CVS Flashcards
Causes of primary hypertension
Unknown. Combination of environmental and genetics. (95%)
Causes of secondary hypertension
(5%)
1. Renal disease 2. Endocrine - Conn’s syndrome; Cushing’s 3. Drugs (NSAIDs etc) 4. Rare tumours (eg. adrenal)
Drugs that cause hypertension
NSAIDs Combined oral contraceptive Coricosteroids Ciclosporin Cold cures e.g. phenylephedrine SNRI antidepressants Some recreational drugs such as cocaine and amphetamines
Lifestyle causes of hypertension
In order of effectiveness to decrease BP: Obesity (weight) Salt in diet Alcohol Exercise Stress
What is the main pathology of hypertension in white people
Changes in mechanisms that control total peripheral resistance. Eg. RAAS. Elevated Renin, Angiotensin II, Aldosterone.
May also be changes in CO, but this pathology is not as much of a driver as TPR changes, hence, treatment is more RAAS, rather than CO, targeted.
MAP = CO x TPR
What is the pathology of hypertension in black people
Increased TRP - but not driven by low renin profile.
Still target TPR over CO as first line, but not ACE inhibitors.
What is malignant hypertension and what are the complications
BP that is in the ~180-200/120-130 range.
Precipitates acute renal failure, heart failure and encephalopathy. Medical emergency.
What are the signs/ symptoms of malignant hypertension?
Rapid rise in BP.
Vascular damage - papillodema (although may not be present).
Headaches, visual disturbances.
What are signs of End organ damage in hypertension, how would you test for these to quantify risk
- Eyes - retinopathy - thick/ narrow arteries/ hemorrhage/ optic disc swelling (look at arteries in back of eye/ look for swelling)
- Cardiac - LVH - (ECG, echo, history of MI)
- Renal - protein in urine (Urine analysis)
Symptoms of hypertension
Usually asymptomatic. May be headache. Not v diagnostic.
How would you diagnose hypertension & stage it
Ambulatory testing / home testing - 1 week. <135/85 + no sign of EOD = no Rx <135/85 + EOD = Rx >135/85 + 20% Qrisk = Rx (Stage 1) >150/95 = Rx (Stage 2)
Outline treatment options for white pt with hypertension
Step 1: ACE / ARB
Step 2: ACE / ARB + CCB
Step 3: ACE / ARB + CCB + Thiazide like diuretic
Step 4: All above + (BB, alpha agonist, centrally acting drugs -moxonidine etc…)
Outline treatment options for black pt with hypertension
CCB first line. rest is the same as Caucasian treatment steps.
What would you use to manage blood pressure in a pregnant pt?
Methyldopa
What hypertension meds are contraindicated in pregancy
All? definitely ACE inhibitors - teratogenic
Methyldopa only safe one
How does methyldopa work?
Decreases DA synthesis - required for NA synthesis = decrease NA = decrease sympathetic = decrease CO & vasoconstriction
Name a centrally acting anti-hypertension (4th line)
moxonidine
Symptoms of HF
SOB
Fatigue
Swelling/ odema
Signs of HF
3rd heart sound
Swelling/ odema
Types of HF
HFREF - EF ~40%, systolic problem
HFPEF - EF ~50%, diastolic problem
Acute HF - medical emergency
Causes of HF
- IHD
- Hypertension
- Alcohol
- Cardiomyopathy
- Values
- Dysrhythmias
Causes of acute HF
- Decompensated - from existing pathology
2. New onset - MI, etc
Treatment targets chronic HF
Vasodilation: ACE inhibitor (+BB - low dose) Aldosterone inibitor
Symptomatic relief of congestion
Diuretic
Treatment targets for acute HF
Congestion - diuretics
NOT BB, or any vasodilators, unless already on these and require for another condition. b/c vasodilators will add to congestion, and BB could take EF into more dangerous level
Drug treatment chronic HF
Triple therapy + diuretic
ACE inhibitor + BB + aldosterone inhibitor
Lifestyle changes HF
Stop smoking
Low salt
Optimse weight & diet
Investigations HF
Bloods - BNP
ECG - hypertophy (long QRS), tall R wave, dysrhythmias
Echo - valve, EF
CXR - eliminate SOB differentials, infection , PE etc
Important diagnostic markets for HF
- BNP >100 ng/L
- Paroxysmal nocturnal dyspnea (only see this in HF or mital valve disease)
- 3rd heart sound
How do you diagnose HF
Eliminate other causes
BNP
PND
3rd heart sound - all good diagnostic indicators
Where is atherosclerosis most likely to form and what are the 3 main consequences
Medium - large arteries: peripheral or coronary arteries.
