Newman Questions Flashcards
Two determinants of O2 demand
Heart Rate, Systolic BP
2 Categories of Pressure Overload
Systemic HTN, Outflow Obstruction (Aortic Stenosis, Asymmetric Septal Hypertrophy)
2 categories of Volume overload
Regurgitant Valves, High-Output States (Anemia, Hyperthyroidism)
2 Major Humoral Manifestations of Renin-Angiotensin
Most potent vasoconstrictor in body; Aldosterone secreted by adrenals
3 Causes of Aortic Regurgitation
Ischemia, Infection, Dissection
3 Causes of Volume Overload
Regurgitation, Anemia, Hyperthyroidism
3 Drugs associated with delayed after-depolarizations
Procainamide, Quinidine, Digoxin
3 Major Clinical Manifestations of RV HF
SOB, Elevated JVP, Hepatojugular Reflex
4 Clinical Manifestations of LV Failure
SOB/Orthopnea/PND; Fatigue/Confusion; Nocturia; Chest Pain
4 Neurohumoral changes with CHF
Increased sympathetic (NE), Renin release, Vasopressin, Cytokines (IL-1, Enodthelin)
5 Causes of Acute Pericarditis
Infection (TB, Viral); CT Disease; Malignancies; Thyroid Dz; metabolic
5 Common Causes of CHF
Volume Overload, Pressure Overload, Loss of Muscle, Loss of Contractility, Restricted Filling
5 complications of MI
HF, Arrhythmia, Shock, Bradycardia, Nausea/Vomiting
5 main etiologies of LV Failure
Volume/Pressure Overload, Restricted Filling, Myocyte Loss, Decreased Contractility
Afterload is the pressure that
the LV needs to overcome for aortic valve to open
Angina Pectoris is characterized by
> 5 mins; Pressing, tightness
Angina, Syncope, HF
Aortic Stenosis
Anterior Leads
V1-V6
Auscultation of STEMI
S4 may be present
AV block can be seen in some congenital disorders:
MD, Tuberous Sclerosis, Maternal SLE
Blowing systolic murmur
Mitral Regurgitation
Bundle Branch Block leads to what on ECG
Widening of QRS Complex
Cardiac Adaptation to Regurgitation
Eccentric Hypertrophy (Dilatation): Cardiac fibers multiply in series –> Output increased (sterling’s law)
Cardiac Adaptation to Stenosis
Concentric Hypertrophy, Normal Volume and Size
Cardiac exam findings in LV Failure
Displaced, Sustained PMI, S3, S4
Causes of Mitral Prolapse
Infection, Infarction, Myxomatous Degeneration, CT disorder
Changes of Calcium function in LV HF
Delivery of Ca to contractile apparatus and reuptake of Ca by SR are slowed
Changes to beta-adrenergic receptor in LV HF
Densensitization
Changes to myosin and troponin in LV HF
Re-expression of fetal and neonatal forms of myosin and troponin
Changes to Systolic Isovolumetric curve in LV Diastolic Dysfunction
None
channels disrupted in prolonged QT
(Ca and/or) K
Clearing throat murmur in systole
Aortic Stenosis
Contractility of Myocytes in LV Diastolic Dysfunction
Preserved
Cytokines released in CHF lead to
IL-1 –> Myocyte hypertrophy; Endothelin –> HTN in pulmonary arteries, mycoyte growth, collagen deposition
Decrease in PR interval means
WPW
ECG in WPW
Short PR, Delta Wave
Echo for MI vs Pericarditis
Segments not contracting vs Effusion
Ejection Fraction =
SV / EDV
EKG Features of Ischemia
Inverted T Wave, ST Depression
Elevated Atrial Pressures indicate
Preload is adequate but ventricular function is decreased, or fluid is accumulating in venous system
Elevated RR, HR, Cold Clammy Skin, Pulsus Alternans, Displacement of PMI, Lung Rales, S3, S4 audible
Left Heart Failure
First Degree AV Block
Abnormally long conduction time (PR > 0.22s)
