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Acute Heart Failure

title: Acute Heart Failure tags: #FFICM #cardiac #HF #Pulm_HTN #ACS notebook: 🌑-FFICM type: anki

category: [[Acute Coronary Care]]

[[Acute Heart failure]]

Acute Heart Failure: Spiralling Failure and Pathophysiology

  1. Myocardial Dysfunction
  2. Reduced Stroke Volume
  3. Increased Ventricular Diastolic Pressure and Wall Stress (Less pumped out so more remains when filling)
  4. Reduced Coronary Perfusion Pressure (Coronaries fill in diastole)
  5. Increased Myocardial Dysfunction (less coronary perfusion is more coronary ischaemia) [@devices_critical_care]

The body attempts to combat this with sympathetic nervous stimulation, RAAS, inflammation. [@devices_critical_care]

Inflammation here is rising:

  • Cytokines
    • IL-1, IL-6, TNF Alpha (resulting in impaired microcirculation and also reduced oxygen extraction)
      • With microthrombi
  • Nitric Oxide Synthase (resulting in more nitric oxide, resulting in vasodilatation, hypotension) [@devices_critical_care]

The problem here might be that fixing the macrociculation won't necessarily fix the microcirculation. [@devices_critical_care]

Flashcard type:basic
What inflammatory mediators are being released in heart failure? Nitric Oxide Synthase
IL-1 + IL 6
TNF Alpha
What does Nitric Oxide do to the vasculature? Vasodilation

LVF

In a LVF state. LVF results in increased preload, and also in increased pulmonary pressures (from a backload sense). MAP is unaffected or even high, but HR increases to compensate for the weak ventricle. Because of the reduced stroke volume, CO still is down (stroke volume is obviously down). Because of everything else that goes along with LVF, in the state of overload, your venous compliance is going to be down (because all the vessels are stretched out). Arterial O2 content and global O2 delivery go down as expected from a reduced CO.

Presenting symptoms

  • Chest pain
  • Shortness of Breath
  • Fatigue
  • Peripheral Oedema 2

Categorising Acute Heart Failure

AHF can be split into:

  1. Warm vs Cold - Perfusion Status

  2. Wet vs Dry - Congestion 2

  3. Majority of patients (>95%) present "Wet" with congestion.

  4. Minority (~5%) present "Cold" with perfusion. 2

Treatment depends on presentation.

Flashcard type:cloze
Acute Heart Failure can be subdivided by {{c1::perfusion}} into {{c2::Warm Vs Cold}} and by {{c1::congestion}} into{{c2::Wet Vs Dry}}

Flashcard type:basic
In Acute Heart Failure, when looking at Perfusion and Congestion status, the majority of patients present "Warm and Wet"

Cardio-Renal Syndrome

The other presentation to be aware of in Acute Heart Failure is cardio-renal syndrome. 2

Congestion in kidneys means kidneys are being hurt in two ways: 2

  • the physical congestion
  • the reduced oxygen delivery 2

So you might need to off load through diuresis or RRT 2

Needing RRT is a poor prognostic sign 2

Theres a balance between working out how much renal injury is acceptable, from diuretic induced vascoconstricion, nephrotoxicity, etc. 2

Flashcard type:basic
What is the broad defn of cardio-renal syndrome? Acute Kidney Injury due to Heart Failure
What is the pathology causing AKI in cardio-renal syndrome? Physical Damage from Congestion plus damage from reduced oxygen delivery

Assessment of Acute Heart Failure

[[Shock]]

Presenting Symptoms

  • Hypotension (later than all the symptoms below)
  • Persistent tachycardia
  • Confusion
  • Tachypnoea
  • Impaired Peripheral Perfusion
  • Progressive Metabolic Acidosis 2

NYHA Classifivation:

  1. Class I - No Symptoms/No Limitation in Ordinary Activity
  2. Class II - Mild symptoms (SOB/Angina)/Slight Limitation During Ordinary Activity
  3. Class III - Marked Limitation on less than ordinary activity (20-100m).Comfortable only at rest.
  4. Class IV - Severe Limitations. Symptoms at Rest. Bedbound.

