Cardiovascular Flashcards
which ECG leads do you look at for atria
I
II
AVR
what does rigth atrial enlargement look like on an ecg
Tall p, pointed p in the limb leads
Don’t sit on a pulmonary problem, its pointy!
what does left atreial enlargement look like on an ECG
Notched/m shaped p wave in limb leads
M for mitral in the left side
what is Wolf-Parkinson-White Syndrome and how is it identified on an ECG
Short PR interval - (accessory pathway bundle of Kent is working so its conducting too quickly)
how is a first degree heart block shown on an ECG
Long PR
what are the three criteria for left ventricular hypertrophy
Sokolow and Lyon Criteria:
(S in V1) + (R in V5 or V6) > 35mm
Cornell criteria:
S in V3 + R in AVL > 28 in men or 20 in women
Modified Cornell:
R in AVL>12
how long should the PR interval be
120-200ms
how wide should teh QRS be
no wider than 110ms (3 small squares)
on whihc leads should teh QRS always be upright
I and II
in whihc lead are all waves negative
AVR
how do the chest leads change and what are teh best at looking at
QRS complex
* R wave increases in size from V1-V4, S wave grows from V1 to 3 and is absent in V6
what should teh ST segment look like in the leads
ST segment is isoelectric in all leads except V1 and V2 where it may be slightly raised (very raised is bad)
in which leads should the p and t wave be upright in
I II V2-V6
what is teh rule for q waves in i, ii, V2-V6
There should be no Q short waves larger than 0,04s in I, II, V2-V6
how many ms is a big and a small box worth on an ecg
big - 0.2ms
small - 0.004 ms
how to remeber whihc colour of elecrode goes to which limb
snow on grass, smoke on fire (remember white is right)
how do you meausre rhythem on an ECG
meausre teh distance between teh Rs
how do you measure the heart rate on an ECG
300/number of boxes between each R
which leads looks at the inferior section of the heart
II
III
AVF
whihc leads looks at the lateral section of teh heart
I
AVL
V5
V6
which leads look at the septal portion of the heart
V1
V2
which leads look at the anterior portion of the heart
V1
V2
V3
V4
how do you work out the heart rate on an ecg, gor both methods
300/1500 method:
this si or regular rhythems
count teh number of big boxes between two QRS complexes and then do 300 divided by this number.
Or cound te small boxes and then do 1500 divided by this number.
10 second rule:
for irrculagr rhythems, you need to cound teh number of qrs complexes on each sheet, as its a 10 second peicie, multiply it by 6 and this gets a pulse.
how much is a big square and a small square worth on an ECG
small - 0.04
big - 0.2
how does one work out the heart axis
looks at lead 1 and avf QRS complex
they should be both positive whihc means its in teh normal range
If lead 1 is negative it might mean that there is a a right axis deviation
if lead avf is negative then it is left deviated
what is the normla heart axis
-30 to +90
what is teh 10 step process to reading an ECG
PS really randy alligators play quickly, sex quickly too.
Patient details
Situation details
Rate
Rhthm
Axis
P-wave and P-R interval
Q-wave and QRS complex
ST segment
QT interval
T-wave
what are the infections caues of pericarditis
- Virus - enterovirusl adenovirus, herpesvirus, parovirus
Bacteria - mycobacterium tuberculosis
what are the most common non infections causes of pericarditisq
NEOPLASTIC - secondary metastatic tumours
automimmne conditions - rheumatoid arthiritus, sjogren syndrome
metabolic - ureamia, myoxedema
trauma and iantrogenic - penatrating injury, radiation injury, postmyocardial infarction syndrome,
other - aortic dissection or chronic heart faliure
what are the three most commen causes of pericarditus
Virusus
Neoplasms
Iantrogenic form stents and surgery
what is a key feature of pericarditis
pain is worse when lying doen and better when sat sitting forewards
what is pulses paridoxis
- Pulsus paridoxis - an exagerated drop in blood pressure during inspiration
what is pericardial effusion
Pericardial effusion - A condition in which extra fluid collects between the heart and the pericardium
what are teh people who ace inhibitors shouldnt be given to, and who are teh people beta blocker cant be given to
ace - prgnant ladies
beta - severe asthma
what is teh main side effect of ace inhibitors
dry cough
what does an incrased PR interval mean
a heart block
what does a saw tooth pattern mean on an ECG
atrial flutter
what are teh 4 types of Angina
Stable - induced by effort such as exercise
Unstable - increased severity, it occurs at rest as well
Decubitus - occurs when lying down
Nocturnal - occurs when asleep and may wake people up
wht is vasospastic angina
Vasospastic angina is also known as prinzmetal angina, variant angina or coronary artery spasm. It develops when a coronary artery supplying blood and oxygen to your heart goes into spasm and suddenly narrows.
what are teh risk factors for angina
Smoking, obesity, exercise, diet, alcohol intake sedentary lifestyle.
Hypertension, diabeties , hypercholesteremia, depression
Age, family history , gender, ethnicity
Stress, low social interaction
pathophysioology of angina
An imbalance between the supply of oxygen to cardiac muscle and the demand
Athelerocscalorsis causes a narrowing of the coronary arteries which cuases ischemia and pain. The plaque gets bigger and bigger and once its 50% of the lumen size it cant compensate anymore, this leads to remodelling and thee vessle becoming narrowing.
Thjis then imposes inot the lumen and runs the risk of hemmoraging
At first a fatty streak forms, which leads to macrophages forming foam cells, and the smooth muscle grows over eth top of the fat.
The consequences of this are occluiion du to thrombus, chronic narrowing of the vessles, aneuyerism changes
what are teh signs of angina
Chets pain comes on and is reslolved by rest or GTN spray
Exasubated by cold, anger and excitement
This can be scored by
Central tight chest pain radiating to arms, neck and jaw
Precipitated by exertion
Relieved by rest or GTN spray
3/3 – typical angina
2/3 – atypical angina
1/3 – non-anginal pain
what are teh symptoms of angina
Pain in chest, arms, neck and jaw.
Dyspnoa - shortness of beath
Palpitations
Syncope - fainting
differential diagnosis for angina
Pericarditis, pulmonary embolism, chest infection, GORD< dissection of the aorta
what are teh zero to finals reatments for angina -
- There are three principles ror manageent - imiediate ef, long term relief and then secindary orevention of CV duiseases.
- Immediate - use GTN spray, if there is still pain after 5 mins take again, if there us still pain after 5 mins call an ambulance
- Long term - beta blocker tor calcium channel blocker
- Secondary prevention - asprin, atorvastain, ACE inhibitors, beta bloker
- RAMP managemeeeeeshould also be used. R- refer to cardiolgy, advise them about the diagnosis manegement and when to call an ambulance, medical treatmentm procedural/surgical interventions.
what are the drug treatment for angina
Treat underlying conditions such as hypertension and diabeties mellitus
Glyceryl trinitate spray - 1st line treatmen which is taken when needed to relive pain
Beta blockers - (bisoprosol, propanalol) reduce the heart rate and the force of contractipn, its negitivly ionotrophic and chronotropic . DON’T use in pateints with asthma or a heart block
Calcium channel blocker - amlodapine,
Anti platelet - asprin inhibits platelet aggregation, by inhibiting COX. Clopidogrel can also be used.
Statins - reduce cholesterol levels, atorvastatin, simvastatin.
ACE inhibitors - for blood pressure controll such as ramapril
Ivabradine - ibibits the pacemaker current in the SAN and therefore reduced heart rate and decreased blood pressure
what are the social traeatments for angina
Work out the Qrisk, this takes into account BP, age, smoking status, cholesterol, rhemuatid arthiritus, diabetes mellitus, BMI
Weigth loss, quit smoking, more exercise
what are teh surgical treatments for angina
Percutaneous cononary intervention - stentin or balooning of the artery, however this runs the risk of restenosis. Drug eluting stents slowly release medication t oprevent blood clots.
