Cardio Flashcards
What does an atherosclerotic plaque consist of
Necrotic core
Connective tissue
Fibrous cap
Lipids
Which layer of the vessel does athlersclerotic plaque form
Intimal layer of arteries
Mechanism of clot formation: step 1
Formation of fatty streak. In first 2 decades.
LDL deposited in intimal layer. Gets modified into oxidised LDL.
Causes endothelial damage that secretes chemoattractants. Monocytes and T lymphocytes.
Modified LDL taken up by macrophages that become lipid ladent macrophages.
Fatty streak formed of:
Lipid Ladent macrophage and T lymphocytes
Athlesclerotic clot forming. After fatty streak. Step 2
Formation of intermediate lesions.
Macrophages become foam cells.
Platelet adhere
T lymphocytes and foam cells secrete interferons that causes smooth muscle cells to accumulate.
Foam cells. T lymphocytes. Smooth muscle cells and platelets
Atherosclerotic clot formation step 3
After intermediate lesions
Formation of plaque.
Foam cells die and form necrotic core
Platelets secreting platelets derives growth factors that’s causes smooth muscle proliferation and progresses into fibrous cap
Fibrous cap has collagen- strength- and elastin- flexible
Atherosclerotic clot is constantly growing and reciding. What are the 2 main complications that could cause
1 lumen narrowing- plaque stenosis. Covers 50-75% of coronary=SCAD. Or peripheral vascular disease
2plaque rupture. Atherothrombotic occlusion.
Exposure of basement membrane. Activated massive clotting cascade= infarcts. Either in location or downstream. Causes ACS or stroke
Where are atherosclerotic plaque likely to form
Areas of turbulent flow. Bifurcation. Changes in diameter or thickness
Outcomes of a plaque
Plaque erosion- emboli. Causes infarct. Second most prevalent cause of coronary thromboses
Athlersclerotic aneurysm. Rupture of a AAA
Risk factors for atherosclerotic plaque
Hypertension Diabetes M Obesity Family history Hyperlipidemia Age Smoking
Stable angina pathophysiology
Coronary artery’s are low resistance and microvessles have variable resistance
Atherosclerotic plaque forms
Perfusion dropped.
Dilation of small vessels as much as possible to normalise flow.
During exertion. Required perfusion increases.
Small vessels unable to dilate anymore as they are maximally dilated.
Required flow in normal Q=3m/s. In exertion Q=15m/s
Anginal pain
Anginal chest pain typical qualities
Central crushing chest pain radiating to jaw and arm.
Pain onset by exertion.
Pain improves with rest or GTN
3=typical anginal pain
2=atypical
1= non anginal
What is the rating of anginal pain compared against
CAD risk probability.
Compares score with age to asses likeliness of ACS
Investigation after assessing risk of angina
Low risk. Move onto another differential
Medium risk- stress echo or exercise test.
Very high risk then progress to management of SCAD
Primary prevention of angina/atherosclerosis
Reduce risk factors, Obesity, diet smoking
Statins
Antihypertensives
Better control of diabetes
Secondary prevention of angina
Same as primary prevention plus anti platelets. Aspirin and clopidogrel
First line management of SCAD
Symptomatic -GTN PRN and how to use it
Disease modifying.
B blockers, or CCB.
(These are first line and reduce symptoms)
Antiplatelet
Preventative
Antihypertensives- CCB or ACEi
Information on lifestyle
Statins
What can aggravate angina
Exertion
Large meal
Emotion
Weather
Name B blockers used for angina and ACS and their CI/ SE
Bisoprolol
Atenolol
For anginal
Atenolol
Propranolol
Metopranolol
For post MI
CI- asthma. Prinzmetal angina. COPD. High doses in HF. Bradycardia
SE fatigue. Hypotension, bradycardia, sexual dysfunction
what are CCB
name a few types
method if action
and their uses
Amlodipine
L-Type CCB
smooth muscle dilators (-ve Ionotropic)
These are arterodilaters. Reduced after load and energy needed to produce same CO. Reduces heart workload.