First thing to do with Pericardial Effusion
Palpate pulse and watch breathing
Giant V Wave
Acute Mitral Regurgitation
Giant V Wave =
Mitral Valve Prolapse
Height of QRS is usually
2 boxes
Hemodynamic changes in Aortic Regurg
Increased Preload, Increased SV
Hemodynamic changes in Diastolic Dysfunction
Diastolic PV curve shifts left, Increase in LV EDP
Hemodynamic changes in systolic dysfunction
Isovolumic Systolic Pressure curve shifts down; SV and CO reduced
Hemodynamics in acute regurgitation
Pressure in LA markedly elevated
High QRS on ECG indicates
Ventricular Hypertrophy
How do CO2, O2, Acidity, and Temp affect Automaticity
CO2, Acidity, and Temp increase, O2 decreases
How do we determine severity of Mitral Stenosis
LV vs Pulmonary Capillary Wedge pressure (should be identical)
How do you distinguish between Aortic Regurgitation and Stenosis
Regurg produces diastolic murmur, wide pulse pressures, brisk pulse
How do you dx Pericardial Tamponade
Pulsus Paradoxis: Upon inhalation, pulse disappears
How does heart respond reduced SV in LV Systolic Dysfunction
Increased return of blood (preload), Increased release of catecholamines, Cardiac Muscle Hypertrophy
How does K+ affect automaticity
Decreased K+ –> Increased automaticity
How quickly can V Fib lead to SCD
Few seconds
How to increase murmur in HOCM
Valsalva or standing –> Decrease IV volume –> Murmur increases
If QRS is wide, what is abnormal
Ventricular activation
Increase in NE during HF can lead to
increased preload and afterload, which can worsen HF
Increase in PR interval means
Heart Block
Increased SV, Brisk Arterial Pulse, Whooshing decrescendo murmur after S2
SV, Pulse, Mumur in Aortic Regurg
Inferior Leads
II, III, aVF
Is S3 present in Systolic or Diastolic Dysfunction
Can be present in either
Key finding in acute regurgitation
Loud murmur without hypertrophy
Key to clinical assessment of Valve Stenosis
Pressure difference on either side of valve
LA pressure in Acute vs Chronic Regurgitation
Elevated in Acute, Normal in Chronic
Long QT results from
Reduced function of K channels -> Prolonged plateau period
Loud S1
Mitral Stenosis
Loud S1 (snaps shut), Diastolic Rumble
Mitral Stenosis
LV Diastolic Dysfunction is caused by any disease that
Causes decreased relaxation, decreased elastic recoil, or increased stiffness of ventricle
May be responsible for Pulmonary HTN, Myocyte Growth, and deposition of interstitial collagen
Role of Endothelin in HF
Midsystolic Click
Mitral Valve Prolapse
Morphological Changes in Aortic Regurg
Ventricular Dilation (Eccentric Hypertrophy)
Morphological Changes in Aortic Stenosis
Concentric Hypertrophy
Morphological Changes in Mitral Regurgitation
If chronic, LV and LA Dilation; Not in acute
Most common cause of mitral regurgitation
Mitral Prolapse
Most common cause of stroke
A Fib
Most common finding
Displaced Apical Impulse (PMI)
Most potent vasoconstrictor
AngII
Most prolonged QT is caused by
drugs
Mumur in Aortic Regurgitation
Decrescendo following S2
Mumur of Aortic Stenosis
Clearing throat in systole
Murmur for Mitral Regurgitation
Holosystolic Blowing Murmur
Murmurs for Mitral Stenosis
Opening Snap, Diastolic Rumble
Murmurs, Sounds in Mitral Stenosis
Loud S1 (snaps shut), Diastolic Rumble
Narrow QRS means
Arrhythmia originating at or above AV node
NE released in CHF leads to
Increased Preload and Afterload
Normal JVP
