Presentation on theme: "Naisan Garraway. 45 yr old lady admitted for work up of chest pain and SOB. ICU called as she is now on 80% FiO2. When she is assessed she looks comfortable,"— Presentation transcript:
45 yr old lady admitted for work up of chest pain and SOB. ICU called as she is now on 80% FiO2. When she is assessed she looks comfortable, with RR of 26 but sats are 93%. She has L and R chest pain that does not radiate. She has not voided in 2 hours.
Her past Hx is significant for primary pulmonary hypertension (Mild), type 2 DM, ORIF of L femur # 1 year ago, and smokes 1 PPD, 1-4 marijuana, and crack (when she can afford it). On exam, she is obese, diaphoretic, temp 38.5 o C, BP 90/40, HR 120. Chest has decreased A/E RLL, heart sounds: normal S1 & S2 with grade 3 pansystolic murmur is heard along the lower left sternal border. Jugular venous distention with a prominent V wave. RUQ fullness but no tenderness on abdo exam.
Labs: WBC 15, Hb 100, plt 250, Na 141, K 5.1, Creat 189, Trop I 5.1, lactate 5. Liver enzymes are elevated. ABG: 7.34/25/69/17. ECG shows sinus tachy, and CXR is clear except possible RLL infiltrate and an enlarged heart silhouette and loss of PA window.
What is the differential dx? Respiratory Cardiac Sepsis
What is associated with an elevated Troponin in the critically ill?
As you bring her down to the Unit her sats drop to 88% and her pressure drops to 80/40! You intubate her (grade 2 airway) but her sats are still 90% on FiO2 1.0 and her BP is 84/37. Question 3. What physiological effect does mechanical ventilation and PEEP have on the R ventricle?
in patients free of previous cardiorespiratory disease, mechanical ventilation with a normal Vt does not have any discernible hemodynamic consequences In the presence of a pulmonary or cardiac disease PPV related adverse hemodynamic effects may seriously complicate respiratory support.
On the one hand, tidal ventilation or PEEP application changes in transpulmonary pressure directly affect RV outflow impedance. On the other hand, tidal ventilation or PEEP increase in pleural pressure increases RV effective elastance, a factor limiting diastolic filling.
Bedside echo show a very dilated R ventricle and mod-severe TR. Her septum is D shaped and PA pressures estimate to be 50 mmHg. Her L ventricle has some decreased function but is also empty. There is no wall motion defects noted.
Yes: it is possible evidence suggests that despite the differences between the ventricles in structure and function, right ventricular dysfunction in septic shock closely parallels left. Ventricular function in both sepsis and septic shock is characterized by ventricular dilation and decreased L/RVEF. In septic shock survivors, these changes resolve over 7 to 14 days.
Multiple cytokines are potentially responsible for the cardiac dysfunction, possibly through NO and cGMP pathways. TNFa IL-1b IL-2 and IL-6 IFN-gamma Cytokine synergy also may play a major role in septic myocardial depression
Survival from septic shock is associated with acute, reversible left ventricular dilation and decrease in LVEF. Nonsurvivors only undergo this process inconsistently. Reversible right ventricular dilation and decrease in EF also are seen, but the prognostic significance is uncertain
RV and LV dysfunction in sepsis are not thought to be caused by coronary hypoperfusion But…. RV more at risk of hypoperfusion than left (coronary perfusion is 50% in systole vs only 20% on left side) RV very dependent on systolic pressure. Even worse in RCA disease
1. Volume overload 2. Direct compression of the RV pericardial effusion, pericardial fibrosis, tumor, massive pleural effusion 3. Lower extremity edema due to extrinsic compression of venous or lymphatics, renal failure, alterations in the renin-angiotensin system, or drug therapy
You try to float a PA catheter but are unable even with fluoroscopy and anesthesia assisting (true story). Your resident gets the central line in and asks if you want to bolus the patient
RV may have some compensatory reserve so volume loading may improve RV output. excessive volume loading may paradoxically worsen RV contractile function through RV dilation impediment to LV filling through the interventricular septum or through pericardial restriction Leads to low CO and RV hypoperfusion
Post hoc analysis showed that treatment with levosimendan was associated with a greater reduction in those hepatic markers of right- ventr Padley, J et al; Journal of Cardiac Failure, Volume 13, Issue 6, Pages S142-S142
Minimize hypoxia/hypercarbia Diuretics Anticoagulants Atrial Septostomy very high associated morbidity and mortality in critically ill patients with severe right ventricular failure not be performed when mean right atrial pressures is >20 mm Hg, significant hypoxemia, and a PVR index >4400 dynes sec/cm 5 /m 2
Treatment is started and there is some improvement on echo of her R ventricular function and PA pressures. That night her Hb dropped to 80 and she was transfused 2 U by the resident on call. She dropped her sats 2 hours later and her CXR looked like bilateral “white out”.
She does not progress well over the next few days and it is apparent her L ventricular function is worse now. Your resident suggests contacting CV surgery about implanting an “assist devise”. Question 10. What are the different categories and mechanisms of assist devises for the heart?
TypeDevicesPulsatile?Energy source Partial vs Total ECG? Complicatio ns Monitoring IntraAortic Balloon Pump PulsatileExternal Driveline (Pneumatic) -Partial -left only Yes-Leg ischemia (ad 10%) -infection -Augmented diastolic -MAP ImpellaNo, but heart can eject External driveline Partial -L : percut -R or Bi: open Yes- Leg Ischemia -Infection - misplacement RPM α CO VAD: 1st Generation -Thoratec -BVS 5000 -AB 5000 -Novacor Pulsatile- Pneumatic - Mechanical /electric Partial to total L, R or BiVAD Yes-Infection -Emboli -Thrombosis -Vej x rate = CO LVAD : Axial flow Pumps -Heartmate II -Micromed DeBakey Non Pulsatile, but heart could eject External Driveline Partial to total Yes-Thrombosis -Infection -Thrombosis of Ao Valve RPM α CO ECMOHeparin coated canulae and oxygenators Non Pulsatile, Heart can eject Biomedicus pump (Centrifugal) Partial to total, central or peripheral Yes-leg ischemia (leg perfusion) RPM α CO (until heart unfilled) Total Implantable Heart -CardioWest -Abiocor Pulsatile- External driveline -transcutaneous transmission TotalNo-infection - Bleeding CO = Vej x Rate
Thoratec: Anticoag, intra or paracorporeal Thoratec Heartmate: No anticoag, long term (Used at SPH) Novacor: anticoag, Big, long term BVS 5000: Good for transport, 10 days max AB5000: Anticoag, long term
If cardiac arrest: May be in asystole and have a pulse If have a pulse: no CPR If no pulse: CPR may generate a pulse (and/or more problems…)
Heartmate II (Used at SPH) Micromed DeBakey
If cardiac arrest: May have asystole and no pulse but have a normal cardiac output If monitor indicates adequate flow, give pressors for desired mean art pressure ( invasive measurment only ) If asystole and no flow: CPR may generate flow Make sure no flow before CPR (may cause damage)
CardioWest Used in Canada Abiocor -14 cases worldwide: all dead -Abiocor II in construction
Asystole: Normal Pulseless: use hand pump at bedside, if does not work - find etiology fast No CPR (useless, rigid plastic box)
She finally responds to treatment enough to be extubated and is sent to the ward. She will be assessed by the transplant team while in hospital. Bonus question : What is the long-term survival of heart lung transplant patients for Pulmonary HTN and heart failure?