Right heart failure + CV Surgery Flashcards
Contrast the right and left ventricle. What’s different about the shape, inflow/outflow tracts, geometry?
T/F: The right ventricle pumps at the same stroke volume as the LV and changes in RV preload and afterload affect the geometric chape and wall thickness
The rigt ventricle has a more complex geometry than the LV, and also has a crescent shape, and distinct outflow/inflow tract
True. (see below)
T/F: The pressure volume loop for the right ventricle looks about the same as that of the LV
Falsehood. The RV has a different geometric shape (which affects how things flow) but more importantly its contractions are peristaltic as opposed to those of the left ventricle
Contrast the following between the right and left ventricle
(wall thickness, stroke volume, contraction pattern)
RV is thin walled, has the same SV as the LV (has a lower EF because it does less work), and it has an atypical contraction pattern
Which can the right ventricle handle better - volume overload or pressure overload? Why?
The right ventricle can handle volume overload better than it can handle volume overload and that is due to the effects of wall stress. Since it’s thin walled, it can only handle so much pressure
Why does LV failure lead to RV failure? (3 reasons) (hint: think about what happens if there’s a pressure problem in the LV and what that does to pulmonic pressures. What happens if the LV becomes mad dilated?)
If there’s pressure problems in the LV, that’ll cause this pressure back up that affects the pulmonary circulation >> affects RV
LV dilation means restriction of space for RV filling
Myopathic process
What mechanisms can lead to the development of right heart failure?
Apparently these aren’t really known.
Some possibilites:
RV ischemia
Microvascular endothelial cell dysfunction
Apoptosis
Wall tension
An occlusion of the right coronary artery can cause what kind of myocardial infarction?
How would this manifest? (3)
An RCA occlusion can cause an inferior rigt ventricular myocardial infarction
Can manifest as stunning of the RV (temporary, reversible loss of contractility), hypotension, and increased jugular venous pressure
***
Increased jugular venous pressure is more commonly seen with right ventricular myocardial infarction
Hypotension, because there’s restricted flow/lower pressure out to the left side from the right ventricle so overall systemic pressure drops
With temporary loss of contractility in RV myocardial infarction, RV depends upon ___ to generate stroke volume (hint: it’s the reason why you should be careful about giving nitroglyecrin)
What would be the benefit of giving inotropes for this condition? why do we avoid systemic vasodilators?
With temporary loss of contractility in RV myocardial infarction, RV depends upon volume to generate stroke volume (and not on contractility anymore.
***Meds you want to be careful about: nitroglycerin (venodilator) – reduces preload (and in the case of RV ischemia you have reduced contractility already and nitrates lower contractility so need to be careful about worsening things)***
***
Also can give inotropes coz that will help to increase/maintain stroke volume
Cannot give systemic vasodilators because you can’t increase stroke volume because your heart has a fixed degree of contractility/ability to pump. Since you won’t be able to pump any better, if you give systemic vasodilators, that’ll cause hypotension
Another cause of RV failure is ___ (hint: can be a saddle)
What does this condition manifest as? How would you treat it?
Another cause of RV failure is pulmonary embolus
Manifests as an acute pressure overload causing a marked increased in wall tension
Can be treated w/ anticoagulants/thrombolytics +/- surgery
What are the steps of managing RV failure? (4)
Optimize volume status
Reduce RV afterload - give pulmonary artery vasodilators
Enhance contractility
Treat underlying condition
How would you manage volume overload in acute RV failure?
Maintain CVP in medium range (8-12mmHg)
For most causes of acute RV failure, diuretics are indicated
Which drugs would you give to enhave contractility? (hint: they’re both inotropes)
Dobutamine
Milrinone
Describe the mechanism of action of dobutamine and milrinone
How would you reduce afterload in acute RV failure?