Use in coronary spasm( prinzmetal angina)
Cause odema in legs since they are arterodilaterers. CI in HF
give an example of a Short acting nitrates and its method of action
GTN sublingual
Venodilators
give an example of a long acting nitrates and its method of action
Veno and arterio dilators
Nicorandil
HCN channel slower
Ivabidrine
Surgical management for angina
Pericuteanous coronary intervention.
Indications are poor response to meds. Previous MI
Treatment to include with PCI
Drug illuding stents
Dual antiplatlet
Prinzmetal angina
ECG changes
Cause and treatment
Coronary artery spasm Shows ST elevation as pain occurs and subsided with it Pain occurs at rest CCB Amlodipine Long acting nitrates ivabridine. CI: B blockers and aspirin
ECG of SCAD
Normal or ST Depression plus T Wave inversion
Aspirin and clopidogrel drug class
COX inhibitor and GP2b3A agonist
Type of chest pain associated with ACS and presentation
Central crushing chest pain. Radiating to jaw and arms. Persistent pains. SOB Palpitations Nausea and sweating
Patients presents with suspected ACS
Investigations
12 lead ECG
Cardiac enzymes
Bloods FBC U&E Glucose Lipids
CXR looks for oedema, HF sign, cardiomegaly
Name cardiac enzymes
Troponin
Creatine kinase
Cardiac isoenzyme
Lactate dehydrogenase
Signs of ACS
Distress, anxiety, pallor, sweatiness
Bp HR up or down
4th heart sounds.
Signs of HF( oedema JVP 3rd heart sounds) Pansytolic murmurs (papliary muscle dysfunction)
Complications of ACS on presentation
Syncope, low BP
Oedema
Epigastic pain
Vomiting
Emergency treatment if ACS
MONA Morphine Antiemetic Oxygen if hypoxia Nitrates. GTN Antiplatlets- aspirin 300mg
Results for NSTEMI/UA ECG
Normal
ST Depression
T wave inversion
Both of the above
ACS ECG shows NSTEMI/UA
Troponin=-ve
-ve cardiac enzymes=UA
No permanent damage occurred
No necrosis
ACS NSTEMI/ UA with +ve cardiac enzymes and T wave
Suggests NSTEMI. There could be necrosis
T wave inversion also shows necrosis
ACS without stemi treatment
Dual antiplatelt therapy
Anticoagulation (antithombosis) LMWH or warfarin
Anti ischemia agent (anginal treatment) B blockers (not biseprolol) or CCB + GTN
General management for ACS
Antiplatelet Anticoagulation Bed rest for 48 hours continue B blockers Secondary prevention Antihypertensives Aldosterone antagonist if evidence of HF Statins Better DM Stop smoking Exercise Diet
Assessing risk for ACS NSTEMI/UA
Grace score
Surgical treatment for NSTEMI/UA
Unstable= PCI is CABG
STEMI ECG
And results
T wave peaking pointy St elevation T inversionI Deep Q wave- suggests full thickness infarct Weeks after Q&T wave still show
New LBBB pattern
Troponin and enzymes elevated
Creatine kinase
Management for STEMI
Reperfusion therapy.
If patient presents within 90 minutes of STEMI then PCI
Followed by dual antiplatelet
After 90 mins to 12 hours then fibrolytic therapy. Alteplase/reteplase tpa
Rescue PCI if fibrolytic.