Coronary = heart attack
Carotids = stroke
Peripheral = gangrene/ limb ischemia
Risk factors for atherosclerosis
- Age (exponential increase in plaques over 55 years)
- Tobacco Smoking (tobacco - endothelial irritant)
- High Serum Cholesterol
- Obesity (increased fat around the heart)
- Diabetes (high blood sugar, damages endothelium)
- Hypertension (sheer forces)
- Family History
Where are plaques most likely to form
Where there is a change in blood flow.
Bends, bifurcation etc.
Describe the mechanism of athersclerosis
Inflammatory mechanism.
1.Stimulus (irritant) gets into endothelial (intima layer) and oxidises. This triggers an injury response by the endothelium.
2.Chemokines (maybe IL-1) released by endothelium to attract neutrophils.
3.Adhesion & migration of neutrophils into intima.
4. Neutrophils then attract more WBCs including macrophage. AT THIS POINT = FATTY STREAK, only inflammatory cells, macrophage & lipidsATTY
5.Macrophage engulfs LDL/ stimulant.
Over time, macrophage dies & get fat spill = necrotic fatty core.
Smooth muscle migrates to intima layer to form a fibrous cap. NOW INTERMEDIATE LESION W CAP FORMING.
6.This either stabalises (inflammation stops) or continues to be resorbed/ deposited & at risk of rupture (if inflammatory reponse continues). FIBROUS CAP/ ADVANCED ATHEROMA - this is the stage you will see patients - prone to rupture stage.
How is a plaque most likely to rupture
Deposition (bc of inflammatory response being continuously triggered) or hemorrhage
Summarise the stages of atherosclerosis
Fatty streak (think layer of inflammatory cells, macrophage & fat in intima) Intermediate lesion (some smooth muscle recruited to intima) Advanced atheroma (prone to rupture) - large necrotic core with fiberous cap - stage where you see patients
Outline the treatment for atherosclerotic plaques
SECONDARY PREVETION
Surgical: If detected at advanced stage & caused an acute coronary event, stroke or peripheral vascular disease = PIC (percutaneous coronary intervention) +/- stent, with anti-thombus drug on stent.
Pharmacological = statin
PRIMARY PREVENTION
Patient at risk, eg over 55 years, QRISK score 20% heart disease in next 10 years = statin.
What blood pressure is indicative of hypertension
140/90 - clinic
135/85 - home
What is the normal length of an R wave on ECG - at what length would you interpret hypertrophy on an ECG
Under 11-13 mm
In exceeds this - hypertrophy
(or hyperkalemia?)
What is the mechanism of Digoxin
Na+/K+ pump inhibitor
= Increase Na+ in cell
Na+/Ca2+ pump becomes inactive (bc no gradient driving Na+ into cell)
=Increase in Ca2+ in cell
This, = more ions in cell = more binding of troponin C = force of contraction
T/F digoxin is Positive Inotrope, bc contractility increased
Also increased parasympathic to heart - Ach - so negative chronotrope
What is heart conditions is Digoxin indicated for
Heart failure - bc decreases heart rate and increases contractility Arrhythmias - ↓ AV nodal conduction (parasympathomimetic effect) ↓ ventricular rate in atrial flutter and fibrillation
What type of calcium channels do CCB inhibit
L type - long Ca2+ voltage dependent channels - the ones that control Ca2+ sustaining contraction
What should verapamil not be used for and why
Heart failure
Because it is a negative inotrop - decreases contractility so may make HF worse
How do amlodipine and verapamil differe pharmacologically
Both target L type Ca2+ channels
Amlodipine targets them at rest = tonic vasodilation - smooth muscle
Verapamil targets during contraction = negative inotrope (contractility) - decreases work of the myocardium - acts on heart muscle more than smooth muscle
What additional property of propranolol means it is used to treat arrhythmia after heart attack
Sodium channel block
What transporter does furosemide block in the LoH to treat HF
NKCC2
Na+/K+/ 2Cl transporter
What is the mechanism of nitrates in treating angina
venodilation - reduce preload
What is the mechanism of CCB in treating angina
arteriodilator - reduce afterload of heart
List two second line anti-anginals and their mechanisms
Nicorandil - mixed venous and artery dilation
Ivabridine - block F type Na+ to lower HR (pacemaker currents) -ve chronotrope
What is the action of atenolol
Peripheral beta blocker
What is the action of doxazosin
Alpha-1 adrenoreceptor blocker - blood vessels
Indicated in hypertension
Can be used during pregnancy
Which antihypertensive is most likely to cause postural hypotension
CCBs
Which anginal drug causes tolerance
Nitrates
What is the mechanism of action for BB in HF
Blocking reflex sympathetic (NA) input to heart
What are the complications of IHD (atherosclerosis)
Angina, Myocardial Infarction, Heart failure
Cardiac causes of syncope
Ventricular tachycardia (very fast HR) Complete heart block (very slow HR) Both = unable to maintain cardiac output
Disruption to ventricular outflow
Aortic stenosis
Hypertropic cardiomyopathy
Symptoms of HF
Tiredness, lethargy - due to poor perfusion
SOB
Odema