Flashcard type:basic
The classification of heart failure by symptoms caused is New York Heart Associtation (NYHA) Score
The NYHA Scoring system is for Classifying Heart Failure by symptoms caused
The NYHA scoring system goes from I to IV

Flashcard type:cloze
Class {{c1::I NYHA}} is where there {{c2::are no symptoms or limitations to ordinary activity}} from {{c3::heart failure}}
Class {{c1::II NYHA}} is where there {{c2::are mild symptoms or limitations to ordinary activity}} from {{c3::heart failure}}
Class {{c1::III NYHA}} is where there {{c2::is marked limitations to ordinary activity and you are comfortable only at rest}} by {{c3::heart failure}}
Class {{c1::IV NYHA}} is where there {{c2::are severe limitations to ordinary activity and symptoms at rest}} from {{c3::heart failure}}

When assessing a patient with Circulatory Failure, remember:

  1. Acute Heart Failure is not a diagnosis!
  2. Acute Heart Failure may be causing the admission, or caused by something else.
  3. Hypotension is NOT the first sign in circulatory failure - tachycardia, confusion, tachypnoea, being 'shut down', acidosis - will occur earlier
  4. Different categories of shock can occur at the same time
  5. You can use a central line oxygen saturation of blood (internal jugular/subclavian) to work out if global oxygen delivery is enoughfor global tissue oxygen demand. Even though it's not a "true mixed" sample it's still useful. ScvO2 (Central Venous Saturations of Blood) < 70% can be concerning that demand is greater than supply. >70% doesn't = everything being fine though, as if metabolically the tissues can't extract oxygen the number will stay high. If <70% consider an approach to increase global oxygen delivery (through increasing cardiac output). Pay more attention to trend than to number. 2

Mixed Venous Sats

  • 75% + = Increased O2 provision or decreased 02 utilisation (like sepsis causing shunt)
  • 50-75% = can be normal or compensation
  • 30-50% = O2 demand is greater than supply
  • 25-30% = severe lactic acidosis
  • < 25% = cellular death [^@cardiac_output]

Central Venous Sats

  • This requires CVC rather than PA catheter.
  • It's usually 2-7% less than SvO2
  • In non-shock it correlates well with SvO2
  • In shock it can be more than SvO2 [^@cardiac_output]

Flashcard type:basic
What blood sample can estimate the relative supply and extraction of exygen from blood? ScvO2 (Central Venous Saturations)
A Central Venous Saturations (ScvO2) can allow you to estimate what? The relative supply and extraction of oxygen from blood
When can a central venous saturation (ScvO2) be falsely raised? If tissues are fucked and can't extract the oxygen
What does a mixed venous saturation of O2 of 75%+ mean? Increased O2 provision or cells unable to use O2
What does a mixed venous saturation of O2 of 50-75% mean? Either normal, or body compensating
What does a mixed venous saturation of O2 of 30-50% mean? O2 demand def greater than supply
What does a mixed venous saturation of O2 of 25-30% mean? Severe Lactic Acidosis
What does a mixed venous saturation of O2 of less than 25% mean? Cells are dying
How low a mixed venous saturation of O2 means cellular death? Less than 25%
What mixed venous saturation of O2 means that there is some severe lactic acidosis? 25-30%
What mixed venous saturation of O2 means that O2 demand is DEFINITELY greater than supply? 30-50%
What mixed venous saturation of O2 could either be normal, or the body compensating? 50-75%
What mized venous saturation of O2 suggests over supply of O2, or failure of cells to use O2? greater than 75%
What is the numerical difference between a mixed venous saturation of O2 and a central venous saturation of O2? Central Venous should be lower, around 2-7% lower
Which should be higher, mixed venous O2 or central venous O2? By how much? Mixed Venous Higher, about 2-7%
When do mixed venous O2 sats and central venous O2 sats have a sensible correlation? When patient not shocked
What can shock do to relationship between mixed venous and central venous O2 saturations? Mess up the relationship. Central venous should be lower, in shock it can be higher.
What is the symbol used for mixed venous sats? SvO2
What is the symbol used for central venous sats? ScvO2
What does ScvO2 mean? Central Venous Saturations
What does SvO2 mean? Mixed Venous Saturations
Where do you sample blood to get a central venous saturations? From a central line!
Where do you sample blood to get a mixed venous saturations? From a PA Catheter
If you take a blood sample from a PA catheter to look at O2 saturations, what type of sample is that? A mixed venous saturations
If you take a blood sample from a central line to look at O2 saturations, what type of sample is that? A central venous saturation

