SEM 2 Lab 2: Exercises Flashcards
Discuss the Forrester classification of CHF
CARDIOGENIC SHOCK
Forrester classifications of cardiogenic shock classifies patient into Warm or Cold and Wet or Dry.
These categorizations have direct implications for prognosis and treatment.
• Patients who are warm/wet may often be managed with volume removal and/or vasodilation to reduce their afterload (vasodilation shifts fluid out of the lungs without affecting the total body volume).
• Patients who are cold/dry may often be managed by fluid administration
classic presentation of cardiogenic shock: patients who are cold & wet
• Cardiogenic shock may be roughly conceptualized as requiring two components:
• (1) Systemic hypoperfusion due to low cardiac output (cold).
• (2) Filling pressures are elevated (wet).
• Patients in cardiogenic shock cannot be fixed with volume administration or removal.
• Giving volume will worsen their pulmonary congestion (making them wetter).
• Removing volume will worsen their systemic hypoperfusion (making them colder).
• Management of cardiogenic shock usually requires interventions to improve cardiac function (e.g., inotropic medications, revascularization, or a mechanical support).
• Cardiogenic shock patients may look deceptively OK, but they are indeed critically ill.
• Early recognition facilitates appropriate ICU management.
• The patient with unrecognized cardiogenic shock will generally fail to respond to non-intensive therapy, running in circles (typically the patient is initially diuresed, then develops worsening renal failure, then is given fluid back, then develops pulmonary edema, then transferred to ICU).
Wet=presence of pulmonary congestion due to elevated filling pressures, dry=no pulmonary congestion. Fluid administration vs fluid removal and BiPAP (reduces preload and afterload)
IABP is used as a supportive treatment tool in a clinical context that will improve (bridging therapy) due to recovery or treatment
-cardiogenic shock
-post bypass
-post MI
-cardiomyopathy
-severe IHD awaiting surgery or stenting
-severe acute MR awaiting surgery
-prophylactically in high risk patient pre-stenting/ cardiac surgery
-miscellaneous (i.e. post myocardial contusion which is expected to recover with time)
Intra-Aortic Balloon Pumps have also been inserted as a last-ditch measure to stop haemorrhage from the aorta or its branches (e.g. massive GI haemorrhage)
IABP-SHOCK II trial (2012) showed no 30-day mortality benefit from IABP insertion for cardiogenic shock following MI when early revascularisation was planned.
LVAD can also improve secondary organ function prior to transplantation, reduce pulmonary hypertension, and enable improvement in nutritional status, all of which are associated with improved post-transplant survival. Nowadays, 80–85 per cent of patients are alive a year after having an LVAD fitted and 70–75 per cent after two years. Patients who have been too unwell to walk around are quickly able to get up and about. Many patients can soon return to other normal activities like driving and going on holiday; some of them even return to work. Nearly one-third of patients die or have a persistently poor quality of life over the year after LVAD. integrating quality of life outcomes into the definition of a poor outcome is particularly relevant in these challenging and complex patients with end-stage heart failure.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4985017/
Assessment findings in a Pericardial Tamponade
Beck’s Triad: sinus tachycardia, elevated JVP, hypotensionPeripheral vasoconstriction or mottlingPulsus paradoxusMuffled heart sounds
- Tachycardia is almost always seen (unless suppressed by medication or conduction system disease).
- Narrow pulse pressure may be a relatively early sign of falling cardiac output (pulse pressure <25% of the systolic blood pressure; this generally suggests a low cardiac output state).
- Hypotensionoccurs in the later stages of tamponade – and if present this is a very concerning finding.
- Hypertensioncan occur early on, due to a compensatory sympathetic response. If antihypertensives are given to “control” the hypertension, this may be catastrophic.
-Tamponade may occur withanyblood pressure (low, normal, or high).
Low voltageElectrical alternans
Restricted Na+ and H2O intake daily means that sudden fluid losses (vomiting, diarrhea, blood loss) can quickly result in hypovolemia.Increased K+ retention and hypocalcemia can negatively impact cardiac function.Decreased renin production leads to chronic hypotension.Decreased nephron function leads to reduced EPO production and anemia.Impaired kidney function leads to H+ ion retention and inability to generate HCO3
Discuss ECG changes commonly found in PE
The ECG changes associated with acute pulmonary embolism may be seen in any condition that causes acute pulmonary hypertension, including hypoxia causing pulmonary hypoxic vasoconstriction.