*see image below*
You can reduce afterload by using pulmonary arterial vasodilators
Review this slide on the causes of chronic RV failure
Describe the pathophysiology of pulmonary hypertension as illustrated below
The progression of RV failure following pulmonary HTN:
The right ventricle hypertrophies a little bit at the onset of pulmonary hypertension to compensate
The RV hypertrophies even further and the lumen of the pulmonary arteries is very small >> pt will be dyspneic, hypertensive etc
How do you treat cor pulmonale? (3)
Oxygen but that only works is hypoxic
Diuretics - improves biventricular function
Reducing salt consumption (helps with fluid control
WE DO NOT BETA BLOCKERS OR ACE INHIBITORS FOR CHRONIC RV FAILURE. THEY MAKE THINGS WORSE!!
What is the effect of hypoxia in right ventricular failure? (hint: what happens to the pulm arteries and why?)
Hypoxia leads to pulm artery vasoconstriction, to shunt blood away from hypoperfused areas to functional ones
How can LV failure lead to RV failure?
Likely through ventricular interdependence (since the ventricles share the intraventricular septum and fibers that connect them what happens in one ventricle can affect the other)
Describe tricuspid regurgitation
Tricuspid regurg is often a functional problem (as in it’s a muscle problem, not valve problem)
Basically when blood shoots back into the right atrium from the rught ventricle
**might not always do surgery**
Another cause of RV failure is ___ (hint: involves pulm arteries)
What is the effect of an increase in this on stroke volume?
Another cause of RV failure is pulmonary hypertension (caused by abnormal increase in pulm arterial pressure)
Rapid increases in pressure cause significant reduction in stroke volume
Define cardiogenic shock
What are some expected clinical symptoms of cardiogenic shock? (remember this is shock involving the heart)
Cardiogenic shock is a state of severe hypotension, dimished myocardial contractility, and low cardiac output
**see below**
Hypotension
End organ hypoperfusion
Cool extremeties (low perfusion to extremities)
Altered mental status (low perfusion to brain)
Other things in lab values: elevated Cr, liver enzymes etc
Briefly describe how the following technologies work in cardiogenic shock:
IABP
Temporary LVAD
ECMO
IABP: balloon that contracts during systole to reduce afterload and expands during diastole to provide coronary perfusion
A temporary LVAD is a pump typically placed through the femoral artery that goes thru the aorta into the ventricle and pumps blood from the ventricle to the aorta
ECMO – extracorporeal membrane oxygenation – compact bypass machine
Describe the difference between VV ecmo and VA ecmo
Under what circumstances woud you use either one?
VV ecmo – veno-venous echmo (blood taken from vein >> machine >> oxygenated and CO2 removed >> back to pt) – provides no hemodynamic support
VV eccmo is a good option for folks with pulmonary failure
VA ecmo – blood from vein >> machine (again O2 in, CO2 out) >> artery >> back to pt (provides blood pressure in addition to oxygenation; supports pts perfusion)
What are the clinical indications of ECMO? (3)
Pts that have cardiogenic shock
Pts with cardiac arrest that is refractory to CPR
Those with respiratory failure
What are the contraindications to ECMO? (5)
Active bleeding or intracranial hemorrhage
Folks on mechanical ventilation for a long time
*Multisystem trauma pts
Folks with irreversible organ dysfunction
Folks with a DNR/DNI
What are the clinical conditions that are amenable to ECMO? (7)
Cardiac arrest
Cardiogenic shock
Respiratory failure (mainly due to ARDS)
Trauma/pulmonarycontusion
Toxic ingestion
Pulmonary embolus
Hypothemia
What are the main treatment options for patients with end stage CHF? (2)
Cardiac transplantation
LVAD
What is the best therapy for end stage heart failure?
What regions of the heart would you anastamose throughout a heart transplant procedure?
Cuurently, the best therapy for end stage heart failure is a heart transplant
Anastamoses: LA>>IVC>>PA>>Aorta>>SVC
What are the major causes of death for recepients of heart transplants? (several but name 3)
Graft failure
Infection
Multi organ failure