PND - paroxysmal nocturnal dyspnoea
Signs of heart failure on an x ray
A - alveolar odema B - Kerley B line C - cardiomegaly D - distension of pulmonary vessels E - pleural effusion
How do you calculate HR off an ECG
Count the number of ‘big’ square (5mm = 0.2 sec) between the R waves and divide the number by 300
How can you identify normal, right and left heart axis
Normal:
I R wave positive
II R wave positive
III R wave 1/2 and 1/2
Right:
I R wave negative
II R wave positive
III R wave positive
Left:
I R wave positive
II R wave negative
III R wave negative
Signs of arrhythmia
Chest pain
Hypotension
Impaired consciousness
Pulmonary oedema
What is sinus bradycardia
Low HR - below 60 beats per minute
List the different types of sinus bradycardia and the causes
- Athletes
- Drugs - beta blocks, digoxin, antiarrhythmic drugs
- Intrinsic problems of the heart: MI/ infarction to the SA-node; fibrosis of the SA node
- Sinus sick syndrome - when your heart intermittently drops one or two beats (2s). On ECG, see bradycardia, that intermittently drops out. P waves lost for 2s = 10 big squares)
What are the complications of sinus node dysfunction
Thromboembolism - blood flow slows down - clot forms and travels into systemic circulation
What are neural causes of sinus bradycardia
Vasovagal - fainting and bradycardia
Carotid sinus syndrome
What is the immediate and longer term treatment for sinus arrthymias
Atropine (adrenaline) IV from 500 micrograms to 3mg - contraindicated in myasthenia gravis
Pace maker
What are the common causes of heart block
Coronary artery disease
Cardiomyopathy (elderly)
Fibrosis of conducting system (elderly)
AV or BoH –> Atrioventricular block
Lower than BoH –> Bundle branch block
What are the different types of AV block
1st - long PR interval - AV node conduction is slow
2nd - i) increasing PR interval, p wave drops out, cycle starts again - AV node problem
ii) PR interval normal - p waves drop out 2:1 P to QRS - think BoH level
3rd - complete heart block. p and QRS independent. Thin QRS = problem in BoH, Wide = purkinje
Type of Bundle branch block
RBBB - MaRRoW V2 - V6
LBBB - WiLLiaM V2 - V6
Decribe the patter as ‘deep slurred S waves’ on ECG in eg V5, V6 leads
How would you identify AV block from an ECG
Look at relationship between p and QRS - does P always come before QRS, if so, is it prolonged, changing/ constant?
Do QRS drop out?
Are they completely separate?
What is the most common arrhythmia
Atrial fibrillation
How long does Atrial fibrillation last
No more than 7 days
What are the complications of atrial fibrillation
Stroke - thromboembolus clot (or MI, or PVD)
Acute heart failure - bc of inadequate cardiac output from ventricles
What are the symptoms of atrial fibrillation
May be asymptomatic Palpitations Fatigue - if cardiac output is affected Acute HF signs if progressed to this SOB
How does atrial fibrillation look on ECG
Regularly irregular - no clear p waves
Describe the pathology of atrial fibrillation
Damage to the atrial myocardium = generation of ectopic beats, happens through:
Change in ion channels (eg post MI; or ischemia)
Change in Ca2+ regulation (as above)
Structural change (eg hypertrophy - hypertension, CAD ischemia etc)
Neural dysregulation - eg fibrosis of conducting tissue - age, hypertension, ischemia, hypertrophy
List some of the causes of structural remodelling of the heart
Aging, hypertension, valve disease, heart failure, myocardial infarction, obesity, smoking, diabetes mellitus, thyroid dysfunction, and endurance exercise training all cause structural remodeling
When would digoxin be indicated as rate control over a beta blocker
Patient with asthma
Patient that is sedentary
What is the mechanism of action of amioderone - how does it act as a rate control medication
Its a K+ channel inhibitor
Slows down the movement of K+ out of the cell as a part of repolarisation of membrane potential
Takes longer for cell to repolarise
Outline the treatment of Atrial fibrillation
- are they haemodynamically stable? If no - start heparin
- If stable:
- Rate control - BB
- Rhythm control - convert to sinus rhythm by electrical CD cardioconversion then rate control
Can do add on rate control with CCB, K+ inhibitors, depending on underlying heart condition
In which cardiac condition should negative inotropes not be used
Heart failure
BB are - but this is bc of their negative chronotrope effects
What assessment should always be done on a patient who had atrial fibrillation
Assessment for anticoagulation
How is atrial flutter treated
Most cases can be treated with radiofrequency catheter ablation of the re-entry circuit
+ Rate control with BB
Summarise cardiac medicine - what are the general groups
- Those that target the HEART:
Chronotropes - rate (BB, Digoxin)
Inotropes - contractility (CCB, Amioderone, Digoxin, Na+ blockers)
2.Those that target TOTAL PERIPHERAL RESISTANCE
ACE inhibitors
CCBs
Diuretics
Causes of infective endocarditis
abnormal valve
regurgitant or prosthetic valves are most likely to get infected.
