Cardiac Flashcards
Physiology of Coronary artery disease
plaques form in coronary arteries due to atherosclerotic deposits
this occludes the coronary artery supplying the heart
less blood flow to heart → myocardium necrosis due to lack of oxygenation anwd blood flow → acute MI
Difference between subendocardial and transmural infarct
subendocardial: NSTEMI - plaque ruptures to cause partial occlusion to artery, infarct to subendocardial myocardium→ myocardial ischaemia + angina
transmural: STEMI - complete occlusion of artery, → myocardial necrosis + MI
What drug classes are contraindicated in HF?
NSAIDs
CCBs
Trimethoprim
Antidepressants
Drugs causing hyperkalemia
What is angina definition?
temporary loss of blood supply to heart, causing chest pain
What causes angina pectoris (stable)?
stable plaque
chest pain brought on by exertion (exercise)
What causes unstable angina?
haemodynamically unstable plaque
What are the 3 stages of atheroma formation in atherosclerosis?
3 stages of atheroma formation:
1) fatty streak formation - lipids deposited in tunica intima layer → deposits + vascular injury → inflammation, ↑ permeability and WBC recruitment to site. Macrophages phagocytose the lipid → foam cell production
2) fibrolipid plaque formation - lipid in tunica intima layer stimulated fibrocollagenous tissue formation → thinning of muscular media
3) complicated atheroma - plaque calcifies as lipid deposits acquire Ca2+ → rupture activates thrombosis (clot formation)
partial occlusion → myocardial ischaemia + angina
complete occlusion → myocardial necrosis + MI
Primary v secondary MI?
1°: primary coronary artery event due to atherosclerosis
2°: secondary due to imbalance in myocardial O2 supply and demand w/o atherothrombosis (eg severe anaemia, coronary artery spasm)
What are causes of left-sided heart failure?
CAD
HTN, aortic valve disease, mitral valve disease - ↑ workload (afterload)
MI = ↓ myocardial mass
cardiomyopathy eg amyloid, sarcoid
What are causes of right sided heart failure?
Pulmonary HTN
tricuspid valve disease
pulmonary valve disease
Conditions which increase afterload in Right sided HF:
increased afterload:
pulmonary HTN - pulmonary vessels are constricted idiopathic
PE in the pulmonary circualtion - inc pressure in pulmonary artery (similar to pulmonary HTN)
cor pulmonale 2 ° to COPD - less ventilation due to hypoxic vasoconstriction of pulmonary vessels (eg capillaries in alveoli), pulmonary artery pressure increases, therefore RV afterload increases as RV must pump more blood to overcome the pulmonary pressure, causes right-sided hyeprtrophy
What is SV?
amount of blood ejected from LV ventricle with each contraction
Pathophysiology of HF with reduced ejection fraction (HF-rEf) - SYSTOLIC
occurs in LV myocardium where blood accumulates in the LV (blood cant get pumped out of heart)
increased preload (FS LAW)
reduced contractility (due to thin, weak myocardium)
Ef less than or equal to 40% (proportion of blood being pumped out of the ventricle)
overall reduced CO
What is preload?
increase in ventricular filling = increased in myocardium stretch = increased venous return
What 3 physiological factors affect SV?
preload (∝ to SV)
contractility (∝ to SV)
afterload (NOT ∝ to SV)
What is pulse pressure?
difference between systolic and diastolic BP
What is afterload?
pressure that ventricles must overcome to push blood into aorta
CO equation
CO = HR x SV
(amount of blood pumped in 1 min) = (no of times heart beats in 1 min) x (amount of blood ejected from LV ventricle with each contraction)
afterload is same as what pressure?
diastolic BP
Equation for CO
CO = HR x SV
Physical exam signs of Right-sided HF
oedema in feet, ankles, legs (sacrum if bed bound)
ascites (fluid in abdo cavity)
hepatomegaly (enlarged, palpable, tender)
raised JVP
Exercise intolerance
Signs and symptoms of Left-sided HF
Dyspnoea
Orthopnea (dyspnoea when lying down)
PND
Bibasal creps
Cardiomegaly (displaced apex beat)
Pulmonary congestion and oedema (crackles)
Exercise intolerance
Physiology of Diastolic HF or ‘HF with Preserved Ejection Fraction (HF-PEF)’
HF when the myocardium is near-normal
Ef greater than or equal to 50%
the issue lies in filling - decreased filling activity (preload)
increased afterload
myocardium is stiff, non-compliant (doesnt want to stretch)
Conditions which cause decreased preload in diastolic HF?
can occur 2° to ischaemic Heart disease/MI
- muscle replaced with fibrous tissue in ischaemic heart disease
- this stiffens muscle
restrictive cardiomyopathy (amyloidosis)
- muscle infiltrated with light chains called amyloid deposits accumulate in the myocardium
- myocardium loses ability to stretch/contract
cardiac sarcoidosis
- rare conditions where immune cells accumulate into granulomas and deposit
- causes muscle wall to stiffen
constrictive pericarditis
- when granulation tissue forms in the pericardium
- causes loss of pericardial elasticity
- this leads to restriction in the ventricular filling
Conditions which increase afterload in diastolic HF?
