Cardiovascular Flashcards
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
What is the pathophysiology of ACS
Acute coronary syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
When a thrombus forms in a fast flowing artery its is made up mostly of platelets
This is why anti-platelt medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment
What are the 3 types of ACS
Unstable angina
ST elevation myocardail infarction (STEMI)
Non-ST elevation myocardial infarction (NSTEMI)
How is suspected ACS investigated
ECG
-ST elevation or new LBBB - diagnoses of STEMI
-No ST elevation then perform troponin blood test
– If raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
– If troponin levels are normal and the ECG does not show pathological changes, the diagnosis is either unstable angina or another cause such as MSK chest pain
Perform all investigation normally arranged for stable angina:
-Physical exam (heart sounds, signs of heart failure, BMI)
-ECG
-FBC (check for anaemia
-U and Es (prior to ACEi and other meds)
-LFTs (prior to statins)
-Lipid profile
-TFTs
-HbA1C and fasting glucose
Plus:
-Chest xray to investigate other causes of chest pain and pulmonary oedema
-Echo after the event to assess the functional damage
-CT coronary angiogram to assess for coronary artery disease
How does ACS present
Central, constricting chest pain associated with:
-Nausea and vomiting
-Sweating and clamminess
-Feeling of impending doom
-Shortness of breath
-Palpitations
-Pain radiating to jaw or arms
Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.
What are troponins
Proteins found in cardiac muscle
The specific type of troponin, the normal range and diagnostic criteria vary by lab so check policy
Diagnosis off ACS typically requires serial troponins.
A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle
Troponins are non specific so a rise does not automatically mean ACS. Alternative causes may be:
-chronic renal failure
-sepsis
-myocarditis
-aortic dissection
-PE
What is the acute STEMI treatment
Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
-Primary PCI (if available within 2 hours of presentation)
-Thrombolysis (if PCI not available within 2 hours)
The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).
WHat is PCI
Percutaneous Coronary Intervention (PCI) involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage. This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage. Usually a stent is put in to keep the artery open.
What is thrombolysis
Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.
What is the acute NSTEMi treatment
BATMAN
B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
Give oxygen only if their oxygen saturations are dropping (i.e. <95%).
What is the GRACE score
This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:
- <5% Low Risk
- 5-10% Medium Risk
- > 10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.
What are the potential complications of MI
DREAD
D – Death
R – Rupture of the heart septum or papillary muscles
E – “Edema” (Heart Failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome
What is Dressler’s syndrome
AKA post-myocardial infarction syndrome
Usually occurs around 2-3 weeks after an MI
Caused by a a localised immune response and causes pericarditis (inflammation of the pericardium around the heart)
Less common as the management of ACS becomes more advanced
Presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation.
Can cause a pericardial effucion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function)
A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echo (pericardial effusion) and raised inflammatory markers (CRP and ESR)
Manage with NSAIDs (aspirin/ibuprofen) and in more severe cases steroids (prednisolone)
May need pericardiocentesis to remove fluid from around the heart
What is the secondary prevention medical management for ACS
6 As
-Aspirin (75mg OD)
-Another antiplatelet (clopidogrel or ticagrelor for upto 12 months)
-Atorvastatin (80mg OD)
-ACE inhibitors (ramipril titrated as tolerated to 10mg daily)
-Atenolol (or other beta blocker titrated as high as tolerated)
-Aldosterone antagonist for those with clinical heart failure (epleretone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted due to higher risk of thrombus formation in different stents
What is the secondary prevention lifestyle management
Stop smoking
Reduced alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (eg diabetes and hypertension)
What are the ECG changes in ACS
STEMI:
-ST segment elevation in leads consistent with an area of ischaemia
-New left bundle branch block
NSTEMI:
-ST segment depression in a region
-Deep T wave inversion
-Pathological q waves (suggesting a deep infarct - a late sign)
What is acute left ventricular failure
When the left ventricle is unable to adequetely move blood through the left side of the heart and out into the body.
This causes a backlog of blood that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs.
The vessels in these areas are engorged with blood due to the increased colume and pressure that they leak fluid and are unable to reabsorbe fluid from the surrounding tissues, causing pulmonary oedema.
What is pulmonary oedema
Where the lung tissues and alveoli become full of interstitial fluid.
This interferes with the normal gas exchange in the lungs, causing SOB, O2 desaturation and the other signs and symptoms
What are the triggers for LVF
Iatrogenic (aggressive IV fluid in frail elderly patient with impaired left ventricular function)
Sepsis
Myocardial infarction
Arrhythmias
How does acute LVF present
Typically rapid onset breathlessness that is exacerbated by lying flat and improves on sitting up.
Causes type 1 respiratory failure (low o2 without an increase of CO2 in the blood)
SOB
Looking and feeling unwell
Cough (frothy white/pink sputum)
Increased resp rate
Reduced o2 sats
Tachycardia
3rd heart sound
Bilateral basal crackles (sound wet) on auscultation
Hypotension in severe cases (cardiogenic shock)
May also have signs and symptoms of underlying cause (chest pain, fever, palpitations)
May also have right sided heart failure (raised JVP, peripheral oedema)
How should suspected LVF be investigated
History and exam
ECG (for ischaemia and arrhythmia)
ABG
Chest Xray
Bloods:
-infection markers
-kidney function
-BNP
-troponin (if ?MI)
echo
What is BNP
B-type natriuretic peptide is a hormon that is released from the heart ventricles when the cardiac muscle (myocardium) is stretched beyond the normal range.
Finding a high result indicates the heart is overloaded (with blood) beyond its normal capacity to pump effectively
The action of BNP is to relax the smooth muscle in blood vessels. This reduces the systemic vascular resistance making it easier for the heart to pump blood through the system. It also acts on the kidneys as a diuretic to promote the excretion of more water in the urine to reduce the circulating volume helping to improve the function of the heart.
Testing for BNP is sensitive but not specific which means that when negative it is useful in ruling out hear failure, but when positive rsult can have other causes:
-Tachycardia
-Sepsis
-PE
-Renal impairment
-COPD
What is ejection fraction
Main meausure of left ventricular function
The presentage of the blood in the left ventricle which is squeezed out with each ventricular contraction
An ejection fraction above 50% is considered normal
What is cardiomegaly on chest xray
A cardiothoracic ratio of more than 50%
When the diameter of the widest part of the heart is more than half the diameter of the widest part of the lung fields