Outcomes of Acute Heart Failure

Outcomes of AHF are poor.

Most will survive first admission, but 25% 1 year mortality for acute decompensated heart failure, and 50% 1 year mortality for those presenting with cardiogenic shock. 2

Flashcard type:basic
What is the 1 year mortality for someone presenting with acute decompensated heart failure? 25%
What is the 1 year mortality for someone presenting with cardiogenic shock from decompensated heart failure? 50%

Aetiology

Causes of Acute Heart Failure:

  • Coronary Artery Disease
  • HTN
  • Cardiomyopathy
  • Valvular Disease 2

Causes of Acute Heart Failure in Critical Care

The most common cause is cardiac, but there are non cardiac causes too. 2

Also important to work out if this is the primary problem, or secondary to another issue, or even not an issue at all (instead being a pulmonary or systemic sepsis) 2

Start Point can be: CHAMP

  1. C - acute Coronary syndrome - treat w/ recascularisation
  2. H - Hypertensive emergency - treat w/ BP reduction w/ vasodilators and diuretics
  3. A - Arrhythmias - treat w/ pharmacological/electrical/pacing
  4. M - Mechanical causes - due to ischaemia + necrosis/ruptures - treat w/ surgery/percutaneous
  5. P - Pulmonary embolism - treat w/ systemic/localised thrombolysis 2

Should you thrombolyse a sub-massive PE when there's some echo or CT evidence of heart strain? Or raised biomarkers? - Challenging, no convincing evidence for systemic thrombolysis. 2

  • Infection
  • Drugs - BBlockers, Calcium Antagonists, Cytotoxic, Alcohol, Cocacine
  • Hypoxaemia
  • Metabolic - Acidaemia, Thiamine Deficiency, Thyrotoxicosis, Hypocalcaemia, Hypophosphataemia
  • Myocardial Contusion (Trauma)
  • Myocardial Infiltration (Tumour, Sarcoid, Amyloid)
  • Vasculitis
  • Neuromuscular (Duchenn, Friedrich, Myotonic Dystrophy) 2

Metabolic things that make contractility worse:

  • Hypoxia (pO2 < 8)
  • Acidaemia (pH < 7.35)
  • Hyperkalaemia (> 5.5)
  • Hypomagnasaemia (< 0.9)
  • Hypocalcaemia (< 1)
  • Hypophosphataemia (< 0.8)
  • Anaemia (< 8)
  • Thiamine Deficiency (B1) 2

Flashcard type:basic
What acronym can be used to give the most common causes of acute heart failure / cardiogenic shock? CHAMP
What is the disease process is the CHAMP acronym for remembering? Most common causes of acute heart failure / cardiogenic shock
What does the C in CHAMP (Causes of Acute Heart Failure Acronym) stand for? Coronary Syndrome
What does the H in CHAMP (Causes of Acute Heart Failure Acronym) stand for? Hypertensive Emergency
What does the A in CHAMP (Causes of Acute Heart Failure Acronym) stand for? Arrhythmias
What does the M in CHAMP (Causes of Acute Heart Failure Acronym) stand for? Mechanical Causes
What does the P in CHAMP (Causes of Acute Heart Failure Acronym) stand for? Pulmonary Embolism
What do each of the letters in CHAMP (Causes of Acute Heart Failure / cardiogenic shock Acronym) stand for? Coronary Syndrome
Hypertensive Emergency
Arrhythmias
Mechanical
Pulmonary Embolism
Whilst CHAMP gives some of the most common causes of Acute Heart Failure + Cardiogenic Shock, what important causes does it miss? Infection
Drugs
Metabolic
Infiltrative
Inflammatory
Which B Vitamin deficiency makes heart contractility worse? Thiamine
Under or over active thyroid makes heart contractility worse? Over (Thyrotoxicosis)
Low or high pH makes heart contractility worse? Low (Acidosis)
Low or high potassium makes heart contractility worse? High (5.5 plus)
Low or high calcium makes heart contractility worse? Low (less than 1) (Hypocalcaemia)
Low or high phosphate makes heart contractility worse? Low (Hypophosphataemia) (less than 0.8)
Low or high magnesium makes heart contractility worse? Low (less than 0.9)
Main drug categories that makes heart contractility worse? B Blockers
CCB
Chemotherapy
Alcohol
Cocaine

