cardio Flashcards
what is included in acute coronary syndromes (G)
unstable angina, STEMI, NSTEMI
acute coronary syndromes- occlusion, infarction (G)
OCCLUSION
- ua- partial of minor coronary artery
- NSTEMI- partial of major or total of minor coronary artery
- STEMI- total of major
INFARCTION
- ua- no infarction, just ischaemia
- NSTEMI- subendothelial infarction (area far away from coronary artery occlusion dies)
- STEMI- transmural infarction
acute coronary syndromes- ECG, troponin and creatinine kinase MBn (G)
ECG
- ua- normal, may show some ST depression/ T wave inversion
- NSTEMI- ST depression and T wave inversion, no Q waves
- STEMI- ST elevation in local leads (2+), Q waves (pathological) after some time
TROPONIN AND CREATININE KINASE MB
- ua- normal
- NSTEMI- elevated (increased with infarction)
- STEMI- elevated (increased with infarction)
troponin vs creatinine kinase mb for ACS (G)
troponin has a shorter half life than CK-MB so CK-MB better after a few days
coronary artery anatomy (G)
aorta -> RCA, LCA
RCA supplies the RA, RV, inferior LV, posterior septal area
LCA -> circumflex, LAD
Circumflex -> LA, posterior LV
LAD -> anterior LV, anterior septum
unstable angina definition (G)
Myocardial ischaemia at rest or on minimal exertion with the absence of myocardial injury- cannot be relieved with GTN or rest
unstable angina aetiology (G)
atherosclerotic plaque rupture and subsequent thrombosis and inflammation
unstable angina risk factors (G)
non-modifiable: age, gender, race.
Modifiable: hypertension, obesity, high LDL, smoking
unstable angina pathophysiology (G)
atherosclerotic plaque ruptures and thrombus forms around the ruptured plaque, causing partial occlusion of the minor coronary artery, causing reduced blood flow → myocardial ischaemia → angina
unstable angina key presentation (G)
central crushing chest pain, radiates to arms, neck and jaw. Is not relieved by GTN or rest, persists longer than 20 minutes, crescendo chest pain (frequent, easier to provoke)
unstable angina other symptoms (G)
sweating, dyspnoea, nausea, fainting, palpitations
unstable angina investigations (G)
1st: history
gold: ECG (ST normal or depression, NO ELEVATION), biomarkers (no troponin increase)
other: CT angiography- shows extent of occlusion
unstable angina differential diagnosis (G)
stable angina, pericarditis, myocarditis
unstable angina / NSTEMI management- immediate and long term (G)
immediate- MONAC
-morphine
-oxygen (if sats <94%)
-nitrates (GTN)
-aspirin (300mg)
-clopidogrel (75mg)
GRACE score- (6 month risk of death or repeat MI after NSTEMI)
prevention: 6As
-aspirin (300mg initial -> 75mg life)
-another antiplatelet: clopidogrel (75mg 12 months)
-atorvastatin (80mg life)
-atenolol or other BB eg metoprolol (BB or CCB)
-ACEi
-aldosterone antagonist if clinical heart failure (eg eplerenone once daily)
low risk: modify risk factors and monitor
high risk unstable angina, always for NSTEMI: invasive coronary angiography and PCI
unstable angina complications (G)
MI, stroke, heart failure
why is diabetes a major risk factor for silent MIs
-diabetic neuropathy
-patients don’t feel the anginal pain so may misdiagnose and die from sudden collapse
MI- type 1 vs type 2
T1- IHD- MI due to acute coronary event
T2- increased demand / reduced supply of oxygen or ca vasospasm
T3- sudden cardiac death/ cardiac arrest
T4- Associated with procedures eg PCI, stenting, CABG
NSTEMI definition (G)
non ST elevated MI. Acute ischaemic event causing myocardial cell necrosis and troponin release
NSTEMI aetiology (G)
rupture and thrombosis of atherosclerotic plaque causing partial occlusion of major CA or total occlusion of minor CA
NSTEMI risk factors (G)
non mod: age, male, race. Modifiable: hypertension, diabetes, obesity, high LDL, smoking
NSTEMI pathophysiology (G)
atherosclerotic plaque rupture and thrombosis causes partial occlusion to the coronary artery, this causes necrosis of cardiac tissue and infarction to the subendothelium
NSTEMI key presentation (G)
central crushing pain, radiating down arm, neck and jaw. Not relieved by rest or GTN spray. It persists for over 20 mins, feeling of impending doom
NSTEMI signs (G)
tachycardia
high/low BP
4th heart sound
NSTEMI other symptoms (G)
sweating
N+V
dyspnoea
fatigue
palpitation
NSTEMI investigations (G)
1st/gold
-ECG- ST depression, T wave inversion. Also R wave regression and biphasic T waves
-Biomarkers- elevated troponin
other: CT angiography, bloods
NSTEMI complications (G)
heart failure,
ruptured infarcted ventricle,
ruptured interventricular septum,
mitral regurgitation,
arrhythmias,
heart block,
post-MI pericarditis (Dressler syndrome)
STEMI definition (G)
ST elevated myocardial infarction. Ischaemic event leading to death of heart tissue and troponin release
STEMI aetiology (G)
rupture and thrombosis of plaque causing complete occlusion of major coronary artery lumen
STEMI risk factors (G)
non-mod: age, male, race.