2mmHg
Opening Snap, Diastolic Rumble
Murmurs for Mitral Stenosis
Physical findings in Mitral Stenosis
RHF: JVD, Ascites, Edema
Pressures in Constrictive Pericarditis
All diastolic pressures in heart equal
Principal Physical Findings in Constrictive Pericarditis
Pulsatile Neck Veins; Systemic Congestion; No Pulsus Paradoxis
Prolonged QRS could be
(1) Ventricular Escape Rhythm; (2) Bundle branch block
Pulmonary edema with no enlargement of chambers
Mitral Valve Prolapse
QRS 6 boxes high on V6
Ventricular Hypertrophy
QRS should be less than
0.12 seconds
Range for QTc
0.38-0.42
Renin released in CHF leads to
AngII –> Aldosterone, Vasoconstriction –> Increased afterload, reduction in CO
Result of Endothelin release in CHF
HTN in pulmonary arteries, Myocyte growth, Collagen deposition
Result of IL-1 release in CHF
Myocyte Hypertrophy
Role of Endothelin in HF
May be responsible for Pulmonary HTN, Myocyte Growth, and deposition of interstitial collagen
Role of IL’s in HF
May accelerate myocyte hypertrophy
Role of TNF in HF
May play role in hypertrophy and myocyte death
S4 is best heard at
PMI
S4 occurs concomitantly w/
Atrial Contraction
Sawtooth pattern on EKG
A Flutter
Second Degree AV Block
Some, but not all, atrial impulses are conducted to ventricles
Sign in Acute Mitral Regurgitation
Giant V Wave
Signs in Aortic Stenosis
Throat-clearing (C-D) murmur, Pulsus Tardus, Pulsus Parvus
Sinus tachycardia accompanying MI may be indicative of
Cardiogenic Shock
Skin findings in Left Ventricular Failure?
Pale, Cold, Sweaty
SV, Pulse, Mumur in Aortic Regurg
Increased SV, Brisk Arterial Pulse, Whooshing decrescendo murmur after S2
Symptoms of Aortic Stenosis
Syncope, Angina, HF
Systolic LV dysfunction reduces
SV (decreased CO)
Throat-clearing (C-D) murmur, Pulsus Tardus, Pulsus Parvus
Signs in Aortic Stenosis
Triad of Aortic Stenosis
Angina, Syncope, HF
Type of HF w/ Pulsus Alternans possible
LV HF
Valve disease associated with Stable Angina
Aortic Stenosis
Vicious circle:
Continued hyperactivity of Renin-Angiotensin system leading to severe vasoconstriction, increased afterload, and further reduction in CO and GFR
Weak and Delayed Arterial Pulse
Aortic Stenosis
What causes nocturia in LHF
Decreased renal perfusion gets better at night
What causes ventricular dilation in Aortic Regurg
Increased Preload
What is characteristic of Aortic Stenosis
Weak Arterial Pulse (parvus)
What is mechanism behind Torsades de Points
Delayed Depolarizations
What is probably the most common cause of LV Failure
MI
What is the Hepatojugular Reflex
Pressing on liver for 5 seconds causes increase in JVP
What on ECG indicates ventricular hypertrophy
High QRS
What usually causes acute mitral regurgitation
Infection, Ischemia
When Apical Impulse (PMI) is displaced =
LV Volume is Increased as compensatory mechanism of HF
When Apical Impulse (PMI) is sustained =
Suggests increased LV volume or mass
When bundle branches are disease, EKG change:
QRS becomes wide
Where is S3 best heard
Apex
Which type of heart failure presents with abdominal pain
Right
Why do patients with Left Sided Failure have Orthopnea
Now operating on steep portion of Diastolic Pressure-Volume Curve = Any increase in blood return leads to marked elevations in ventricular pressures
Width of QRS is usually
3 little boxes
Workup of Stable Angina
Stress Test, Echo, Coronary Angiogram