CardioResp Flashcards
6 key cardiology symptoms
Plapitations Chest Pain SOB Orthopnea Ankle swelling/ oedema Syncope/ dizziness
Describe the NYHA Heart Failure Classification system
1-4 1 = no limitation 2= mild PA limitation (mild HF) 3= marked PA limitation (moderate HF) 4= symptoms at rest (severe HF)
Final part of cardiology history?
System view e.g. just Bowel and water works Anything i missed? What have you been told so far? ICE
Cause of third heart sound? describe sound
a-stiff-wall
lub dub dee
Cause of forth heart sound? describe
Slosh-ing-in
Dilation
Low pitched
Causes of third and forth heart sound
Both caused by HF MI Cardiomyopathy Hypertension
Grading of murmurs describe
1-6 (last three with a thrill) 1- barely audible 2 soft 3 heard easily 4 loud with thrill 5 very loud with thrill, may be heard with streph partially off 6 same as 5
Causes of mitral stenosis
Rheumatic fever (chorea) in 50% Age and calcification
Signs of mitral stenosis
Pulmonary oedema signs
AF (highly associated due to atrial changes)
RHF late
Malar flush
How does ausculation change with mitral stenosis progression
Earlier the murmur/ mitral ‘snap’ with more severe disease due to Left atrium hypertrophy
Followed by low rumbling - bell at apex with patient lying on left side
Chest Xray mitral stenosis
Pulmonary hypertension- upper lobe diversion, bat winging, loss of menisci
LAH
ECG mitral stenosis
RVH - lead to right axis deviation and tall R in V1/2
AF
Bifid P wave - LAH causing left atrial delay
Mitral Regurg causes:
More common than MS Rheumatic heart disease Papillary muscle necrosis (MI) Cardiomyopathy CT disorders - Ehlers Danlos - Marfans - Osteogenesis Imperfecta Endocarditis
Mitral regurg signs
Malar flush
Displaced apex beat (volume overload)
Palpable thrill
Pansystolic murmur radiating to axilla “burr” - not gap before S2 unlike AS
Mitral regurg xray and ECG
Cardiomegaly (grows more to maintain BP desite loss of blood the wrong way, V and A) Left displacement (S in V1 and tall R in V5/6) Bifid P wave
AS causes
<65 bicuspid valve
>65 Calcification age related
Rheumatic heart disease
AS symptoms
Syncope on exercise
Angina
SOB
Poor prognosis without surgery
Signs of AS
Collapsing pulse Slow rising character Low volume - small PulseP Forceful apex beat Eject systolic mkurmur to cartids lub-whoosshhh (pause) dub
CXR and ECG of AS
Enlarged aorta (post stonotic dilatation) LV straign pattern - depressed ST with inverted T in all ventricular facing leads
AR causes
Bifid aortic valve
Rheumatic valve disease (commonest)
infective endocarditis
Marfan’s (CT causes regurg)
AR signs and ECG
Loudest at 4th intercostal space left sternal edge, sitting forward and breathing out.
High pitched early diastolic murmur. (think other MR is high pitched too “burrr”) lub taaarr
Collapsing pulse (wide pulse pressure)
Pistol shot femorals - femoral artery
low volume pulse
Quincke’s sign - capillary pulsation in the nail beds
De Musset’s sign - head nodding with each heart beat
(all three to do with PULSITATION / wide PP)
Displaced apex beat (LVH)
ECG - LVH - LAD,
Angles of limb leads
I 0 II 60 aVf 90 III 120 aVr -150 avL -30
Placement of chest leads
V1: Fourth intercostal space, right of the sternum.
• V2: Fourth intercostal space, left of the sternum.
• V3: Directly between leads V2 and V4.
• V4: Fifth intercostal space at midclavicular line.
• V5: Level with V4 at left anterior axillary line.
• V6: Level with V5 at left midaxillary line.
Why is the rhythm of atrial flutter normally around 150, 100 or 75bpm?
