blood  goes  round  and  round,  and  sometimes  it  

doesn’t

PGIM  EM  Teaching  Colombo,  November  2015

Dr  Nick  Taylor  MBBS  FACEMVisiting  Emergency  SpecilaistETU,  Teaching  Hospital  KarapitiyaSenior  Specialist  and  Co-­DEMT,  The  Canberra  Hospital

HEART  FAILURE

Goals

•Understand  basic  circulation  physiology•Describe  the  cause  and  effects  of  left  and  right  heart  failure

•Classify  Left  Ventricular  Failure•Learn  the  principles  to  treat  acute  left  ventricular  failure  and  cardiogenic  shock

The Physiology of the

Circulation

Blood  goes  round  and  round...

Schematic  of  circulation

Fully  labelled...all  you’ll  ever  need

A  few  equations

•CO=

•BP=

•CO=HR  x  SV

•BP=CO  x  TPR

What  is  preload?

•Preload  is  the  initial  stretch  of  myocytes before  they  contract•It  is  often  described  by  a  surrogate:  the  volume  of  blood  in  the  left  ventricle  at  the  end  of  diastole  (LVEDV)

What  is  afterload?

•Afterload  is  the  Left  ventricular  wall  stress  [the  wall  tension  (pressure  x  radius)  divided  by  wall  thickness]

• It  is  often  thought  about  as  the  pressure  the  LV  must  overcome  to  eject  blood

• It  is  closely  related  to  Aortic  pressure

What  is  inotropy?•Inotropy  is  a  preload  independent  increase  in  the  rate  of  force  and  pressure  generated  by  the  LV

•It  leads  to  higher  velocity  of  ejection

•It  increases  stroke  volume  by  decreasing  End  systolic  volume

Ahh….  Messers  Frank  and  Starling

RVEDP/V//LVEDP/V//preload

Stroke  Volume

Increased    inotropy,  decreased  afterload

Increased  afterload,  decreased  inotropy

Increasing  SV

•Increasing  preload and  inotropy and  decreasing  afterload increase  stroke  volume•Raising  afterload decreases  stroke  volume•Only  preload  is  free

•CO=HR  x  SV

•BP=CO  x  TPR

Heart Failureblood  goes  round  and  round,  

and  sometimes  it  doesn’t

Right  heart  failure:  Causes

Left  Heart  Failure

Pulmonary  Disease

Right  Heart  Machinery  failure:  Valves,  Muscle,  Circulation

Right  heart  failure:  Effects

Raised  JVP

Congested  liver,  pulsatile  liver,  ascites,  portal  hypertension

Peripheral  oedema

Left  Heart  Failure:  Causes

Left  Heart  machinery  dysfunction:  Muscle,  valves,  circulation

AFTERLOAD  problems

PRELOAD  problems

Left  Heart  Failure:  Effects

Acute  Pulmonary  Oedema

End  Organ  Dysfunction:  ‘shock’

Right  heart  failure

Left  Heart  Failure:  3  types

•Hypertensive:  SBP>140•Normotensive:  SBP  90-­‐140

•Hypotensive:  SBP<90

CARDIAC  FAILURE  vs  VASCULAR  

FAILURE  

CARDIAC  FAILURE  PATHOPHYSIOLOGY

• Patients  with  CHF  represent  the  old  school  textbook

• A  patient  with  chronic  heart  failure  who  develops  intravascular  volume  overload  through  a  variety  of  mechanisms  (eg,  medication  noncompliance,  dietary  noncompliance,  acute  kidney  injury).

• Their  weak  LV/RV  cannot  tolerate  increases  in  intravascular  volume,  so  oedema develops  in  the  lungs  and  periphery

• In  general,  symptoms  develop  gradually  in  the  patient  with  this  type  of  ADHF.  

Normotensive  Left  Heart  Failure  “CLASSIC”  CHF

•Fluid  overload.  Some  LV  dysfunction

•Often  iatrogenic,  non  compliant,  another  cause  eg  RF  

•Rx  with  diuretics,  preload  reduction  (venodilators  eg  nitrates),  NIV

•The  inpatient  granny  on  ortho

VASCULAR  FAILURE  PATHOPHYSIOLOGY

• Patients  with  vascular  failure  have  an  sudden  increase  in  vasoconstriction  and  afterload.

• This  sharp  increase  in  afterload  occurs  via  neurohumoralpathways  involving  the  sympathetic  and  renin–angiotensin–aldosterone  axes.

• Patients  with  vascular  failure  typically  present  acutely  often  lack  the  classic  signs  of  peripheral  edema,  and  generally  have  preserved  cardiac  function.  

