Murmurs and Shock Flashcards
descrive the 4 heart valves
Aortic Valve (three leaflets) – between PV and aorta
Tricuspid Valve (three leaflets) – between RA and RV
- Pulmonic Valve (three leaflets) – between RV and PA
- Mitral Valve (two leaflets) – between LA and LV
explain the grades of murmurs
- Grade 1 – very soft heard after careful auscultation
- Grade 2 – readily heard soft murmur
- Grade 3 – moderately loud, not associated w/ palpable thrill
- Grade 4 – Loud, no or intermittent palpable thrill
- Grade 5 – loud associated w/ palpable pericardial thrill. Murmur not audible when stethoscope is lifted from thoracic wall
- Grade 6 – loud murmur associated w/ palpable pericardial thrill and heard when stethoscope is lifter from thoracic wall
define sclerosis, stenosis, regurg
- Sclerosis – valve thickening and calcification without significant pressure gradient (<2 m/sec)
- Stenosis – valve thickening and calcification with significant pressure gradient (>2 m/sec)
- Regurgitation – inadequate closure of the valve leaflets, causing back flow of blood into the ventricle
thinking symptom wise where will right and left sided heart failures be noted
- RIGHT side of Heart – back up into body
- Lower extremity edema
- Ascites
- LEFT sided – pulmonary associated symptoms à backs up into lungs first
define preload vs after load
preload - volume in ventricles at end of diastole
after load - resistance left ventricle must overcome to circulate blood
what causes an increase in preload vs afterload
preload
hypervolemia
regurg of cardiac valves
HF
afterload
vasocontriction
HTN
describe effects of special tests on preload and afterload
valsalva
Squatting from standing
Standing from Squatting
Legs raise (passive)
Handgrip exercise
INCREASES preload -
quatting from standing
leg raise
DECREASE preload
Standing from Squatting
valsalva
INCREASED afterload - handgrip
DECREASE afterload - valsalva
most common valvular dz?
Aortic regurg
most common causes of AR and AS in:
developed countries
developing countries
DEVELOPED countries - Calcific disease
developing countries - rheumatic valve disease
valvular dz assoc w/ sx:
- Exertional dyspnea
- Exertional angina
- HF symptoms – orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema, lower extremity edema
- Awareness of heart beats due to dilation**
AR
describe physical exam findings for AR vs AS
AR
Wide pulse pressure in BP (140/50)
- Displacement of apical pulse laterally and inferiorly
- Prominent pulsation/thrill over sternal notch – aortic dilation
- Bounding pulse due to arterial pulse falling off rapidly
AS
- Carotid pulse DEC in amplitude
- Split S2 (pulmonic valve closing prior to aorta) or deceased S2
As has similar si/sx as AR but we more frequently see:
•Pre-syncope or syncope
AR: aware of heart beats due to dilation
describe patho of AR vs AS
AR
Increases volume overload in LV -> increase in LV capacity to ensure ventricular compliance -> ventricular wall thickness increases in proportion to increase in chamber radius -> eccentric hypertrophy
AS
Increase afterload in LV à LV needs to generate more force to overcome afterload à thickening of LV à less LV compliance and impedes filling à concentric LV hypertrophy
gold standard for dx of valvular dz?
Echo – TTE w/ Doppler
tx of AR/AS
Limited physical activity
Tx underlying CV dz
HTN tx challenging
HF management - Low dose diuretic w/ ACE
Palliative care
surgical options
surgical tx of AR and AS
SURGICAL
AVR or SAVR – open heart surgery
TAVR – done via femoral, axillary artery or directly via aorta –> Originally used for high-risk pts but not approved for all
F/u
•2-4 wks after discharge, then every 3-6 mo eventually transition to 6-12 mo
Asymptomatic pt monitoring: exam + echo in pts w/ AS
- Mild AS w/o calcification 2-3 yrs
- Mild AS w/ significant calcification – yearly
- Moderate AS – yearly
- Severe AS – every 6 mo
Exercise stress tests are used to dx AS/AR in what pt population
•pts w/ severe AS who live sedentary life
metabolic dz such as Paget’s, Fabry’s Lupus are assoc w/
AS
sx of MS
- Exertional dyspnea/ exercise intolerance
- Paroxysmal or persistent Afib
- Chest pain – due to portal HTN
- Fatigue
- Ascites
•Lower extremity edema
- Thromboembolism
- Hemoptysis – INC pressure in pul. system
- Hoarseness – increase in L atrial size that compresses recurrent laryngeal n.
sx of MR
Asymptomatic –
•sx don’t occur until late in dz –> develop due to LV enlargement, systolic dysfunction, pHTN or Afib
then develop same sx as MS
Most common cause of MR in developed and developing countries
developed –MVP and CAD
developing –rheumatic heart disease
MVP is associated w/ an ______ in sudden cardiac death
INCREASE in sudden cardiac death
most common cause of MR
MVP
Ct disorders such as Marfans, OI and Ehlers Danlos are associated w/ what valvular dz?