Depends on ratio of A:V dependent on how many beats AVN is conducting (degree of block)
VT ECG appearence
Wide QRS
Concordance pos or neg
Fusion or capture beats (normal or semi normal beats)
No relation to P waves
No delta wave (would make it WPW)
No BBB (would make it SVT with abberancy or BBB)
120-180 bpm
VF ECG
Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF -> fine VF)
concordance - all limb leads show either positive or negative
Capture or fusion beats
capture beats - occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
Treatment of Broad complex tachycardias
Haemodynamically unstable - DC shocks followed by amioderone
IF stable and regular
- asssume VT and give amioderone and K/ Mg if needed
- If known history of SVT and BBB consider adenosine (as it’s likely to be that).
If irregular:
- AF with BBB (treat same as AF)
- Pre excited AF (amioderone)
- Polymorphic VT (e.g. Torsade de pointes - varying axis, long QT syndrome) high dose BB for torsade/ May need to correct hypokalaemia and give Mg sulfate
4 causes of wide complex reg tachy:
1) SVT abberancy
2) WPW
3) SVT with BBB
4) VT
When and why do you never give adenosine? When could you give it?
1) VT - blocking AVN wont help
2) Pre-excited SVT (e.g. AF) - narrow complex or broad as may be abberant/ BBB as it may force it down accessory pathway, (think pre-exciting must refer to the possibility of an accessory pathway).
3) SVT - impossible to tell if there is an accessory pathway however… consider if regular and there is a history of SVT and BBB (as you know it is not pre-excited)
(“pre-exitiation refers to contraction of ventricles viva an accessory pathway”- by definition isn’t this broad complex so wouldn’t adenosine help block pathway? i.e. can’t force down accessory pathway by blocking AVN as it is already going down?)
No P waves in narrow complex tachy?
AVNRT - simulatieous contaction? think Somani diagram
Causes of narrow complex tachycardia?
AFib Aflut AT JET: -AVNRT -AVRT All causes of SVT
Treatment of NC tachy?
AF/ flutter - normally
multifocal AT (ectopics) - most common in COPD, correct hypoxia and hypercapnia. If normal AT normally due to digoxin toxicity.
SVT - haemodynamically stable 1- Vagal 2 - adenosine 3 - Verapamil 4 - atenolol or sotalol 5 - DC cardioversioon
If unstable
-DC cardioversion
Main causes of LAD and RAD
LAD:
- LVH
- Ischaemia of LBB
RAD
- RVH
Causes of werid P waves
Left atrial enlargement e.g. MS or HYT
Bifid P wave (P mitrale) - enlarged
Tall P wave (P pulmonale):
Right atrial dysfunction e.g. pulmonary hyt, COPD, congenital HD (TOF, Pulmonary stenosis)
Names of 2nd degree HB
Mobitz I (Wenckebach) - prolongs progresively Mobitz II - failure of AVN to conduct all
Causes and presentation of 3rd degree HB
Total failure, bradycardia (30-50)
Stokes-Adams attack (sudden collapse/ syncope due to the brady)
MI
AVN fibrosis or bundle of hiss
Drugs - digoxin, diltiazem (especially with BB)
ECG signs of LVH
Englarged S wave in V1 (35mm or 3.5 squares)
Englarged R wave in V5/6 35mm
Possible T wave inversion in V5/6 at late stage
Sokolow-Lyon Voltage criteria
Note no axis deviation really?
ECG sings of RVH
Right axis deviation
Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
QRS duration < 120ms (i.e. changes not due to RBBB).
Desribe ECG BBB
Normal QRS duration is 0.12s (3 small squares)
o Widened in Bundle Branch Block (BBB)
o If the major deflection in V1 is up then it is Right
BBB, if down then Left BBB
o Remember WiLLiaM and MaRRoW
o LBBB: W in V1 and a M in V6
o RBBB: M in lead V1 and a W in lead V6
What does ST deepression up sloping mean?
ST depression that is Upsloping is rate related, not ischaemia
Changes in ECG post MI?
Hyperacute T waves first
ST elevation
Pathological Q waves (at least 1/4 of QRS height) hours-days
T wave inverison
Describe the territories of MI
v1-2: septal v3-4: anterior v5-6: lateral avL-I: high lateral avR, II, III: Inferior
v1-v3 depression: posterior
Describe ECG changes in PE
Tachycardia most common S in I = large Q in III = large T in III = large SIQIIITIII
P HYT can cause RAD
ECG changes of hyperkalaemia
Broad Bizarre QRS
Hyperacute T wave
Low flat P wave
Slurring into ST segment
Causes of HF in order of likelihood
70% IHD
30% Non ischaemic cardiomyopathy (genetic, alcohol, drugs)
5% hypertension
also: Valve disease Pulmonary pathology Hyperdynamic circulation (increased volume) - anaemia, thyrotoxicosis, Paget's Pericarditis/ Pericardial effusion Alcohol and drugs CHD Arrhythmias including AF and heart block
Pathophysiological changes in HF and subsequent mechanisms to maintain CO broadly. Early and late mechanisms.
