Cardiovascular Flashcards
(119 cards)
What is sudden cardiac arrest
A sudden state of circulatory failure due to a loss of cardiac systolic function.
What are the 4 cardiac rhythm disturbances which cause cardiac arrest
Ventricular fibrillatio
Pulseless ventricular tachycardia
Pulseless electrical activity
Asystole
What is tornadoes de pointes
A sub-group of polymorphic VT in patients with an underlying prolonges QT interval, sometimes related to hypomagnesaemia
How does cardiac arrest present
Patient unresponsive
Absence of normal breathing
Absence of circulation (no pulse)
Cardiac rhythm disturbance
What are the risk factors for cardiac arrest
Strong:
-Coronary artery disease
-Left ventricular dysfunction
-Hypertrophic cardiomyopathy
-Arrhythmogenic right ventricular dysplasia
-Long QT syndrome
-Medications which prolong the QT interval or cause electrolyte disturbances
-Acute medical or surgical emergency
-Illicit substances
Weak:
-Brugada syndrome
-Valvular heart disease
-Smoking
-History of eating disorders
What are the investigations for suspected cardiac arrest
1st line:
-Continuous cardiac monitoring
-FBC
-Serum electrolytes (electrolyte imbalances, esp hyperkalaemia or hypokalaemia)
-ABG
-Cardiac biomarkers
-Point of care ultrasound
Consider also:
-ECG
-Coronary angiography
-Echocardiogram
-Chest x-ray
-Toxicology screen
-Cardiac MRI
-Signal-averaged electrocardiogram (SAECG)
-Electrophysiological study
How is a cardiac arrest managed
Basic life support:
Give naloxone in suspected opioid overdose
Give adrenaline to increase rate of achieving spontaneous circulation and to increase short term survival
In patients with sudden cardiac arrest due to torsades de pointes, giving magnesium may restore a perfusing cardiac rhythm
Assessment for and treatment of any suspected reversible causes of cardiac arrest
ACLS:
Shockable rhythms:
-Pulseless VT and VF
-BLS in community
-Give adrenaline
-If no spontaneous circulation resolves and a shockable rhythm identified, one shock should be delivered followed by 5 cycles (2 mins) of CPR
-IV or IO access obtained without interupting CPR
-Reassess pulse and rhythm, is no change then shock again along with amiodarone or lidocaine and continue CPR for 5 cycles
-Reasses, if no change restart at stage of adrenalin administration
-Continue until spontaneous circulation achieved or resus measures are terminated
Non-shockable rhythms:
-Pulseless electrical activity or asystole
-BLS
-If spontaneous circulation is not restores, and a non-shockable rhythm is identified, 5 cycle of CPR are provided
-IV or IO access is obtained without interrupting CPR
-Give adrenaline asap and every 3-5 mins after
-Check response after every 5 cycles (2 mins) of CPR
-Continue this cycle of giving CPR and adrenaline until spontaneous ciculation is attaned or resus is terminated
What post-resuscitation care can be provided in cardiac arrest
If spontaneous circulation is achieved, immediately commence post-resuscitation care:
-monitoring
-organ support
-correction of electrolyte imbalances and acidosis
-safe transfer to a critical care environment
-thorough search for potnetial aetiology
-modify/treat risk factors for sudden cardiac arrest
12 lead ECG to determine signs of STEMI and if present then emergent coronary angiography with or without PCI should be performed. In some cases can also be done in those with ACS but no sign of STEMI.
Anoxic brain injury is a frequent complication of sudden cardiac arrest and targeted temperature management protocals can be used to improve survival and neurological outcome.
What is targeted temperature management
Used in post-resuscitation from cardiac arrest.
AIm for between 32 and 36 degrees C
Three phases of Induction, Maintenance, Rewarming
Induction and/or maintenance achieved by:
-Icepacks with or without wet towels
-Cooling blankets or pads
-Water or air-circulating blankets
-Transnasal evaporative cooling
-Intravascular heat exchanger
-Extracorporeal circulation
Rewarming should be achieved slowly (0.25°C to 0.50°C of warming per hour) to avoid rebound hyperthermia, which is associated with worse neurological outcomes
When can resuscitation of a cardiac arrest be terminated
Pre-hospital guidance. Must meet all:
For BLS EMS
-EMS did not witness the arrest
-The patient had no ROSC before transport
-No shock was administered before transport
For ALS EMS:
-Arrest not witnessed
-No bystander CPR was provided
-The patient had no ROSC before transport
-No shock was administered before transport
Resuscitative measures should be terminated if there is documentation of a valid “do not resuscitate” order
Terminating resuscitative measures may also be considered on the basis of the following:
-Delayed initiation of CPR in unwitnessed cardiac arrest
-Unsuccessful resuscitation after 20 mins of ACLS guideline-directed therapy
-conditions that compromise the safety of the emergency care providers
What are the potential complications of cardiac arrest
Death
Rib and sternal fractures
Anoxic brain injury
Ischaemic liver injury (shock liver)
Renal acute tubular necrosis (ATN)
Recurrent cardiac arrest
What is the prognosis following cardiac arrest
Generally poor
Early provision of CPR, including compressiononly CPR, by bystanders during out-of-hospital arrest increases the rate of survival from sudden cardiac arrest
Even those who do survive to hospital admission do not always survive to hospital discharge and those who do survive to hospital discharge often have neurological, pulmonary, cardiac, hepatic, renal or MSK complications
What is myocardial infarction
Myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand
What is STEMI
ST-elevation myocardial infarction
Caused predominantly by complete atherothrombotic occlusion of a coronary artery
Diagnosed clinically when there is new (or increased) and persistent ST-segment elevation in at least 2 contiguous leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off points are:
- ≥2.5 mm in men <40 years old
- ≥2 mm in men >40 years old
- ≥1.5 mm in women regardless of age
(1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).)