MVP
describe primary vs secondary causes of mitral valves dz
Primary – due to valve dysfunction
- Degenerative dz
- Rheumatic heart dz
- Endocarditis
- Congenital
Secondary is due to other factors
- CAD
- Dilated CM
- HCM
- RV pacing
HF symptoms more common in MR / MS / MVP
MS
- Crackles in lungs
- Peripheral edema
- Ascites
Mitral facies are associated w?
MS
Mitral facies – pinkish/purple patches on cheeks
tx of Mitral dz
Asymptomatic – routine monitoring by cardiologist
Medical management of sx – mostly HF sx
ACE, ARB, BB, aldosterone antag
•Diuretics
surgical procedures:
FIRST line – Mitral Valve Balloon valvotomy
- Asymptomatic to severe MS
- Severe MS w/out MR
Transcatheter mitral valve clip
- MR only
- Femoral vein access w/ transseptal puncture
Surgical repair / replacement
- Failed balloon valvotomy
- Other surgical issues MR or MVP
- MS w/ MR
describe the different procedures assoc w/ MS vs MR
FIRST line – Mitral Valve Balloon valvotomy –> MS
- Asymptomatic to severe MS
- Severe MS w/out MR
Transcatheter mitral valve clip –> MR only
split S2 is associated w/
AS and PS
describe the displacement of apical pulse in MR vs AR
AR - laterally and inferiorly
MR - Leftward displacement
Mitral valve dz Non-surgical candidate monitoring:
routine echo yearly
- Mild – echo every 2-3 yrs
- Moderate – echo every 1-2 yrs
- Severe – echo every 6-12 mo
Non ejection click is assoc w/
MVP
diagnostic imaging of choice for mitral valve dz?
Echo –
- usually TTE w/ doppler
- but TEE is suboptimal
CXR of valvular dz show?
aortic - widened aortic notch
mitral - Nonspecific LA and LV enlargement
tricuspid - Cardiomegaly from RV enlargement & Pleural effusions
pulmonary - Cardiomegaly w/ RV enlargement
si/sx of tricuspid dz
- Neck pulsations (JVD)
- Palpations
- Edema (peripheral)
- Ascites
- Abdominal pain/bloating
- Sx related to cause
NO LEFT SIDED sx such as pre-syncope or syncope
Opening snap can follow murmur in what valvular dz
TS
JVD- Kussmal’s sign is associated w/
TS and TR
•Lack of or decrease or rise in JVP
sx associated w/ tricuspid dz
Edema - – ascites, peripheral and occasional anasarca
Hepatomegaly
JVD
RA and RV dilation (pHTN, chronic PE, severe COPD) are all causes of:
TR
tx option of choice for most pts w/ tricuspid dz
Surgical repair or replacement
tx of TS
percutaneous balloon valvotomy
medical management of tricuspid dz
Med management aimed at sx - Diuretics / aldosterone antag
sx of??
Asymptomatic
- Exertional dyspnea
- Fatigue
- Syncope
- Chest pain
- Right HF sx (edema, abdominal bloating)
pulmonary valve dz
tx for PS and PR
Should undergo annual screening and monitoring
Correct any underlying issues
- Pulmonary artery vasodilators
- HF medication
Congenital PS – fixed in infancy w/ surgery or balloon valvotomy
Symptomatic or severe PR –> Surgical intervention tissue or mechanical valve
name the systolic murmurs
occur b/w S1 and S2
AS
MR
MVP
TR
PS
name diastolic murmurs
AR
MS
TS
PR
what murmurs are heard best over apex
MS - held in expiration
MR
MVP
what murmur is heard best ar ERb’s
AR
what murmurs INCREASE w/
squatting and leg raises
AR / AS
MR / MS / MVP
AR vs MR special test differnetiation
AS vs MS
AR - handgrips inc murmur
MR - hangdrips no effect
AS - handgrips decrease
MS - inspiration decreases
hangrips have what effect on these 2 murmurs?