Give them anti coagulation
Post 12 house- dual antiplatlet+ anticoagulation
Complication of MI
Atrial or ventricular arrhythmia LBBB Heart failure occurs in 40% mural thrombi drsslers
Pt presents with signs and symptoms of MI but ECG and chest X-ray are clear. Describe the pain as tearing. What is differential
Suspect Dissection. Use emergency CT. correct in surgery
Stages of hypertension
Stage 1 140/90
Stage 2 160/100
Severe 180/110
Requirement to treat hypertension
If stage 1 plus organ damage
Stage 2 or severe
Diagnosing hypertension
Ambulatory blood pressure monitor if elevated Biochemistry U&E LFT FBC GFR glucose Fundiscope for hypertensive retinopathy HBA1C
Treating hypertension pharmacological
Over 55 or Afro cardibean = CCB
Under 55 anything else = ACEi
ACEi untolerated then ARB
Then B blockers
Then CCB
Then thiazides like diuretics
Treating hypertension conservative
Main 3
Lose weight
Drink less booze (booze BP)
Reduce salt intake
Smoking, reduced stress. Coffee
Hypertension prevalence
One quarter of adults and half of those over 60
Complications of hypertension
Biggest one is stroke
MI Aneurism renal dysfunction heart failure
CI: oral contraception and antidepressants
Medication stopped before surgery
Hypertrophic cardiomyopathy.
inheritance pattern
prevalence
pathophysiology
Autosomal dominant
Prevalence 1 in 500
Mutations cause hypertrophy of ventricles and septum
Causing LVOT obstruction
Signs and symptoms of hypertrophic cardiomyopathy
Asymptomatic. First symptom can be sudden death. 6%
Signs. Crescendo de crescendo early systolic murmur
Syncope
Dyspnoea
Chest pain
Ejection systolic murmur due to LVOT
Jerky carotid pulse
S4 heart sounds due to crack when atria contract
Causes of ejection systolic murmur
Obstruction or stenosis
Pansystolic murmur is a sign of
Mitral regurgitation.
VSD
Pansystolic murmur is a fixed volume sounds that’s occurs between S1 and S2 since as blood is ejection it goes up into across: leaky mitral valve, septum
Differentiate HCM and Aortic stenosis since they both have the same ejection systolic murmur
Patients does valsalva or stand up from squatting since this (reduces filling) decreases preload so less blood in LV. (reduced CO)
Murmur is louder in HCM since less blood pressing back against ventricle wall so obstruction is larger
Murmur is quieter in aortic stenosis since less blood is leaving past stenosis
Investigation for HCM
ECG- shows T wave inversion Q wave AF
Gold standard is echo or cardiac MRI
HCM treatment
Symptomatic treatment
B blockers or CCB vamirpil. Reduce HR cause more filling time so less obstruction
If AF of Vt then add amiodarone plus warfarin
Preventing sudden death
If high risk then Implantable cardiac defibrillator
Screening in relatives
Dilated Cardiomyopathy
Autosomal dominant
Cytoskeleton abnormality leading to dilated ventricles
Presentation of dilated cardiomyopathy
Presentation similar to HF since dilation can cause HF
Symptoms SOB
Fatigue
Signs oedema Raised JVP Pleural effusion S3 heart sound. Physiological in young people sound of blood hitting LV after mitral valve opens. Pathological means dilated ventricle
Investigations in Dilated cardiomyopathy
Echo- gold stander- shows dilation
CXR
Treatment of dilated cardiomyopathy
Transplant since 40% mortality in 2 years
Digoxin ACEi ICD diuretics
Arrhythmogenic cardiomyopathy details
Autosomal recessive
Mutation in Desmosomes causes fibrosis which causes arrhythmia
Presentation is arrhythmia or sudden death
cardiac MRI shows fibrosis
B blocker for symptomatic
Amiodarone
ICD
Commonest sites for aneurysm
Abdominal aorta Iliac Poptial Femoral Thoracic
Prevalence of AAA
5% in over 60
5m=F
Screening program for AAA
Men aged 65-75 echo
Presentation and treatment of AAA
Severe pain Epigastic radiating to the back Hypotension Tachycardia Anemia Sudden death