Introduction of infectious material into the blood stream or directly onto the heart during surgery
Have had IE previously
IE presents with what 3 things
Fever + additional infection signs
Murmur - new, or worse
Emboli signs - splinter haemorrhages, Janeway’s lesions etc
What imaging would you do for IE
Transthoracic echo Transoesophageal echo (better sensitivity than first but unpleasant for patient)
Peripheral signs of IE - but remember not that common
Petechiae 10 to 15%,
Splinter hemorrhages
Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits)
Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole
Roth spots on fundoscopy.
What ECG changes might you see with IE
Prolonged PR interval
AV block
bc of anatomical relation of aorta abscess to AV node.
What is the best imagine test for confirming IE
TOE
Treatment of fungal IE
Amphotericin
Antibiotics for IE
Think - gentamicin
Prosthetic valcue - gentamicin + rifampicin, + either vancomycin or flucloxicillin (if staph confirmed)
Native valve - gentimicin, fluclox, ampicillin, or when confirmed for stap - just fluclox
Diagnosis for IE
2 Major
1 major + 3 minor
5 minor
Describe the diagnostic criteria for IE
MAJOR
- 2 positive cultures of typical pathogen
- 3 or 4 positive cultures of atypical pathogen >12 hours
- Single positive for coxiella burnetti
MINOR
- Prosthetic valve
- > 38
- Vascular signs - haemorrhages, janeway’s lesions etc
- Immunological signs - olser’s nodes, glomerulonephritis
- +ve blood cultures that dont meet criteria above
Investigations for IE
Blood cultures: 3 sets (6 bottles), from different sites at different times FBC - normocytic anaemia neutophillia CRP/ ESR Rheumatoid factor Serology - viruses
Urinalysis - haematuria
ECHO - TOE, or TTE if can’t tolerate but may not be able to see anything is smaller than 2 mm
Can do CT if needed
CXR
Regular ECG
Signs and symptoms of IE
Infection signs - fever, malaise, rigor, weight loss etc
Cardiac signs - murmur, breathless, chest pain
Emboli signs - vasculature, micro haematuria
Immunological signs - osler’s nodes
Risk factors for IE
Prosthetic valve - strep viridens
Prolapsed valve - strep viridens
IV drug user - R side of heart - risk of septic PE - staph a
Hickmen line/ long time - anyone in hospital - fungal
Catheters - enterococci
What is a bifid p wave - what pathology does it show
‘m’ shaped p wave - shows left atrial hypertrophy P mitrale
Peaked p wave - right atrial hypertrophy - P pulmonale
biphasic is where it goes up and down - also sign of left atrial pressure/ hypertropy
Changes to the PR interval indicate what conditions/ pathology
WPW syndrome - short PR, delta wave
Long = AV block - 1st?
What differentiates between type I and II 2nd degree heart block
PR interval
Type I = prolonging PR until resets
Type II = no change in PR
What are the signs of left ventricular hypertrophy on ECG
VI - S
V5,6 - R
If >35 mm = hypertrophy
How would you differentiate between supraventricular and ventricular tachycardia from an ECG
Supra - QRS usually normal (unless causing BBB)
Ventricular - wide based QRS
Inherited LV hypertrophy
Hypertrophic cardiomyopathy (HCM - SARCOMERE PROTEIN 1 in 500
Symptoms of HCM
HCM may cause angina, dyspnoea, palpitations, dizzy spells or syncope
Dilated cardiomyopathy
Dilated cardiomyopathy (DCM) – often caused by cytoskeletal gene *Presents with HF DCM - LV/RV or 4 chamber dilatation and dysfunction
Arrhythmogenic
Arrhythmogenic cardiomyopathy (ARVC/ALVC) – desmosome gene mutations
Inherited channelopathies
Inherited arrhythmia (channelopathy) caused by ion channel protein gene mutations These usually relate to potassium, sodium or calcium channels Channelopathies include long QT, short QT, Brugada and CPVT *Have structurally normal heart*
Present with syncope
Inheritance pattern of ICCs
Dominant
