Download Pharmacotherapy of Cardiogenic Shock_Master

CS
Therapeutic Discussion
Pharmacotherapy of Cardiogenic Shock
What are the different types of shock?
- Hypovolemic
- Distributive
- Cardiogenic
- Obstructive
What is cardiogenic shock?
- ↓ cardiac output in the presence of adequate intravascular volume
- State of end organ hypoperfusion due to cardiac failure
o Brain: ↓ LOC
o Kidneys: ↓ U/O
o Skin: cool and clammy, ↓ cap refill
o Lactate: elevated (caveat: if in liver failure, lactate will be high due to ↓ clearance)
o ↓ScVO2/SVO2
- ↓CI, ↑PCWP, ↑↔SVR
o MI can cause SIRS, which results in low-normal SVRs (inappropriate vasodilation)
- Do not rely on the BP to tell you if a patient is in shock!
o In animal studies, MAP < 60 has been shown to be detrimental to cellular processes
o Patients with HTN may require a higher MAP to maintain tissue perfusion
What is the definition of cardiogenic shock?
- Persistent hypotension (SBP 80-90 or 30mmHg lower than baseline x 30 minutes)
- Reduction in cardiac index (normal = 2.5-4)
o <1.8L/min/m2 without support or <2-2.2L/min/m2 with support
- Adequate/high LV filling pressures  This means that there is blood left over in the ventricles after contraction
(not contracting adequately to eject all of the blood)
o LVEDP > 18mmHg or RVEDP > 10-15mmHg
What is the pathophysiology of cardiogenic shock?
- Mostly due to LV pump failure
- The heart benefits from low blood pressure and also suffers from low BP
o Low BP reduces afterload (easier for heart to pump); Low BP results in compromises in coronary flow
- Unpredictable who will go into shock
o Severe impairment of contractility does not always lead to shock
o Sometimes moderately depressed LVEF leads to shock
↓CO
↑SNS
↑HR
↑Contractility
↑Myocardial O2
Demand
↑Myocardial O2
Demand
↑RAAS
Vasoconstriction
↑Afterload
↑ADH
Vasoconstriction
↑Volume
↑Volume
↑Afterload
↑Venous
Return/Preload;
worsens
pulmonary
edema
↑Venous
return/Preload;
worsens
pulmoanry
edema
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority
CS
What is the incidence of cardiogenic shock?
- 5-8% of STEMI, 2.5% of NSTEMI
- Incidence has been in decline with increasing uses of primary PCI for MI
o The only way to prevent cardiogenic shock secondary to MI is to ensure early perfusion therapy
 Randomized trial of early in-ambulance lytic = primary PCI for the development of CSCirculation.
2003;108:2851–2856.
CC/HPI
PMHx
Meds
Objective
On
Exam
Lab
Dx
How do patients typically present with cardiogenic shock?
Lightheadedness, SOB, chest pain, palpitations, cardiac arrest
What are some causes of cardiogenic shock?
- Any cause of acute, severe LV or RV dysfunction
- MI with LV failure (5-8%STEMI, 2.5% NSTEMI)
- Mechanical complications: ventricular septal rupture (87%; highest mortality), contained free
wall rupture, papillary muscle rupture  women and elderly at high risk
- Suspect non-mechanical complications in those with non-anterior MI or first MI
- MI + additional factor: hemorrhage, infection, bowel ischemia
- In the absence of CAD: myocarditis/pericarditis, takotsubo cardiomyopathy (4.2%)
- Acute mitral regurgitation (endocarditis, chordal rupture due to trauma or degenerative
disease)
- LV outflow tract obstruction: aortic stenosis, hypertrophic obstructive cardiomyopathy
- Aortic dissection  severe aortic insufficiency
- Cardiac tamponade
- Massive PE (pulmonary congestion)
- Tension pneumothorax (obstruction of venous return)
- Left atrial myxoma: cardiac tumor that blocks flow
- Pheochromocytoma
Risk Stratification
- Mortality due to CS ~50% (used to be as high as 80-90%)
- Mortality ranges from 10-80% depending ln the demographic, clinical and hemodynamic
factors: age, clinical signs of peripheral hypoperfusion, anoxic brain damage, LVEF
- Hemodynamic factors only predict short term mortality
What are risk factors for cardiogenic shock?
- Older age
- Anterior MI: V leads (LAD, LCx, LM)
- HTN, Diabetes
- Multi-vessel coronary artery disease
- Hx MI/Angina, HF
- STEMI, LBBB
- Acute treatment of MI may ↑ the risk of CS in those who are predisposed
- 75% of those with CS complicating MI develop CS after hospital presentation
- Diuretics: MI results in acute pulmonary edema, but circulating volume may be low, ↓ preload and ↓ intravascular volume
- ACEI: ↓ preload and intravascular volume, ↓ SVR
- BB: Lowers cardiac output
Vitals: ↓BP, ↑HR, ↑RR, ↓O2 sats
CNS: decreased LOC
CVS: new murmur (ruptured myocardium/papillary muscles), ↑ JVP
Resp: diffuse crackles
GI: reduced u/o
MSK: cool and clammy, cap refill < 3s
↓Na, ↑ Trop, ↑ BNP, ↑SCr
EKG
Ischemia, ST elevation, T wave changes, LBBB
CXR
Pulmonary edema
Echo
Visualize movement of the ventricles, rule out valve problems, check pressures
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority
CS
Pathophysiology of Cardiogenic Shock
What is the treatment approach to cardiogenic shock?
