CV integration lab Flashcards
Venous return to the RV _____ during normal inspiration and a ____ in venous return to the LV.
Venous return to the RV increases during normal inspiration (increases in vol) and decreases in venous return to the left ventricle (reduction of vol)
These changes in venous return can alter intensity of murmurs and heart sounds, primarily those that
During inspiration, there is an increase in the splitting of:
S2 as A2 and P2 are separated (due to longer RV ejection time compared to LV ejection time during inspo)
Describe S3 and S4 heart sounds of RV origin w/ inspo and expo:
decrease with expo
increase with inspo
Describe S3 and S4 from left side of heart with inspo and expo:
increase with expo
decrease with inspo
Describe tricuspid stenosis with inspo and expo:
opening snap decreases with expo
opening snap increases with inspo
Describe mitral stenosis with inspo and expo:
opposite of tricuspid
opening snap increase wit expo
opening snap decreases with inspo
Pulmonary ejection sounds with inspo and expo:
decrease in inspo
Inspiration increases the intensity of murmurs originating from the ___ of the heart.
What are they also?
R side of the heart
Murmurs= tricuspid stenosis, pulmonary regurg, systolic murmur of tricuspid regurg (cavallo’s sign) and presystolic murmur of ebsteins anomaly)
What happens in MVP?
inspiratory decrease in venous return to the left side of heart reduces LV volume
In what pathological heart issue does murmur and click occur earlier and may diminish?
Mitral valve prolapse
When might a loud first heart sound be heard?
fever or exercise (hyperdynamic)
mitral stenosis
atrial myxoma
When might a soft first heart sound be heard?
low CO @ rest, HF
tachy
severe mitral reflux (caused by destruction of valve)
What would produce a variable intensity in the first heart sound?
atrial fibrillation
complete heart block
What is a second heart sound?
audible expiratory spitting means >30 msec difference in timing of the aortic (A2) and pulmonic (P2) components of the second heart sound
Where is splitting of S2 best heard over?
over 2nd left ICS
normal P2 is often softer than which sound? where is it rarely audible
normal P2 is often softer than A2
rarely audible at apex
If P2 is audible over apex what is the diff dx?
significant pulmonary HTN
Atrial septal defect
Second heart sound findings should always be present in what positions?
upright and supine
normal subjects may have expiratory splitting when recumbant that disappears when upright
When can you hear a loud aortic component of second second?
systemic HTN
dilated aortic root
When can you hear a soft aortic component of second second?
calcific aortic stenosis
What kind of second heart sound would you hear with pulmonary htn?
loud pulmonary component of second sound
What shock is caused by failure of the heart as a pump to deliver adequate perfusion to peripheral tissues
cardiogenic shock
What shock is caused by failure of arterial circulatory bed to maintain adequate perfusing pressure to peripheral tissues?
distributive shock
What shock is caused by significant reduction in cicrculating vascular volume, resulting in reduced perfusing pressure to peripheral tissues
hypovolemic shock
What regulates HR?
autonomic NS
what influences stroke volume?
LV preload, afterload, and myocardial contractility
Systemic Vascular resistance is governed by:
arterial tone, arterial volume, and structural integrity of vessels themselves
Example of someone running up hill and CV performance of what happens:
runner experiences ruge in serum catecholamines–> increased SNS output–> increased HR–> increased myocardial contractility–> increased CO; arteriolar tone will increase as result of VC effects of catecholamines–> increase in perfusion pressure–> adequate blood flow to joggers LE and diaphragm
When does shock typically occur?
when there is a massive perturbation of one or more of the processes (HR/ stroke vol/SVR, etc.) that cannot be compensated for by adoptions in other areas
What components are the main ones that go into tissue perfusion pressure?
CO (HRx SV)
SVR (arterial tone/volume/integrity)
A patient presents with unexplained sinus tachy and a BP of 90/75 (hypotensive BP), what would the main differential that you would think about be?
shock
could also consider cardiac tamponade..
If you see a pt with shock who has bradychardia (or lower than expected HR), what should you consider doing next?
ways to increase HR
In a patient with suspected shock, it is critical to check what early?
arterial blood gases and lactate levels
What is associated with better outcome in a patient with cardiogenic shock and what should you exclude immediately?
exclude acute MI immediately
EARLY revascularization is assoc with better outcomes!
What would be a cause of a wide, fixed splitting S2
atrial septal defect
What would be a cause of wide split S2, varying with inspo
pulmonary stenosis, RBBB
What would be the cause of paradoxical splitting of S2
hypertrophic cardiomyopathy
If you see diffuse ST elevations on all leads(and/or sometimes PR depression), what should you suspect?
acute pericarditis
How would you describe a pericardial friction rub?
a three component scratchy rub that is loudest over the left sternal border
The dx of acute pericarditis requres presence of at least 2 of the following criteria:
typical chest pain
pericardial friction rub
widespread ST segment elevation
new or worsening pericardial effusion
Common clinical features of cardiac tamponade include:
Dyspnea Hypotension Tachy Jugular venous distention Pulsus pardoxus of >10 mmHg
Constrictive pericarditis can complicate any pericardial dz (acute pericarditis or cardiac surgery). How do these pts typically present?
progressive dyspnea
edema
ascites
cachexia
elevated JVP, pulsus paradoxus, Kussmauls sign, and/or pericardial knock
In a pt with acute pericarditis, the sharp pleuritic chest pain typically IMPROVES when the pt:
sits up and leans fwd
Where is pericardial friction rub heard best upon auscultation?
scratchy sound best heard with diaphragm and loudest over left sternal border
Pts with suspected pericardial dz should undergo initial evaluation with:
ECG, CXR, and Echo
Pericardial effusion and cardiac tamponade on ECG:
low QRS voltage (bc fluid in bw heart and ECG leads) and sometimes electrical alternans (QRS reflecting swinging in heart in pericardial fluid)
What ECG findings would you find in constrictive pericarditis?
no specific findings
nonspecific ST and T waves changes are common
What is the CXR in acute pericarditis?
Pericardial effusion ?
constrictive pericarditis?
acute pericarditis= typically NORMAL
Pericardial effusion (with or w/out tamponade) = cardiomegaly with clear lung fields
Constrictive pericarditis= pericardial calcification (uncommon)
What test should you perform rapidly if you suspect tamponade?
echocardiography
normal in acute pericarditis unless assoc. with pericardial effusion
What test has a major role in IDENTIFICATION of a pericardial effusion and in assessing its hemodynamic significance?
Echocardiography
What is the treatment for cardiac tamponade?
immediate removal of pericardial fluid