Ventricular dilation Myocyte enlargement Neurohumeral: Increased ANP Increased symp activation Increased peripheral vasocnstriction Increased fluid retention
Early
- Normally Low CO counteracted by increase in VP and starlings curve
- Mild HF, Low CO counteracted by increase in VP and HR, decreased ejection fraction.
Late
- CO maintained by large increases in VP and sinus tachy, not in exercise. Increase in VP causes signs and symptoms
Severe HF - decreased CO at rest even with VP and HR.
How do the physiological response to HF increase the damage?
Chronic activation of RAAS and adrenergic systems causing vasoconstriction and Na and water retention increase afterload and preload and increase cardiac work leading to further myocyte damage
Signs and symptoms of LHF
Symptoms: o Fatigue (common) o Exertional dyspnoea o Orthopnoea / PND • Physical signs are few and not prominent until a late stage or if LV failure is acute: o Displaced Apex Beat Cardiomegaly o Gallop Rhythm on Auscultation 3rd heart sound heard o Features of Mitral Regurgitation Dilatation of the mitral annulus o Crackles at Lung Bases Pulmonary oedema o Dependent Pitting Oedema Activation of RAA
Causes of RHF
- Chronic Lung Disease (Cor pulmonale)
- PE or Pulmonary Hypertension
- Tricuspid / Pulmonary Valve Disease
Also:
o Left-to-Right shunts e.g. ASD / VSD
o Isolated Right Ventricular Cardiomyopathy
Symptoms and signs of RHF
• Symptoms: o Fatigue o Dyspnoea o Anorexia / Nausea • Physical signs are usually more prominent than the symptoms: o ↑ Jugular Venous Distension ± V waves of tricuspid regurgitation o Cardiomegaly Dilatation of the right ventricle produces cardiomegaly ...and may give rise to functional tricuspid regurgitation o Hepatic Enlargement Tender and smooth o Ascites Development of free abdominal fluid o Dependent Pitting Oedema
Diagnosis and staging of HF
Diagnosis of Heart Failure should not be solely based
on history and examination
• Evidence of cardiac dysfunction must be
demonstrated
• Investigations include
o Bloods
o CXR
o Echocardiogram
• The underlying cause must be established in all
patients
NYHA Heart Failure Classification
Symptoms
Class I - No limitation of physical activity
Class II - Slight limitation of physical activity
(symptomatically mild heart failure)
Class III - Marked limitation of physical activity
(symptomatically moderate heart failure)
Class IV - Symptoms at rest
(symptomatically severe heart failure)
Management of HF
General Management
• Low level exercise
• Low salt diet
• Stop smoking
• Education
• Vaccination
Medical Management
1. Diuretics
o Step 1: Furosemide (loop diuretic) 40mg and
titrate up if needed.
o Step 2: Change to Bumetanide (loop diuretic)
if Furosemide not working.
o Step 3: Add a Thiazide for complete diuresis
…must watch U&E’s
2. Ace Inhibitor (ACEi)
o Trials have shown ACEi in heart failure
improves symptoms and prognosis.
o Replace with an Angiotensin II receptor
antagonist if patient gets a dry cough.
3. β-Blockers
o Used in chronic stable heart failure.
o Should be initiated in confirmed heart failure
due to left ventricular systolic dysfunction after
diuretics and ACE-I therapy.
4. Spironolactone (aldosterone antagonist)
o 30% reduction in all-cause mortality when
added to conventional treatment in patients
with moderate to severe HF.
5. Inotropic agents
o Dopamine & Dobutamine. - IV Inotropes are frequently used to support myocardial function in
patients with acute left ventricular failure with hypotension.
o Digoxin. - Patients who are hospitalized or present with severe heart failure in spite
of therapy with vasodilators, beta-blockers, diuretics (and also patients
with rapid AF), may benefit from digoxin.