If small then risk factors and surveillance (every 3 months) small is less than 5.5 cm diameter. If larger than 5.5 or rapidly growing then operate
If large then surgical repair of gortex graft or stent
Risk factor of AAA
Age Male gender Hypertension Smoking Hyperlipidemia Atherosclerosis
Aortic dissection
what is it
presentation
Investigation
Treatment
A tear in the intimal layer of artery causing blood to enter medial layer and the intimal layer gets cleared
Rf and causes: ehler danlos syndrome, Marfans (eaker connective tissue) Male over 50
Sudden onset chest pain. Not radiating. Tearing pain Pulse defect Left right BP different Syncope, Hyper or Hypotension Develop aortic regurgitations Coronary ischemia and tamponade
ECG, CXR and CT angiography
Surgery is corrective
tetralogy of fallots pathophysiology
misaligned VSD
overriding aorta
RV hypertrophy
Pulmonary stenosis/block of RVOT
essentially get a Right to left shunt
what does maternal alcohol or infection cause
alcohol= septal defect infection= PDA and valvar defect
explain foetal circulation
umbilical vein (ligementum teres) to IVC via ductus venosus (ligementum venosus) then foramen ovalue and Ductus arteriosis (ligamentum arteriosis)
signs of congenital heart disease
Central cyanosis clubbing due to prolonged cyanosis pulmonary hypertension syncope eisenmenger syndrome growth failure squatting
explain central cyanosis
right to left shunt as complete mixing of ventricular blood- in fallots
explain pulmonary hypertension and eisinmenger syndrome
SD or VSD (eisinmengers complex) causes left to right shunt which causes increased pressure on pulmonary causing pulmonary hypertension which causes RV hypertrophy which causes right to left shunt
fallots presentation
Squatting
cyanosis
syncope on exercise
fallots treatment
O2 if cyanosed
squat as this +PVR -VR -Right to left shunt
B blockers as reduce strain and surgery
Ventricular septal defect prevalence
most common conginetal heart defect. 1 in 500
Ventricular septal defect
presentation, signs, symptoms and murmur
treatment
presents with pulmonary plethora (radiological finding, patinet looks pink ), increased perfusion to lungs. symptoms include SOB Tachypnoea Tachycardia cardiomegaly.
pansystoloc murmur, smaller the hole, less serious the disease, more sound
Treatment surgical
shunts right to left and left to right
left to right is how it usually starts of, except fallots due to overriding aorta, L to R causes pulmonary plethora and pulmonary hypertention which then starts to become R to L which gives cyanosis
atrial defect
Interatrial defects
atrioventricular spetal defects
L to R shunts, pulmonary plethora, SOB, increased RR and HR
big hole in heart common in downs, breathlessness can get eisinemgers syndrome needs corrective surgery
patent foramen ovale is associated with what
associated with increased risk of paradoxical embolism from stroke
where does ductus arterosis insert into aorta
between brachiocephalic and L common carotid
coarction of aorta
pathophysiology
signs symptoms complications and diagnoses
Narrowing of aorta at ductus arteriosus upper body hypertension lower body hypotension radiofemoral delay kidney injury scapular bruti, buzz CT/MRI diagnostic
Patent ductus arteriosis
pathophysiology
signs symptoms complications and diagnoses
DA in fetus shunts PA to aorta. in adult it shunts from aorta to PA. causes Pulmonary plethora, SOB tachypnoea/cardia low BP.
can cause LA LV dilation and RV hypertrophy
ECHO diagnostic
what causes ventricular dilation and hypertrophy
dilation is caused when there is excess blood entering the ventricle or atria, this can be due to increased entry or a back flow, as a result the heart dilates to accommodate flow and ends up being too dilated can lead to heart failure as it will stop pumping properly
Hypertrophy is caused when there is excess force to pump against, eg hypertension or increased after load.