HTN: high pressure in the aorta so the ventricle increases cardiomyocyte size to compensate =more sarcomere = bigger cell = more power = more blood needing to be pumped out
aortic stenosis (aortic valve disease): aortic valve stiffens, LV requires more contractile force to pump blood past it, and myocyte increases
Diastolic HF can easily progress into systolic HF
What happens if you constantly increase preload in right sided HF?
constantly increased preload
over time myocardium constantly hypertrophies
loses contractility
myocardium weakens over time → RIGHT HF
Conditions which increase preload in right sided HF:
Pulmonary valve regurgitation: if pulmonary valve damaged, instead of going to the pulmonary vasculature, will accumulate in RV, expand muscle, RV weakens over time
Tricuspid valve regurgitation: tricuspid valve damage, more blood backs into RA and leaks into RV, expands muscle, RV weakens over time
How can inferior MI result in HF?
MI: rupture of coronary artery plaque/thrombosis
this decreases perfusion to that region of the myocardium
therefore less contractility of that
leads to HF
Why are IV drug users at risk of getting infective endocarditis?
IV drug users have weak tricupid valve
infective carditis (bacteria eg S.aureus targets valves as they have poor blood supply, over time valves degenerate) → Right HF
IE weakens already weak valves
leads to Right HF
Compensatory mechanisms in response to low CO (sympathetic NS)
low CO from heart = low arterial BP = less blood getting around body = less tissue perfusion = risk of becoming hypoxic and eventually necrotic
ELECTRICAL ACTIVITY:
carotid sinus detects low BP - sends signals to medulla - activates sympathetic NS - tries to raise HR, contractility
SA node stimulated → increases HR →, therefore, CO increases
therefore body becomes tachycardic
CONTRACTILITY:
fibres stimulate b1 receptors → increases myocardiocyte contractility → inc SV → inc CO → inc BP
VENOUS/ARTERIAL:
a1 receptors on SMC → inc norepinephrine released → inc vasoconstriction → inc venous returns → inc preload → inc SV → inc CO → inc BP
Management of person with confirmed HF-rEF?
step 1
ACEi (or ARB in pts non-compliant with ACEi) and B blocker
step 2
MRA (eg spironolactone) in addition to step 1
check Na and K before starting MRA , assess renal function
step 3
Replace ACEi with sacubitril valsartan if the ejection fraction is less than 35%.
SGLT2i - Dapagliflozin
Lifestyle management
What is Peripheral arterial disease (PAD)?
narrowing of arteries resulting in restricted blood flow
What are 2 types of PAD?
Occlusive - build of plaque (atherosclerosis) or embolus - narrowed artery - reduced tissue perfusion
Functional - blood vessels not working properly - intermittent arterial constriction - decreased diameter - less tissue perfusion (eg Raynauds disease - causes numbness in digits)
Signs of HF on CXR
A
B
C
D
E
Alveolar oedema - fluffiness and grey
Kerley B lines - small lines of pocket of fluid
Cardiomegaly
Upper lobe diversion - upper lobe pulmonary venous congestion - elevation of left atrium
Pleural effusion
When would you start ivabradine (Specialist) for HF pts?
NYHA class II to IV stable chronic HF with systolic dysfunction AND
who are in sinus rhythm with a heart rate of 75 bpm or more AND
who are given ivabradine in combination with standard therapy including beta-blocker therapy, ACEi and MRAs, or when beta‑blocker therapy is contraindicated or not tolerated AND
Ef less than 35%
What would you give a patient with LV systolic dysfunction if symptoms persist even after taking ACE inhibitors and Beta-blockers?
MRAs
When to give sacubitril valsartan in chronic HF pts?
Sacubitril valsartan is recommended as an option for treating symptomatic chronic heart failure with reduced ejection fraction, only in people:
with New York Heart Association (NYHA) class II to IV symptoms and
with a left ventricular ejection fraction of 35% or less and
who are already taking a stable dose of angiotensin‑converting enzyme (ACE) inhibitors or ARBs
What does specialist management of HF-REF involve after steps 1 and 2?
Replace ACEI with sacubitril valsartan if Ef <35%
An SGLT-2 inhibitor (empagliflozin or dapagliflozin).
Ivabradine for people in sinus rhythm with a heart rate over 75 bpm AND Ef less than 35%.
Hydralazine and nitrate (especially if of African-Caribbean descent).
Digoxin for people in sinus rhythm to improve symptoms.
Aortic stenosis pathophysiology
calcification of aortic valve
left blood passes fromLV to aorta
LV hypertrophy over time
LA also enlarges
if left untreated can cause HF
Changes to ECG Leads II, III and aVF are associated with with artery?t
Right coronary artery
What is pathiphysiology of STEMI?