6. Nitrates
o Reduce preload and afterload.
o Short and long acting nitrates (e.g. Glyceryl Tri-
Nitrate (GTN) and Isosorbide Mononitrate (ISMN)).
o With chronic use, tolerance develops, hence
administered at 0800 and 1400 hours BD.
7. Anticoagulation
o Can be considered as HF is associated with a
4x increase in stroke risk.
Non Pharmacological Management
• Revascularization
• Biventricular pacemaker or Implantable Cardioverter
Defibrillator (ICD)
• Cardiac Transplantation
• LVAD (Left Ventricular Assist Device) and Artificial
Heart
Management of a STEMI
Airway, Breathing, Circulation • IV access • 12-lead ECG • Give: • Oxygen • Nitrates (GTN spray 2 puffs sublingually) • Aspirin (300mg) • Diamorphine (2.5-10mg IV, plus antiemetic) Investigations • Bloods: o FBC, U&E, LFTs, glucose, lipids, CK, troponin I • Portable CXR
Indications for thrombolysis in ACS
o < 12 hours onset pain \+ any 1 of the following: o ST elevation >1mm in 2+ consecutive limb leads o ST elevation >2mm in 2+ consecutive chest leads o Posterior infarct o New onset LBBB
Thrombolysis containdications
Haemorrhagic stroke or Ischaemic stroke < 6 months CNS neoplasia Recent trauma or surgery GI bleed < 1 month Bleeding disorder Aortic Dissection
Relative
Warfarin
Pregnancy
Advanced Liver Disease
Infective Endocarditis
Indications for primary PCI
(<90mins from pain onset) • Indication: o Same as thrombolysis indications. o If does not fulfil thrombolysis criteria or thrombolysis contraindicated. o If symptomatic post-thrombolysis or develops cardiogenic shock.
Complications of STEMI
S - Sudden death or from VF P - Pump failure / Pericarditis - First 48hours Following transmural MI Worse lying plat Pericardial rub Pericardial effusion R - Rupture papillary muscles or septum E - Embolism A - Aneurysm / Arrhythmias D - Dressler’s syndrome
What is Dressler’s syndrome?
2-6 weeks after MI Autoimmune reaction against proteins in recovering myocardium Fever Pleuritic pain Pericardial effusion Raised ESR Treat with NSAIDs
Discharge management for STEMI
Aspirin • Clopidogrel • ACE inhibitor • β-blocker • Statin • Address modifiable risk factors • 1 month off work • Need to inform DVLA – no driving for 4 weeks.
Management of NSTEMI.
Close monitoring with ECG Aspirin 300mg Nitrates - GTN or sublingual morphine for chest pain O2 if sats <90?% of SOB Clopidogrel 300mg and continued for 12months
PCI or thrombolysis if indicated.
Fondaparinex or enoxaparin, oral BB or enoxaparin if waiting for angiotraphy
Long term same as stemi (probably):
Aspirin • Clopidogrel • ACE inhibitor • β-blocker • Statin • Address modifiable risk factors
When would PCI be considered in NSTEMI
96hr of first admission if 6 month mortality above 3% or if clinically unstable
Very high Trop I
Symptoms dispite maximal medical therapy
<6 months since last PCI
Heart failure/ poor LV function
Haemodynamically unstable
Based on GRACE score
Signs and symptoms of Acute LVF
Acute breathlessness
o Cough & frothy pink sputum
o Orthopnoea, paroxysmal nocturnal dyspnoea
o Collapse, arrest, cardiogenic shock
Distressed, pale and sweaty
o Tachycardic
o Fine crepitations bilaterally
o Gallop rhythm: 3rd heart sound
Cause of Acute LVF
Myocardial ischaemia
o Hypertension
o Aortic stenosis or aortic incompetence
o Mitral incompetence
Management of Acute LVF
• Airway, Breathing, Circulation • Sit upright • 100 % O2 via non-rebreather mask • IV access and monitor ECG • Morphine 2.5-5mg IV (with antiemetic) Other: • If SBP >100mmHg – Nitrate (GTN) IV infusion • Furosemide 40-80mg IV • CPAP
Investigations of acute LVF
ECG: Arrhythmia, tachycardia, MI, LVH • Bloods: FBC, U&E, CK, Troponin I • CXR • ABG • Echo
Radiological signs of heart failure
ABCDE Airspace shadowing Kerley B lines (septal lines) Cardiomegaly Diversion of blood to upper lobes Effusions
3 ways tachhy arrythmias are produced
Accelerated automaticity o An area of myocardial cells depolarises faster than the SA node 2. Triggered activity o Myocardial damage 3. Re-entry o Propagating action potential keeps meeting excitable myocardium. o There must be 2 pathways around an area of conduction block.
VT Precipitating factors
Metabolic (low K or Mg) • IHD • Cocaine • Cardiomyopathy • MI
SVT Precipitating factors
- IHD
- Thyrotoxicosis
- Caffeine
- Alcohol
- Amoking
AF Precipitating factors
Same as SVT & also: • Mitral valve disease • Hypertension • Lung disease • Post op • Pericardial disease • Cardiomyopathy
Normal bug in infective endocarditis
Usually bacterial
o Streptococcus viridians
Upper respiratory tract commensals
• Others
o Staphylococcus aureus – Skin infections,
abscesses, central lines, IV drug abusers…
• And more…
Pathophysiology of infecive endocarditis
1 Endothelial damage/ damaged valve
Platelets andfibrin deposition (Sterile fibrin-platelet vegetation)
3 Bacteraemia
4 Adherence and colonisation of bacteria
5 Fibrin aggregates protect the bacteria vegetation from host defence mechanisms
• Consequences
o Disruption of the valve cusps, commonly
leading to mitral or aortic regurgitation.
o Vegetations embolise.
o Deposition of immune complexes.
Clinical presentation of infective endocarditis
HEART MURMUR + FEVER • Four processes causing the clinical picture: o Systemic infection o Valvular / Cardiac damage o Embolisation o Immune vasculitis 1. Systemic infection o Malaise o Pyrexia o Myalgia o Weight loss o Fatigue 2. Valvular / Cardiac damage o Changing Murmur Aortic regurgitation Mitral regurgitation o Heart failure o Conduction Abnormalities 3. Embolisation o Cerebral o Pulmonary o Coronary o Renal (haematuria) 4. Immune Vasculitis o Roth spots (Retinal infarcts with surrounding haemorrhage) o Oslers nodes o Janeway lesions o Clubbing o Splinter haemorrhages o Glomerulonephritis
Diagnosis of infective endocarditis
A. Positive blood culture for Infective Endocarditis:
o Typical organism in 2 separate cultures.
OR
o Persistently positive cultures (3 sets, at different
times, from different places, at peak temperature).
B. Evidence of Endocardial involvement:
o Positive echocardiogram (Vegetation, abscess,
prosthetic valve damage).
OR
o New valvular regurgitation.
- Predisposition
- Fever >38°C
- Vascular / Immunological signs
- Positive blood culture (But does not meet Major criteria)
- Positive echocardiogram (But does not meet Major criteria)
2 Major OR 1 Major, 3 Minor OR 5 Minor
Investigation infective endocarditis
Bloods - full work up - emboli damage
Urinalysis
Treatment infective endocarditis
Airway, Breathing, Circulation – Stabilise the patient
• Always involve a microbiologist and a cardiologist
• Depends on organism
• Empirical treatment is:
o BENZYLPENECILLIN & GENTAMICIN
• Treatment can often be at least 4 weeks IV antibiotics
Prevention of infective endocarditis/ prevention
Who’s at Risk?
o Structural congenital heart disease
o Acquired valve disease
o Prosthetic valves
o Previous endocarditis
• Explain to patient:
o Benefits and risks of antibiotic prophylaxis, and
why antibiotic prophylaxis is no longer
routinely recommended.
Importance of maintaining good oral health.
o Symptoms of infective endocarditis and when
to seek expert advice.
o Risks of undergoing invasive procedures,
including body piercing or tattooing.
Explain the anatomy of heart layers
Myocardium Visceral pericardium Pericardial space (with 15-50ml of pericardial fluid) Parietal pericardium Fibrous layer
Visceral pericardium: An inner serous membrane
made of a single layer of mesothelial cells.
• Pericardial fluid drains via the thoracic duct and right
lymphatic duct into the right pleural space.
Presentation of acute pericarditis
Acute pericarditis is an inflammation of the pericardium characterized by: o Chest pain o Pericardial friction rub o Serial ECG changes
Substernal or left precordial pleuritic chest pain with radiation to the trapezius ridge, which is relieved by sitting up and bending forward and worsened by lying down
dry cough, fever, fatigue, and anxiety
Pericardial pain: 5 features o like pleurisy: 1. Sharp 2. Worse on inspiration o like angina: 3. Central chest pain 4. Radiating to left shoulder o specific: 5. Eased sitting forward • +/- Dyspnoea, especially with tamponade • +/- Fever
Pathophysiology of pericarditis
xPericardium is acutely inflamed. • Infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularisation. o May develop constrictive pericarditis Exudates & adhesions encase the heart within a non expansile pericardium. o May develop a pericardial effusion Serous or haemorrhagic. May lead to cardiac tamponade.
Causes of pericarditis
Viral (most common) o Particularly Coxsackie Viruses o Treatment is symptomatic, with observation for the development of pericardial tamponade. • Idiopathic • Tuberculosis • Bacterial o Causes purulent pericarditis. o Requires antibiotics for at least 4 weeks and drainage of pericardial fluid. o Develops from: Direct pulmonary extension Haematogenous spread Myocardial abscess Endocarditis Penetrating injury to chest wall (trauma or surgery) Subdiaphragmatic suppurative lesion • Cardiovascular disease o Myocardial infarction o Dresslers Syndrome • Neoplasm o Lung tumours o Metastatic disease • Renal failure o Before dialysis, pericarditis developed in 35- 50% of patients with uremia and chronic renal failure. o Often died within a few weeks. o Requires intensive dialysis. • Inflammatory o Rheumatoid Arthritis o Sarcoidosis o Systemic Lupus Erythematosus (SLE) etc...
Examination of pericarditis
• Tachycardia + Tachypnoea + Fever
• Pericardial friction rub
o Auscultate with diaphragm over the left lower
sternal edge
• If constrictive pericarditis:
o Right heart failure
↑JVP, severe ascites, hepatomegaly, Kussmaul’s
sign (JVP ↑ with inspiration)
o Hypotension, Pulsus Paradoxus (↓ in palpable pulse
and ↓ in systolic BP on inspiration)
• Loud high-pitched S3 (pericardial knock)
Investigations pericarditis
Bloods: FBC, U&E, LFT, CRP, CK, Troponin I • Further investigations: o Virology screen o Blood cultures o Antistreptolysin titre o Rheumatoid factor o Antinuclear antibodies (ANA) o Anti-DNA antibodies o Tuberculin testing o Sputum for acid-fast bacilli
Echocardiography (ECHO)
o If pericardial effusion or tamponade is
suspected.
o If there is a pericardial effusion, you may see
right ventricle compression as this is
compromised first.
• CT / MRI
ECG changes in pericarditis
Classic acute pericarditis evolves through 4 stages:
o Stage 1: Saddle shaped ST elevation (Diffuse
concave upward ST elevation, except aVR and V1 (usually
depressed).
o Stage 2: Occurs several days later. ST
segment returns to baseline, followed by T
wave flattening.
o Stage 3: T wave inversion.
o Stage 4: ECG returns to the pre-pericarditis
baseline weeks to months after onset.
• All 4 stages are only present in 50% of patients.
• T wave inversion may persist indefinitely with the
chronic inflammation observed with Tuberculosis,
Uremia, or Neoplasm.
Pericardial effusion/ Cardiac tamponade definition
• Pericardial effusion
o Pericardial effusion is an abnormal
accumulation of fluid in the pericardial cavity.
• Cardiac Tamponade
o Pericardial effusion causing haemodynamically
significant cardiac compression.
Pericardial pressure increases inhibiting
venous return to the heart.
This results in reduced cardiac output,
hypotension and shock.
PEricardial effusion/ Cardiac tamponade aetiology and grouping
• ‘Acute’ o Trauma o Iatrogenic (cardiac surgery / catheterisation / anticoagulation) o Aortic dissection o Spontaneous bleed (uraemia / thrombocytopenia) o Cardiac rupture post-MI • ‘Subacute’ o Malignancy o Idiopathic pericarditis o Uraemia o Infection (including TB) o Radiation
Presentation of pericardial effusion/ tamponade
• Depends on speed at which fluid accumulates! • Commonly o Cardiac arrest o Hypotension o Confusion o Shock • Slowly developing tamponade o SOB o Cough, hiccups, dysphagia Signs • Beck’s triad: o ↑ JVP o ↓ BP o Muffled heart sounds • Tachycardia • Kussmaul’s sign (JVP ↑ with inspiration) • Pulsus paradoxus (↓ in palpable pulse and ↓ in systolic BP on inspiration)
Treatment of PEricardial effusion/ Cardiac tamponade
ABC
IV acess
ECG
Bloods
Get senior help
• Pericardiocentesis
o Needle inserted at level of Xiphisternum, aim
for tip of left scapula, aspirating continuously.
o Blind – complication risk 5-50%, only if
emergency.
o USS guided – relatively safe.
o Send the pericardial fluid for microbiology and
cytology.
• A drain may be left in temporarily to allow sufficient
release of fluid
Side effects if beta blockers
GI disturbances; bradycardia; fatigue;
cold peripheries; heart failure; hypotension; dizziness;
sexual dysfunction; peripheral vasoconstriction;
bronchospasm.
CI to beta blockers
asthma; marked bradycardia;
heart block; uncontrolled heart failure; PVD - peripheral vasc disease;
Prinzmetal’s angina; hypotension; cardiogenic shock.
Types of CCBs and functions/ indications
Non-dihydropyridines
o Verapamil & Diltiazem
Negatively inotrophic / chronotrophic but DO NOT
USE IN HEART FAILURE
• Dihydropyridines
o Amlodipine, Felodipine, Nifedipine
Dilates peripheral arteries, ↓ after-load, dilates
coronary vessels, act on vessels > myocardium
Indications:
o Verapamil: fast AF, SVT, hypertension.
o Dihydropyridines: hypertension; to prevent
angina.
Side effects of CCBS
o Verapamil & Diltiazem: constipation; N&V;
flushing, headache, dizziness; fatigue.
o Dihydropyridines: abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue.
Contraindications of CCBs
Verapamil & Diltiazem: HF, 2nd or 3rd degree
heart block, cardiogenic shock.
o Dihydropyridines: Unstable angina, significant
AS.
Nitrates contraindications
• Contraindications: hypersensitivity to nitrates;
hypotensive conditions; hypovolaemia; hypertrophic
obstructive cardiomyopathy; AS; MS; cardiac
tamponade; constrictive pericarditis; marked anaemia.
Nitrates side effects
postural hypotension; tachycardia;
throbbing headache; dizziness.
o TOLERANCE
ACE MoA
Action: Inhibits conversion of angiotensin 1 into
angiotensin 2, therefore inhibiting angiotensin 2 having
its effects:
o Increasing sympathetic activity.
o Fluid retention by kidney – via Increase in
aldosterone and direct action.
o Arteriolar vasoconstriction.
o Stimulating ADH secretion causing increased
fluid retention.
ACE inhibitors also cause:
o Reversal of left ventricular hypertrophy.
o Reversal of endothelial dysfunction.
Side effects ACE
renal impairment; persistent dry cough;
angioedema; rash; hypotension; pancreatitis;
hyperkalaemia; GI effects.
Containdications to ACEi
hypersensitivity to ACEi
(angioedema); renal artery stenosis; pregnancy; aortic
stenosis; toxicity.
May adversely affect fetal and neonatal BP control and renal
function; possible skull defects and oligohydramnios; toxicity.
Treatment of pericarditis
• If a cause is found, this should be treated!
• Bed rest and oral NSAIDs
o High-dose aspirin, indometacin or ibuprofen.
o But NOT post-MI: NSAID associated with
myocardial rupture.
o Corticosteroids have been used when the
disease does not subside rapidly.
• Further Treatment:
o Pericardial window
o Pericardiectomy
Causes of reversible cardiac arrest
Hypoxia
Hypovolaemia
Hypokalaemia
Hypothermia
Tension Pneumothorax
Tamponade
Thromboembolism/ PE
Toxicity