Mod: hypertension, diabetes, obesity, high LDL, smoking
STEMI pathophysiology (G)
atherosclerotic plaque rupture and thrombosis causes complete occlusion of coronary artery leading to transmural injury and infarct to the myocardium
STEMI key presentation (G)
central crushing chest pain, radiates to the arm, jaw and neck. Not relieved by rest or GTN spray, it persists >20 mins, feeling of impending doom
STEMI signs (G)
tachycardia, high/low BP, 4th heart sound
STEMI symptoms (G)
sweating
dyspnoea
N+V
fatigue
palpitations
STEMI investigations (G)
1st/gold:
ECG (ST elevation, after some time: T wave inversion, deep broad Q waves, left BBB)
biomarkers: elevated troponin
other:
CT angiography
bloods
STEMI management (G)
Acute treatment: MONA (morphine, oxygen <92%, nitrates, aspirin)
Primary PCI if available within 120minutes of first medical contact or within 12hours of symptoms,
if unavailable, fibrinolysis to break down clot (e.g., alteplase). Consider PCI if this fails
Secondary prevention: aspirin, clopidogrel (antiplatelet), statin (atorvastatin), metoprolol (BB or CCB), ACEi, modify risk factors
STEMI complications- acute (G)
Heart failure due to ventricular fibrillation
rupture of infarcted ventricle,
rupture of interventricular septum,
heart block,
cardiogenic shocl
arrhythmias,
mitral regurgitation/ incompetence,
STEMI complications- long term (>2 weeks) (G)
-Dressler syndrome (autoimmune pericarditis)
-heart failure
-left ventricular aneurysm
how does an ECG change after MI (G)
-hyperacute T waves
-pathologically deep Q waves
-LBBB
what is indicated by pathological Q waves
transmural infarction- typically appear 6 or more hours after the onset of symptoms
stable angina definition (G)
A symptom of IHD
-central crushing pain due to decreased coronary artery blood flow,
-causes oxygen supply/ demand mismatch in exertion
stable angina aetiology (G)
narrowing of coronary artery by atherosclerosis.
Rare: reduced O2 carrying capacity (anaemia), peripheral resistance (LV hypertrophy), coronary artery spasm
stable angina risk factors (G)
non-mod: age, male, FHx, race
mod: obesity, T2DM, HTN, smoking, cocaine use, high LDL
stable angina pathophysiology (G)
-high oxygen demand on exertion. Narrowing of coronary arteries from atherosclerotic plaque
-reduces blood flow → myocardial ischaemia → angina
-atherogenesis: fatty streak → intermediate lesions → fibrous plaque
stages of atherogenesis
fatty streak
-appears in intimal walls (v early, less than 10 years old
-T cells and lipid laden macrophages- foam cell
intermediate lesions
-foam cells (bigger, taken up more lipid), T cells and vascular smooth muscle cells
-platelets also aggregate and adhere to the side, inside the vessel lumen
fibrous plaques
-advanced
-large lesions (foam cells, T cells, smooth muscle, Fibroblasts, lipids uptake with a necrotic core)
-they develop fibrosis cap over the top of lesion
atherogenesis in stable angina (G)
-symptoms start when 70-80% of lumen is occluded
-fibrous cap is strong and less rupture prone.