• These  patients  are  frequently  hypertensive  upon  ED  presentation  and  can  be  either  euvolemic or  hypovolemic.  

Hypertensive  Left  Heart  Failure

• LVEF  relatively  preserved• Redistributive• Too  much  afterload

• Rx  with  veno/arteriodilators  eg  GTN,  SNP,  Hydrallazine;  NIV

• Generally  don’t  need  much  diuretic  (Frusecide)  unless  obviously  overloaded

• The  elderly  female,  stiff  ventricle,  ‘diastolic  dysfunction’,  most  common

TREATMENT  of  ADHF

Morphine

• Available  evidence  is  weak  but  shows  higher  rates  of  ventilation  and  ICU  and  mortality

• No  trials  have  shown  benefit

• Review:  Sosnowski MA.  Review  article:  lack  of  effect  of  opiates  in  the  treatment  of  acute  cardiogenic  pulmonary  oedema.  Emerg Med  Australas 2008;20:384–90.  

• Weak  dilator:  resp depressant,  sedative  why  use??

Frusemide

• Traditional  mainstay  of  pharmacologic  therapy  for  patients  with  ADHF.  

• Because  the  majority  of  acutely  ill  ED  patients  with  ADHF  are  not  volume  overloaded,  indiscriminate  administration  of  diuretics  could  be  harmful.

• Adequate  renal  perfusion  is  necessary  for  these  medications  to  be  effective.  

• As  a  result,  the  role  of  diuretics  in  the  ED  management  of  patients  with  ADHF  is  limited.

• No  difference  between  bolus  vs  infusion,  high  dose  vs  low  dose

Digoxin

• Has  little  to  no  effect  on  systemic  blood  pressure  and  renal  function,  and  has  many  protective  neurohormonal effects.  

• It  has  not  been  shown  to  reduce  in  heart  failure,  despite  symptom  relief  and  improvement  in  hemodynamics.

ACE-­‐I

• ACE  inhibitors  are  effective  at  reducing  afterload  and  have  been  used  in  the  ED  treatment  of  patients  with  ADHF.  

• Several  small  studies  on  ACE  inhibitors  in  patients  with  ADHF  demonstrated  improvement  in  hemodynamic  markers.

• A single-­‐center  study  demonstrated  reduced  rates  of  intubation  and  intensive  care  unit  admission  for  patients  who  received  sublingual  captopril  in  ED

• Current  ACEP  guidelines  include  ACE  inhibitors  in  the  treatment  options  for  ED  patients  with  ADHF

• Captopril  or  enalapril

Nitrates

• .At  low  doses,  nitroglycerin  reduces  preload  primarily  through  its  dilatory  effects  on  the  venous  system.  

• At  higher  doses,  nitroglycerin  causes  arterial  dilation,  thereby  also  reducing  afterload.

• Initially,  nitroglycerin  can  be  given  SL  route  (400  mcg  every  5  minutes)  

• The  infusion  often  begins  at  20  mcg/min,  

• It  is  critically  important  to  titrate  the  infusion  rapidly  to  clinical  improvement.

• In  general,  the  dose  of  GTNcan be  increased  by  40  mcg/min  every  5  minutes  to  a  maximum  of  200  mcg/min.  

SNP

• Sometimes  needed  for  afterload  reduction  in  severe  HTN

• Nitroprusside is  given  IV  at  a  starting  dose  of  0.100  to  0.125  mcg/kg  per  minute.  The  infusion  can  be  increased  by  0.1  mcg/kg  per  minute  every  5  minutes  until  a  maximum  dose  of  400  mcg/min  is  reached.

• Importantly,  nitroprusside is  metabolized  to  cyanide,  which  can  accumulate  rapidly  in  patients  with  renal  dysfunction.  

• It  is  associated  with  increased  mortality  in  AMI

NIV

• NPPV  reduces  afterload  by  reducing  the  transmuralpressure  across  the  left  ventricle.

• In  addition,  NPPV  increases  intrathoracic pressure,  thereby  reducing  venous  return  and  preload  

• Through  these  mechanisms,  NPPV  reduces  the  work  of  breathing  and  improves  oxygenation.  

• Cochrane  review  :compared  with  standard  medical  therapy  alone,  NIV  resulted  in  significant  reductions  in  the  rates  of  in-­‐hospital  mortality  and  intubation  in  patients  with  ADHF.

• Neither  CPAP  nor  BiPAP has  been  shown  to  be  superior.  