Coronary artery bypass graft - good preognosis but longer recovery
what are the three acute coronary syndromes
Unstable angina - cardiac chest pain with a creshendo pattern
STEMI - a major occlusion of a coronary arterym full thickness muscle damage,
Diagnosed by ECG at resintation
NSTEMI - occurs by developing a complete occlusion of a minor coronary artery or partial occlusion of a major coronary artery previously affected by atherosclerosis
what is teh pathophysiology of acute coronary syndromes
Rupture or erosion of fibrous cap of a coronary plaque with subsequent formation of a platelet rich clot, inflammation, and vasoconstriction produced by platelet release of serotonin and thromboxane A2
Unstable angina differs from NSTEMI because in NSTEMIs the occluding thrombus is sufficant to cause myocardial damage and an elevation in serum markers of myocardia injury (troponin and creatine kinase)
The main causes if the rupture of atherosclerotic plaque, and consequent arterial thrombosis. The more uncommon causes of it care coronary vasospasm, drug abuse, dissection of coronary artery.
what are teh tests for acute coronary syndromes
ECG:
UNSTABLE ANGINA - there is a normal one or slight T depression
STEMI - ST elevation and tall T waves, will produce pathological Q waves sometime after an MI
LEFT BRANCH BUNDLE BLOCK. Remember WilliaM - V1 is W and then M is for V6
NSTEMI - a retrospective diagnosis - will see ST depression and/or T wave inversion
Ischemia - ST depression, T wave flattening or inversion
Q waves - evidence of previous infarction, pathological Q waves are wider than normal, >35% QRS hight and wider than one small square) the larger the infarction is the more likely it will result in a pathological Q.
what are the tests for unstable angina
History
FBC – anaemia aggravates it
Cardiac enzymes (troponin normal) – excludes infarction
ECG – ST depression when patient is in pain
CT Coronary angiography
Risk assessment (QRISK2) – if low risk do an elective stress test
what are the 9 treatment catogorys for unstable angina
Risk Factor modification
Stop smoking
Lose weight
Healthy diet
Exercise
PCI (if risk assessment score is medium/high) and CABG
Aspirin (300mg initially then 75mg daily) – irreversibly inhibits COX-1 🡪 less production of thromboxane A2 🡪 less platelet aggregation
Anti-coagulants – Heparin interferes with thrombus formation at site of plaque rupture by inhibiting factors II (prothrombin), VII, IX and X and reduces risk of ischaemic events and death
Fondaparinux (synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin
Nitrates – GTN spray or IV infusion
Beta blockers – metoprolol, bisoprolol
Statins – Reduce cholesterol e.g. atorvastatin, simvastatin
ACE inhibitors - Ramipril
Calcium channel blockers (if beta blocker contraindicated) – amlodipin
what are the three cardiac enzymes to test for
TROPONIN T and I, highly sensitive to cardiac muscle injury. It will show a rise within 3-12 hours, peak at 24-48 hours. Normal troponin rules out MI.
CREATINE KINASE- catalyses the conversion of creatine ad it will rise and can be used to determine reinfarction
MYOGLOBIN - cardiac enzymes which rises when heart damaged
what are teh complications of acute coronary syndromes
DARTH VADER
Death
Arrhythmias
Ruptured septum
Tamponade
HF
Valve disease
Aneurism of ventricle
Dressler’s syndrome - pericarditis and effusing after 2-12 weeks
Embolism
Reoccurrence of ACS
define MI
Necrosis of cardiac tissue due to prolonged myocardial ischemia due to complete occlusion of an artery by a thrombus
MI risk factors
Age, make, history of coronry heart diseas, DM, hypertension, hyperlipidemia, family history
MI pathophysiology
Due to the rupture of an atherlosclarotic plaque which leads to a clot formation in one of the arteries
Rupture - thrombus - occlusion of artery - myocardial cell death
MI key presintations on an ECG
STEMI - ST elevation, Tall T waves, pathological Q waves
NSTEMI - ST depression and t wave inversion
MI signs
Longer than 20 mins, not relieved by GTN spray, pain may radiate to the left arm, pulse and blood pressure may vary, patient is gray and sweaty, 4th heat sound
MI symptoms
chest pain, sweating, dysponea, fatuigue, nausea, vomiting
MI tests
History, ECG
STEMI - ST elevation and tall T waves
NSTEMI - ST depression and T inversion
Cardiac enzymer - Troponin T, creatine Kinase, myoglobin
CT angiogra,
FBC, U&E
Blood glucose and lipid level
MI diffrentai diagnossi
Angina, pericarditis, endocarditis, pulmonary embolism, pneumothorax, aortic aneurism
actute and secondary manegement for MI
Acute management:
MONA - Morphine, oxygenine if low sats, nitrates, Asprin
12 lead ECH and cardiac moniter
Beta blocker for IV, contraindicated in hypotension, HF, bradycardia and asthma
Referral to PCI
Thrombolysis - alteplase
Secondary:
Modification of risk factors
75mg asprin daily
Clopidogrel, ticagrelor
Statins
Beta blocker, ace inhibitor or calcium chanel blocker
Return to work after 2 months if suitable to, and take it easy!
complications of MI
MAPDUM
Myocardial rupture
Arrhythmia
Pericarditus
Dresslers syndrope
Unalive
Mitral incompetance
causes of heart disease
schaemic heart disease, hypertension, cardiomyopathy, valvular heart disease, congenital heart disease, alcohol and chemotherapy, arrhythmias anaemia, pregnancy, obesity, hyperthyroidism.
risk factros for heart diease
Age, obesity, male, previous MI.
explain systolic and diatlic heart faliure
- Systolic - faloure to contract, ejectio fraciton in less than 40%
This is cause by MI, HTN,IHD, cardiomyopathy (walls are wrong)- Diastolic - inibility to relax and fill- because tehre is reduced preload and the ejaction fraction is greater the 50%
Caused by constrictve pericaritis, cardiac tamponade, hypertension
- Diastolic - inibility to relax and fill- because tehre is reduced preload and the ejaction fraction is greater the 50%
explain low output and high output heart faliure
Low output heart faliure is cuased by pump faliure, excessive preload, chonic ncreased afterload
High output HF - anaemia, pregnancy, hyperthyroidism
what are teh compensatory mechanisms of heart faliure
- SYMPATHETIC STIMULATION - increased HR and contractility, increasing the preload, incrases afterload which causes redcued CO eventually
- RAAS - fall in CO leads to diminished renal perfusion, activation of RAAS, increased salt and water retention which leads to oedema
- Angiotensin II causes arteriolar constriction leading ot increased after load
- VENTRICLAR DILATION - the ventricles become stretched due o the increased preload, but too much and so they cant pump as effectivly
- MYOCYTE HYPERTROPHY
what are teh pathologys caused by teh compnsatory mechanisms of heart faliure
- Increased preload - faliure of the heart leading to more blood being left behind which stretched the myocyted more
- Increased afterload
- Salt and water retention, this increases the afterload
- Myocardial remodelling - due to myocyte damage and increased interstitial fibrosis
what are teh 3 cardina signs of heart faliure
- Dyspnea
- Fatigue
Ankle swelling
- Fatigue
what are teh chest xray signs of heart faliure
A- alveolar oedema (bats wings in the gaps)
B Kereley B lines
C-Cephalisation of the blood vessles
D - dilated upper lobe vessles
E - pleural eflusions
what are teh 4 test to be doen for heart faliure
ECG - may show underlying causes such as arrhythmias, hypertrophy and hypertension
Bloods - BNP - brain natriutc peptide maybe be secreted by the ventricles when in stress
Cardiac enzymes - Toponin T, creatine Kinase, myoglobulin
CXR
heart faliure treatment
ifestyle factors
Ace inhibitors
Beta blockers
Diuretics
Ventricular assistance device
Surgery heart transplant
If it is an acue condition give 100% oxygen and nitrate spray as well, and some IV opiates
Fr chronic treat in the same maonor as other hyoertensives, ABCD method
what are 4 acyte heart faliure causes
- Hypertension