-If plaque is prone to rupture -> prothrombotic state; platelet adhesion and accumulation
-results in progressive luminal narrowing
stable angina key presentation (G)
central crushing chest pain radiating to neck, arm, jaw. It is relieved by GTN spray or 5 mins rest. Brought on by exertion
stable angina other symptoms (G)
dyspnoea, nausea, sweating, fainting, fatigue. Symptoms worsen with time
stable angina investigations (G)
1st line: ECG (normal)
gold: CT angiography (shows presence of luminal narrowing/ plaque)
other:
echo with exercise tolerance test (resting is normal, exercise is ischaemia
invasive angiography- shows pressure gradient across stenosis showing atherosclerotic arteries
stable angina differential diagnosis (G)
ACS
stable angina management (G)
Immediate symptomatic relief – GTN spray
Long term relief:
1st line – education/ lifestyle.
Beta blockers and/or CCB (amlodipine. Do not combine BB with non-dihydropyridine CCB). + other antianginal (long-acting nitrates, e.g. isosorbide mononitrate) (1st: CCB/BB → CCB + BB → CCB + BB + another antianginal)
Procedural intervention if pharmacological unsuccessful : PCI (less invasive but risk of stenosis), CABG (better prognosis but more invasive)
Secondary prevention: Aspirin, Atorvastatin, ACE inhibitor
stable angina complications (G)
MI, stroke, heart failure
Prinzmetal angina definition (R)
angina due to coronary vasospasm aka vasospastic angina
prinzmetal angina aetiology (R)
does not correlate with exertion. May be precipitated by smoking, cocaine, marijuana, emotional stress, extreme cold weather
prinzmetal pathophysiology (R)
coronary artery spasms and suddenly narrows
prinzmetal angina key presentation (R)
central crushing chest pain at rest which resolved with GTN spray
prinzmetal angina symptoms (R)
dyspnoea, sweating, nausea
prinzmetal angina investigations (R)
1st: ECG (ST elevation during acute episode), biomarker (not elevated)
gold: coronary angiography (ACh used to provoke spasm)
prinzmetal angina management (R)
1st: GTN spray
other: calcium channel blockers and long acting nitrates
stop smoking, reduce risk factors
AAA definition (G)
dilation of the abdominal aorta >50%,
diameter >3cm,
typically infra-renal,
in elderly men
AAA epidemiology (G)
elderly men
20% rupture anteriorly (very bad)
80% rupture retroperitoneal (less bad)
AAA aetiology (G)
mainly idiopathic
atheroma, trauma, infection
connective tissue disorders: Marfan’s and Ehlers-Danlos syndrome
AAA risk factors (G)
smoking,
atherosclerosis,
obesity,
hypertension,
increasing age
AAA pathophysiology (G)
inflammation and degradation of smooth muscle cells in all layers of vascular tunic →
loss of structural integrity of the aortic wall → widening of the vessel →
mechanical stress (HTN) acts on weakened wall tissue →
dilation and rupture may occur with leukocyte infiltration.
Dilation may disrupt laminar flow and turbulence causing thrombi to form in the aneurysm, and thromboembolism
true vs pseudo AAA
all 3 layers of vascular tunica (intima, media, adventitia)
pseudo- not all 3
inflammatory AAA (G)
usually in younger patients who are smokers
-atherosclerosis in arteries
-same symptoms with pyrexia
AAA key presentation (G)
-normally asymptomatic until rupture
-palpable pulsatile mass in abdomen
-often incidental finding
unruptured AAA other signs (G)
tachycardia, hypotension
Cullens and Grey turners sign in some cases
ruptured AAA symptoms (G)
-sudden epigastric pain radiating to flank
-loss of consciousness
-N+V
-hypovolemic shock
AAA investigations (G)
1st line:
abdominal USS
>3cm, if ruptured- immediate management. Used to assess aorta- cheap, easy, sensitive and specific
gold:
CT angiography
AAA differential diagnosis (G)
acute pancreatitis- typically more associated with grey turner/ cullens sign
appendicitis
AAA management if ruptured (G)
stabilise ABCDE,
Resuscitation measures (oxygen, fluids, aiming for lower than normal BP during fluid resus as higher BP may increases blood loss- known as permissive hypotension)
urgent surgery EVAR (stent through femoral arteries) or open surgery (laparoscopic).
