Pitcher- CV and PV Flashcards
A 28 y/o female seen in the ED with chest pain that worsens with deep breathing and is quite uncomfortable lying down. She reports a dry cough the last 4 days, have a 2 and 5 y/o at home and is a social worker in a teen homeless and suicide prevention center. She is on an oral contraceptive and states her grandfather had a stroke from poorly controlled hypertension last year.
key factors: oral contraceptives–> hypercoagulable state
close to tachycardia
What could lead to pericarditis? pneumonia, for example.
Order troponin, d-dimer
amount and color of sputum could be useful; high volume - bacterial,
CBC with left shift might represent baterial
What are we looking for in peripheral pulses?
How they feel, if you can feel them, and how symmetric they are help in diagnosis
Pulses: superficial temporal artery, facial artery, common carotid artery, brachial artery, radial, femoral, popliteal, posterior tibial, dorsalis pedis
Inspection/Palpation
Supine with head/chest elevated 30 degrees, inspect and palpate precordium for thrills, significant changes in pulse amplitude. If amplitude is elevated, this is felt as a heave. A thrill feels like a vibration and is from a valve problem.
Auscultation
Supine, head up 30 degrees to accentuate sounds best
Use diaphram and bell (with light pressure)
Always identify S1 and S2
different places to hear special things
leaning forward– accentuates aortic murmurs and pericarditis
left lateral decubitus- accentuates mitral murmurs
Murmur
Defined as turbulence across a valve causing sound.
Can be High, Medium or Low pitch
Blowing, Harsh, Musical, Rumble
Occur in systole, diastole or both
Any of 4 valves in either or both phases
Can vary in intensity
May be increased or caused by changes in velocity of flow across normal valves, ie, exercise or hyperthyroidism.
Low viscosity blood causes murmurs at normal velocity with normal valves, ie, anemia
Bruit
Similar noise from turbulence within an artery outside the heart itself.
Typically lower pitch and softer
Usually best heard with the bell (do not press hard)
Grading Murmurs
1/6 Very faint
2/6 Quiet, but can easily be heard if in quiet room
3/6 Moderately loud
4/6 Loud, with palpable thrill
5/6 Very Loud, Thrill, can be heard with stethoscope partially off chest
6/6 Very Loud, Thrill, can be heard with stethoscope
OFF the chest
Murmurs or Bruits– common and less common causes
Benign or Innocent: Stills typically infants Valvular problems papillary muscle tear or rupture chordae tendoneae rupture congenital malformation fibrosis annulus or leaflet (infection) Patent ductus (Aorta-Pulm A) Septal defects ASD, VSD Artery stenosis
less common causes:
Tetralogy of Fallot: Pulmonic Stenosis + VSD + Aorta overriding VSD + RVH
Abdominal Aneurysm
Hyperthyroid state
Obstructive Hypertrophic Cardiomyopathy (IHSS)
Heart Sounds
S1 : Mitral and Tricuspid closures. Signals onset of systole
S2: Aortic and Pulmonic closures. Signals onset of diastole
Anything that causes a separation in the closure of paired valves is called
a split heart sound
Split S1: may be normal variant or abnormal from RBBB or PVC (premature ventricular contraction)
Probably normal if heard LSB
If both split, or consider RBBB and premature ventricular beats (PVC)
Changing the conduction characteristics changes contraction timing , changing valve closure timing: bundle branch blocks
Abnormal valve characteristics also can change closure times: prolonged in stenosis
Split S2 can vary with respiration, Split S1 does not.
LSB = left sternal border RBBB right bundle branch block
Split S2
Split S2: may be normal variant increasing with inspiration, decreasing with expiration or abnormal in pulmonic stenosis or RBBB again
So to be more certain, listen at pulmonic area and have patient take a deep breath and hold it, split should change in normal variant.
S1, S2, S3, S4
S1 and S2 are normal valvular sounds caused by the closure of matching valves during normal heartbeat.
“Lup Dup”
S3 and S4 are NON-valvular sounds occurring in diastole caused by some form of non-compliance of a ventricle
Indicates possible pathology
S3
S3 Early Diastole, closely follows S2 Best at apex in left lateral decubitus May be normal up to age 30 yr “Kentucky” Pathology (etiology still uncertain) Occurs at the ** transition of rapid to slow ventricular filling as the ventricular wall reaches the extent of diastolic excursion of the muscle that is inadequate to accommodate the inflow of blood. This causes a reverberation defined as an S3. Most common: LV myocardial damage (CHF, MI) causing systolic dysfunction from dilated cardiomyopathy. Due to sudden limitation of normal ventricular relaxation during filling stage in diastole.***
Often present in hemodynamically significant chronic mitral regurgitation Over fills LA = more blood flow back into LV An important early finding in heart failure due to a dilated myocardium (more often systolic failure) Early detection (BNP, Pro-BNP, doppler echocardiogram) allows treatment that might improve prognosis for asymptomatic patients
S4
Just before S1, very late diastole just after atrial contraction
Best at apex in left lat decubitus
Caused by *** vibration of LV from the atrial kick trying to pump the last of the blood in but instead hitting poorly compliant ventricular wall.