- Acute pulmoar oedema
- Cardiogenic shoc
Septic shock
causes of lft heart faliure
IHD
HTN
Cardiomyopathy (dilated where the chamber grows and wall thins, or restrictive where the heart become stiff)
Aortic Stenosis (narrowing of the aortic valve)
symptoms of left heart faliure
Exertianly dyspnoea
Fatuigue
Weight loss
Notcurnal cough
Dysnpena when lying down
signs of left heart faliure
Cardiomegaly
Pulmonar oedema
3rd and 4th heart sounds
Pleural effusion
Tachycardia
right sided hear faliure causes
- Left ventricular fliure - it cuases a fluid bulid up in the lungs
- HTN
- Pulmonary stenosis
- Lung disease (cor pulmonale) there is increased pressure in the lungs which means its harder to pump the blood into
AV shunt -
right heart faliure syptoms
- Dyspnoea
- Peripheral oedema
- Ascites (fluid build-up in the abdomen)
- Nausea
Anorexia
right heart faliure signs
- Raised JVP
- Hepatomegaly
- Pitting oedema
Fluid weight gain
Aortic aneurism defornition
Permanent localised dilation of an artery to 1.5 - 2x the normal diameter
Aortic aneurism causes
Trauma
Atheroma
Connectives tissue disorder - Marfans (fibrillin 1 is affected), Ehlers Danols syndrome - collagen
Aortic aneurism risk factors
Smoking, family history, age, male, HTN, trauma, COPD, Hypercholesteremia
Aortic aneurism pathophysiology
- It affects all three layers, and has a saccular r fusiform shape
- Most common arteries: aorta, iliac, popliteal, femoral, thoracic
Fake aneurisms are where blood collects under the adventia (outer layer) and happens after trauma
Aortic aneurism symptoms
sually asymptomatic and picked u[ on a scan
Sometimes there is pain due to pressure on other structures
Aortic aneurism signs
Pulsile abdominal swelling
Expansile aorta epigastic pain and hypovoleamic shock
Hypotension
Collapse
Aortic aneurism tests
CT or MRI angiogram
Abdominal ultrasounds
diffreenntial diagnosis for aortic anuerism
GI bleed
Perforated ulcer
Appendicitis
Pyelonephritis
aortic anyerism tx
Monitoring
Surgery to put in a graft
symptoms of a thoraccis anyerism
Asymptmetic
Cough if pressing on phrenic nerve, dysphagia
differenticlal diagnosis of thorassic anyerism
MI
bakc pain
aortic dissection epidemiology
Males more than females
Common emergency
Aortic dissection causes
Chronic hypertension
Connective tissue disorders
Anyerisms
Infection
Atherlosclarosis
Trauma
Aortic dissection pathophysiology
Tear in the intima, blood flowing into the intima in high pressure, this creates a flues lumen and splits is leading to occlusion in branches of the aorta
Aortic dissection types
Tear in the intima, blood flowing into the intima in high pressure, this creates a flues lumen and splits is leading to occlusion in branches of the aorta
Aortic dissection signs
Absent peripheral pulse
Unequal pulse
Neurological signs
Aortic regurgitation
Cardiac tamponade
Compression of other arteries - renal subclavian
Aortic dissection symptoms
Sever tearing central chain pain radiating down back and arms
Aortic dissection manegemt
Type A - surgical repair
Type B - surgical repair, medication or control blood pressure
atrial flutter
Definition
Aetiology
Risk Factors
The atria is in random extreme tachycardia, it is due to circular current running through the atrium. It is a regular but sped up beating, it is less severe than atrial fibrillation.
They often have underling heart problems such as - coronary heart disease, heart valbve disease, congenital heart disease, high blood pressure
Increased age
Valvular dysfunction
Atrial septal defects
Atrial dilation
atrial fibrillation
Definition
Aetiology
Risk Factors
Chaotic rhythem with no regularity
Hypertension
Heart faliure
Coronary artery disease
Rheumatic heart diseas
Thyrotoxicosis
Most common supraventircular arrhythmia
AVRNT Definition
Aetiology
Risk Factors
AV Node re-entry tachycardia, they have an extra electical conduction pathway that causes tehheart t beat more
Three are two pathways this cuases xtra heartbeets due to a circualr fashion.
They are electrical bondes which means that it loops back round
Twice as common in women than in men
Caffine, alcohol
Exertion
AVRT defornition, and causes
AV re-entering (or reciprocating) tachycardia
Its caused by extra connection between the atria and centricels
They are electrical bondes which means that it loops back round
Aortic dissectionatrial flutter
Pathophysiology
Key presentations
A heart rate of between 250-320 bpm and it is fluttering, it is shown on an ECG as a sawtooth pattern most commonly shown in II, III, aVF, V1
Palpitations
Fatuigue
Light-headedness
Jugluar venous pulsation
Chest pain
Worsening heart faliure
atrial fibrillation
Pathophysiology
Key presentations
Atrial activation 300-600 a mmin
Only a small propotion travel to the ventircles
Aysmptomitic
Palpitations
Fatuigue
Dyspnoea
Heart faliure
AVNRT
Key presentations
Regular rapid palpations
Neck pulsation 9JV pulsations)
Polyuria due to release of ANP
Chest pain and SOB
AVRT
Pathophysiology
Key presentations
There is extra electircal condiiction pahway which send signals back into the atria and into the ventrcles againe
This is wolff parkinson white syndrome, the extra bundle here is called the bundle of kent, this cuases a short pR interval
There is a slurred start to te hQRS interval
Palpitatoins
Diziness
Dysponea
Chest pain
Syncope
atrial flutter
Tests and treatment
ECG - will show as sawtooth patterns
Full blood count
Thyroid function tests
Renal function and serum electrolytes
Troponin T levels
If its an emergency- electrical cardioversion to shock the heart back into working
Give antigoagulation to prevent lots form forming in the artium
Treat the underlying cases - beta blockers
Catheter ablation - putting tubes through blood vessles into the heart to destory atches of the tissue
arial fibrillation
Tests and treatment
ECG - irregular waves, no clear p, irregular QRS complex
Rate control- reduce the heart rate by ising beta bi=locker, and anti arrhythias such as amiodarone
Cardioversin therapy
If they don have heart disease yo ucan use sotalol
CHADSVASC score to asses if they are at risk form a sroke and give anti coaguletns as appropriate
Atrial fibriallation can causes thrombs to form - warfrin, heparin, rivaroxiban
AVNRT
Tests and treatment
Blood test
Thyrpid function test
Ecg - p waves not visable or immediately after QRS complex.
Holter monitoer- a portable ecg you wear for eth whole day
Echocardiogram
Listen for bruit - a breathy vaaaa sound,
Most don’t require management
Vagal manoeuvres - dunking head in water, carotid sinus massage
Beat blockers
Calcium channel blockers
AVRT Tests and treatment
Blood test
Thyrpid function test
Ecg - p waves not visable or immediately after QRS complex.
Holter monitoer- a portable ecg you wear for eth whole day
Echocardiogram
Listen for bruit - a breathy vaaaa sound,
Vagal manouvers
IV Adenosine - causes a complete heart block for a fraction of a second which leads to termination of the crcuit K
Ventricular ectopic defornition and causes
Type of arrhythmias where there is an extra beat every so often
Infection, muscle disease, channel ion disease, electrolyte imbalence
Ventricular ectopic signs and symptoms
Diziness
Fainting
#palpitation
Tiredness
Cold peripheries
Dyspnoa
Ventricular ectopic tests
ECG to took for it
Echocardiogram
Exercise stress test
Blood test for infection markers
ventricular ectopic treatment
Beta blockers
Calcium channel blockers
what is toursaire de pintes: defornitoin, symptoms, causes, treatmetn
Toursardes de pointes - a complicatio hwat causes the ventricles to beat out of time with the atria. It will case a very raplily up and down ECG, butu blood ion tests should also be conducted. It can causes sudden cardiac death
Symptoms include:
Heart palpitation
Diziness
nausuea
Cold sweats
Chest pain
Shortness of breath
Rapid pulse
Low blood pressure
Syncope
Cardiac arrest
It is often brought on by stress and exercise, and also some types of drugs.