Contiguous ECG leads lie next to each other anatomically and indicate a specific myocardial territory
How does an MI present
Common:
Chest pain
Dyspnoea
Pallor
Diaphoresis
Cardiac risk factors
Nausea and/or vomiting
Dizziness or light-headedness
Distress and anxiety
Palpitations
Uncommon:
Abnormal breath sounds
Additional heart sounds
Cardiogenic shock
Reduced consciousness
Hypotension
Atypical location or nature of pain
What is the chest pain described in MI
Central
Retrosternal, crushing, heavy, severe, and diffuse in nature
May be described by the patient as “pressing or squeezing”
May occur at rest or on activity
May be constant or intermittent, or wax and wane in intensity
Sometimes radiating to the left arm, neck or jaw
May be associated with nausea, vomiting, dyspnoea, diaphoresis, lightheadedness, palpitations or syncope
What investigations should be performed in suspected STEMI
ECG
Coronary angiography
Cardiac troponin
Glucose
FBC
U and Es
CRP
Serum lipids
Consider also:
ABG
Chest X-ray
Point of care transthoracic echocardiogram
Emerging tests:
Cardiac myosin-binding protein C (cMyC)
What are the differentials in suspected STEMI
Unstable angina
N-ST-EMI
Aortic dissection
Pulmonary embolism (PE)
Pneumothorax
Pneumonia
Pericarditis
Myocarditis
GORD
Oesophageal spasm
Costochondritis
Anxiety or panic attack
What is the criteria for acute, evolving ot recent MI
Either one of the following criteria:
-Typically rise of biomarkers of myocardail necrosis (troponin or creatine kinase-MB) with at least one of the following:
– Ischaemic symptoms
– Development of pathological Q waves on ECG
– ECG changes indicative of ischameia (ST-segment elevation or depression)
– Coronary artery intervention
-Pathological findings of acute MI
What is the criteria for established MI
Any one of the following:
-Development of pathological Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardail necrosis may have normalised, depending on the length of time that has passes since the infarct developed
-Pathological findings of healed or healing MI
-Cardiac MRI with delayed enhancement imaging showing a classic sub-endocardial or transmural infarct in a coronary artery distribution
How is STEMI managed
Give all patients with suspected acute coronary syndrome a single loading dose of aspirin as soon as possible, unless they have aspirin hypersensitivity
Make a clinical diagnosis of STEMI and start treatment if the patient has sighns and symptoms of myocardial ischaemia plus persistent/increasing ST elevation in two or more contiguous leads on ECG (do not wait for cardiac troponin to confirm)
Perform all the following in tandem as soon as a clinical diagnosis of STEMI has been made:
-Immediately assess eligibility for coronary reperfusion therapy
-For most patients the best option will be primary percutaneous coronary intervention (PCI); fibrinalysis is reserved for those without timely access to primary PCI
– if eligible, take steps to ensure reperfusion is administered asap
– If not, offer conservative medical management
-Gain IV access and start continuous haemodynamic monitoring and pulse oximetry
– Avoid cannula insertion obstructing access to the right radial artery (common entry site for primary PCI)
-Give pain relief
– IV opioid plus concomitant IV anti-emetic
-Give O2 only if sats <90%
-Give dual anthplatelt therapy by adding a P2Y12 inhibitor to aspirin
– If having PCI, use prasugrel if not already taking an oral anticoagulant, or clopidogrel if they are already taking oral anticoagulation
-Consider an IV nitrate if the patient has:
– persistent chest pain despite sublingual GTN
– Sustained hypertension
– Clinical and/or radiograpgic evidence of congestive heart failure
-Seek immediate specialist input from the interventional cardiology team
– if you are managing the patient at a non-PCI, contact the interventional cardiology team at your designated PCI-capable hospital to discuss immediate transfer
If the STEMI patient has cardiogenic shock, seek urgent senior support - coronary angiography ± PCI is indicated
When should IV nitrate not be given in STEMI
Hypotension secondary to any of:
-right ventricular infarction (usually complicating an inferior or extensive anterior STEMI)
-severe aortic stenosis or left ventricular outflow tract obstruction
-pre-existing cardiomyopathy
Persistent hypotension secondary to another cause
Use of phosphodiesterase-5 inhibitor (eg avanafil, sildenafil, tadalafil, vardenafil) for erectile dysfunction within the last 48 hours
When should and shouldn’t antivoagulant therapy be given in STEMI management
Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI
Anticoagulation will be started by the interventional cardiology team in the catheterisation lab
If the patient is having fibrinolysis, start anticoagulation at the same time. Use enoxaparin or unfractionated heparin (unless streptokinase is used for thrombolysis, in which case choose fondaparinux). Continue anticoagulation until revascularisation (if fibrinolysis is followed by PCI) or for the duration of hospital stay up to a maximum of 8 days
How should patients who have had a return of spontaneous circulation after an out of hispital cardiac arrest be managed
Primary PCI is the treatment of choice if there is STEMI on post-ROSC ECG or life-threatening arrhythmia
If no ST-segment elevation then:
- Exclude non-coronary causes of cardiac arrest
-Perform urgent Echo
-Strongly consider a referral to cardiology for urgent angiography if there is a high index of suspicion of ongoing MI despite no St-segment elevation
When deciding whether to take a survivor of cardiac arrest (with or without ST-segment elevation) to the cath lab for urgent angiography ± PCI:
- Consider each case on its individual merits and seek senior advice
- Take account of factors associated with the cardiac arrest that will influence the chance of a good neurological outcome