Low pitch. Quieter. Best with bell. “Tennessee”.
Pathology (etiology still uncertain)
Aortic/pulmonic stenosis , HTN (elevated afterload) , wall damage from MI from remodeling or tissue death cause *** thickening of ventricular walls from a higher work load, and some stiffening. This also leads to non-compliance of the ventricle as the atria pump the last of the blood from the chamber to the ventricle.
Decreased ventricular distensibility Hypertension Aortic valve stenosis Pulmonic valve stenosis Hypertrophic cardiomyopathy
First 3 result in muscle hypertrophy due to increased work load. Hypertrophic cardiomyopathy is a genetic disorder.
Gallop” Rhythm technically refers to
either pattern of S1…S2S3 Or S4S1…S2 Or S4S1…S2S3
Ejection Click
An ejection click is a sound occurring at the moment of maximal pressure with sudden tensing of a valve root.
Aortic Ejection Click:
Early systolic: at onset of left ventricular ejection, aortic root suddenly stretched. (Second right interspace)
Pathology:
Dilated aneurysm of aortic root, coarctation of aorta, HTN all can dilate aorta and change the root dimensions.
Aortic valve stenosis, and aortic regurgitation also can change the dynamic of the aortic root.
Anything that can cause over working of the root of the aortic valve can over-distend it and cause click.
Aortic Stenosis:
Systolic crescendo-decrescendo pattern,
medium pitch, typically harsh
Transmits sound to carotid arteries.
Pathology: Rheumatic disease (progressive fusion), congenital bicuspid valve, calcification of valve.
Symptoms: None until severe, then dyspnea on exertion, angina and syncope. Left ventricular enlargement can occur, creating hypertrophic, poorly compliant muscle and an S4
Aortic Regurgitation
“Austin-Flint” murmur associated (mitral diastolic flow murmur)
Early diastolic, high pitch blowing decrescendo murmur from initial high pressure back flow through a more narrow orifice
What position can enhance the sound?-
Dilates the left ventricle (S3!) and can cause high pulse pressure and brisk carotid pulse
Pathology:
Rheumatic disease, congenital bicuspid valve, endocarditis (Strep, Staph, Haemophilius..)
Pulmonic Ejection Click
Pulmonic Ejection Click:
Sudden root tensioning. Very early systole.
(Second left interspace)
Pathology:
Pulmonary HTN, aneurysm dilating the root
Pulmonary valve stenosis or regurgitation can alter stress on root of valve causing click.
Pulmonary Stenosis:
Systolic crescendo-decrescendo murmur when severe enough to hear, 2nd left interspace more harsh as severity worsens = pulmonic post
Most are asymptomatic and if mild, usually will not progress. If more severe, progressive stenosis occurs.
Symptoms:
Include exertional dyspnea, chest pain, syncope. Can dilate the right ventricle , thicken muscle, causing right heart failure symptoms, including poor muscle compliance creating an S4
Etiology: Usually congenital, rarely associated with carcinoid tumor. Infrequently affected by rheumatic fever or infective endocarditis. Most pathology is from pulmonary hypertension dilating the artery affecting the valvular ring for either stenosis or regurgitation.
Pulmonary Regurgitation
Graham Steell Murmur occurs
with increased pulmonary artery pressure causing higher
velocity regurgitant flow.
Identical to aortic regurgitation, not as loud.
Identify best by which post it is most clear. Softer diastolic decrescendo
Pathology:
Anything that causes pulmonary HTN: mitral stenosis, LV failure, obstructive sleep apnea, emphysema, idiopathic pulmonary hypertension
Tricuspid Valve Stenosis:
Diastolic low pitch rumble, best heard with bell, with inspiration
Opening snap may be heard over tricuspid area.
Distinguished from mitral stenosis by location and that it is accentuated by inspiration, increasing heart filling dynamics.
Pathology:
Rheumatic valvular disease, congenital heart disease, carcinoid tumor.
Impeding right ventricular filling increases central venous pressure.
Symptoms of decreased cardiac output since blood not able to get into the cardiac/pulmonary system effectively
Physical: look for elevated JVP; RA enlargement