Treating  the  patient  with  APO

• Sit  up• High  flow  O2,  monitor,  arrange  CXR/USS• IV  access,  12  lead  ECG  ASAP• S/L  GTN  300-­‐600mcg  unless  hypotensive• CPAP  start  with  PEEP  5-­‐10,  max  15cm  H2O• Frusemide IV  if  obviously  overloaded  (20-­‐40mg)• No  morphine  • GTN  infusion  start  low  and  increase  rapidly;  titrate  to  response  and  blood  pressure  Rx  for  ACS  if  required

CARDIOGENIC  SHOCK/HYPOTENSIVE  

HF

PATHOPHYSIOLOGY

• The  primary  insult  is  typically  an  infarct  causing  either  reversible  ischemia  or  irreversible  injury  to  the  LV

• Coronary  perfusion  decreases,  followed  by  cardiac  output.  

• The  drop  in  cardiac  output  results  in  hypoperfusion,  triggering  catecholamine  release  to  improve  contractility  and  blood  pressure.  

• This  increases  myocardial  oxygen  demand.

• The  result  is  a  vicious  cycle  of  decreasing  myocardial  blood  supply  with  increasing  myocardial  oxygen  demand,  that  can  manifest  as  rapid  clinical  deterioration.  

REMEMBER

•We  can  cause  shock  by  injudicious  use  of  medications

• Be  particularly  cautious  with  negative  inotropes  in  arrhythmias  with  LV  dysfunction  and  diuretics  and  dilators  with  RHF

TREATMENT  OF  CARDIOGENIC  SHOCK:  revascularise  ASAP

• Revascularization  addresses  the  underlying  pathology  by  restoring  coronary  blood  flow  to  perfuse  myocardial  tissue  that  is  still  viable.  

• Time  is  of  the  essence:  animal  models  have  demonstrated  that  nearly  50%  of  salvageable  myocardium  is  lost  within  the  first  hour  of  coronary  artery  occlusion,  and  two-­‐thirds  within  3  hours.  

Inotropes

• Endogenous  catecholamine  release  itself  is  part  of  the  “vicious  cycle”  of  cardiogenic  shock.

• When  using  inotropes  to  treat  cardiogenic  shock,  need  to  find  a  balance  between  excessive  myocardial  oxygen  demand  and  total  cardiovascular  collapse

DOPAMINE

• Dopamine  acts  via  ß-­‐adrenergic  receptors  to  increase  inotropy and  heart  rate,  and  at  higher  doses  induces  peripheral  vasoconstriction  via  alpha-­‐activation.

• Downsides  are  its  propensity  to  cause  arrhythmia  and  increase  myocardial  work

DOBUTAMINE

• Dobutamine is  a  synthetic  agent  that  was  developed  to  activate  ß-­‐adrenergic  receptors  without  causing  peripheral  vasoconstriction  or  triggering  the  release  of  endogenous  catecholamines.

• Dobutamine can  effectively  increase  cardiac  output  and  reduce  left  ventricular  end-­‐diastolic  pressure,  but  hypotension  may  result  because  of  unopposed  peripheral  ß2  stimulation,  

• Tachycaridaand  proarrhythmic,  and  tolerance  is  observed  with  pro-­‐ longed  infusions

Noradrenaline

• Norad is  an  endogenous  adrenergic  agent  that  acts  at  A-­‐and  B-­‐receptors,  and  causes  an  increase  in  inotropy,  chronotropy,  and  peripheral  vasoconstriction.  

• When  compared  with  dopamine  in  cardiogenic  shock,  norepinephrine  was  found  to  be  as  effective  as  dopamine  in  improving  hemodynamic  parameters,  but  carried  less  risk  of  adverse  arrhythmias  and  improved  28-­‐day  mortality.

• Based  on  the  available  evidence,  norepinephrine  is  the  preferred  first-­‐line  adrenergic  agent  in  cardio-­‐genic  shock.  

• De  Backer  D,  Biston P,  Devriendt J,  et  al.  Comparison  of  dopamine  and  norepinephrine   in  the  treatment  of  shock.  N  Engl J  Med  2010;362:779–89.  

Phosphodiesterase  Inhibitors  

• Milrinone is  a  noncatecholamine inotropic  agent  that  inhibits  the  breakdown  of  cyclic  AMP  and  promotes  an  increase  in  intracellular  calcium  in  cardiac  myocytes.  

• Similar  to  dobutamine,  milrinone improves  contractility  and  cardiac  output  at  the  risk  of  increased  systemic  hypotension.  

• It  has  not  been  shown  to  improve  outcomes  when  routinely  used  in  acute  exacerbations  of  congestive  heart  failure.