It is treated by beta blockers, pacemakers, implantabe cardioverter defibrillator
Prelonged QT syndrome defornition and risk factors
Prolonged qt interval on an ECG which ma be congenital or aquired
It can lead to sudden cardiac death due to ventricular tacharrhythmias
PT interval prolonging drugs (amioderone)
Gene mutations
Prelonged QT syndrome pathophysiology
In congenital - they have gene mutaions affecting ion channles which prevent the signals passing on
Prelonged QT syndrome key presintation sna dsymptoms
History of gene mutations
Drugs or circumstances known to prelong QT
Syncope dueing heighted adrenergic tone
Syncope during arousal or surprise
Dizziness
Angina
Fatigue
Oliguria
Prelonged QT syndrome tests
ECG!!!
Echocardiogram
Genetic testing
Exercise tolerance test
Prelonged QT syndrome treatment
Beta blockers
Implantable cardioverter defibrillator
Lifestyle modification
type 1 heart block
Definition
Aetiology
Delayed AV conduction that causes a prolonged PR interval
- LEV disease
- IHD - scar tissue forms myocyte blocks the conduction pathway
- Myocarditis
- Hypokalaemia
- Drugs such as beta blockers
- Increased vagal tone
type 1 heart block key presintations, and manegemnt
asymptomatic
no manegement heheheeh what a prank card lol
1st degree heart block ECG findings
ECG - prolonged PR interval of over 0.22 seconds
type 2 heart block moblitz 1 defornition and aitiology
2- Mobitz I - prolonged PR which increases until a QRS is missed and then the cycle restarts
you make my heart miss a beat (or a ventricular contraction)
Moblitz I (wenckebach)- caused by AV node block and results in progressive PR interval prolongation until a p wave fails to conduct and a QRS is skipped. Its normally cyclical and the QRS is missed every n times.
Caused by MI, drugs, increased vagal tone, hyperkalaemia
type 2 heart block moblitz 1 key presintations and ECG findings
light headedness, diziness, syncope
increasing PR interval length untill a beat is skipped
type 2 heart block moblitz 1 treatment
Atropine if it causes bradycardia or hypotension
type 2 heart block moblitz 2 defornition and cause
2 - Mobliz II - just a missed QRS every so often
Some atrial impulses fail to reach the ventricles
Mobitz 2 (hay) - there is no incrased PR interval, just an intermittent QRS missing. Sometimes a fixed ratio of missing QRS.
Structural heart disease, MI or fibrosis, cardiomyopathy
Its gerally seen in serious changes to the hearts structure.
type 2 heart block moblitz 2 key presintations and ECG findings
Chest pain, dyspnoea, syncope. Postural hypertension.
○ QRS is widened and QRS complexes are dropped without PR prolongation
○ FBC to look for electrolyte imbalance
type 2 heart block moblitz 2 treatmetns
NEVER GIVE ATROPINE
Stopping medication that slow nodal conduction (beta blocker/digoxin/calcium channel blocker)
Adress electolycte imbalances
Pacemaker
type 2 heart block moblitz 2 complications
Risk of sudden death, risk of asystole, needs a pacemaker placed
Don’t give atropine!! It can increased the chance f complete heart block or asystole
type 3 heart block defornition and causes
3 -
Occurs when there is complete dissociation between atrial and ventricular activity. E.g. atrial BPM is 60, ventricular is 30 BPM
CHD
Infection
Hypertension
Myocaridal infarction
type 3 heart block key presintations and EXG findings
Syncope
Dysnpnoea
Chest pain
Confusion
ECG - p waves that don’t lead to QRS ever and more p waves than qrs
Ventricular contaction is sustained below the sight of block in the pathway
If the HIS system is changed i
type 3 heart block tx
Dopamine, adrenaline, IV atrpopine
Pacemaker insertion
BBB defornition
BBB - complete block f a bundle branch oto eiter the left or the right, which leads to late contraction of theventricle
causes of LBBB
Left:
Coronary artery disease
High blood pressure
Heart valve disease
Enlarged or weakened heart muscle (cardiomyopathy)
Heart infection (myocarditis)
Heart attack
Congenital heart defects
Certain heart rhythm medicines
Causes of RBBB
Right:
Myocarditis.
Trauma to your chest.
Heart attack (myocardial infarction).
Right heart catheterization or other procedures.
Changes in branch structure, such as stretching.
Pulmonary hypertension
Pulmonary emobolism
Copd
ecg results for left and right BBB
ECG - WiLLiaM MaRRow
For a left bundle branch block, there is a W in V1 and an M in V6 in the right bundle branch block there is M in lead 1 and W in V6
Wide QRS which is lasting longer
treatment for bbb
pacemaker!
hypertension criteria
140/90mmhg on at least two separate occasions
hypertension causes
95% of cases - is a primary origin
Secondary - renal, endocrine (cushings, acromegally), coarctation of the aorta, preeclampsia occuring in the third trimester, drugs
hypertension risk factors
Family history
Old age
Low birthweight
Male
Afro-caribean heritage
Unhealthy diet
Lack of physical activity
Obesity
hypertension pathophysiology
Vascular changes - atherosclerosis which causes thickening og the media of muscular arteries
Heart changes
Nervous system - intracerebral haemorrhaging
Kidneys - renal disease can causes water retention
Malignant - raised diastolic blood pressure, progressive renal disease,
hypertension key presintations
Asymptomatic apart from in malignant
May cause the occasional headache
hypertension tests
Take the blood pressure - if it is >140/90 confirm on a second reading and use a 24 hour ambulatory BP monitor, and a multiple hoe BP monitoring
Test to asses end organ damage - urine analysis to check the kidney function
ECG and echo
Fundoscopy to check hypertension retinopathy
Bloods - creatine, eGFR, glucose
Clinical history of previous MI
hypertension manegemtne
Calculate the QRISK of heart attack!!
If there is end organ damage or high QRISK then it needs to be treated
Lifestyle changes - smoking cessation, low fat diet, reduced alcohol and salt, increased exercise, Weigth loss
Drugs - ABCD
Ace inhibitor - ramopril
Beta blocker - bisoprolol, propanol
Calcium channel blockers - amlodipine
Diuretics - furosemide
what is malignant and severe hypertension
Malignany hyertention - ca rapid rise in BP cuain vascular damagem and might give sympotms of headache and visual disturbances
Severe hypertentions of > 200/130
It ca cuase hypertensie emergancies wych as acute kidney injury and HF
Treat with sodium nitroprusside!!
Deep vein thrombosis defornition
Occlusion in normal vessles most commenl deep I the vien so te leg. Thet often occur after periods of imobalisation
Deep vein thrombosis risk factors
Age
Obesity
Vacrose veins
Long haul flights
Immobility and bed rest
Plasminogen deficiency
Pregnancy
Deep vein thrombosis causes
Surgery
Immobility
Leg fractures
Oral contraceptive pill
Long haul flights
Pregnancy
Deep vein thrombosis key oresintations
Calf pain and swelling
Warmth
Redness
Ankle oedema
Pitting oedema
Gangrene
cyanotic discoloration
Deep vein thrombosis tests
- Look for the D dimer - this si a protien reeased form eth breakdown of clots which if its there it ight be DVT and if its nt, it excludes VDT
- FBC including plateltes
- Doppler - compression ultrasound which uses sound waves to see the blood flow through the vessles, looks at the poplitel vein
Deep vein thrombosis treatmetns
The main aim is to prevent PE
* LMW heparin (enoxaparin) to inactivate factor Xa and stop the clotting * Warfarin - antagonist of 1 9 7 2 clotting factors * Direct acting oral anticoagulants; apixaban, rivaroxaban , they work by inhibiting Xa factors but don’t need monitoring like warfin does
Prevention:
* Compression stockings
* Early mobilisation
Leg elevation
Deep vein thrombosis complications
PE
Post thrombolytic syndrome - damage to the veins and valves causes ulcers and pain, vacrose veins and swelling
Reoccurrence of thrombosis
pulmonary emoblism - dfornition causes and risk factors
Dislodged thrombi occludes pulmonary vasculature, it might causes right sided heart failure and cardiac arrest
Deep vein thrombosis
Increasing age
Obesity
Surgery
pulmonary emoblism test and assesment scoring system
CTPA
Echocardiogram
D-dimer test t to look for clot proteins
Full blood count
ARTIERIAK BLOOD GAS
Chest x ray
ECG - sinus tachycardia
Looks for Prescence of DVT
Use the wells score for diagnosis-
Clinical signs and symptoms of DVT +3
PE is #1 diagnosis OR equally likely +3
Heart rate > 100 +1.5
Immobilization at least 3 days OR surgery in the previous 4 weeks +1.5
Previous, objectively diagnosed PE or DVT +1.5
Haemoptysis +1
Malignancy w/ treatment within 6 months or palliative +1
SOCRE OF >4 MEAN PE LIKELY
pulmonary emoblism - key presintations
Dyspnoea
Chest pain
Signs of DVT
Risk factors
Cough
Fever
pulmonary emoblism - diffreentila diagnosis
Unstable angina
NSTMI
STEMI
Pnumonia
bronchitis
Pericarditis
Cardiac tamponade
pulmonary emoblism tx
HEAMODYNAMICALLY UNSTABLE:
* Give oxygen
* give thrombolytics to break it down
* It can cause low blood pressure so giving salone (500ml/0.9%) or hartmans solutinon
* Anticoagulation - given to haemodynamically stable patients - apixaban, rivaroxaban, or LMWH.