AAA graft surgery- replace weakened wall.
100% mortality with no immediate treatment
AAA management if unruptured (G)
symptomatic- urgent surgical repair (EVAR or open surgery).
If asymptomatic- surveillance and risk management (smoking, diet, exercise, HTN)
If asymptomatic but aneurysm > 5.5cm/ rapidly growing/ 4cm for over a year- elective surgery (EVAR or open)
EVAR vs open surgery (AAA) (G)
EVAR- endovascular repair- stent inserted through femoral/ iliac artery, less invasive but more post operative complications.
Open surgery- fewer complications but more invasive
AAA complications (G)
ruptured aneurysm,
thrombosis, embolism,
abdo compartment syndrome
AAA prognosis
80% mortality if ruptured
AAA screening (G)
men in England are offered an ultrasound at age 65 to detect asymptomatic
Aortic dissection definition (G)
Tear in the intima of the aorta allowing blood to dissect the media,
forming a false lumen between the inner and outer layers of the media. (separating the layers apart)
-surgical emergency
Stanford classification for aortic dissection (G)
Type A –
affects ascending aorta and arch before brachiocephalic artery.
Proximal to left subclavian (2/3 are type A)
Type B – affects descending aorta distal to the left subclavian (descending thoracic).
Most common location:
sinotubular junction where aortic roots becomes tubular aorta (type A), (main one)
just distal to the left subclavian in descending aorta (B)
aortic dissection epidemiology (G)
men aged 50-70
aortic dissection aetiology (G)
Mainly mechanical wall stress due to risk factors.
Also, connective tissue disorders (Marfan’s and Ehlers-Danlos syndrome)
aorta conditions (bicuspid aortic valve, coarctation of the aorta, CABG)
aortic dissection risk factors (G)
hypertension,
smoking,
trauma,
raised LDL,
obesity,
sedentary lifestyle,
male,
increasing age,
family history,
AAA
aortic dissection pathophysiology (G)
Tear in the intima causes blood to pass through the media creating a false lumen where blood can pool.
As the dissection spreads, flow through the false lumen can occlude flow through branches of the aorta
including coronary, brachiocephalic, carotid, intercostal, renal and visceral > ischemia of supplied regions > organ failure and shock
aortic dissection key presentation (G)
sudden and severe ripping/ tearing pain in chest
aortic dissection other signs and symptoms (G)
-Asymmetrical blood pressure in arms (>20mmHg),
-hypotension/ shock,
-radial pulse deficit (radial pulse in one arm is decreased/absent and doesn’t match apex beat),
-diastolic murmur, aortic regurgitation,
-focal neurological deficit eg syncope (e.g., muscle weakness/paralysis – carotid and spinal arteries),
-interscapular and lower pain,
-cardiac tamponade
-chest and abdo pain
aortic dissection investigations (G)
1st:
-ECG (may have ST depression)
-CXR- shows widened mediastinum >8cm is suspicious
-transthoracic echocardiogram (intimal flap in acute, 2 lumens in chronic
gold:
-Transoesophageal echocardiogram
-CT angiogram (used when patient is haemodynamically stable
both look for intimal flap and false lumen
TTE vs TOE for aortic dissection
TOE is more invasive but more specific for AD and very sensitive
aortic dissection DD (G)
MI, cardiac arrest, pericarditis
aortic dissection management (G)
1st line- immediate surgery;
Type A- open surgery to replace aortic deficit with stent
type B- TEVAR (thoracic endovascular aortic repair
maintain haemodynamic stability- fluids, adrenaline, transfusion esp if hypotensive
medical:
Beta blocker (labetalol)
or
Non dihydopyridine CCB (diltiazem/ verapamil)
^^ to prevent reflex tachycardia and lower BP
vasodilator- sodium nitroprusside
aortic dissection complications (G)
cardiac tamponade
aortic regurgitation
pre-renal AKI
aortic dissection prognosis (G)
high mortality from rupture
DVT definition (G)
formation of thrombus in deep vein system
DVT aetiology (G)
virchow’s triad: venous stasis, endothelial injury, hypercoagulability
DVT/ PE risk factors (G)
Virchow’s triad:
Venous stasis (immobility, long haul flights, surgery. Stasis → aggregation of clotting factors).
