Cardiogenic Shock - ECG lesson 2 Flashcards
Cardiogenic Shock
A clinical condition of inadequate tissue (end organ) perfusion due to the inability of the heart to pump an adequate amount of blood.
Reduced cardiac output results in clinical and biochemical signs of end organ HYPOperfusion.
Causes of Cardiogenic Shock?
- Acute Coronoey Syndrome (ACS)
- Arrhythmias
- Acute decompensated Heart failure.
- Various mechanical causes including acute mitral incompetence (Valve issues) , ventricular septal defect and Cardiac wall rupture
Compensatory Methods: for Cardiogenic Shock?
- via the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) <— increased water retention, enables increased volume of blood and therefore increased perfusion.
Baroreceptors and Chemoreceptors:
- chemoreceptors -> noradrenaline and adrenaline —> raises blood pressure —> Vasoconstriction allows more blood to perfume through body
Baroreceptors -> SA NODE -> increased heart rate = more perfusion
Clinical signs and symptoms of Cardiogenic shock?
- tachycardia
- Hypotension
- Delayed CRT
- Tachypnoea
- reduced SP02
- Reduced GCS
- Oliguria (reduced urine output) <— reduced blood flow to kidneys prevents kidneys working properly.
- Pallor/ clammy
Sensitive organs?
Brain & Kidneys
Management of Cardiogenic shock?
- Aim to restore end-organ perfusion
• Re vascularisation —> PPCI —> platelet agglutination Inhibitor
• After-load —> MAP lower than 75 —> Norepinephrine (vasopressin) = raises BP , Vasodilators —> Nitro = lowers BP
FINISH THIS CARD
How to reliably measure end organ perfusion ?
- Blood pressure:
below 90 Systolic or, below 65-75 Mean Arterial Pressure (MAP) - GCS:
of less than 15 (without alternative explanation; such as dementia) <— evidence of reduced perfusion.
Aim to restore normal GCS and blood pressure.
Medical History
Family history:
- FHx of Cardiac Disease
- FHx of sudden Cardiac death
Does PT have any of the following:
- Hyperlipidemia
- Hypertension
- Ischaemic Heart Disease
- known Arrhythmia
- pacemaker
Effects of Atropine
Atropine blocks Parasympathetic (slows things down ) influences in the heart , improving AV conduction and increasing heart rate.
Atropine blocks parasympathetic system and enables heart rate to increase.
Atropine dosages: 500mcg/600mcg <— can give a maximum of 6 500mcg dosages and a maximum of 5 600mcg doses
Indications for atropine?
- absolute Bradycardia <40bpm
-Systolic blood pressure below normal parameters for age
- Paroxysmal ventricular arrhythmias requiring suppression
- inadequate perfusion causing confusion.
- Bradycardia following return of spontaneous circulation
Contraindications:
- Should NOT be used to treat Bradycardia if PT has suspected HYPOthermia <— normal response for heart to slow down if PT is HYPOthermic
- Do NOT give to PT’s who have had a Cardiac transplant <— high degree AV block or Sinus Arrest may occur
Transcutaneous Pacing
Used for Bradyarrythmias
- non invasive pacing which means:
• can be established easily
• easy to perform and requires minimal training
Currently not a skill for Paramedics in UK , except for SPCC <— as they have advanced ECG training.
Reason for paramedics not being able to do this treatment , is lack of ECG reading skills.
Transcutaneous pacing, is 2 pads on patients chest that transmits pulses between each other , this stimulates heart to contract at a designated rate.
Tachyarrhythmias
Do guidelines
Cardioversion
Similar to defibrillation with some important distinctions:
- shock is administered to PT with a pulse
- less energy required in Cardioversion (below 150J)
- shock is delivered during a different part of the cardiac cycle (usually synchronised rather than unsynchronised) , meaning shock is delivered during the QRS wave. In defibrillation , shock occurs whenever button is pressed.
Cardioversion SYNCHRONISES the shock to occur when the QRS complex does.
Valsalva Manoeuvre
- forced expiration against a closed Glottis, mimics many normal activities such as straining for a poo, blowing up a balloon or playing saxophone.
- This activates the vagus nerve, which activates the Parasympathetic nervous system and slows the heart rate.
- Increasing Intrathoracic pressure, stimulates the vagus nerve and causes increased parasympathetic drive, which may slow the heart rate.
Technique used to revert SVT: usually blowing into a 10/20ml syringe (loosened) for 15 seconds. This is ideally done in a supine position , but may be down semi- recumbent if lying flat isn’t possible
Modified Valsava Manoeuvre
- involves tipping patient back after blowing into syringe for at least 15 seconds, lift legs to 45 degree angle for minimum of 15 seconds.
Re-assess rhythm and repeat as necessary, up to 3 times.
Fluid therapy - stepwise approach
1) does PT have adverse signs
2) if adverse signs present , treat underlying cause, e.g; if Bradycardic, administer Atropine
3) if despite treating the underlying cause, the PT is still presenting with “adverse signs” , consider distance to nearest ED/PPCI and discussion with receiving unit R.E fluid therapy.
4) Administer Bolus of IV Sodium Chloride as per the JRCALC clinical guidelines.
5) only consider further Bolus if patient remains unstable, considering distance to hospital.