Causes of Cardiogenic Shock

Flashcard type:basic
How much of cardiogenic shock is caused by ACS? Two thirds
What is the most single most common cause of cardiogenic shock? ACS (2/3)

Treatments of Acute Heart Failure

The aim of treating Heart Failure is to find the balance. Get the heart working hard enough to supply oxygen to other organs, but not so hard that it is damaged further. 2

You can increase efficiency of heart by optimising fluid balance, and vascular resistance, as well as looking specifically at heart. 2

Pillars of treatment are: Diuretics, Vasodilators, Inotropes 2

Flashcard type:basic
What is the most important drug category when it comes to treating acute heart failure? Diuretics

Inotropes

[[Inotropes and Vasopressors]]

Whilst putting an extra strain on heart, can often be required 2

Diagnosis of Acute Heart Failure

Echo

  • A focused echo should be able to give decent information, if even just from one view.
  • You can also use microbubble contrast techniques to improve image quality.
  • If TTE not possible consider TOE. TOE gives good views when you cant get on TTE, but doesn't visualise right heart or apex of LV as well. 2

Echo will give you evidence of: 2

  1. LV Systolic Dysfunction
  2. Heart Failure with Reduced Ejection Fraction (HFrEF - An ejection fraction of less than 40%)
  3. Although increasing afterload with vasopresssors can make the ejection fraction look worse than it would otherwise
  4. Diastolic Dysfunction
    • Heart Failure with Preserved Ejection Fraction (HFpEF) - An ejection fraction greater than 50% in context of left atrial enlargement/increased LV wall thickness
    • Although ok EF doesn't mean ok cardiac output!
    • Up to half of patients with AHF may have HFpEF or mid-range EF (40-49%) (HFmrEF)
    • They have just as bad outcomes as HFrEF patients
  5. Pericardial Effusions/Tamponade
  6. Just because an effusion is small doesn't mean no tamponade, it's all about the speed of accumulation
  7. Space Occupying Lesions Obstructing Heart - Pleural Effusions/Gas Trapping/Pneumothoraces
  8. Volume of Preload/Fluid Responsiveness - Do a fluid challenge
  9. Valvular Heart Disease (Particularly: Aortic Stenosis, Mitral Regurg)
  10. Septal Defects
  11. Intracardiac Thrombus
  12. Pulmonary Hypertension - Measuring PASPs
  13. RV Size and Function (Particularly for PEs) 2

Flashcard type:basic
What percentage counts as a reduced ejection fraction on echo? Less than 40%
What percentage counts as a mid-range ejection fraction on echo? 40 to 50%
What percentage counts as a preserved ejection fraction on echo? Greater than 50%
Why can vasopressors make the heart look worse on echo? Increasing afterload will increase the pressure the heart has to pump against

Biomarkers

Flashcard type:basic
What are the two main biomarkers to look at when it comes to heart failure/cardiogenic shock? BNP
Troponin
What counts as a "normal" BNP? Less than 100pg/ml
What are the three types of cardiac troponin? TnI
TnT
TnC
What is troponin inside heart cells? Part of the contractile apparatus, with actin and tropomysin.
What three proteins are part of the contractile apparatues in heart cells? Actin
Troponin
Tropomyosin

