CARDIO Flashcards
ECG signs
- Q-waves are associated with a previous myocardial infarction (Q waves are pathological if present in V2-V3, or >0.1mV for 0.03s or more in 2 contiguous leads)
- Delta waves are associated with WPW Syndrome, alongside a short PR and prolonged qrs
- Saddle ST elevation is associated with pericarditis
- ‘J’ wave - small hump at the end of the QRS complex, assoc with hypothermia
Length:
PR 3-5, QRS 2-3
Signs of hypothermia on ECG
The following ECG changes may be seen in hypothermia
bradycardia
‘J’ wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
What is AF?
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia. It is characterised by uncoordinated atrial activity on the surface ECG can be due to ectopic foci or re-entry circuit.
Chaotic and irregular atrial arrhythmia, the prevalence of which increases progressively with age.
Causes significant morbidity and mortality including palpitations, dyspnoea, angina, dizziness or syncope, and features of congestive heart failure, tachycardia-induced cardiomyopathy, stroke, and death.
ECG shows absent P waves, presence of fibrillatory waves, and irregularly irregular QRS complexes. Also order electrolytes, cardiac enzymes (Myocardial ischaemia can be a cause or consequence of AF) and TFTs (thyroxtoxicosis can present with AF).
Mx: If haemodynamically unstable -> DC cardiovert (GA)
Most patients presenting with new-onset or ‘acute’ atrial fibrillation (AF) do not require immediate cardioversion
Most patients will require medical therapy to control ventricular rate using CCB/ b blocker. Check for RA thrombus using echo and anticoagulate with DOAC if needed. If CHADVASC is 2 or more add in heparin to antihypertensives.
When do use cardiac catheter ablation?
NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.
Technical aspects
the aim is to ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium. The procedure is performed percutaneously, typically via the groin both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue
Anticoagulation
should be used 4 wks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per there CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended
Outcome
Complications:
cardiac tamponade (fluid in the pericardium builds up, resulting in compression of the heart)
stroke
pulmonary valve stenosis
success rate around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patient who’ve undergone multiple procedures around 80% are in sinus rhythm
MI complications
MI COMPLICATIONS:
Cardiac arrest
This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.
Cardiogenic shock
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the ‘mechanical’ complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump.
Chronic heart failure
As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure.
Tachyarrhythmias
Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia.
Bradyarrhythmias
Atrioventricular block is more common following inferior myocardial infarctions.
Pericarditis
Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
Left ventricular aneurysm
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
Left ventricular free wall rupture
This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.
Ventricular septal defect
Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed.
Acute mitral regurgitation
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.
How to deal with choking?
Ask the pt “are you choking” if they answer verbally yes then it is mild. If they nod/don’t respond -> severe.
If mild airway obstruction
encourage the patient to cough
If severe airway obstruction and is conscious:
give up to 5 back-blows
if unsuccessful give up to 5 abdominal thrusts
if unsuccessful continue the above cycle
If unconscious
call for an ambulance
start cardiopulmonary resuscitation (CPR)
Causes of infective endocarditis
(historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries.)
INFECTIVE, CULTURE POSITIVE:
1 Staphy aureus is now the most common cause of infective endocarditis. Acute presentation & IVDUs
2.Staphylococcus epidermidis -commonly colonize indwelling lines, prosthetic valve surgery
3.Strep viridans ~20% of cases. found in the mouth ?poor dental hygiene/dental procedure
4. Streptococcus bovis - associated with colorectal ca
INFECTIVE, CULTURE -VE: Haemophilus, Coxiella eetc.
Non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditis
Digoxin Toxicity ECG signs
ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardiaHF 3rd line treatment
Third-line treatment should be initiated by a specialist.
1. ivabradine
criteria: sinus rhythm > 75/min and a left ventricular fraction < 35%
2. Sacubitril-valsartan
criteria: left ventricular fraction < 35%
is considered in heart failure with reduced ejection fraction who are symptomatic on ACE inhibitors or ARBs
should be initiated following ACEi or ARB wash-out period
3.Digoxin
digoxin has also not been proven to reduce mortality in patients with heart failure. It may however improve symptoms due to its inotropic properties
it is strongly indicated if there is coexistent atrial fibrillation
4. hydralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients
5.cardiac resynchronisation therapy
indications include a widened QRS (e.g. left bundle branch block) complex on ECG
How do we diagnose HTN?