PDA is a good demonstrator because there is increased blood flow into the left atria and ventricle there is LA LV dilation and because the pressure in pulmonary artery has increased there is RV hypertrophy
bicuspid aortic valve
prevalence and assosiations
usually tricuspid, 1-2% it isn’t, its the most common congenital valve defect
associated with coarction and aortic stenosis
what causes ventricular dilation and hypertrophy
ventricle pumps against pressure= hypertrophy
ventricle overload= dilation
in dilation there is displaced apex beat
what does s4 represent
contraction of a stiff ventricle, due to HCM, aortic stenosis
what does S3 represent
contraction of a stiff atria, high pressure atrial contraction against a ventricle, mitral stenosis, dilated cardiomyopathy CHF
What is the commonest valvar heart disease and its causes
aortic stenosis as caused by Bicuspid aortic valve.
degeneration and calcification, inflammatory proccess or rheumatic heart disease
risk factors for aortic stenosis
male diabetes hypertension smoking hyperlipidemia
pathophysiology of aortic stenosis
valve stenosis due to inflammatory process
causes increased after load and LVOT obstruction so LV hypertrophy so LA hypertrophy pulmonary oedema (cardiac failure)
presentation of aortic stenosis
dyspnoea
angina
syncope on exertion
signs of aortic stenosis
pulsus tardus - retarded- slow pulse
pulsus parvus -poor, weak pulse
S4- due to hypertrophic ventricle contraction
ejection systolic murmur
investigations and diagnoses of aortic stenosis
CXR may show calcification
ECG shows Hypertrophy
echo-diagnostic, can see LVOT obstruction
2 Treatments for aortic valve stenosis
valve replacement or TAVI
trans catheter aortic valve replacement
infective endocarditis prophylaxis
vasodilators are CI since wouldn’t change afterload, would lower BP and cause syncope
mitral stenosis pathophysiology what it causes and presentation, treatment
caused by calcification, rhematic heart disease or IE
LA hypertrophy, pulmonary oedema - presentation = SOB
pulmonary oedema- RHF
diastolic murmur.
diagnose by echo and treat with replacement valve
mitral regugitation
pathophysiology what it causes and presentation, treatment
rhematiod heart disease, calcification and IE.
bacflow during systole, causes LA dilation, LV dilation, displaced apex,
progressive HF
SOB oedema fatiuge lethargy
increased risk of IE
pansystolic murmur
replacement
Aortic regurgitation pathophysiology what it causes and presentation, treatment
LV dilation, Early diastolic decrescendo murmur
causes LVF and this causes symptoms of oedema, chest pain, fatigue, syncope, chest pain due to reduced coronary perfusion
management are vasodilators, B blockers.
causes of Heart failure
MI
Dilated cardiomyopathy - valve disease
Hypertension
most to least common
pathophysiology of HF, compensatory mechanism that try to keep patient alive
treat it like you have just lost blood. BP dropped:
RAAS activated, increased fluid reabsorbed=oedema
symathetic system activated adrenaline, positive chronotropic and ionotropic.
constriction of periphral vessles.
increase venous return .
all these do is make situation worst
release of naturetic peptides
function of naturetic peptides
inhibit ADH inhibit RAAS vasodilators decrease water reabsorption lower BP
signs of fluid overload
pulmonary oedema- SOB and orthopnoea ascites periphral oedema hepatomegally raised JVP
LV HF with preserved EF symptoms
SOB, orthopnoe.. fluid overload
fatiugue wheeze,
Nocturnal couch with pink sputum
nocturia- get up to pee, sign that daytime urine filtration is low
signs of LVHF
tachycardia, S3 and S4 cardiomegaly pleural effusion fluid overload symptoms(5)
what is the classification and staging of heart failure
new york heart assosiation classiification
I: asymptomatic
II: slight limitation mild HF
III:Marked limitation Moderate HF
IV: unable to carry out physical activity without discomfort Sever HF
Investigation and diagnoses of HF
bloods - Nauturetic peptides CXR- cardiomegaly pleural effusion and pulmonary oedema ECG- identify cause of MI Echo- assesmnet of LV function biochemistry- GFR, U&E Thyroid LFT
management of LV HF Pharmacological symptomatic treatment
Diuretics
start on thiazide (DCT) diuretic - bedfroflumothiazide
then loop diuretic - Furosemide
lastly aldesterone antagonist- spironolactone
management of LV HF Pharmacological control
ACEi-ramipril, SE is hypotension so administer v slowly
B Blocker, bisoprolol, Slows HR reduces work load, risk of hypotension so again start slow.