Natriuretic Peptides - BNP

In myocardial wall stress, ventricular myocytes release proBNP, which is split into BNP (B-type natriuretic peptide) and N-terminal fragment (NT-proBNP) 2

BNP is active, NT-proBNP isn't. (NT-proBNP is the c-peptide to BNP's insulin) 2

BNP is useful to exclude heart failure, with a cut-off of 100pg/ml (Sensitivity 90% Specificity 70%) 2

But like every other marker it goes up in a range of things, including age, renal failure, sepsis, etc. 2

Troponins

Troponin are usually inside the myocyte as part of the contractile apparatus (with actin and the tropomysin). They're only released with myocyte necrosis. 2

  • TnI - Binds to actin, preventing actin interacting with myosin
  • TnT - Binds to tropomyosin
  • TnC - Mops up calcium. Allowing troponin-tropomyosin interacting with myosin. 2

Again though, that necrosis doesn't necessarily mean MI. It does generally mean badness though, raised levels associated with increased risk of mortality. 2

Troponin in Ischaemia
  • 50% of peak released in first 4 hours
  • Peaked by 12 hours
  • Back to normal 10 days later 2

Flashcard type:basic
When does troponin levels peak in blood in cardiac ischaemia? 12 hours
When should half of the troponin be released in cardiac ischaemia? 4 hours
When should troponin levels be back to normal in blood after cardiac ischaemia? 10 days

Cardiogenic Shock

Cardiogenic shock is the clinical state following circulatory failure due to left, right, or biventricular dysfunction. The clinical state is of end-organ hypoperfusion, resulting into multiorgan dysfunction. [@devices_critical_care] 2

Cardiogenic shock is diagnosed by presence of:

  • Persistent Hypotension (Systolic < 90, or MAP > 30 below baseline, or requirement of vasopressors to keep systolic > 90)
  • Signs of impaired organ perfusion despite normo/hypervolaemia [@devices_critical_care]

Flashcard type:basic
What is the definition of cardiogenic shock? "Circulatory failure due to heart dysfunction, resulting in end-organ hypoperfusion"
Give four ways you can recognise the presence of cardiogenic shock Systolic less than 90
MAP more than 30 below baseline
Requirement of vasopressors to keep systolic more than 90
Signs of impaired organ perfusion despite adequate volume status (like a raised lactate)

Prognosis

1% of UK population have heart failure but 5% of hospital admissions. [@devices_RCA]

If critical care interventions are delayed until there already is other organ failure, underlying pathology is often irreversible. 2

Management (3 Steps)

Step 1 - Assessment/Salvage Phase

Rapid investigtion with:

  • Hx
  • Examination
  • Bloods
  • ECG
  • echo [@devices_critical_care]

Monitoring with:

  • Art line allows for:
    • Target MAP (65+)
    • ABG + Lactate
    • Pulse Pressure Variation (for fluid responsiveness)
    • Waveform analysis for cardiac output (Inconsistent pervormence) [@devices_critical_care]
  • CVC allows for:
    • Access for fluids inotropes and pressors
    • Central Venous Pressure
    • Central Venous Oxygen Saturation
    • Central Venous CO2 Pressure [@devices_critical_care]
  • echo allows for:
    • Repeated evaluation of left and right ventricular function
    • assessing valve function
    • investigating other mechanical complications
    • estimating cardiac output [@devices_critical_care]
[[Inotropes and Vasopressors]]

Vasopressors:

Noradrenaline recommended for cardiac shock. Dopamine might cause increased ischaemic events. [@devices_critical_care]

Add in vasopressin when norepinephrine is > 0.2micro/kg/min. This will reduce rates of AF and RRT [@devices_critical_care]

Don't use adrenaline, it increases lactate, increases oxygen usage, increases rates of arrythmias, and has association with higher mortality. Also, noradrenaline is better at hitting haemodynamic goals in cardiogenic shock. [@devices_critical_care]

Inotropes:

Can be added to improve stroke volume after vasopressor has stabilised BP a bit. [@devices_critical_care]

Dobutamine recommended at (2.5micro/kg/min) [@devices_critical_care]