AR - increase
AS - decrease
in a MS murmur (inspiration / expiration) increases murmur while (inspiration / expiration) decreases murmur
expiration increases
inspiration decreases
inspiration increases and decreases what murmurs
increases TS and TR
decreases - MS
HOCM vs AS
AS
DECREASES
- Valsalva
- Standing
HOCM will do opposite
As radiates to carotid, HOCM does not
standing or valsalva decreases what murmurs
AR and AS
MS and MR
what murmurs radiate to axilla
MR and MVP
murmur that is described as blowing sound
AR
descrecendo
early-diastolic
murmur described as harsh
AS
crescendo-descresendo (soft-loud-soft)
murmur described as rumble (3)
MS - loud S1 followed by decresc-cresc, low pitched
MR - medium to high pitch, rumble increases twoard end
TS- opening snap may follow, decresc-cresc, low pitched, rumble increases twoard end
murmur described as non-ejection click
MVP - low pitched
murmur described as continuous blowing
AR - early diastolic
TR - systolic
murmurs heard best on LSB
AR - 3rd and 4th ICS
TS - 3rd to 5th ICS (bell)
murmur described as pulmonary ejection click
PS - systolic, Crescendo-decrescendo
murmurs described as
Crescendo-deccrescendo
Decrescendo-Crescendo
Crescendo-deccrescendo
AS and PS
Decrescendo-Crescendo
MS and TS
what murmur can radiate to neck and carotids
AS
describe chemoreceptors and their role
- specialized areas in the medulla oblongata, aortic arch, and carotid arteries that are sensitive to concentrations of O2, CO2, and H+ ions (pH) in the blood
- Decrease in arterial oxygen or pH and/or increase in carbon dioxide → smooth muscles to contract → vasoconstriction → increase in BP
describe baroreceptors and their role
- major stretch receptors located in the aorta and carotid
- Respond to changed in smooth muscle fiber length by altering their rate of discharge
- Increase in arterial BP → increase rate of baroreceptor firing → travel afferent nerves → medulla → slows the heart rate via vagus nerve → decreases myocardial contractility → increases arteriolar and venous dilation → reduces BP
define orthostatic hypotension
Tx?
changes in vital signs taken within 3 minutes of position change (supine to sit or sit to stand)
- Decrease in SBP >20
- Decrease in DBP >10
- Increase in HR >20 bpm
give fluids - if resolve ortho hypo!
tx undeerlying dz
Increase salt in diet
Increase fluid in diet
Elevation of head in bed
Medication changes
define hypotension
Sustained symptomatic systolic blood pressure (SBP) <90 mmHg
•or an acute drop in SBP of >30 mmHg from baseline
name 4 types of shock
distributive
cardiogenic
hypovolemic
obstructive
causes of distributive vs obstrucitve shock
distributive -
septic shock
SIRS
- Neurogenic shock – TBI, spinal cord injury
- Anaphylactic shock
- Drug and toxin-induced shock – insect bite
- Endocrine shock – Addisons, Myxedema
obstructive
Mechanical
- Tension pnuemo
- Pericardial tamponade
- Constrictive pericarditis
- Restrictive CM
Pulmonary vascular
- PE
- Severe pHTN
si/sx of shock
look sick
hypotension
tachycardia
Oliguria (<30-50cc/hr)
tachypnea - reduce acidosis
Cool, clammy, cyanotic skin
Metabolic acidosis – “high ion gap metabolic acidosis
automaticaaly think??
shock
Hyperlactatemia correlation w/ mortality w shock
- Normal lactate is 0.1-3mmol/L
- **higher the lactate higher the mortality
management of shock
recognize
identify probable cause
oxygen >94%
•Maintain IV access at ALL times
give fluids
maintian ABCs
- Vasopressors – levophed, phenylephrine, vasopressin
- Inotropic support – dobutamine, epinephrine
- Mechanical support for cardiogenic shock
- Intra-aortic balloon pump
- Advanced cardiac mechanical support
appropriate fluid for type of shock
- LV ischemia or depressed EF: 500-1000cc
- RV ischemia or sepsis: 2-5L à preload dependent, RA need fluid or it will collapse
- Hemorrhagic shock: 3-5L
complications of shock
- Limb ischemia – can lead to dry gangrene which would require amputation
- Acute respiratory distress syndrome (ARDS)
- Death – high mortality associated with some causes of shock
- Permanent organ damage or death
Distributive shock is due to
due to severe peripheral vasodilation
cardiogenic vs hypovolemic shock due to
card -due to intra-cardiac causes of cardiac pump failure that results in reduced cardiac output
hypovol -due to reduced intravascular volume, which in turns, reduced CO
obstructive shock is due to
due to extra-cardiac causes of cardiac pump failure and is often associated with poor RV output