these reverse effect of activated sympathetic drive and RAAS to normalise flow and reduced workload on heart
if HF with AF the Digoxen
management of LV HF Pharmacological conservative
diet
smoking
weight loss
activity
who is at risk of a silent MI
Diabetics and Hypotensive patients
risk factors for infective endocarditis
previous IE Had prosthetic valve replacement congenital heart defect IVDU Bad dental health VSD PDA, any abnormal heart structure or valve disease
3 pathogens that can cause IE
Strep Viridans
Staph aureus
Enterococci
2 factors that lead to IE
Abnormal cardiac structure and bateremia
cause of Complications of IE
IE causes platelet and fibrin or bacterial accumulation.
these can be projected distally into anywhere in the body causing peripheral stigmata.
think of IE as a Heart disease that’s ejecting gunk everywhere
Complication/signs of IE
Stroke, AKI, PE or Peripheral stigmata:
petechiae, red spots
splinter haemorrhage, spots under nails
Oslers nodes- tender subcutaneous nodules in digits
Janeways lesions- nontender subcutaneous nodes in digits
Roth spots on fundescope- retinal infarct
Criteria used to diagnose IE
Modified dukes criteria
Investigations for IE
Echo cardiogram is gold standers Transeosphageal echo if looking at prosthetic valves Blood cultures FBC= low Hb high WBC High CRP High U&E CXR= pulmonary odema or PE ECG=PR elongation/heart block Increased INR
Treatment for IE
Initially IV antibiotics then continue oral antibiotics for 4-6 weeks
antibiotics- Benzlypenicilin & gentamyosin
MRSA= Vancomyosin
surgery if extensive
treat any complications
Prevention of IE
Good dental care, education of Risks like surgery and non medical procedure like tattoo and piercings
3 Diseases that class as Pericarditis
acute pericarditis
pericardial effusion & Cardiac tamponade
constrictive pericarditis
What is acute pericarditis and its cause
Inflammation of pericardium often idiopathic or due to viral Coxsackie B- Enterovirus
or post MI as Dressler’s syndrome
Diagnoses of acute pericarditis
2 out of these 3
characteristic chest pain
friction, pericardial rub
ECG changes
define pericardial chest pain
sharp central retrosternal and pleuritic- worst by movement and inspiration, made better by leading forwards . radiates to back and shoulder due to phrenic involvement
ECG changes of Pericarditis
PR depression and diffuse or wide ST elevation
signs and symptoms of pericardial effusion
Signs of PE or tamponade- Dysponea
cough, dry
hiccups
plus pericarditis signs
Investigations in Pericadial effusion
CXR- normal or effusion
troponin- normal
ECG- main diagnostic
difference between ECG of STEMI and pericarditis
STEMI- ST elevation is convex upwards
Pericardits - ST elevation is Concave upwards+ PR Depression
remember if you had an MI you’d be conVEXED too
Management for pericardial effusion or acute pericarditis
treat underlying issue.
NSAIDs or Colchoicne- reduces reoccurrence
cardiac tamponade
signs symptoms investigation and management
Dysponea, raised JVP Pulsus paradoxis
muffled S1 and S2. Tachycardia but hypotensive
ECG and Echo diagnostic
if small, manage like pericarditis if large then urgent draining
constrictive pericarditis
what is it how is it diagnosed and whats the treatment
calcification of pericardium
causes heart failure
diagnosed by CT or MRI
surgical treatment
causes of soft S1
Mitral regurgitation
causes of loud S1
mitral stenosis
causes of soft S2
Atrial Stenosis
What does S3 in old person suggest
Dilated ventricle