HEAMODYNAMICALLY STABLE:
Anticoagulation and monitor closely for signs of becoming haemodynamically unstable
pulmoary empbolism complications
Heart failure
MI
peripheheral vascular disease 4 stages
Legs most commonly affected
4 stages:
1. Asymptomatic
2. Intermittent claudication (pain in the arms or legs that occurs when the blood supply s narrowed)
3. Rest pain or nocturnal pain
Necrosis/gangrene
peripheheral vascular disease causes and risk factors
ATHERLOSCLAROSIS!
Smoking
Diabetes
Dyslipidaemia- increased fat levels in the blood
Hypertension
peripheheral vascular disease pathophysiology
If its in the hip or buttocks - aorta or iliac
Thihgh - common femoral
Upper 2/3rd of calf - superior femiar aryert
Lower 1/3 of calf - popliteal artyer
Fooot - tibeal ot peroneal artyer
The pain is cases by the released of adenosine in response to muscle ischemia
There is a narrowing of the vessles which occludes the blood flow leading to ishecemia and pain
peripheheral vascular disease signs and symptoms
Absent pulses
Punched out ulcers
Cramping pian in calves ,thighs and buttocks
Pain is relieved by rest
Postural colour change - buegers test (foot turns white when elevated and red when lowered)
There are 6 Ps of limb ischemia
* Pain
* Pallor
* Pulseless
* Perishing cold
* Paraesthesia
* Paralysis
peripheheral vascular disease tests
- Ankle brachial pressure index - this is the difference in pressure between the ankle and the arm. The blood pressure is measured using a cuff and sopper ultrasound device. The ankle should normally have a higher blood pressure than the arm, but in peripheral vascular disease the ration changes. It is ankle/arm which should be less than 0.9 to be abnormal.
- COLOUR DUPLEX USS - quick and non invaseive, can show the vessles and blood flow within them
- AUSICLATIONS - bruits due to the turbulent blood flow
- Creatine kinase MM - a marker that shows muscle breakdown
peripheheral vascular disease differentials
diabetes mellitus, arthritis, anaemia, renal disease
peripheheral vascular disease tx
Risk factor modification - smoking, hypertension, cholesterol, improves diabetes, diet
Medications - antiplatelet therapy (clopidogrel)
Exercise programs - improve blood flow
Percutaneous transluminal angioplasty (stent)
pericarditis causes
- Idiopathic
- Infection - mainly viral but could by TB or fungal
- MI
- Autoimmune - SLE, sjoogrens
- Dressler dynrom - inflamation of the pericardium after the MI damagining it, a delayed response
- Iantrogenic - caused by surgery or medications
- Uraemia - build p of toxins due to kidney faliure
- Malignancy - breast lung leukeamia
pericarditis key presintations, signs, sympotoms
Pericardial rub
Pain worse when lying flat and reilved when sat forewards
Raised JVP
Chest pain, sever, sharp and not with a crushing feeling
Dysnopea
Hiccups and cough due to phrenic involvement
Fever
pericarditis tests
ECG - sadle shapped ST in all leads
PR depression
PeRicardiTiS
Bloods - cardiac enzymes
C reative pritiens
FBC
Echocardiogram
CXR - show water bottle shape and cardiomegaly f there is effusio
pericardidits pathophysiology
It become inflamed with peripher vascularisation and infiltraiotn y polymorphonuler leukocytes
pericarditis tx
NSAIDS
Colchine - inhibits migration of neutrophils
f=drainigle of fluid
Rest
Treat underlying cuases- steriods for autoimmune cases
pericarditis complications
Pericardial effusion
Cardiac tamponade - there is so much pericardial effusion that the heart can no longer beat anymore
Chroninic constricitve pericarditis - there is a rigid pericardil sack which prevents diastolic filling f the ventricels
what is constricitve pericarditis
Constrictive pericarditis:
Normally idiopathic or restrictive cardiomyopathy
Signs and symptoms simmilar to right sided heart faliure, Juglar veouns distention, dependant oedema, hepatomegaly, ascites
Kussmals sign - JVP rises with inspiration
Pulsus paridoxus
AF
Pericardial knock
Chest xray - show norma heart and ericardial calcification
CT or MRI - diagnostic to show pericardial thickening
echcardiogram
pericardial effusion and cardiac tamoponade defornition
Effustion - fluid in the space
Tamponade - effcects on the hearts ability to pump
pericardial effusion signs
Effusion obsucres apex beat
Hypotension tachcardia
Elevated JVP
Pulsus paridosis - a blood pressure fall of more than 10mmHg during inspiration
Causes more venous return to eh right side of the heat
pericardial effusion tests
Echocardiogram
Chest xray
ECG - shows low voltage complexes with sinus tachycardia
#
- Pericardial effusion
○ CXR – large heart
○ ECG – low voltage QRS complexes and sinus tachycardia
○ Echocardiogram - Cardiac Tamponade
○ CXR – large heart
○ Beck’s triad
§ Falling BP
§ Rising JVP
§ Muffled heart sounds
○ ECG
Echocardiogram
pericardial effusion and cardiac tamponade manegemtnet
Effusions normally resolve themselves
Tamponade requires emergency pericardiocentesis
If effusion reoccurs excision of pericardial segment allows fluid to be absorbed through plural and mediastinal lymphatics
infective endocarditis defornition
Infection of the heart valves and endocardial lining within the heart
infective endocarditis epidemiology/risk factors
Elederyly
IV drug abusers
Congenital heart disease
Poor dental hygiene
Prosthetic valves or pacemakers
More commen in men
infective endocarditis bacterial causes (name teh bacteria)
S.aureus is the most common
Pseudomonas aeruginosa
Streptococcus viridians (from dental problems)
infective endocarditis key presintations
FROM JANE
Fever
Roths spots
Oslers nodes
Murmur
Janeway lesions
Aneamia
Nailbed splinter hemmorages
Emboli - MI storke PVD
There are two main diagnostic criteria - bugs grown form cultures and evidance of endocarditis on an echo or new valve leak
There are 5 minor ones:
Risk factors
Fever
Vascular or immue phenomena
Equivocal blood cultures
infective endocarditis sympotms
Fever + prosthetic material in heart, risk factor, newly developed arrhythmias
Headaches
Fever
Malaise
Confusion
Night sweats
infective endocarditis signs
Splinter haemorrhages
Roth spots (haemorrhages in the retina)
Osler nodes in fingers (tender nodules in the fingers)
Janeway lesions - haemorrhages and nodules in fingers
Clubbing
infective endocarditis tests
Transoesophogel echo - diagnostic
Transthoraci echo
ECG
CXR
Blood cultures
infective endocarditis treatment
Antimicrobials - IV for 6 weeks
If not staph use benzylpenicillin and gentamycin
If staph use vancomycin and rifampicin
Always treat with 2 antibiotics at the same time so it’s a broad specturm.