Vascular injury (smoking, trauma - damaged endothelium cannot secrete anticoagulant chemicals).
Hypercoagulability (pregnant, COPD, obesity, malignancy, sepsis, oestrogen therapy, inherited thrombophilia – predispose to clots, e.g. antiphospholipid syndrome)
DVT pathophysiology
The major of thrombi occur in the lower legs below the calf which can impede minor veins eg ant/posterior tibial.
More serious (life threatening) DVT occur above the calf and can occlude major veins, e.g., superficial femoral, impeding distal flow.
The thrombus can embolise from the deep veins to the vena cava > right side of heart > pulmonary arteries and cause a pulmonary embolism.
DVT key presentation (G)
-unilateral calf swelling,
-tenderness,
-pitting oedema,
-dilated superficial veins,
-colour changes to leg,
-warm,
-erythema,
-cyanosis if complete occlusion of a large vein known as phlegmasia cerulea dolens
DVT investigation
Wells score (risk of patient having DVT or PE. <2 = unlikely.)
- If unlikely (<1), order D-dimer test (looks for fibrin breakdown products and clotting problems).
If D-dimer is raised, order doppler ultrasound of leg. If not raised then not PE. - If DVT likely >1, order doppler ultrasound.
doppler- if unable to compress vein = clot
(eg pitting oedema is 1 point, calf swelling 3cm more than other leg is 1 point)
DVT DD (G)
compartment syndrome, cellulitis, acute limb ischaemia
DVT management (G)
1st line – DOAC anticoagulation: apixaban or rivaroxaban.
Long term: LWMH, DOAC or warfarin, compression stockings, treat underlying cause.
LMWH 1st line in pregnancy
DVT monitoring
prevention- hydration, mobilisation, compression stockings, LMWH
DVT complications (G)
PE
what is cellulitis- definition and symptoms
-skin infection, typically staph aureus and strep pyogene
- tender, inflamed swollen calf with pronounced demarcation
Cellulitis investigations
-FBC shows leukocytosis (infection)
-DVT would have normal levels
how can DVT cause ischaemia
RARE
acute oedema > DVT > causes pressure higher than perfusion pressure of arteries > ischaemia
complication of arterial thrombosis in coronary/ cerebral/ peripheral circulation
- coronary circulation → myocardial infarction
- cerebral circulation → stroke
- peripheral circulation → peripheral vascular disease and gangrene
how to differentiate between PE, pneumothorax and pneumonia
They all present with pleuritic chest pain
do CXR
PE is normal, pneumonia and pneumothorax are diagnostic
what is a D-Dimer
-measure of clot burden: D-dimer is
a small protein released into the blood when a blood clot is fibrinolysed
-sensitive- rules PE in
-not specific- raised in many conditions so not diagnostic
PE definition (G)
-blood clot forms in the pulmonary arteries, usually as a result of DVT in the legs which has embolised to the lungs.
-DVTs and PE are called venous thromboembolism
PE pathophysiology, how it causes cor pulmonale (G)
Clots in the pulmonary arteries block blood flow to lung tissue and create strain on the right heart.
PE can cause cor pulmonale due to increased pulmonary resistance > increases strain on right heart > right ventricle hypertrophy > right heart failure.
PE key presentation (G)
sudden onset pleuritic chest pain, dyspnoea, haemoptysis
PE other signs and symptoms (G)
Haemoptysis, pleuritic chest pain, hypoxia, tachycardia, tachypnoea, DVT (leg swelling and tenderness), hypotension, cyanosis, increased jugular venous p,
cough, fever, dizziness, syncope
PE investigations (G)
1st line: Wells score (risk of DVT or PE). (DVT evidence= 3pt, tachycardic= 1.5 pt etc.)
1. <4 = unlikely PE. Order d-dimer (looks for fibrin breakdown products and clotting problems).
If d-dimer raised, order CT pulmonary angiogram (visual of thrombus), if not raised it’s not a PE.