1. Re-vascularize as soon as possible
a. Give some fluid to make sure not hypovolemic
b. If can’t revascularize and hemodynamically unstable:
i. IABP
ii. Mechanical ventilation: PEEP ↓ preload and afterload, ↓ work of breathing
iii. Inotropes
iv. Vasopressors
v. LVAD as a support to heart transplant
2. Avoid negative inotropes and vasodilators initially
3. Normalize glycemic control: Reduces mortality in those who are hyperglycemic
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority
CS
Treatments/Benefit
PCI/CABG
-
Reperfusion
-
Comments
Revascularization provides benefit at all levels of risk
Post PCI TIMI flow grade and time of symptom onset to PCI are independent predictors of
mortality
Reduces mortality and interrupts the vicious circle
Elderly patients benefit from PCI!
SHOCK Trial
- ST elevation, LBBB, Q-wave MI, HR<90, end organ hypoperfusion (cold extremities,
decreased U/O, ↑ HR), cardiac index < 2.2, PCWP>15mmHg
- Emergency revascularization (PCI/CABG within 6h) vs. Medical stabilization
- Outcome
o 30d mortality (46.7% vs. 56% NSS)
o 50% vs 63% @ 6m SS, 53% vs 66% SS (ARR 13%! NNT = 8)
o This benefit is seen whether the revascularization is via PCI or surgery
o Those who were > 75y: results were NSS (but there were baseline differences in EF
in these older patients)
Lytic
Reperfusion
Mechanical
Support: IABP
↑ coronary perfusion
pressures
Relieve cardiac
ischemia, support
circulation
Inotropes and
Vasopressors (low
doses)
-
Thrombolytic therapy is less effective but can use if PCI is impossible or if will be delayed
or if it is used within 3h of MI
- GISSI 30 day mortality = 70% in 146 pts with shock treated with streptokinase or placebo
- ISIS mortality 65% in 93 patients with shock treated with streptokinase, 78% in 80 patients
treated with tPA
- GUSTO N=315 with shock, SK = tPA for mortality (56% vs. 59%)
Reasons for ↓ efficacy
- ↓ arterial pressure limits penetration of lytic into a thrombus
- Passive collapse of infarct artery in the setting of hypotension
- Acidosis inhibits the conversion of plasminogen to plasmin (prevents endogenous clot
breakdown)
- Mainstay of therapy for CS, does not ↑ myocardial oxygen demand
- Improves coronary and peripheral perfusion via diastolic balloon inflation
- Augments LV performance via systolic balloon deflation with an acute ↓ in afterload
- Accurate timing of inflation and deflation provides optimal support
- Not everyone has a hemodynamic response to IABP, but response predicts better
outcomes
- Should be inserted quickly, even before revascularization if possible
- Causes mechanical breakdown of platelets  need anticoagulant/antiplatelet on board
- Temporarily improve CO and peripheral perfusion, but do not interrupt the downward spiral
- ↑ myocardial O2 consumption
- Use until IABP is placed or afterwards while waiting for heart function to improve
- SOAP II trial (15% CS) NE = Dopamine for mortality, but more arrhythmias with dopamine
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority
CS
↑ contractility and
maintain tissue
perfusion
-
LVAD
(Left Ventricular
Assist Devices)
Improves circulation
of oxygenated blood
Bridge to transplant
and cardiogenic shock patients did better with NE than dopamine
Dopamine and NE have some inotropic effects, but sometimes dobutamine is needed in
addition
NE: +++ alpha, ++ B1, Used to think that this causes harm, but because of SOAP II,
started using NE, easy to titrate, rapid acting
Often use combo vasopressors, but start with NE
Dopamine: ++ alpha, ++ B1, tend need to use larger doses in cardiogenic shock (more α)
Dobutamine: ++B1, + B2 (vasodilation = decreased afterload, decreased pre-load,
decreased BP initially before BP goes back up), Good for chronic HF.
-
Device drains blood from L side of the heart and returns blood to the systemic arteries with
pulsatile or continuous flow
- Surgically implanted LVADs removed blood through a cannula placed at the LV apex and
return blood to the ascending aorta
- Percutaneous LVADs are also allowed
- May cause irreversible organ failure
- Device-related complications
- Need anticoagulation for percutaneous LVADs but are optional with surgically placed
LVADs
- Hemodynamics improve better with LVAD vs IABP, but more multiorgan system
dysfunction (?SIRS) and similar mortality rates
TandemHeart® (Percutaneous LVAD)
- Cannula placed through femoral vein and intra LA via trans-septal puncture
- Blood removed from LA  Blood returned to systemic artery (femoral) with retrograde
perfusion of the abdominal and thoracic aorta
Impella®
- Placed across the aortic valve and spins blood up and out of the LV
ECMO
- Extracorporeal circulation of blood through a membrane oxygenator
- Relieves R and L heart
- Venoarterial (for heart failure) and venovenous (for lung failure)
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority
CS
Mechanical Revascularization Algorithm
What is the pathophysiology and general treatment approach in RV failure?
- General treatment: fill the tank
o Want to ensure adequate preload to ensure perfusion of the rest of the body
o Aggressive fluid resuscitation may be detrimental if the RV pressures get too high
- Elevation in RV pressure may result in shifting of the interventricular septum towards LV
- ↑ L atrial pressure and impairs LV filling due to the mechanical effect of the bowing of the septum into the LV
- RV failure  LV failure
- Target RV pressure = 10-15mmHg (any higher or lower is no more beneficial)
- Treatment option: nitric oxide to lower pulmonary vascular resistance and promote forward flow
Prepared by Erica Wang Pharm.D. (Updated 2-May-17)
Cardiac Services, Kelowna General Hospital, Interior Health Authority