Cardiology Flashcards
Arthrogenesis RF
- Modifiable
- Non modifiable
Modifiable
- High cholesterol
- Smoking
- Alcohol
- Obesity
- Sedentary lifestyle
- Hyperlipidaemia
- HTN
- DM
Non mod
- Male
- Family hx
- Age
Atherosclerosis pathogenesis
-Endothelial injury
-endothelial dysfunction
-endothelium releases chemoattractants
-Leukocytes accumulate and migrate into vessel walls releasing inflamm cytokines
IL-6
IL-1
IFN-Gamma
LDL - can pass in and out of arterial wall when in excess
Accumulation leads to glycation and oxidation
Stages of atherogenesis
- fatty streak
- Intermediate lesions
- Fibrous plaques
- Rupture of fibrous plaque
- Erosion
Complonents of Fatty streak
Foam cells and T-lymphocytes
Components of Intermediate lesions
Foam cells
T lymphocytes
Vascular SM
Aggregated platelets
Fibrous plaque components
Central necrotic tissue Foam cells T - lymphocytes Vascular SM Fibrous cap - Fibrin+Elastin
Primary prevention of CVD
- QRISK 3 Score If score >10% innitate STATINS - Stop Smoking -Stop drinking Alcohol -Tx Co-morbidities - Diet -Excercise -Weight Loss
Secondary prevention of CVD
After CVD development A - Asprin + Clopidogrel (12m) A - Atorvastatin A - Atenolol - Bisoprolol (Titrated) A - ACEi (Titrated) - Ramipril
Titrated to max tolerable dose
Complications of atherosclerosis
- TIA
- MI
- Peripheral vascular disease
- Strokes
- Chronic Mesenteric Ischaemia
- Angina
What is stable angina
Chest pain due to reversible myochardial Ischaemia Mismatch in O2 demand and supply Exacerbated by excercise Relieved by rest +GTN Spray Radiation: Neck,Jaw,Arm Exacerbating factors: - Cold weather - Emotion - Heavy meal
Types of Angina
Stable
Unstable
Prinzmetal - C.A vasospasm
Decubitus - Precipitated by lying flat
Causes of Myochardial Ischaemia
- Decrease B.F –> Atheroma
- Decrease O2 carrying capacity –> Anaemia
- Decrease O2 availability –> Hypoxia
- Increase distal resistance –> L.V hypertrophy
What percentage occlusion does a rapid decline in perfusion occur
Diameter stenosis > 70%
Stable angina Investigations
ECG
- ST depression/ T-wave inversion
- Excercise ECG - ST depression
Bloods
- FBC/U+E/HbA1c/LFT
CT Coronary Angiogram
- GOLD - Diagnostic
- Shows narrowing
Stable Angina Management
Secondary prevention
- Weight loss
- Diet
- Smoking/Alcohol
- Hyperlipidaemia –> Statins
- 75mg Asprin
Short term Sx relief
- GTN Spray
5mins - repeat - pain - 999
Long term sx relief
- Bisoprolol
-CCB –> Amlodopine
Either or used in combo if sx not controlled
What are the methods for revascularisation
- Percutaneous Coronary Intervention
- Coronary Artery Bypass Graft
PCI
- Procedure
- Advantages
- Risks
- Ballon inflated in stented vessel + Stent (Drug eluting)
- DAPT (Asprin + Clopidogrel) Decrease risk of instent thrombosis
A:
Less invasive
Short recovery
D:
DAPT
Risk of stent thrombosis
Not for compex cases
CABG
- Procedure
- Advantages
- Disadvantages
Use ITA to bypass stenosis in LAD/RCA
A:
Good prognosis
Complex cases
D:
Invasive
Risk - Stroke,Bleeding
Long recovery - Hospitalised
What is ACS
Umbrella term for Unstable angina and MI
- Result of rupture of a fibrous cap –> Platelet aggregation –>thrombus formation from an atherosclerotic plaque blocking a coronary artery
Dx STEMI
ST elevation
New LBBB
Tall T-waves/T-wave inversion
Pathalogical Q-wave
Troponin T+I elevated
Creatnine Kinase elevated
Dx NSTEMI
Normal ECG
ST depression
T-wave inversion
Pathalogical q-wave
Troponin T+I elevated
Dx Unstable Angina
ST - depression