If reading of >140/90 offer ABPM. If <135 monitor. If 135-150 that is stage 1 HTN. If >150 this is stage 2 HTN - treat immediately. If stage 1, treat if > 80 and they have a complication such as: end organ damage, q risk ~ 10% or more, diabetes, renal disease or established CVSD
If the blood pressure is >= 180/120 mmHg: you need to admit if they have chest pain or eye HTN signs. If not, urgently investigate.
How to assess prognosis most MI?
GRACE score
Age
SBP
HR
Creatinine (serum)
CHF (killip classes 1: No CHF, 2: Pulmonary rales/ jugular venous distension, 3: Pulmonary oedema 4: Cardiogenic Shock )
Other diagnostic factors: ST deviation, Cardiac arrest on presentation, Tropnins raised
PESI
PESI to see if they’re high risk. Or simplified PESI one point or more -> admit for anticoagulation: (one point). Score 0 - 1.1% mortality at 30days. Score above 1 - 30 day mortality is 9%.
Tachycardia (>110)
History of cancer
Eighty (age > 80)
Systolic hypotension (<110)
Oxygen sats below
Ninety percent
PE Mx
Stable
Apix/Rivaroxaban would be offered for haemodynamically stable PE, as DOACs are now increasingly used in PE.
Submassive:
PE that have led to RV dysfunction without haemodynamic collapse (i.e. BP<90 for 15 min despite resus)
RV dysfunction -> +ve troponin, ECG changes, Echo, raised BNP (signs of myocardial stretch), CTPA suggesting heart strain.
Tx: Admit, if you think they’re high risk give IV LMW and HDU monitor for at least 3d. Thrombolyse if deteriorate. Needs inpatient echo due to evidence of RH strain. Inpatient for 3-5days
Massive:
Systolic <90 for over 15 min despite resus attempts or systollic drop > 40mmHg -> THROMBOLYSIS in ITU/RESUS/HDU
Periarrest/has arrested - 50mg stat atleplase (tPA) and then prolong resus (30-60 min CPR).
If no peri-arrest/arrest (hypotensive but no periarrest), give 10mg aleplase over 1-2min and then 90mg over 2 hours.
Complications: Haemorrhage, hypotension, anaphylaxis
Absolute CI: ICH, stroke in past 6 months, SAH, plts <30 (but absolute CI can become relative CI in life threatening cases, need 2 consultants involved)
Relative CI: TIA, already on oral anticoags, severe uncontrolled HTN, pregnancy, plts 30-60
Inferior vena cava filters may be offered in people who have recurrent PE despite anticoagulation.
Infective Endocarditis Diagnostic Criteria
Duke’s Criteria
• 2 major
• 1 major + 3 minor
• All 5 minor
MAJOR:
1. +ve blood culture
• Typical organism in 2 separate cultures, or
• Persistently +ve cultures, e.g. 3, >12h apart
2. Endocardium involved
• +ve echo (vegetation, abscess, valve dehiscence) or
• New valvular regurgitation
MINOR:
- Predisposition: cardiac lesion, IVDU
- Fever >38
- Emboli: septic infarcts, splinters, Janeway lesions
- Immune phenomenon: GN (glom nephritis), Osler nodes, Roth spots, RF (rheumative fever)
- +ve blood culture not meeting major criteria
Other symptoms:
Splenomegaly, clubbing, splinter haemorrhages, janeway lesions, new/changing murmur, AV block, LVF
Post MI treatment
- ACEi: start w/i 24hrs of MI (e.g. lisinopril 2.5mg)
- β-blocker: e.g. bisoprolol 10mg OD (or, CCB)
- Cardiac rehabilitation (group exercise and info)
- DVT prophylaxis until fully mobile
- Continue for 3mo if large anterior MI
- Statin: regardless of basal lipids (e.g. atorv 80mg)
Advice • Stop smoking • Diet: oily fish, fruit, veg, ↓ sat fats • Exercise: 30min OD • Work: return in 2mo • Sex: avoid for 1mo • Driving :avoid for 1mo
NB. Continue clopidogrel for 1mo following STEMI Continue aspirin indefinitely.
NYHA classification
- No limitation of activity
- Comfortable @ rest, dyspnoea on ordinary activity
- Marked limitation of ordinary activity
- Dyspnoea @ rest, all activity → discomfort