Calcium  Sensitizers  • As  the  name  implies,  calcium  sensitizers,  such  as  

levosimendan,  enhance  cardiac  contractility  without  actually  increasing  intracellular  calcium  levels.  

• Levosimendanhas  been  shown  to  improve  cardiac  output,  increase  lactate  clearance,  and  reduce  norepinephrine  requirements  in  decompensated  heart  failure.

• At  least  one  meta-­‐ analysis  has  suggested  it  may  reduce  overall  mortality  in  critically  ill  patients,  although  the  data  are  mixed.

• The  SURVIVE  trial  compared  levosimendanwith  dobutamine in  acute  decompensated  heart  failure,  and  found  no  difference  in  all-­‐cause  mortality  at  6  months.  

Intra-­‐aortic  Balloon  Pump  

• The  IABP  uses  the  principle  of  counterpulsation to  augment  systolic  function  and  promote  myocardial  oxygen  delivery..  

• In  principle,  IABP  seems  like  a  logical  way  to  manage  cardiogenic  shock.

• The  SHOCK-­‐II  trial,  among  others,  failed  to  demonstrate  benefit  when  routinely  used  in  the  setting  of  cardiogenic  shock  and  acute  MI

• However,  the  BCIS-­‐1  trial  showed  a  long-­‐term  mortality  benefit  in  patients  with  severe  cardiomyopathy  under-­‐going  PCI.

LVAD

• Several  different  ventricular-­‐assist  devices  (VADs)  have  been  developed,  

• The  most  common  type  in  current  practice  involves  a  continuous-­‐flow  pump  that  enhances  output  from  the  left  ventricle  (LVAD).  

• The  relatively  small  INTrEPID trial  demonstrated  signif-­‐icantmorbidity  and  mortality  benefits  for  patients  ineligible  for  transplant  who  underwent  LVAD  placement  versus  medical  therapy  alone.

Extracorporeal  Membrane  Oxygenation  

• Extracorporeal  membrane  oxygenation  (ECMO)  combines  a  centrifugal  pump,  a  heat  exchanger,  and  an  oxygenator  to  provide  cardiac  and  respiratory  support.  

• Veno-­‐ venous  and  venoarterial forms  exist;  the  former  provides  only  pulmonary  support,  whereas  the  latter  is  true  cardiopulmonary  bypass.  

• ECMO  has  been  used  in  a  variety  of  settings,  including  cardiogenic  shock,  acute  respiratory  distress  syndrome,  and  the  periarrest period.  

• There  is  evidence  to  suggest  that  ECMO  may  improve  short-­‐ and  long-­‐term  survival  compared  with  conventional  CPR  in  the  setting  of  in-­‐ hospital  cardiac  arrest,  particularly  for  patients  with  primary  heart  disease

Hypotensive  Left  Heart  Failure/Cardiogenic  shock

• ‘Pump  failure’  (poor  LVEF)

• Rx  with  inotropes/volume  challenge

• Rx  with  NIV/IPPV

• eg  LAD  infarct,  myocarditis

SUMMARY• Hypertensive:  SBP>140:  

• Vascular  Failure

• Most  common  mode  of  ED  presentation

• Not  Volume  overloaded;    Thus  Dilate

• Normotensive:  SBP  90-­‐140

• Chronic  LV  dysfunction  with  volume  overload

• Targeted  diuresis/dilatation

• Hypotensive:  SBP<90

• Difficult  clinical  problem

• Revascularization  is  key

• Inotropic  balance  

References

• Michael  C.  Scott,  MDa,b,  Michael  E.  Winters  Congestive  Heart  Failure  Emerg  Med  Clin  N  Am  33  (2015)  553–562  

• Joshua  B.  Moskovitz,  MD,  MPH,  MBA*,  Zachary  D.  Levy,  MD,  Todd  L.  Slesinger,  Cardiogenic  Shock.  Emerg  Med  Clin  N  Am  33  (2015)  645–652  

• Susan  R.  Wilcox,  MD*;  Christopher  Kabrhel,  MD,  MPH;  Richard  N.  Channick,  MD.  Pulmonary  Hypertension  and  Right  Ventricular  Failure  in  Emergency  Medicine.  Annals  of  Emergency  Medicine  Volume  66,  no.  6  :  December  20

• David  M  Viau,  Javier  A  Sala-­‐Mercado,Marty  D  Spranger,  Donal  S  O’Leary,  Phillip  D  Levy  .  The  pathophysiology  of  hypertensive  acute  heart  failure  Heart  2015;101:1861–1867.  

• .  

THANKYOU

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