Don't use levosimendan and milrinone as they will cause more vasodilation. [@devices_critical_care]

Fluids/Bloods:

Target Hb >8 to optimise O2 delivery in cardiogenic shock. [@devices_critical_care]

Flashcard type:basic
What should be the trigger for starting vasopressin in cardiogenic shock? When noradrenaline is greater than 0.2 micro/kg/min
What should be the starting dose for dobutamine in cardiogenic shock? 2.5 micro/kg/min

Step 2 - Optimisation/Stabilisation

In this stage you may need advanced haemodynamic monitoring:

  • Pulmonary Artery Catheters [@devices_critical_care]
  • Transpulmonary Thermodilution Systems [@devices_critical_care]

Advanced Haemodynamic Monitoring

The key variables for vent function are:

  • RAP
  • MAP
  • HR
  • LAP
  • PAP
  • CO

The first three are able to be clinically assessed, the last three need some kind of cardiac output monitor like a PA catheter.

What are the key questions?

  1. Is more volume needed?
  2. Is CO too low for global oxygen delivery?
  3. Is dilator, constrictor, or inotropic needed?

[[pa_catheter]]

Transpulmonary Thermodilution Systems

Can measure intermittently, or continuous. [@devices_critical_care]

Recommended for severe shock and ARDS. [@devices_critical_care]

They measure:

  • Pulse Pressure Variation (for volume responsiveness)
  • Global End Diastolic Volume (For Preload)
  • Cardiac Function Index (For Systolic Function)
  • Global Ejection Fraction (For Systolic Function)
  • Extravascular Lung Water (for pulmonar oedema) [@devices_critical_care]

Flashcard type:basic
In cardiac output monitoring, why might you want to measure someone's global end diastolic volume? To estimate preload
In cardiac output monitoring, why might you want to measure someone's cardiac function index? To estimate systolic function
In cardiac output monitoring, why might you want to measure someone's global ejection fraction? To estimate systolic function
In cardiac output monitoring, why might you want to measure someone's extravascular lung water? To estimate pulmonary oedema
In cardiac output monitoring, why might you want to measure someone's pulse pressure variation? To estimate volume responsiveness

[[Acute cardiac syndrome]]

Heart Failure Drugs

Diurese, diurese, diurese!

Reduce Afterload
  • Nitrates / Alpha Blockers / PDE-3 inhibitors / ACEi
  • These will all work as arteriolar dilators
Increase Contractility
  • Remove negative inotrope-y* : Acidaemia/Hyperkalaemia/Drugs 2
  • Add positive inotrope-y
Increase Heart Rate
  • Increase the heart rate in HF will improve cardiac output
  • Up until the point of 100, less time for filling at that point
  • If you get to more than 110, you should slow it down
  • Oh's says to do that with conversion etc,
  • It doesn't talk much about diuresis
  • However Acute Heart Failure team at GJNH emphasise diurese and diureses
  • Amiodarone is good for this but remember is also negative inotrope

Flashcard type:basic
What's a good heart rate when treating someone with acute heart failure? Around 100
What's a bit too slow heart rate when treating someone with acute heart failure? Less than 100, as up to 100 you can improve cardiac output
What's a bit too fast heart rate when treating someone with acute heart failure? Greater than 110, as there's not enough time for heart filling

Sources

[@devices_critical_care]: Mechanical Circulatory Support Devices for Cardiogenic Shock: State of the Art. Ludhmila Abrahao Hajjar and Jean-Louis Teboul

[@devices_RCA]: Ventricular assist devices. Paul Harris. Lakshminarasimhan Kuppurao

[Acute Coronary Care]: "Acute Coronary Care" [Acute Heart failure]: "Acute Heart Failure"

[Inotropes and Vasopressors]: "Inotropes and Vasopressors" [Inotropes and Vasopressors]: "Inotropes and Vasopressors"

[Acute cardiac syndrome]: "Acute cardiac syndrome"

  1. Wikipedia! ↩

  2. Oh's Intensive Care Medicine - Chapter 24 - Acute Heart Failure and Pulmonary Hypertension ↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩↩