W12 CARDIORESPIRATORY DISEASE Flashcards
Most common cause of RV failure
pulmonary HTN
most common cause of pulmonary HTN is LV failure
how is RV failure dx
ECG
lactate + BNP markers
echocardio
CT
cardiac MRI
How do lung diseases cause pulmonary HTN
via hypoxia
which causes polycythaemia (increased RBC mass), vasoconstriction and vascular remodelling
in addition to damage of lung parenchyma with loss of vascular bed
how does RHF occur in PE
RV fails to maintain blood flow past an obstructing large embolys
why is the RV more resiliant than the LV during ischaemia
RV has less oxygen demand, coronary perfusion occurring throughout the cardiac cycle and dual blood supply ( the LAD supplies the anterior two thirds of the septum)
sx of RHF
mainly due to systemic venous congestion and or low cardiac output
exertional dyspnoea
fatigue
dizziness
ankle swelling
RUQ abdo pain
How does raised RV pressures impact stroke volume
the increased pressure in the RV, pushes the IVS into the LV and impairs LV diastolic function leading to impaired filling and reduced stroke volume
explain the difference between the RV and LV and the impact of PPV
Fundamentally different
RV preload is extrathoracic
afterload is intrathoracic
LV preload is intrathoracic
afterload is extrathoracic
in PPV inspiration leads to an increased in RV afterload and a decrease in RV preload.
this contrasts with spontaneous resp which has generally lower RV afterload and higher RV preload
this means wherever possible these pts should be maintained in spontaneous respiration and intrathoracic pressures should be minimised
why give adrenaline infusion for shocked PE patient
Beta agonist activity may cause pulmonary vasodilation (much of the haemodynamic deterioration due to PE isnt the clot itself but rather the pulmonary vasoconstrictors which are released in response to the clot, hence why this would help) (oxygen is a pulmonary vasodilator**)
massive PE causes death due to failure of the RV, beta antagonism may improve contractility of the RV thereby improving CO
heparin in PE
prevents additional clots from forming but doesnt break down the existing clot
thrombolysis in PE goal and effects
primary reason is to reduce risk of cardiac arrest
widely accepted standard of care
causes an immediate reduction in pulmonary vascular resistance and immediate improvement to RV function, this reduces risk of acute RVF and haemodynamic deterioration
refractory hypoxemia in PE
causes
this always reflects some sort of shunt
right to left shunting of blood through the FA or atrial septal defect
PE causes an elevation of right sided heart pressures causing a right to left shunt of deoxygenated blood
also could be co existant pulmonary process –> pneumonia, mucous plugging or pneumothorax
what is stertor stridor
due to obstruction in nasopharynx
monophonic on inspiration
mainly a concern in paeds as they are nose breathers
signs for an obstruction around the glottic region
just above the vocal cords / soft tissue airway
when the airway is at its narrowest during inspiration this area of the airway is collapsable therefore you should hear the stridor on inspiration
during expiration when the extrathoracic tissue EXPANDS, you will not hear the stridor
subglottis / tracheal obstruction
FBAO
likely to hear a biphasic stridor