Treat complications - arrhythmias, HF heeart block and embolisation
Stroke rehab abscess drainage
Surgery
shock defornition
Acute circulatory failure where there is inappropriate tissue perfusion resulting in hypoxia. It also causes low BP below 90.
There are compensatory mechanisms:
Hypotension causes baroreceptors in thee aortic arch and carotid sinus to stimulate adrenaline release, this causes vasoconstriction and increase CO.
Reduced perfusion of the renal cortex causes renin release. This incr
shock key presintations
- Pallor
- Rapid weak pulse
- Presuced pulse pressure
- Reduced urine output
- Confusion, weakness, collapse, coma
Reduced capillary r
shock first line tests
○ FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry
shock tx
Airways
Breathing - 100% O2
Circulation - IV acess, fluid for blood loss, stop bleeding, give adrenaline to cause vasoconstiction
define hypovolemic shock
Loss of large amounts of blood
causes of hypovolemic shock
There is a reduced preload. This can also be caused by burns which causes plasma leakage, D&V dehydration, intestinal obstruction, pancreatitis
blood loss
hypovolemic shock kery presintations
inadequate tissue perfiusion
Increased sympathetic tone
Tachycardia
Sweating
Bradycardia
anaphyactic shock causes
IgE - release of histamine
anaphylactic shock key presintations
- Onset of symptoms after antigen exposure
- Swollen tongue, lips
- Laryngeal oedema
- Swollen epiglottis
- `Warm peripheries and hypotension due to profound vasodilation
- Urticaria
- Angio-oedema
- Wheezing and SOB due to bronchospasm
- Upper airway obstruction due to laryngeal oedema
Low BP – due to vasodilation, increased vascular permeability and fluid loss from vascular space
anaphylactic shock treat,ent
- Remove antigen
- Oxygen
- Adrenaline
- Fluids (500ml 0.9 saline)
Observation
septic shock pathophysiology
Vasodilation due to inflammatory cytokines
Systemic inflammatory respnse, temtruture is raised, tachycardia, increased resp rate
Severe sepsis – sepsis with dysfunction of one or more organs
Septic shock – persisting tissue hypoperfusion after a fluid challenge
Endotoxins cuases lower perfusion which causes dameg to endothelium and there is inflamation
There is increased clotting
septic shock key presintations
- Pyrexia and rigors (increased body temptriute which auses the person to feel cold untill they reach it and shake (rigours)
- Nausea and vomiting
- Vasodilation with warm peripheries
Bounding
septic shock tests
BLOOD CULTREIS LOOKING FOR BACTERIA
○ FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry
septic shock treatmetn
- Airways
- Breathing
- Circulation
- Antibiotics
○ Community-acquired pneumonia – ceftriaxone
○ MRSA – vancomycin
○ Pseudomonas – cefepime + metronidazole - Treat underlying cause
- Coagulopathy
- Acute kidney injury
cardiogenic shock pathophysiology
Heart isn’t pumping well
Myocardial flaure signs
* Chest pain
* Respiratory distress
* JV distention
* Hypotensino
* Crackles in lungs
* ST elevation
Gallop rhythem
cariogenic shock causes
MI
Myocarditis
Atrial and ventricular arrhythmias
Bradycardia
Rupture of valve cusp
PE
Tension pneumothorax
Cardiac tamponade
cardiogenic shock tests
○ D-dimers
○ Echocardiogram
FBC
○ Serum creatinine
○ Electrolytes
○ Blood glucose
○ Coagulation
○ Blood gases
Liver biochemistry
what is ARDS
ARDS: caused by : sick, head injury , near drowning, chemical pneumotisk sepsis
- Alveolar capillary membrane injury results in leakage of fluid into alveolar spaces
- There is resulting neutrophil invasion which attracts more neutrophils = Exudative phase
- Eventually, fibroblasts come in and initiate healing = proliferative phase
- Scar tissue then forms due to fibroblasts = fibrotic phase
- Results in severely stiff lungs and therefore severe difficulty in ventilation and O2 blood perfusion
Causes cynosis, tachycardia periphera vasodilation
neurogenic shock pathophysiology
Damage to Ns mean bp can’t be controlled as well, caused norallly by a spinal injury above T6
define cardiomyopathy
Disease in the myocardium which effect the mechanical or electrical function of the heart
hypertropic cardiomyopathy defornition cna causes
Hypertrophic- heart is stiff and doesn’t relax properly.
caused by autosomal dominant mutation
hypertrophic cardiomyopathy key presintations
Angina
Dyspnoea
Palpitations
Dizzy spells
Syncope
Crescendo decrescendo murmur
S4 sound
hypertrophic cardiomyopathy tests
Microscopically - myocyte disary, fibrossi is an electrica insulator and the curretn goes though the fibrosis and casues arrhythmia
ECG - abnormal, deep T wave inversion
Echocardiogram
hypertrophc cardiomyopathy tx
Amidarone - antu arrhythmia
Calcium channel blockers
Beta blocker
Digocin contraindicated
Surgery
dialated cardiomyopathy defornition
Muscle is normal or thin and the chamber is large. This eams that they arent as sting and cant work as effectively
dialated cardiomyopathy causes
diopathic
Infectio
Ischemia
Alcohol
Genetic
dialated cardiomyopathy key presintations
Heart faliure sympotms
Dysponea
Arrhythmias
Increase JVP
dialated cardiomyopathy tests
CXR - learge heart
ECG
Echo
dialated cardiomyopathy treatment
HF and AF treated in the normal way
Left ventricular assist device
Heart transpplant if thinning s too great
Arrthymogenic cardiomyopathy defornition
Presents with arrhythmias
There is a replacement of the heart muscle with fat, therefore it cant beat as well
May be little structural or directly involve RV and LV
Arrthymogenic cardiomyopathy key presintations
Arrhythmia
Syncope
RHF
Arrthymogenic cardiomyopathy tests
Histology - more fatty layers
ECG - in V123, ther eare epsilion wave and t wave inversion
Genetic testing
Echo
Arrthymogenic cardiomyopathy manegement
Beta blockers
Arrhythmias - amiodarone
restrictive cardiomyopathy defornition
Ventricles are stiffer and ledd compleinet
This leads to less CO and HF
Poor dilation of the heart restricts its ability to take on blood and pass it onto the rest of the body
restrictive cardiomyopathy causes
Amyloidosis - misfolded protiens which are insoluble
Acrcoidosis - formation of granulmas I the heart walk
Idiopathc
Endocardia fibrolastosis
Iron overload
restrictive cardiomyopathy key presintations
Similar to constrictive pericarditis
Dysponea, elevated JVP
Heaptomegaly
Acitis
3rd and 4th heart sounds
restrictive cardiomyopathy tests
CXR
ECG
Echo
Cardiac catherisaition
restrictive cardiomyopathy treatments
Treat underlying causes
Heart transplantation
Rheumatic fever defornition
An autoimmune diseae that occurs after a group A strp infection which can affect many systems such as chroic rheumatic disease, without long term pernicillin it can reoccur and cases damage to the cardiac valvular tissues. The antibodies to the bacteria also react and damage the myocardium. It normally occurs 2-4 weeks after infection.
Rheumatic fever risk factors
Less developed countries
Lower income
Family history of rheumatic fever
Genetic susceptibility
Rheumatic fever pathophysiology
Carditis caused by the attack of the immune system. Pericarditis, myo and endo as well.