2. >4 = likely PE. Order CTPA -specific to PE, can rule out PE if not present
gold: CT pulmonary angiogram (direct visual of thrombus in pulmonary artery)
other:
ventilation-perfusion scan (shows area of lungs not perfused)
ECG (shows sinus tachycardia, S1Q3T3 pattern = cor pulmonale, pathognamonic, T wave inversion Y1-4, new RBBB)
ABG (low O2 and CO2)
normal CXR
PE DD (G)
MI
pneumonia
pneumothorax
PE management (G)
Massive PE, (hypo <90 sys) haemodynamic compromise = thrombolysis (streptokinase/alteplase)
Non-massive PE (most common) = anticoagulation – apixaban, rivaroxaban or LMWH
Long term: LMWH, DOAC or warfarin. LMWH 1st line in pregnancy
PE complications (G)
pulmonary infarction, cardiac arrest
hypertension definition (G)
High BP over 140/90 in clinic or 135/85 for ambulatory or home reading
hypertension epidemiology (G)
biggest risk factor for CVD
hypertension aetiology (G)
primary: essential hypertension. Idiopathic, 95% of cases
secondary: known cause hypertension. ROPE renal disease, pregnancy. pre-eclampsia, endocrine (Conn’s), obesity. 5% of cases
hypertension risk factors (G)
non-modifiable:
increasing age, FHx, ethnicity (Afro-Caribbean).
Modifiable:
alcohol, sedentary lifestyle, diabetes, smoking, salt intake, overweight, stress
hypertension key presentation (G)
asymptomatic, mostly found on screening
what is malignant hypertension and how does it present
-very high diastolic - 180/120
-mostly in black males aged 30-40
-chest pain, heart failure
-headache, seizures
-visual disturbances
-haematuria, renal failure
hypertension classification (G)
stage 1:
-clinic reading: 140/90
-ambulatory reading: 135/85
stage 2:
-clinic reading: 160-90
-ambulatory reading: 150/90
stage 3:
-clinic reading: 180-120
-start immediate treatment
secondary causes of hypertension
-renal disease
-phaeochromocytoma
-Cushing’s
hypertension investigations (G)
1st: clinic BP
gold: ambulatory BP (worn for 24 hours)
other: Assess end organ damage:
-fundoscopy- retinopathy, papilledema
-urine albumin: creatinine (proteinuria),
-dipstick (haematuria) for renal failure
-bloods (HbA1c, GFR, lipids)
-ECG/ echo (abnormalities, LVH)
hypertension DD
chronic kidney disease, Cushing’s, phaeochromocytoma
hypertension management
1:
-T2DM or >55: ACEi
-black/ Afro Caribbean heritage: CCB
2: (for both^)
ACEi + CCB
3: ACEi + CCB + thiazide- like- diuretic (TLD) eg indapamide
4: ACEi + CCB + TLD + other drug
-if potassium > 4.5 : spironolactone
-if potassium < 4.5 : alpha/ beta blocker
if the patient has T2DM and is black/ afro and over 55- diabetes takes precedence so give ACEi
hypertension monitoring (G)
treatment targets:
age < 80 = 140/90 mmHg
age > 80 = 150/90 mmHg
hypertension complications (G)
heart failure,
big increase in IHD risk,
CKD,
increase in cerebrovascular accident risk
heart failure general definition (G)
Heart failure is the inability of the heart to deliver oxygenated blood to tissues at a satisfactory rate for the tissues metabolic requirements- syndrome not a diagnosis
systolic heart failure definition (G)
failure of heart to contract efficiently to eject adequate volumes of blood.
Ejection fraction <40%. Heart failure with reduced ejection fraction. HFrEF
diastolic heart failure definition (G)
inability of the ventricles to relax and fill normally, causing increased filling pressures. Ejection fraction >50%. Heart failure with preserved ejection fraction. HFpEF
right sided heart failure definition (G)
inability of the right ventricle to pump adequate amount of blood leading to systemic venous congestion and peripheral oedema.