Complete occlusion of one or more coronary arteries due to a thrombus (made up of aggregated platelets and thrombin)
reduces oxygen perfusion to myocardium
= transmural infarction
Management of STEMI?
MONA is a mnemonic for the initial management of a STEMI.
Morphine
Oxygen (saturations under 94%)
Nitrates
Aspirin (300mg loading dose)
What produces ST elevation in the precordial leads (V1-3)
Left anterior descending (LAD) occlusion
What produces ST changes in the inferior leads (II-III-AVF)?
Right coronary artery (RCA) occlusions
What produces ST elevation in the lateral leads (I, AVL and V5-6)
Left circumflex artery (LCA) occlusion
Which heart sound is associated with aortic stenosis and how to accentuate, where does it radiate?
Mid-systolic ejection murmur
Ask pt to sit forward better heard on held inspiration
Radiates to carotid
Which heart sound associated with mitral regurgitation and how to accentuate, where does it radiate?
Holosystolic murmur
Best heard in left lateral decubitus position
Radiates to left axilla
How would you detect and diagnose pts with AF?
Perform manual pulse palpation to assess for an irregular pulse if there is a suspicion AF. This includes people presenting with any of the following:
breathlessness
palpitations
syncope or dizziness
chest discomfort
stroke/TIA
12-lead ECG to cofnirm AF diagnosis
ECG Features of AF
Irregularly irregular rhythm
No P waves
Narrow QRS complex (120 ms)
What is orbit bleeding score for?
bleeding risk in AF pts on anticoags
What is HAS-BLED score for?
Estimates risk of major bleeding for patients on anticoagulation to assess risk-benefit in AF care
WHat causes holosystolic murmur?
whooshing sounds
occurs due to mitral/tricuspid regurg, VSD
Common causes of mitral regurgitation?
Rheumatic fever
ischemic heart disease
mitral valve prolapse
Common causes of tricuspid regurgitation?
Rheumatic fever
Infective endocarditis
What is ventricular septal defect (VSD)?
congenital abnormality causing blood to flow between RV and LV due to hole in AV septum
How is aortic stenosis murmur best describe and where is it best heard?
crescendo-decrescendo
2nd ICS, right sternal edge border
radiates to carotid
How is mitral valve prolapse best described and where is it best heard?
mid-systolic click, followed by a mid or late-systolic murmur
Heard loudest at the apex
How is tricuspid regurgitation murmur best described and where is it best heard?
pan systolic murmur, heard loudest at 4th ICS
Lower left sternal border
Warfarin moa
inhibits epoxide reductase
this prevents the reduction of vitamin K to its active hydroquinone form
this in turn acts as a cofactor in the carboxylation of clotting factors II, VII, IX and X and protein C.
T or F - Leftsided HF leads to right-sided HF?
true
Which vessel connects the aorta and pulmonary artery in foetal life?
Ductus arteriosus
What is Staling law?
The Frank-Starling law states that the force or tension developed in a muscle fibre depends on the extent to which the fibre is stretched.
In a clinical situation, when increased quantities of blood flow into the heart (increasing preload), the walls of the heart stretch.
What does Frank-Staling Law indicate in HF?
SV in a normal heart responds to changes in preload. the greater the EDV in LV, the higher SV should be
due to stretch in the cardiac myocytes.
This effect only occurs up to a point, as can be seen in HF, which prevents this response from occurring due to excessive stretch of the cardiac myocytes.
What is ejection fraction defined as?
SV/EDV = the amount of blood (as a percentag) that is pumped out of a filled ventricle with each heartbeat.
What is preload defined as?
the stretch of myocardium or end-diastolic volume of the ventricles
A 42-year-old woman presents to the clinic complaining of episodes of dizziness and light-headedness, especially when standing up quickly. On examination, her blood pressure is 120/75 mmHg while sitting and drops to 95/60 mmHg on standing. Her heart rate increases from 70 bpm to 88 bpm upon standing. She has no other significant findings on examination.
What nerve is responsible for this reflex?
Vagus nerve - Vagus nerve is correct. The vagus nerve (cranial nerve X) plays a crucial role in the baroreceptor reflex, particularly in mediating the parasympathetic response. When there is a decrease in blood pressure, the vagus nerve activity is reduced, which leads to an increase in heart rate. This response is part of the body’s mechanism to elevate blood pressure.
Which condition presents with pulsatile hepatomegaly due to the backflow of blood into the liver during the cardiac cycle?
Tricuspid regurgitation
What is Becks triad? (acute and chronic)
hypotension, jugular vein distension, and diminished heart sounds
What is cardiac tamponade?
acute tamponade triad (hypotension, venous distension, and diminished heart sounds)
chronic compression triad (high venous pressure, ascites, and diminished heart sounds)