T- wave inversion
NO PATHOLOGICAL WAVES
NORMAL TROPONIN LEVELS
RF for ACS
Male Obese HTN Smoking Family Hx Age High cholesterol DM
Describe the cardiac enzymes
Troponin T+I
- Myocardial necrosis
- > 30ng/l –> MI
- Rises 3-12hrs after chest pain onset
Creatnine Kinase MB
- Low accuracy present in normal individuals
- Determines re-infarction as levels fall slower than troponin
ACS Sx + signs
Acute central chest pain >20mins
- Nausea
- Sweating
- Vomitting
- S.O.B
- Feeling of impending doom
- Pain radiating to arms/neck/jaw
Signs:
- HR
- BP
- Reduced 4th Heart sound
Signs of silent MI + who experiences them
- Elderley and DM pts
Syncope
Pulmonary oedema
Vomitting
Alternative causes of raised troponins
Sepsis
Myocarditis
Aortic dissection
PE
NSTEMI and UA initial Tx
M- Morphine (5-10mg) O- 02 (SaO2<90%/S.O.B) A- Asprin (300mg) \+Clopidogrel N - Nitrates - GTN spray
Additional:
Beta blockers
Anticoagulant
- LMWH (Enoxaparin)
Risk stratification NSTEMI
GRACE
- 6m risk of death or repeat MI after NSTEMI
- High risk if score>10%
- Consider PCI to tx CAD
TIMI
- Thrombolysis In MI
Risk of dying from a heart event for pts with NSTEMI/UA
STEMI Patho
Plaque rupture thrombus occlusion Infammation Myocardial cell necrosis
STEMI Sx + signs
Sx
- Central chest pain
- Radiates to arm/neck…
- Sweating
- S.O.B
- Palpitations
Signs
- Clammy
- Pale
- 4th heart sound
- Pansystolic murmur
Acute STEMI managment
Morphine
Oxygen
Asprin + Ticagrelor (180mg)
Nitrates - GTN
B- Blocker
- Ensure no: HF/HB/COPD/Shock
STEMI ECG + PCI availabel in 2hrs?
Yes –> PCI
NO –> Fibrinolysis
Fibrinolysis
STREPTOKINASE
Plasminogen activation factors given
Plasmin cleaves fibrin to its degradation products breaking up the thrombus
STEMI Secondary management
Asprin Antiplatelets - Clopidogrel Atorovostatin - (80mg) ACEi - Titrated slowly Atenolol - CI --> CCB
Lifestyle
- Stop smoking + alcohol
- Cardiac rehabilitation
- Optomise tx for other conditions - DM/HTN
- Mediterranian diet
Advice following STEMI
Quit job if:
- Airline pilots
- Drivers
Can return to work in 2 months
Differential Dx STEMI
Cardio: ACS Aortic dissection Pericarditis Myocarditis
Lungs:
PE
Pneumonia
Pneumothorax
GI:
Oesophageal spasm
STEMI Complications
- AV block
- Cardiogenic shock
- LV failure
- PE
- Pericarditis
- Cardiac tamopnade
- Mitral regugitation
- Ventricular septal defect
- Dresslers syndrome
ECG Leads visualisation
1 - Lateral –> Circumflex
2 - Inferior –> RCA
3 - Inferior –> RCA
aVR - Neutral
aVL - Circulflex
aVF - RCA
ECG chest leads
- Heart area
- Vessel
SEE ALL LEADS V1 - Septal --> LAD V2 - Septal --> LAD V3 - Anterior --> RCA V4 - Anterior --> RCA V5 - Lateral --> Circumflex V6 - Lateral --> Circumflex
Rules for ECG
- All waves -ve in aVR
- PR interval = 120-200ms
- QRS <110ms
Heart failure defenition
CO inadequate to meet body’s requirements
Types of HF + Causes
Systolic
- Failure to contract
- EF <40%
- IHD/MI/Cardiomyopathy
Diastolic - Inability to relax and fill - Normal EF as total volume decreased - Reduced pre-load - Tamponade Restrictive cardiomyopathy Constrictive pericarditis Obesity HTN
Calculation for EF
= SV/Total volume
HF Causes
IHD HTN Cardiomyopathy Arrhythmias --> Atrial fibrillation Aortic stenosis Mitral regrug Chronic lung disease
Types of output in HF and causes
HIGH
- Anaemia
- Pregnancy
- HTN
LOW - Decreased CO that fails to increase with exertion - Pump failure Systolic failure due to decreased HR - Anti - arrhthmic drugs - Excessive pre-load FLuid overload Mitral regurg -Chronic increased afterload Aortic stenosis HTN
How does HF occur
As heart begins to fail compensatory changes occur
Overtime these compensatory changes get overwhelmed causing pathological development
Compensatory changes in HF
- Sympathetic stimulation
Increased afterload through peripheral vasoconstriction and Increasing HR/contractility - RAAS
Salt and water retention
Increases afterload and preload through increased volume and vasoconstriciton
-Cardiac Ventricualr dilatation Ventricular remodelling - Myocyte hypertrophy - Interstitial fibrosis
Why is increased preload beneficial in HF
Failure of heart muscle means blood remain after systole resulting in increased preload
This stretches the myocardium
Frank starling
Maintains CO for a short period
Left sided HF Sx
Exertional dyspnoea Fatigue Paroxusmal noctural dyspnoea Cough - Frothy sputum Breathlessness Orthopnea
Left sided HF sings
- Crepitations in lung bases
- Tachycardia
- Heart murmur
- Pulmonary oedema
- Cardiomegaly (Displaced apex beat)
- 3rd/4th Heart sound
- Reduced BP
Rght sided HF causes
- Pre-existing LVF
- Pulmonary stenosis
- Cor pulmonale
- Atrial/ventricular septal defect
Right sided HF Sx
- Nausea
- Anorexia
Right sided HF Signs
- Raised JVP
- Hepatosplenomegaly
- Ascites
- Weigth gain (fluid)
- Pitting oedema
Cause of paroxysmal noctural dyspnoea
- Decreased adrenaline at night
- Resp centres less responsive
- Fluid settles over large S.A
What is used to classify severuty of Sx in HF
New york Heart classification 1. Asymptomatic 2. Slight limitation Comfortable at rest 3. Marked limitations Limiting dyspnoea 4. Dyspnoea present at rest Activtiy leads to discomfort
HF investigations
Bloods:
- Brain natriuretic peptide
Levels correlate with severity
- FBC/LFT/U+E/TFTs
ECG
- Shows underlying causes
- Ischaemia
- LV hypertrophy
- Arrhythmias
If BNP + ECG abnormal –> Echo
Echo - TTE
- Assess cardiac chamber dimensions
- Valvular disease
- Wall abnormalities
CXR
Changes in CXR for HF
A - Alveolar oedema B - Kerley B- lines C - Cardiomegaly D - Dilated upper lobe vessels E - Pleural effusion
HF management
- Lifestyle
Education Loose weight Stop smoking Decrease Alcohol Diet
HF Management Notes
Avoid exacerbating factors eg: Verapamil/ NSAIDs
Tx exacerbating factors
eg: Infection/ Anaemia
Annual flu and one off Pneumococcal vax
Acute HF tx
- 100% O2
- Nitrates - GTN
- IV opiates - Diamorphine
- IV furosemide (fluid overload)
- Consider inotropic drugs
Chronic HF tx
A - ACEi/ARB B- Betal blocker A - Aldosterone antagonist (Spirinolactone) If A + B don't control sx L - Lood diuretics Digoxin
Consider CCB - Amlodopine fro vasodialtion
HF RF
- Age>65
- African desecent
- Previous MI
- Obesity
- Men of Lack of protective effect from oestrogen resulting in early onset IHD
Why does HTN lead to HF
- Increase arterial pressure
- harder to pump in to HTN system
- L.V hypertrophy
- Increase O2 demand and decreased supply from C.A
- Weaker contractions
- Systolic failure
Why does dilated cardiomyopathy lead to HF
- Chmaber grows to increase increase preload
- Increase contraction and strength via FSM
- Overtime muscles get thin and weak
- Systolic failure
How do:
- Aortic stenosis, HTN and hypertrophic cariomyopathy lead to HF
- Concentric myocyte hypertophy
- Muscle crowds in to chamber doom
- Diastolic failure
How does restrictive cariomyopathy lead to HF
- Muscle stiffer and less compliant
- Cant’t fill and stretch
- Diastolic failure
How does IHD lead to HF
C.A atherosclerosis
MI
What is Cor pulmonale
Right sided HF caused by rep disease
Cor pulmonale causes
- COPD
- PE
- CF
- Interstitial lung disease
Cor pulmonale patho
Diseased lung leads to hypoxia
- Hypoxic pulmonary vasoconstriciton
- Increase pulmonary B.P
- Harder for R.V to pump in against
- Hypertrophy and failure
Acute HF
New onset/ Decompensated chronic HF
Charecterised by pulmonary and/or peripheral oedema without signs of peripheral hypoperfusion
Chronic HF
Devlops slowly
Venous congestion is common
Arterial pressure maintained until late
HTN diagnostic BP
Clinic = 140/90
Ambulatory BP = 135/85
HTN - Primary
Essential HTN - Unknown cause - Multifactoral genetic susceptibility obesity sedentary lifestyle old age
HTN - Secondary
R - Renal disease
CKD - DM nephropathy
Renal artery stenosis
Glomerulonephritis
O - Obesity
P - Pregnancy induced HTN
E - Endocrine
- Conn’s syndome
- Cushings syndrome - Hypersecretion of corticosteroids enhances vasoconstrictive effects of adrenaline
- Phaemochromocytoma
Aorta coarctation
Drugs assosciated with HTN
Coricosteroids - Prednisolone EPO Alcohol Ecstacy Cocaine Contraceptive pill (Oestrogen) NSAIDs Vasopressin
HTN RF
Age Male DM Afro-carribean Obeaity Alcohol High salt diet Fam hx
HTN Complications
IHD
HF
Stroke
Haemorrhage
HTN CP
Headache
Visual disturbances
Usually asymptomatic apart from malignant HTN
Signs:
Bilaterral retinal haemorrhages and exudates
Papilloedema
HF main causes (3)
IHD
Dilated CM
HTN
HTN Histological changes and untreated results
Fibrinoid necrosis of the vessel wall in untreated results in end organ damage
Renal - Haematuria/Proteinuria/Progressive Kidney disease
Brain -
Cerebral oedema/Haamorrhage
Retina -
Cotton wool spots/ hard exudates/papilloedema
CV
HF/Aortic dissection
Diagnosing HTN
*Pt has BP >140/90
*Offer ABPM
Calculate Qrisk2 and look for end organ damage
- Fundoscopy - haemorrhage
- Urinalysis - Protein/blood
- Blood tests - eGFR
*ABPM <135/85 NO tx
* ABPM >135/85
tx if Qrisk2>20% or EOD
*ABPM >150/95
TX
When should you always treat HTN
If there is end organ damage
Tests for EOD
Urine analysis *A:C - Proteinuria *Dipstick - Haematuria ECG/Echo - LV hypertophy Fundoscopy Bloods - HbA1c/eGFR/Lipids
Stage 1 HTN
Clinic = >140/90
Ambulatory = >135/85
Stage 2 HTN
Clinic > 160/100
Ambulatory >150/95
Stage 3 HTN
BP > 180/110
Immediate ant-HTN tx
BP equation
CO X TPR
HTN Tx
- Lifestyle
Reduce alcohol reduce salt intake Excercise Loose weight Smoking cessation - CVD risk
HTN tx
- Additional pharamacological tx
Statins - Reduce CVD risk
Optomise glycaemic control in pts with DM HbA1c<53mmol/mol
HTN Tx pathway
<55y/o –> HIGH renin
>55y/o or Black –> LOW renin
A - ACEi
B-ARB
C - CCB
D - Diuretics
Add:
Spirinolacone
Alpha-blocker - hydralazine
Beta-blocker
HTN treatment targets
Under 80 BP<140/90
Over 80 BP <150/90
Common causes of chest pain
Angina
ACS
Pericarditis - Sharp pain aggrevated by movement, respiration and changes in posture
Aortic dissection - Severe chest pain radiating to back
GORD - Exacerbated by lying down
MSK - tender to palpate over affected areas
PE - dyspnoea/ Tachycardia/ Hypotension
What is Bradycardia
Slow HR <60bpm
What is tachycardia
Fast HR>100bpm
Sinus arrhythmia
- Results from fluctuations in autonomic tone
Inspiration –> fall in PNS tone and HR quickens
Expiration –> HR falls
Children and YA
Predictable changes in HR
Sinus bradycardia
- When is it normal
- Extrinsic causes
- Intrinsic causes
- Sleep and athletes
- Extrinsic
Beta- blockers
Anti- arrhythmic drugs
Hypothyroidism - Intrinsic
MI –> Acute ischaemia of SAN
Sever symptomatic bradycardia tx
Atropine
Heart Block common causes
CAD
Cardiomyopathy
Fibrosis of conducting tissue
Heart Block - AVN
- First degree
- Delayed AV conduction
- Every atrial impulse leads to ventricular contraction
- Long PR interval (>0.2secs)
Hear block - AVN
- Second degree
Some atrial impulses do not make it through AVN to ventricles
- Mobitz type 1
- Mobitz type 2
HB - Mobitz type 1
- Defenition
- Causes
Wenckebach phenomenon
- Longer-longer- longer- drop
- Progressive PR interval elongation until beat is dropped and impulse fails to move through to ventriles
- Absent QRS complexes
Causes:
- AVN Blocking drugs
- Inferior MI
Mobitz type 2
- defenition
- causes
- risks
- Tx
- QRS compexes dropped without PR interval prolongation
- Specified ratio (Pwaves:QRS)
Causes:
- Inferior infarction
Risk:
Asystole
tx-
Pacemaker
3rd degree HB
- defenition
- risks
- P waves completely independent of QRS complexes
- Ventricular contractions maintaind by escape rhythms
- Risk of asystole
Causes:
HTN
Endocarditis
IHD –> MI
Aropine
- MOA
- Indications
- S/E
- Inhibits PNS
- Mobitx type 2
- Complete HB
S/E
- Pupil dilatation
- Urinary retention
- Dry eyes
- Constipation
RBBB
- Causes
- ECG findings
- Oscultation
RBB no longer conducts
Late activation of R.V
Causes:
- healthy individuals
- PE
- R.V Hypertrophy
- IHD
- Congenital HD (Fallot’s)
MaRRoW
- M - QRS - V1
- W - QRS - V6
Splitting of S2
LBBB
- causes
- ECG findings
Late activation of L.V
Abnormal Q waves
Causes:
- Aortic stenosis
- HTN
- Cardiac surgery
WiLLiaM
W - QRS - V1
M - QRS - V6
Sinus tachycardia
- Excercise
- Excitement
- Fever
- Pain
- Anaemia
- HF
Narrow comlex tachy
QRS <120ms
- A.Fibrillation
- A.Flutter
- SVT
Broad complex tachy
QRS >120ms
- VT
What is AVNRT
- ECG
AV nodal re-entrant tachycardia
- Fast HR caused by electrical signals that loop back on themselves
- Narrow complex tachycardia
- Self perpetuating electrical loop where the re-entry point is back through the SAN
ECG:
- QRS –> T-wave–>QRS
- No Pwave visible as Atria and ventricles recieve impulses at the same time
What is AVRT
AV re-entrant tachycardia
- Re-entrant loop via accessory pathway
Wolff - parkinson white syndrome
- Incomplete atria and ventrical separation during development
Wolff - Parkinson white syndrome
- defenition
- bundle name
- ECG chnages
- CP
- Tx
- Accessory electrical pathway connecting atria and venticles
- Bundle of Kent
ECG
- Short PR interval
- Wide QRS complex
- Delta wave
-CP Palpitations dizziness syncope dyspnoea
SVT Tx
- Vagal manoevers
- carotis massage
- Valsalva manoevere
- Breath hold - Adenosine
complete HB for 1/4sec - Direct current cardioversion
WPWS Tx
Radiofrequency catheter ablation of accessory pathway
Adeosine
- CI
Slows cardiac conduction through AVN
Resets sinus rhythm
- brief asystole
CI
- HB
- COPD
- HF
Shockable heart rhythms
VT
VF
Ventricular fibrillation
- Defenition
- ECG
- Tx
- Rapid and irregular ventricular activation with no mechanical effect –> NO CO
- Pt is pulseless, unconscious and resp stops –> C.A
- Usually caused by ventricular ectopic beats
ECG:
- Shapeless rapid oscillations
- No organised complexes
Tx:
- Electrical defib
- Cardioverter - defibrillators
AF
- Defenition
- Causes
Chaotic irregular atrial rhythm - 300-600bpm
Intermitent response from AVN so irregular ventricular rate
Sepsis Mitral stenosis IHD Thyrotoxicosis HTN
Risk of AF
Embolic stroke
AF CP
Sx
- chest pain
- palpitations
- dyspnoea
- faintness
Signs
- irregular pulse
- No p waves on ECG
- Rapid irregular QRS rhythm
AF DD
Atrial flutter
Ventricualr ectopics
AF Dx
ECG
- No p waves
- rapid irregular QRS complexes
AF TX
Acute - alcohol toxivity/chest infection
tx provoking cause
- Cardioversion
- LMWH - Enoxaparin - thromboembolism
- Cadioversion fails –> Anti-arrhthmic - Amioderone
What are most patients with AF usually on
warfarin
What is used to calculate the risk of stroke therfore the need for anti-coag
CHA2-DS2-VASc Score C - CCF H - A2 - Age >75 D - DM S2 - Stroke V - Vascular disease A - Age (65-74) Sc - - Female
1 = consider asprin or anticoag 2 = oral anti-coag required
Atrial flutter
- Definition
- causes
Abnormal but organised atrial rhythm
250-350bpm
Idiopathic HTN HF Pericarditis COPD Obesity CHD
Atrial flutter CP
Palpitations chest pain dizziness syncope fatigure breathlessness
Atrial flutter Dx
saw-tooth like atrial flutter waves - F waves
- if not visiable –> carotid sinus massage
Atrial flutter
- radiofrequency catheter ablation
- IV Amioderone - sinus rhythm
- B-blocker - suppresses arrhthmias
Aneurysm defenition
permanent dilation of artery 2x normal diameter
Aneurysm
Symmetrical
Asymetrical
- Fusiform
- Saccular
True aneurysm
- dilations involving all 3 layers of arterial wall Aorta - A + T Iliac popliteal femoral
False aneurysm
hole in B.V allows leakage
blood collects in adventitia
surrounding tissue acts as wall
Where do most aneurysms occur specifically
40% - T
60% - A
* below branching of renal artery but above aortic birfucation
- less elastine so weaker
AAA RF
HTN Familh hx smoking male trauma hyperlipidaemia Male atherosclerotic damage
AAA CP
unruptured - no sx
- pain: abdo/back/loin
- pulsatile abdo swelling
ruptured
- abdo pain
- pulsatile abdomen
- collapse
- tachy
- hypotension
AAA DD
GI bleed
ischaemic bowel
perforated ulcer
appendicits
AAA Dx
- US
- CT/MRI
AAA Tx
RF-
smoking cessation
BP control
Statind
small <5.5cm - monitered
open surgical repair
Endovascular stenting
TAA
- Ascending
- descending
- Marfans/ HTN
- secondary to atherosclerosis
TAA CP
asymptomatic
- chest pain
- aortic regurgitation
- compression of local structures –> IVC
- Cardiac tamponade
TAA Dx
- Transoesophageal echocariography
- US
- CT/MRI
Aortic dissection defenition
- Tear of tunica intima
- blood flows between layers of aorta wall increasing diameter of vessel
- collects in false lumen
AD causes + RF
HTN Stress Pregnancy - increase B.V coarctation of aorta Aneuryrsm Trauma - shearing forces
RF:
Ehlers danlos
Marfans
AD CP
- Tearing chest pain
- pain radiates to back and arms
- HTN
- Hypotension
- shock
- absent peripheral pulses
AD DD
MI ACS Aortic regurgitation MSK pain Pericarditis
AD Diagnosis
CXR - widened mediastinum
CT scan
Transoesophageal echo
MRI
What law is applied to aortic dissections
Laplaces law
- increase diameter
- increase tension
Aortic aneurysm complications
- Aortic insufficiency
pulls on valve as it dilates
blood flows back to ventricles during diastole - high pitched cough
LRL nerve stretched - Blood clots
blood polls in extra lumen space - Headache + can’t flex neck fowards
bleeding into SA space
increases pressure
irritates meninges
Aortic Dissection tx
- analgesia - morphine
- resuscitation
- surgery
replace arch
surgical stenting - control HTN - B-blockers
- GTN
What is peripheral vascular disease
Partial blockage of peripheral vessels by an atherosclerotic plaque resulting in insuffecient perfusion of lower limb
Peripheral vascular disease RF
Smoking obesity HTN DM Sedentary lifestyle High cholesterol
Peripheral vascular disease symptoms
Pain Pallour Perishingly cold Pulseless Paralysis Parasthesia
Pericardium function
Promotes cardiac efficiancy
- limited dilation
Aids atrial filling
- creates a closed chamber
- Decrease external friction
Anatomically fixes heart to sternum and diaphragm
Acute pericarditis aetiology
- Infectious
- non infectious
- Infectious
Viral - coxsackie viruses
- EBV / HIV/ Mumps
bacterial
- Mycobacterium TB
Fungal
- Histoplasa spp –> immunocompromised
- Non infectious
- Rhemuatoid arthiritis
- Uraemia
Acute pericarditis clinical presentation
Fever chest pain - worse with deep breathing - relieved by sitting and leaning foward Hiccups pericardial friction rub - auscalltation tachycardia pain radiates to arm - trapezius ridge
Acute pericarditis DD
Pneumonia angina MI Aortic dissection Pneumothorax
Acute pericarditis diagnosis
- ECG
saddle shaped ST elevation –> ALL leads
PR segment depression
-CXR
rule out effucion (>300ml to be detectable)
Acute pericarditis tx
- NSAIDs
- Colchicine –> 3m course
S/E - Nausea and diarrhoea
How does pericardial effusion lead to tamponade
large volume of fluid collects in pericardial sac
ventricullar filling compramised so decrease in CO
Cardiac tamponade
Pericardial effusion presentation
chest pain dyspnoea muffled heart sounds compression of local structures - Hiccough - phrenic nerve - spasm of diaphragm - nausea - diaphragm
cardiac tamponade presentation
increase pulse decrease BP Increase JVP Kussmauls sign Pulsus paradoxus - large decreases S.V and Systolic BP during inspiration
Pericardial effusion diagnosis
CXR - large globular heart
ECG - low voltage QRS complex
Electrical alternans - Diff heights QRS complexes
Echo - echo free zone
Cardiac tamponade diagnosis
CXR - Big globular heart ECG - Low voltage QRS Electrical altercans Echo - Echo free zone Diastolic collapse - R.A/R.V Bck's triad - Falling BP Rising JVP Muffled heart sounds
Pericardial effusion tx
analgesia
pericardiocentisis –> Send fluid for culture
- ZN stain/ TB culture / Cytology
constrictive pericarditis presentation
Kussmauls sign right HF signs Ascites Oedema Diffuse apex beat
Constrictive pericarditis diangosis
CXR - small heart + calcification
ECG - low voltage QRS
Echo - small ventricular cavaties with normal wall thickness
CT/MRI - distinguish from restrictive CM
Where does infective endocarditis occur (3)
- valves with congenital/aquired defects
RS endocarditis more common in IVDU - Normal valves with virulent organisms
- Prosthetic valves/ pacemakers
Which organism most commonly causes infective endocarditis and descibe it
Viridans streptococci Gram +ve alpha haemolytic optochin resistant low virulence
Where is viridans step found and what type of valves are at risk
found in mouth
attacks previously damaged valves
Where is S.aureus found and which groups of people are at risk from infective endocarditis caused by it
Skin
IVDU
diabetic
surgery
Attacks healthy or previously damaged valves (Tricuspid)
S. epidermidis
- valves
- route of entry
- Prosthetic
- Valve surgery/ IV catheter - HOSPITAL
RF for infective endocarditis
IVDU Poor dental hygeine Dental treatement Prosthetic valve Pacemaker Cardiac surgery congenital heart defects
Infective endocarditis presentation
systemic features of infection
- malaise
- fever
- night sweats
- weight loss
Signs:
- Spliter haemorrhage (Septic emboli deposit)
- Janeway lesions
- Oslers nodes - fingers and toes
- Roth spots - eyes
- Glomerulonephritis
- Arrhythmias
- HF
- PE/Stroke/MI
- Murmur - turbulent flow past damged valve
what presentation of a pt requires infective endocarditis ruling out
Heart murmur and fever
Infective endocarditis diagnosis
Blood cultures - 3 from 3 different sites
- take before Abx
Blood test -
High ESR and CRP
Neutrophilia
Echo - Transoesophageal
ECG -
Long PR intervals
Infective endocarditis initial tx
Presuming not staph
- Benzylpenicillin + Gentamycin
Criteria for infective endocarditis diagnosis
Duke’s classification
Tx for suspected staphylococcus infective endocarditis
Vancomycin swapped for penicillin
Infective endocarditis preventions
- Abx prophylaxis to high risk groups before procedure
Prosthetic valves
Hx of transpalnt
Hx of IE - Good oral health
- Inform pts of IE sx
Aortic valve ausculltation
2nd intercostal space - Right sternal edge
Aortic stenosis aetiology
- Ageing - Degeneration and calcification of normal valve
- Congenital - Clacification of congenital bicuspid valve
- Rheumatic heart disease - scar tissue formation
Aortic stenosis patho
narrowing of valve = obstructed L.V emptying
Increase pressure gradient between aorta and L.V resulting in increased afterload
Increase L.V pressure
Compensatory L.V hypertrophy
- Increased myocardial demand
- relative ischaemia –> Angina / Arrhythmia
Aortic stenosis presentation
Angina
Syncope - exertional
HF
Signs:
- Dizziness
- Decrease carotid pulse - SLOW RISING
- Decrease intensity of 2nd heart sound
- Murmur
Aortic stenosis diagnosis
- Echo - diagnostic
L.V hypertorphy - CXR
- Calcified aortic valve
- L.V hypertrophy - ECG
- L.V hypertrophy
- Depressed ST Segments
Aortic stenosis tx
- Trancutaneous aortic valve implantation - cracks calcification
- Aortic valve replacement
Infective endocarditis prophylaxis
Aortic regurg aetiology
Rheumatic fever
IE
Bicuspid aortic valve
Aortic regug presentation
exertional dyspnoea
palpitations
angina
Signs: collapsing pulse wide pulse pressure Ascites displacement of apex beat
Aortic regurg diagnosis
CXR -
enlarged cardiac silouhette
Aortic root enlargement
ECG -
L.V hypertrophy - tall R waves
Inverted t waves
Echo
Mitral regurg aetiology
- mitral valve prolapse
- papillary muscle damage - post MI
- IE
- LSHF
- Rheumatic fever
Mitral regurg presentation
Exerional dyspnoea
fatigue
palpitations
signs:
AF
Apex beat displaced laterally
Soft S1
Mitral regug diagnosis
- ECG - Severe MR
AF
LV hypetrophy + LA enlargement - CXR - LA enlargement
- Transoesophageal echo
Mitral regurg tx
Mild - serial echos
Meds:
ACEi
B- blockers - HR control for AF
Diuretics for overload
Mitral valve stenosis aetiology
- rheumatic fever
- commisural fission - IE
- Mitral annular calcification
- elderly
- end stage renal disease
Mitral stenosis presentation
Progressive dyspnoea
- pulmonary HTN + Congestion
- worse with excercise/pregnancy
Dysphagia and hoarse voice
- pressure on local structures
Fatigue
chest pain
palpitations
Mitral stenosis signs
Malar flush
Low volume pulse
S1 - loud snap
RSHF
- Increae JVP
- Ascites
- Peipheral oedema
Mitral stenosis diagnosis
ECG:
- LA enlargement - Bifid P wave
- AF
CXR
- LA enlargement
- Pulmonary congestion
ECHO - GOLD
why is lidocaine effective in VT tx
Blocks inactivation gate of the sodium channel