• Sinus tachycardia – the most common abnormality (seen in 44% of patients with PE)
• Complete or incomplete RBB(18%)
• Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF). This pattern is associated with high pulmonary artery pressures (34%)
• Right axis deviation(16%). Extreme right axis deviation may occur, with axis between zero and -90 degrees, giving the appearance of left axis deviation (“pseudo left axis”)
• Dominant R wave in V1– a manifestation of acute right ventricular dilatation
• Right atrial enlargment (p pulmonale)– peaked P wave in lead II > 2.5 mm in height (9%)
• SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III (20%). This “classic” finding is neither sensitive nor specific for PE
• Clockwise rotation– shift of the R/S transition point towards V6 with a persistent S wave in V6 (“pulmonary disease pattern”), implying rotation of the heart due to right ventricular dilatation
• Atrial tachyarrhythmias – (8%)
• Non-specific ST segment and T wave changes, including ST elevation and depression (50%)
STRATEGIES TO MAXIMIZE RV performance in the setting of RV FAILURE
-Caution with fluids: Overfilling causes a decrease in LV filling.
- Decreased LV filling/output can decrease right coronary perfusion worsening ischemia. -Support SBP: LV output determines RV coronary perfusion.
Keep SBP»PAP.
Avoid hypotension, even transiently.
**Lower threshold to start vasopressors (greater effect on SVR than PVR = vasopressin, epi at low or mid doses, norepi at lower doses)
-Decrease PVR: Avoid hypoxia, hypercapnia, and acidosis.
- Inhaled NO2 or Flolan. Inhaled NTG or milrinone (5 mg/ 5 min). Inhaled pulmonary dilators also improve V/Q mismatch which helps correct acidosis through respiratory compensation.
-Increase RV contractility: Inotrope. Cath lab if coronary ischemia
-Caution with intubation: Intubation induction worsens MAP, hypoxia, CO2.
**PPV worsens RV function so target low PIP and low PEEP.
***ECMO might bridge to survival in PE or reversible cause.
Benefits: Better ventricular filling with slower heart rate.
Better ventricular filling in NSR due to atrial contraction (atrial kick).
Reduced MvO2 with slower heart rate.
Risks: Atria may not regain contractility with conversion to NSR so no atrial kick to improve ventricular filling.
Cardiac output will decrease in proportion to heart rate decrease, may worsen hypotension if stroke volume does not increase sufficiently to compensate.
Ischemia-related afib may be resistant to conversion to NSR.
Discuss pulmonary HTN and causes
Causes of pulmonary HTN can be classified into three rough categories which tend to overlap. Pts with RV failure often have some combination of numerous factors. Identifying and treating all causative factors is critical
- Causes of chronic pulmonary HTN (WHO has a long long list)
- Severe diseases which can cause acute pulmonary HTN (PE, sickle cell acute chest syndrome, ARDS, septic shock, post-cardiac arrest)
- Precipitating factors which can make either of the above worse. (negative inotropes, alpha agonists, systemic vasodilators, non-adherence of PH therapies, Hypervolemia, acidosis, arrhythmia *especially A-fib, hypoxemia, hypercarbia, excessive lung volumes, and any and all lung disease)
Pulmonary HTN = Increased pressure in the pulmonary artery – mean pulmonary artery pressure greater than 25mmhg
Pulmonary HTN is concerning for a number of reasons but acute mortality is driven by profound cardiogenic dysfunction and shock. Can be caused acutely with hypoxemia, ARDS, acute PE, sympathomimetic drugs,
What is Ventricular Interdependence
Ventricular interdependence = Share septum, myocardial fibers, and pericardium and dependent on each others function.
What are Clinical features of RV failure
Clinical features of RV failure
- Systemic congestion is almost invariably present (JVD, kussmaul’s sign, peripheral edema, hepatic distention may cause RUQ tenderness)
- Hypoperfusion occurs if RV failure is severe enough to cause shock (cool, clammy extremities, delayed CRF, congestive encephalopathy, congestive nephropathy)
- Frank systolic hypotension
Refractory shock with multiorgan failure (bowel wall edema may promote bacterial translocation and systemic inflammation, adding a component of vasodilatory shock)