heart failure definition (G)
-10% of over 70s
-male > women
-increases with age
-affects 1-2% of the developed world
heart failure aetiology- general (G)
Ischaemic heart disease (main one)
hypertension,
cardiomyopathy,
alcohol excess,
valve disease,
anything increasing cardiac work eg obesity, pregnancy
right heart failure aetiology (G)
-pulmonary hypertension,
-pulmonary embolism,
-COPD,
-cor pulmonale (right heart enlargement as a result of disease of lungs or blood vessels)
left heart failure aetiology (G)
-coronary artery disease,
-valve defect,
-myocardial infection,
-congenital heart defects,
-arrhythmias
what is congestive heart failure (G)
heart failure affecting left and right side
heart failure risk factors (G)
-older
-male
-smoking
-obesity
-previous MI
how can heart failure be classified (G)
-time- acute or chronic
-ejection fraction- preserved or reduced
-NY heart association class 1-4
preserved vs reduced ejection (G)
preserved 50%:
-diastolic failure (heart pump function impaired)
-filling issues
reduced- <40%
-systolic failure (pump fails)
-decreased CO due to pump issues
what is normal ejection fraction
50-70%
NY heart association classification (1-4)
assesses heart failure severity
1. no limit on physical activity
2. slight limit on moderate activity
3. marked limit on moderate and gentle activity
4. symptoms at rest
Frank-Starling mechanism (G)
increased preload = increased afterload = increased
heart failure pathophysiology (G)
Failing hearts have dysfunctional Frank Starling law
-Reduced cardiac output is caused by decreased preload, decreased contractility, increased afterload, decreased heart rate
-When the heart begins to fail, the compensatory mechanisms change to maintain CO:
increased SNS (increased HR and contractility)
increased RAAS (increased aldosterone and ADH so increased fluid retention therefore increasing preload)
natriuretic peptides
ventricular dilation
ventricular hypertrophy
compensatory mechanisms become exhausted and pathological:
SNS and RAAS also cause vasoconstriction and exacerbate fluid overload which increase afterload and myocardial work, damaging myocytes > cardiac remodeling > reduced CO = heart failure
heart failure key presentation (G)
remember SOBAFAST
SOB
ankle swelling (oedema)
fatigue
heart failure other signs (G)
Oedema
(LHF = pulmonary congestion – pulmonary oedema, RHF = systemic backlog – peripheral oedema)
LHF: bibasal pulmonary crackles, 3rd and 4th heart sounds, cardiomegaly (displaced apex beat), tachycardia
RHF: raised JVP, hepatomegaly, pitting oedema, weight gain (fluid)
heart failure other symptoms (G)
LHF: dyspnoea, orthopnoea, poor exercise tolerance, fatigue, nocturnal cough (pink frothy sputum), wheeze, cold peripheries
RHF: peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis
heart failure investigations
1st: ECG
abnormal- may indicate cause
BNP (brain natriuretic peptide)- will be elevated (>400ug/ml). It is released from myocardial walls under stressed- more raised = more severe)
CXR- ABCDE
Alveolar oedema
Kerley B lines
cardiomegaly
dilated upper lobe vessels
(pleural) effusions
gold:
echo- confirm cause eg MI, LV dysfunction
heart failure DD (ECG)
COPD, PE
heart failure management
- ACEi (ramipril) and BB (bisoprolol)
- ^ + aldosterone antagonist (spironolactone) + loop diuretic (furosemide)
- consider cardiac resynchronisation therapy (improves A-V coordination)
surgery - consider revascularisation, LVAD, valve surgery, heart transplant (as last resort)
lifestyle changes
heart failure complications (G)
pleural effusion
AKI
sudden cardiac death
heart failure prognosis
50% die within 5 years of diagnosis
cor pulmonale definition, pathophysiology (G)
-Right sided heart failure caused by resp disease
eg. COPD, PE, CF
-pulmonary hypertension results in RV being unable to pump blood out of ventricle into pulmonary arteries effectively
-Leading to back pressure of blood in RA, vena cava and systemic venous system
cor pulmonale presentation
key: SOB, peripheral oedema, chest pain
others: hypoxia, cyanosis, raised JVP, 3rd heart sound, syncope
cor pulmonale investigations and DD
1st: ABG (hypoxia and hypercapnia), spirometry, chest CT, echo
gold: right heart catheterisation
DD: primary pulmonary hypertension, pulmonary valve stenosis
cor pulmonale management
-treat symptoms and underlying cause
-long term oxygen therapy
-treat heart failure
-consider venesection (reduce RBCs) if haematocrit is less than 55
-consider heart-lung transplantation in young patients
cor pulmonale complications and prognosis
complications: tricuspid regurgitation and cardiac cirrhosis, death
prog: 50% 5 year survival
effusion in pericarditis
-can be wet or dry
-mostly wet- exudative (infection/malignancy)
-wet is associated with haemorrhagic bleeding
-dry = fibous
pericarditis definition (G)
inflammation of the pericardium with/without effusion
pericarditis epidemiology
men 50-70
pericarditis aetiology
main 2:
-idiopathic
-viral (cocksackievirus, HIV, EBV)
-bacterial- TB
-autoimmune eg lupus
-Dressler syndrome (post MI)
-neoplastic -lung/ breast
-cancer
-injury
pericarditis pathophysiology (G)
-inflamed pericardial layers rub against each other (as inflammation causes pericardial space to narrow), this exacerbates inflammation
-can be dry- less bad, no fluid needed to compensate friction
-or effusive- fluid needed to compensate for friction
pericarditis relevant anatomy
-2 pericardial layers with 50ml of fluid between them
-fluid helps the heart to beat with less friction
-potential space between the layers is the pericardial cavity
-separates the heart from the rest of the mediastinum
pericarditis key presentation (G)
-sharp, severe pleuritic chest pain, referred to right shoulder
-worse on inspiration and lying down
-relieved by sitting forward
-low grade fever
pericarditis other signs
pericardial friction rub on auscultation (scratching sound alongside heart sounds when leaning forward)
signs of right sided heart failure (constrictive pericarditis) eg peripheral oedema, SOB, due to granulation formation in the pericardium causing impaired diastolic filling
pericarditis investigations (G)
1: FBC
raised WCC- infective
raised ESR- autoimmune
gold: ECG
wide saddle shaped ST elevation
PR depression
other: CXR
water bottle shaped heart- cardiomegalic
pneumonia in bacterial cases
pericarditis management (G)
idiopathic and viral:
-NSAIDs (2 weeks)
-colchicine (3 weeks), anti-inflammatory to prevent recurrence
-consider steroids (second line) in recurrent cases if inflammatory
-treat cause- Abx for bacterial (RIPE for TB)
pericarditis DD (g)
rule out MI (both have CCC pain)- MI is not associated with lying down and has no pericardial rub
pericarditis complications (G)
pericardial effusion > cardiac tamponade > myocarditis, constrictive pericarditis
pericardial effusion and cardiac tamponade definition (G)
pericardial effusion: accumulation of fluid in the pericardial sac
cardiac tamponade: when pericardial effusion is large enough to increase the inter-pericardial pressure > decreased ventricular filling > decreased cardiac output
pericardial effusion and cardiac tamponade aetiology (G)
exudative effusion:
-causes related to pericarditis: autoimmune, viral, bacterial, neoplastic, idiopathic, trauma
transudative effusions
-there is increased venous pressure which causes restricted pericardial drainage
-congestive heart failure, pulmonary hypertension
bleed in pericardial space
-due to rupture of heart or aorta: trauma, aortic dissection
pericardial effusion and cardiac tamponade risk factors (G)
malignancy
purulent pericarditis
aortic dissection
pericardial effusion and cardiac tamponade pathophysiology (G)
accumulation of fluid in the pericardial cavity causes an inward pressure on the heart making it more difficult to expand during diastole
pericardial effusion and cardiac tamponade key presentation (G)
pericardial friction rub
dyspnoea
Becks triad: hypotension, muffled S1,S2 heart sounds, raised JVP
pericardial effusion and cardiac tamponade other signs and symptoms
pulsus paradoxus: decrease in 10 mmHg systolic on inspiration
orthopnoea
raised pulse
kussmauls sign- paradoxical JVP on inspiration (cardiac tamponade)
dysphagia
hiccups
nausea
hoarse voice
pericardial effusion and cardiac tamponade investigations (G)
1st:
ECG - varying amplitude QRS complexes (due to heart bouncing around in pericardial fluid)
CXR- enlarged globular heart
gold:
echo- echo free zone around the heart
other: FBC
raised WBC and ESR
pericardial effusion and cardiac tamponade DD (G)
constrictive pericarditis, Dressler’s, congestive heart failure
pericardial effusion and cardiac tamponade management (G)
treat the cause
pericarditis:
aspirin, NSAIDs, colchicine
drain the effusion:
-needle pericardiocentesis
-surgical drainage
cardiac tamponade:
-urgent pericardiocentesis
-send fluid for culture
pericardial effusion and cardiac tamponade complications (G)
-haemodynamic compromise
-cardiac tamponade
-death
pericardial effusion and cardiac tamponade prognosis (G)
depends on underlying cause- worse with infection
