers
Both Systolic Outflow Murmurs (Crescendo + Decrescendo)
AS - Increased with Squatting (Increased LV Volume) - Valsalva/Standing Decreases
HCM - Increased with Valsalva + Standing (Decreased Venous Return) = less filling + more resistance to forward flow - Squatting Decreases
Key Cardiac Imaging Planes (2)
Vertical Long Axis - Verticle Cross-Section from Mitral to Apex - Shows Half LA/LV
Short Axis - Horizontal Sections of LV/RV - Most important axis because it gives you volumes
Imaging Uses - CXR - 1
CHF - See Enlarged Mediastinum + Lung Edema + Loss of Bronchi
Imaging Uses - Normal Echo - 2
Valves (Long Axis) + LV Fucntion
Imaging Uses - Transesophageal Echo - 3
Right behind LA - Uses for Endocarditis + ASD + Thrombus in LA before cardioversion
Imaging Uses - Contrast MRI - 1
MI - Area + Size of Infarct
Imaging Uses - Nuclear Imaging/PET - 2
CAD + Myocardial Blood Flow (MBF)
Imaging Uses - Electron Beam CT Angiography - 1
Coronary Artery Calcifaction - Only way to see soft plaques
Baroreceptor Reflex - Pathway + Response to Low BP
Receptors in Aortic Arch (CNX) + Carotids (CNIX) - High BP = High Baroreceptor Signal = Increased Vagal + Decreased Symp. Tone
Low BP = Less Baroreceptor Firing + Less Parasymp stimulation + less symp. blocking
Systolic HTN - Mechanism + Age Group
Elderly HTN - Increased large vessel stiffening with age - increases with life
Diastolic HTN - Mechanism + Age Group + Risk Factors
Young HTN - Increased Systemic vascular resistance - More dangerous + genetic + progressive
Indications of Secondary HTN (3) + Key HTN Risk Drug
1) Resistant (to 3 or more HTN Meds)
2) Diagnosis before age 30 w/o FH or obesity
3) Rapid Changes/Onset
NSAIDs - Can cause HTN!!
Major Cause of Secondary HTN (Pathoma)
Renal Artery Stenosis - Hypoperfusion of the Glomerulus - Thinks you have low blood volume - activates RAAS to increase
Major Use of Wedge Pressure (From Right Swann-Ganz Cath)
Estimates LA Pressure - Also during Diastole LA/LV Pressure Approx. Equal - Allows for estimate of LV diastolic pressure and preload
Continuous Elevated Pulm. Artery Pressure - Normal Pressure + Associated Diseases (3)
Normal = 2-10 mmHg = Wedge + LA too
Diseases - Left HF + Parenchymal Long Disease (COPD) or Pulm. Vascular Disease (HTN/PE)
Reduced Pulm. Artery Pulse Pressure - Associated Diseases (3)
Right Heart Ischemia/Failure + PE + Tamponade
Left Cath. Findings in Pathology (3)
Abnormally High LA-LV Pressure Gradient in Diastole = Mitral Stenosis
Low Systolic Pressure Gradient between Aorta/LV = Aortic Stenosis
Large Systolic v wave on LA JVP = Regurgitation
Modifiable Atherosclerosis Risk Factors (5)
1) Dyslipidemia
2) Tobacco Smoking
3) HTN
4) Diabetes
5) Sedentary
Non-modifiable Atherosclerosis Risk Factors (3)
1) Advanced Age
2) Family History
3) Male (Estrogen protects until menopause)
Markers of Increased Atherosclerosis Risk (2)
Elevated CRP - C-Reactive Protein - Inflammation Marker
Elevated Homocysteine - Increased by low levers of B12, B6. and Folate
Normal Endothelium Features (5)
1) Impermiable to Large Molecules
2) Resists Leukocyte Adhesion
3) Promotes Vasodilation (NO/Prostacyclin)
4) Anti-Inflammation
5) Anti-thrombotic (heparin sulfate + thrombomodulin)
Atherosclerosis Progression (7 Stages)
1) Endothelial Injury
2) LPL Entry/Modification
3) Inflammation via cytokine release
4) Leukocyte adhesion via VCAMs
5) Foam Cell Formation when macrophages take up LPL with scavenger receptors
6) Foam Cell PDGF (Platelet derived growth factor) pulls smooth muscle into the intima
7) Smooth muscle cells use collagen type I to promote extracellular remodeling
Factors Impacting Fibrous Cap Formation in Atherosclerosis (3)
Promote Cap = PDGF + TGF-Beta
Inhibit Cap = IFN-Gamma from Lymphocytes
4 Major Manifestations of Atherosclerosis
1) Stroke (Thrombotic + Embolic)
2) CAD - Angina/Ischemia/MI
3) Aneurysms (AAA - Weakening of vessel walls)
4) Renal Artery Disease = Emboli Occlusion + Renal Artery Stenosis
Primary vs. Secondary Hemostatsis