Rheumatic fever signs and symptos
Fever, joint pain
Recent sore throat, skin infection, chest pain, dyspnoea, heart palpitations, heart murmur, pericardial rub, swollen joints which apperar migratory as different joint get inflamed at different times
Skin lesions - painless nodules, Erythema marginatum rash
Nervous suste involvelemt - chorea which is irreglar uncorntrolled rapid movemt of the limbs
Rheumatic fever tests
Throat swab for bacteria culture
ASO antiboy titres - antibodies againt streptococcus, which indicate recent infection
Echocardiogram
ECG
CXR
Rheumatic fever trteatment
Penocymethypnicillin for 10 days to get rid of infection
NSAIDS for joint pain
Asprin and steroids for carditis
Phrophylactic antibiotics are sued to prevent further steptococcal infections and reoccurance
Rheumatic fever complications
Valvular stenossi (mitral normally)
Chronic heart faliur
Reoccurance of RF
aortic stenosis causes
Due to the narrowing there is obstructed LV emptying which causes a pressure gradient to develop between LV and the aorta which means an incrased afterload whih cleads to left ventricle hypertrophy
Tis then leads to increased myocradial oxygen demand, angina and LV faliure
aortic stenosis risk factors
Congentital bicuspid valve
Old age leading to calcificationa nd degeneration of normal valves
Rheumatic heart disease
aortic stenosis signs and symptoms
○ Exertional syncope
○ Angina
○ Dyspnoea – due to HF
Slow reisinf and weak carotid pulse
Soft or absent 2nd heart sound and preominenet 4th heart sound due to LV hypertrophy
Ejection systilic murmur - sounds like a whooshing noise
Heart faliure
aortic stenosis tests
Chest xray - shows noral heart size, LVH, prominence of ascending aorta and calcular calcification
ECG - may show signs of LV stress patterns and ST depression and T wave invesrsion in aVL V5 and V^
echocardiogram is teh main diagnostic tool!!
aortic stenosis
aortic stenosis treatment
Surgical - aortic valve replacemnet - in symptomatic patiens as onset of symptoms associated with 75% mortality at 3 years
General - dental hygine is important as they are at risk of endocarditis
aotic regurgitation explination
Regurgitation - failure of the valve to work properly
Leakage of blood into LV due to ineffective coaptation of the aortic cuffs
define stenosis
Stenosis - narrowing of the valve to the point where is 1/4th of the normal size. There are three type, supravalvular, sub, and valvular
Aortic Regurgitation causes
Idiopathic
Effective endocarditis
Chronic rheumatic fever
Congenital bicuspic aortic valve
Rheumatic fever
Infective endocarditis - acute
Aortic Regurgitation pathophysiology
Combined pressure and volume overload - LV dilation and LVH
Aortic Regurgitation signs
Collapsing pulse
Wide pulse pressure
Quincke’s sign - capillary bed
De Mussets sign - head nodding with each heart beat
Mullers sign - visible pulsation of uvula
Heart sounds - displaced hyperdynamic apex beat
Early diastolic murmur at left sternal edge in 4th intercostal space - accentuated when eth patient sits forewards and holds breath
Systolic murmur
Aortic Regurgitation symptoms
Exertional dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Palpitations
Angina
Syncope
De Mussets sign - head nodding with each heart beat
Mullers sign - visible pulsation of uvula
Aortic Regurgitation tests
Echocardiogram
ECG - LVH (left ventricular hypertrophy)
CXR - shows a large heart and occasional dilation of ascending aorta
Aortic Regurgitation treatment
IE prophylaxis (antibiotics for infective endocarditis)
Vasodilators
Surgical - pelplace valve before LV disfunction
mitral stenosis defornition
Obstruction of LV that prevents proper filling during diastole
mitral stenosis causes
Rhumatic heart disease causes by rehmatic fever
Infective endocarditis
Mitral annular calcification
Congenital causes
mitral stenosis risk factors
Unreated strep infections
mitral stenosis pathophysiology
Thickening and imobility of valve leads to obstruction of blood flow form the LA to the LV which leadsto increase LA pressure, pulmonary hypertention and right heart dysfunction
Atrial fibrillation is commen due to elevation of LA pressure and dilation
Thrombus may fmor in the dilated atrium and could causes a stroke
Elevated LA pressure can lead to pulmonary embolism
mitral stenosis signs
Mitral facies - extrere cheek flushing due to vasoconstriction
Low volume pulse
Tapping, on disppalced apex beat
Heart souds - loud S1 at apex, if there is a loud S2 with elevated JVP and peripheral oedema it may indicate pulmonary hypertension induing RV overload
Diastolic murmur is a low pitch rumble at the apex and is left heard when the patient is lying on the left hand siede and expiring
mitral stenosis symptoms
Exertional dyspnoea
Coughing up blood
Haemoptysis - coughing up blood
Right heart failure - fatigue, weakness, lower leg swelling
Palpitations due to AF
Chest pain
mitral stenosis tests
Echocardiogram
Chest xray - LA enlargeent, pulmonary hypertension, calcifies mitral valce
ECG - AV and LA enlargement
mitral stenosis tx
Contoell of any AF with beta blockers
Anticpagulents to prevent clot formation in AF
Diuretics for heart faliure
Percutaneous mitral balloon valvotomy to open up the valve more
mitral regurgitation defornition
Backflow of blood from the LV to the LA during systole
mitral regurgitation causes
Myxomatouse degeneration
Rehumatic heart disease
Infective endocarditis
Ishcheamic mitral valve
Dialated cardiomyopathy
mitral regurgitation risk factors
Female
Lower BMI
Age
Renal dysfunction
Previous MI
mitral regurgitation pathophysiology
Pure volume overload due to leakage form LC into LA
Compemsatory mechanisms - LA enargemet
LV hypertrophy
Increased contractility
Preogressive LA dilation and RV dysfunction due to pulmonary hypertension
Progressive LV volume overload leads to dilation and preogressive HF
mitral regurgitation signs
Collapsing pulse with wide pulse pressure
Hyperdynamic and displaced apex beat
Heart sounds
Soft S1
Pansystolic murmur
Diastolic blowing urmur
Austin flint murmur
Systolic ejection murmur
mitral regurgitation symptoms
Exertional dysponea
Fatuige and legarthy
Palpitations
Right sided HF that can lead to congestive failure
mitral regurgitation tests
CXR - enlarged LA and LV
Echocardiogram - LA LV size and function
ECG
mitral regurgitation treatments
Consider IE prophylaxis (a hight dose of antibiotics)
Vasodilators
AF control - beta blockers, calcium channel blocks
Anticoagulant for AF and flutter
Serial echocardiogram to manage flutter
Surgical treatment to replace valve if the patient has symptoms at rest or exercise, or if the left ventricle end systolic diameter is >45mm.
Tetralogy of Fallot defornition
is made up of 4 different heart defects
* Ventricular septal defect * Overriding aorta - aorta positioned over VSD instead of LV * Pulmonary stenosis RV hypertrophy
Tetralogy of Fallot epidemiology
Most common cyanotic cardiac disorder,
10% of all contentive heart defects
Tetralogy of Fallot key presintations
- Frequesnt crying in children
- Toddlers may squat to alleviae some of the L ot R shunt
- Central cynosis
- Low birthweigt
- Dysponea
- Delayed pubity
- Systolic ejecion murmus
- Adults are asymptomatic often
- Dysponea on exertion
- Systolic ejection murmurs
Clubbing
Tetralogy of Fallot test
CXR shows boot shaped heart
ECG shows RBBB
Tetralogy of Fallot treatment
Children knee to chest position and give O2
Full surgial treatment is required due to progressive cardiac debiliy and central thrombosis risk
Often pulmonary valve regurgiation in adulthood and require a redo surgery
coarctation of aorta defornition
There is a narroing in the aorta at the site of the ductus arteriosis
coarctation of aorta epidimiology
Associated with turners syndrome, berry anyerisms, bicuspid acotic valves
More common in male
coarctation of aorta pathophysiology
evere - complete obstruction leading to collapse
Mild - raisd blood pressire, systolic murmur form collateral vessles
Can lead to long term problems sucj as hypertension
Coronary artyery disease
Early stokes, subarrachnoid hemmorage
It requires repeat interverntions and enyerisms can form at the rigth o
coarctation of aorta key presintations
- Often asymptomaic
- Right arm hypertension
- Radio femoral pulse delay (feel the redia pulse before femoral
- Discrepancies in BP in upper body and lower
- Bruits (buzzes) over the scapula form collateral vessels
- murmur
Headache
coarctation of aorta test
CXR- show indentation
ECG - LV hypertrophy
CT - can demonstrate coarcation and quantifty flow
coarctation of aorta treatment
Surgical repair
Percutansous repain
Baloon dilation and stenting
Ventricular septal defect defornition
there is a hole in teh sepum of teh heart taht allow blood flow
Blood moves form left to right
Increased blood blow to the lungs
Ventricular septal defect key presintations
Pulmonary hypertension and eisenmengers complex
Smalll breathless baby
Increased resp rate
Tachycardia
Murmur
Increased risk of endocarditis
Cyanosis
Finger clubbing
Ventricular septal defect treatment
Many will close up naturally
If small no intervention is required
Moderatly sized lesion may need ACE inhibitor, furosemide and digoxin
Consider prophylactic antibiotics for risk of endocarditis
Ventricular septal defect risk factora
Down syndomre
Materal alcohol consumption
Family history
atrial septal defect risk facros
age
male
atrial septal defect what are teh two types
Primium - present earlier
May involve AV node
Affects lowe in eh septum
SECONDUM - the most common, pressure higher in the L than R, causing a left o right shunt
Increased flow to the right hand side and lings
Can lead to right sided heart failure and dyspnoea
Will cause right sided overload and dilation
It can lead to right ventricle hypertrophy and pulmonary hypertension
what is eisenmengers complex
Eisenmengers complex - occurs in VSD or ASD
Reversal of the L too R shunt due to pulmonary hypertension leading to left hypertension
Causes deoxygenated blood to travel around the body and the only cure is a transplant
atrial septal defect - what is Pulmonary artery banding
Pulmonary artery banding - band reduces the flow to the lungs wihc reduces pulmoanry hypertensino and eisenmengers syndrom
atrial septal defect key oresintations
Pulmonary flow murmur
Split second heart sound
Dyspnea
Exercise intolerance
Atrial arrhythmias
atrial septal defect treatmetn
Surgical closure done via keyhole
Patent ductus arteriosus defornition
A connection between the pulmnary artery and the aorta still exists
Patent ductus arteriosus epidemiology
Females more than males
Patent ductus arteriosus pathophysiology
t sould have closed within a few ours of birth but it remins open
It can cuases a left to right shunt and eventulal leads ot plmonary hypertension and eisenmengers sundrome and RS heart faiure due to hypertrophy
Patent ductus arteriosus key presintations
Murmur
Breathlessness
Eisemengers syndrome (differentila cyanosis - clubbed toes which are blue)
Patent ductus arteriosus tests
CXR - large shunts may be preominent
ECG - lA abnormality and LV hypertrophy
Echocardiogram - dialated LA and LV
Patent ductus arteriosus treatmetns
urgical closing
Venous approach has lower complications
Indomethacin (prostoglandin inhibitor can stimulae the duct to close)
what are two conditions that will cuases a systoic murmur
mitral regurgitatoin
aortic stenosis
what are two conditions that will causes a diastoil murmur
aortic regurgitation
mitral stenosis
what is hypohidrosis
A rare condition in which the sweat glands make little or no sweat.
what is atropine used for
tropine is a prescription medicine used to treat the symptoms of low heart rate (bradycardia), reduce salivation and bronchial secretions before surgery or as an antidote for overdose of cholinergic drugs or mushroom poisoning.
what is teh mechanism of atropine
its is an ACTH antagonist so block teh parasympathetic signals allowing the heart rate to increase via teh sympathetic pathway
where is b type natritic peptide secreted form
ventricle myocardium
what do high livels of Btype natriuetic peptide indicate
heart faliure
what are teh two drug classes prescried for heart faliure
beta blocker
ace inhibitors
define ejection fraction
jection fraction (EF) is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction.
what are teh bacteria most likely to causes rheumatic fever
Strep grouop A - staphylococcus pyogenes
these are teh bacteria whihc cuases strep throat
what infections in teh rest of the body will heart faliure incrase the risk of
chest infections and ulcerated cellulitic legs - due ot teh excess fluid collecing
what are teh two types of peripheral vascular disease
- Functional - when your vessels open in exaggeration and thre is no actuall damage to the structure, for example in raynards and tempriture
Organic, meaning that there is a change in structure of your blood vessels,
what are teh three medications to give for peripheral vascular disease
Naftidrofuryl oxylate - peripheral vasodilator
Cilostazol - relax blood vesse and prevent platelets from sticking together
anticoagulation
what is teh treatment algorhythem for hypertension
diabetic - ace inhibitor
what is teh treatment algorhythem for hypertension
non diabetic under 55 or any diabetic type 2 - ace, thn add on ccb or thiazide, then all three togther if still not controlled
diabetic over 55 or afro-caribean - CCB, then ccb and ace, then ccb ace and thiazide like diuretic
what is an easy test to do for aortic dissection
do teh blood pressure on both of teh arms and one arm should be >20mmhg higher than the other.
what is teh diagnostic test for aortic dissection
CT angiogram with contrast dye!
what are teh shockable and non shockabel rhythems
shockable:
ventricular fibrillation
ventricular tachycardia
non shockable:
pulseless electircal activity
asystole
what is pericardiocentisis
Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the heart (pericardium). It’s done using a needle and small catheter to drain excess fluid. A fibrous sac known as the pericardium surrounds the heart.
Pericardiocentesis typically begins with a needle inserted at a 15-degree angle between in the xiphoid process and left costal margin. The needle is then carefully lowered to a horizontal level with the chest and gradually moved towards the point of the left shoulder blade, with the aspiration of fluids.
what is teh way of working out if a person with AF needs anticoagulents
CHADVASC - A scoring system to see if anticoagulets are recommended or not for atrial fibrillation. each is worth 1 point unless stated otherwise. If they score 2 or more give DOAC.
Congestive heart falire
Hypertension
Age over 75
Diabetes
Stroke (this is worth 2 points)
Vascular disease
Age over 65
Sex
what is pulsus paridoxus
- Pulsus parixods is when you’re bp drops more than 20mmgh on inspiration. The normal levels is 8-12mmhg.
It is caused by cardiac tamponade, constrictive pericarditis, atria septal defect, aortic regurgitation.
what is kussmals sign
- Kussmals sign - a paridoxical rise in JVP on inspiraion
- Due to increased volue in thr rhght ventricle
Caused y contrictive pericarditi, restirctive cardiomyopathy, pericardial effusion, severe right sidede heart faliure
- Due to increased volue in thr rhght ventricle
what is teh difference between pericadial effusion, cardiac tamponade and constrictive pericarditis
- Pericardial effusion happns ver time and cuases a slow stretching of the sack, it has kussmals sign
- Tamponade is a sudden accumulation of fluid that constricts the heart, it has becks triad - muffles heart sounds, hypotension and distentin of the juglar viens. This is when there is an anctual pressure on the heart muscle which prevents it from working properly. A sign of it is pulsus paridoxusdue to the large drp in systolic blood pressure during inspiration
- Constrictive pericarditis is when the sack has become all fiberous which cuases kussmals sign, it is a chronic condition and it is caused by viruses, surgery and radiaiton therapy.
what is teh duke criteria
There are two main diagnostic criteria -
* bugs grown form cultures
* evidence of endocarditis on an echo or new valve leak
There are 5 minor ones:
1. Fever > 38 oC
2. Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor)
3. Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjuntival hemorrhage, Janeway lesions)
4. Echocardiography findings (suggestive but not definitive)
5. Predisposition (heart condition or IV drug user)
6. Microbiologic evidence (Positive blood culture but not meeting major criteria)
This is the duke criteria. Definitive Diagnosis requires 2 Major or 3 Minor + 1 Major or 5 Minor
Use the mnumonic of BE FIVE PM ot remember the criteria
what percentage of people wth DVT will deveop PE
10%
what are teh 3 main symptms of DVT
SOD
coughing up blood
pleuric chest pain - pain on breathing in