Primary - Platelet Aggregation mediated by vWF - Not strong enough, needs clotting cascade to secure it
Secondary - Clotting cascade to form a thrombus + secure the original clot with cross-linked fibrogen
Von Wilabran Factor (vWF) - Functions (2)
1) Release Factor VIII to increase Factors IX and X to increase secondary hemostasis
2) Responds exposed collagen in the sub-endothelial matrix - recruits platelets for primary hemostatsis
Vascular Injury - 3 Effects Mediating Hemostatsis
1) Vasoconstriction
2) Collagen Exposure (recruits vWF) + Primary Hemostatsis
3) Tissue Factor Exposed (Binds Factor VII and activates Secondary Hemostatsis)
Primary Hemostatsis - 4 Steps
1) vWF Binds the newly exposed collagen
2) vWF Links with a platelet via the platelet’s GP Ib receptor - Activates the Platelet
3) Activated platelet links to other platelets via its GP IIb and IIIa receptors - Fibrin Link
4) Platelet aradonich acid is activated via COX1 to release TXA2 and recruit more platelets
Secondary Hemostasis - Common Pathway
Meeting point of Intrinsic/Extrinsic Pathways - Xa activates Va which activates IIa (Thrombin) which triggers fibrin cross linking
Factor XIII Performs the Cross-Linking (Activated by Factor IIa)
Secondary Hemostatsis - Extrinsic Pathway
TF Exposed on injured endothelium - Binds Factor VII - Activates Factor X + Common Pathway + IX (Intrinsic Pathway)
Secondary Hemostatsis - Intrinsic Patthway
XII - XI - IX Cascade - Activates More Factor X - Rapid acceleration of the clotting
Tissue Factor Pathway Inhibitor - Mechanism + Types
Mechanism - Activated By Factor Xa - Goes back and turns of TF-VII Complex
Alpha - Circulating Anti-Coagulation
Beta - On endothelium - keep thrombus from spreading
Thrombomodulin Pathway - 2 Effects
On endothelium - Turned on by IIa which it then inactivates
Activates Protein C
Protein C Pathway
Protein C (Protein S Co-Factor) - Inhibit Factor Va/VIIIa
Antithrombin III - Location + Activity
Circulating from Endothelium + Liver
Inhibits Factors II and X - Action enhanced by heparin sulfate
Coagulation Testing - PT vs PTT (4 Possibilities)
PT - Extrinsic Pathway (PeT) - Long = TF, VII, V, X, II
PTT - Intrinsic Pathway (PeTiTe) - Long = XII, XI, IX, X, V, II
Both Long = Common = X, V, II
Both Normal = Outside the Box = VIII, Platelet Function, Fibrinogen, Fibrinolysis
Major Clotting Disorders (4)
Factor 5 Lieden Mutation
Hemophilia A
Hemophilia B
ADAMTS-13
Factor 5 Lieden Mutation
Mutation in Factor V - Activated Protein C (APC) Deficiency - Can’t cleave V to turn off
Hemophilia A
Bleeding Disorder - Factor VIII Deficiency - IIa cannot activate more VII and IX to rapidly expand the clot
Hemophilia B
Bleeding Disorder - Factor IX Deficiency - Loss of the Intrinsic Pathway to rapidly expand the clot - Less serious than Factor VIII (Still have Facto VII expansion)
ADAMTS-13
Responsible for the breakdown of vWF and platelet aggregation - to much = bleeding disorder
Vitamin K Dependent Clotting Factors (6)
Factors II, VII, IX, X + Proteins C/S
Fibrinolysis
Plasminogin - Activates to plasmin via tPA - breaks down the fibrin crosslinking
Balanced by Plasminogen Activator Inhibitor (inhibts tPA)
D-Dimer
Detects PE via looking for small pieces of broken down fibrin from fibrinolysis - indicates clot
Acquired Factor VIII Deficiency - Pathology + Diagnostic Findings
Pathology - Bleeding Disorder - Auto-Immune disorder targets Factor VIII
Findings - Long PTT (Indicates problem with XII, XI, IX, or VIII) + Normal PT (no problems with common pathway) + Does not respond to platelets (should do fine with new factors being replaced but does not because autoimmune still knocks out the new Factor VIII)
DVT without Provocation (2 Causes)
Cancer + Pregnancy
Protein S Level Changes - Cause + Pathology
Cause = Pregnancy
Protein S is normally half bound to C4b - In pregnancy more C4b takes up more Protein S - Reduces the ability of Protein C to inhibit clots - hypercoagulation state
Lethal Fetal Hypercoagulation Disorders (2)
Homozygous Protein C Deficiency + Anti-Thrombin III Deficiency
