Week 5 Cardio Flashcards
(87 cards)
Clinical trial
Evaluation of therapeutic intervention in humans, who are healthy or have a disease
Unbiased, accurate assessment of effect of treatment
Guidlines recommendations for evidence
Class I: General evidence shows treatment is useful/effective
Class II: Conflicting evidence
Class IIa: General evidence showing in favour of efficacy
IIb: Efficacy less well established
Class III: General evidence showing treatment not useful/effective
Level of evidence
A - multiple RCT
B - single RCT
C - consensus of opinion from experts/multiple small studies
AF (def, symptoms, diagnosis
Chaotic rhythm of atrium. Ventricular rhythm is irregular and rate controlled by AV node refractoriness.
Most common sustained cardiac arrythmia
Major risk factor for stroke
Symptoms:
Aysymptomatic, palpitations, SOB, chest pain
Diagnosis:
Irregular pulse
Confirmed by 12 lead ECG
Types: Paroxysmal (stops spontenously)
Persistent (stops with intervention)
Permanent
Investigations:
ECG, Echocardiogram, TFTs, LFTs
Atrial flutter
Circular movement of electrical activity in atrium. Usually 2:1 AV conduction, 300bpm
ECG:
Sawtooth appearence (as P waves don’t always cause QRS due to refractory period. Successive atrial depol (P) waves)
Regular narrow QRS
Treat with catheter ablation
Conditions that pre-dispose AF
HTN
HF
Valvular heart disease
Thyrotoxicosis
Diabetes
Obesity
Coronary artery disease
Treatment AF
Aims:
Prevent stroke, relieve symtpoms, rate control, correct rhythm
Prevent stroke
Warfarin
DOACs: Dabigratan, Apixiban/Edoxaban
- increased risk of GI bleeding
Rate control
HR <110
If symptomatic <80
Pts without HF: (1st line) B-blocker (bisoprol) or Ca2+ antagonist (Verapamil)
2nd line: Digoxin
Rhythm control
Younger pts, pts with symptoms despite rate control
Anti-arrythmic drugs:
Class 1: Na+ channel blocker: Flecainide (contra-indicated with significant heart disease)
Class III: K+ channel anatagonists: Amiodarone
Sotalol (B-blocker with Class III activity)
Multi- channel blockers: Dronedarone
Catheter ablation:
Radiofrequency or cryo-ablation to create scar tissue to destroy areas (pulm. veins) triggering arrthymias
- Indicated for paroxysmal AF
Direct current cardioversion (persistent AF, or pts who present first time with no heart disease, <48hrs)
Risk factors for stroke for pts with AF
CHA2-DS2-VASCs score (out of 9 pts)
Cardiac failure
HTN
Age >75 (2pts)
Diabetes
Stroke (2pts)
Vascular disease
Age 65-75
Sex
HF definition, symptoms/signs, causes, types
When heart fails to pump blood around the body at a rate to meet metabolic demands
Due to abnormality of cardiac funciton or filling pressure
Symptoms:
Dyspnoea, cough, ankle swelling, fatigue
Signs:
Raised JVP
Displaced apex beat (cardiomegaly)
Pulmomary oedema
Peripheral oedema e..g ankles
Causes:
HTN, Coronary artery disease, TB, alcohol. congenital heart disease
Types:
HF-REF (reduced ejection fraction)
Young, males, coronary arteries
H-PEF (preserved ejection fraction)
Old, femle, HTN (filling abnormal)
Chronic/acute
Chronic (congested) - presents for period of time, can be from acute or lead to acute
Acute - usually hospital admin, from chronic or de novo
Causes of HF
Common: coronary heart disease, HTN, idiopathic, toxic (alcohol)
Uncommon: valve disease, infections e.g. Chaga’s, congenital heart disease
HF pathophysiology
Myocardial injury
- LV systolic dysfunction (reduced EF)
- body percieves reduced circulatory vol
- neurohumoral activation (increased sym activation, RAAS, natriuretic peptides)
- systemic vasocontrction, Na+/H2O retention
- LV dysfunction
HF classification
New York Heart Assocation Classifcation (NYHA)
Class I: No symptoms
Class II: Mild symptoms e.g. mild SOB
Class III: Moderate limitation in activites due to symptoms
Class IV: Severe limitations. Symptoms whilst at rest.
General investigations HF and for selected pts
Bloods: FBC, UEs, LFTs, CRP
BNP (brain natriuretic peptide) - released from ventricular myocytes
Echocardiogram (size, systolic/diastolic function)
CXR (exclude lung pathology)
ECG (rate, rhythm, QRS)
Selected pts
Coronary angiogram
Exercise testing
Ambulatory ECG
Myocardial biopsy
Treatment for CHF
B-blockers (Carvedilol) + ACEi (Ramipril)
MRA (spironolactone)
ARB (angiotensin II receptor blocker) - Valsartan, Socubritil (LCZ696) - inhibits renal vasoconstriction, and breakdown of neprilysin, increasing natriuretic peptides
ICD (implantable cardioverter defribillator), Ivrabadine (If current inhibitor, reduces HR)
Digoxin
Isosorbide dinitrate
Cardiac transplant
Suspected Acute HF: identification of aetiology
CHAMP
C acute Coronary syndroe
HTN
A rrythmia
M acute Mechanical cause
PE
Acute HF Wet vs dry
95% AHF pts “wet” - congested
Pulmonary congestion
Raised JVP
Peripheral oedema
5% AHF pts “dry” - hypoperfused
Oligouria
Confusion
Treatment AHF
O2
IV Furosemide
Nitrates
Dobutamine (ionotropic)
Ultra-filtration
Hypertension defintion
Persistent elevation in arterial blood pressure <140/90, without secondary cause
Increases vascular risk in pts such that invervention is needed
Leads to increased risk of coronary artery disease, stroke, HF, peripheral vascular disease, renal failiure
Hypertension pathophysiology
BP = CO x TPR
Genetics + Environment leads to:
Defects in renal sodium homeostasis (increased Na and H2O retention - increased plasma volume - leading to increased CO)
- Functional vasoconstriction
Defects in vascular smooth muscle - leading to thickened vascular wall
- Increased total peripheral resistance
CHF Xray signs
Stage 1: Redistribution
- Redistribution pulmonary vessels (normally vessels in lower lobes larger than ones in upper. If uppe lobe vessels larger than lower lobe vessels - increased pulm venous pressure)
- Cardiomegaly (widest transvere cardiac diameter, divided by wideset transverse diameter lungs. Normally 0.5)
2. Interstitial oedema
- Kerly B lines (setpal lines - fluids leaks into interlobular septa due to oedema)
3. Alveolar oedema
- Consolidation
- Pleural effusions (fluid in parietal space, can obscure heart border)
Alveolar oedema
B - Kerley B lines
C ardiomegaly
Distended upper lobes (redistribution pulmonary vessels)
Pleural Effusion
Effects of HTN and cardiovascular mortality
Cardiovascular disease risk doubles for every systolic 20mmHg increase and diastolic 10mmHg increase
Types of HTN: primary and secondary
Primary: unknow cause (90%)
Risk factors: Age, sex, physical activity, obesity, genetics
Secondary: underlying cause (10%)
Cushing’s syndrome
Hyperaldosteronism
Phaeochromocytoma
NSAIDs
Obstructive sleep opnoea
Diagosis HTN
Multiple out of office BP measurement:
24 hr ambulatory BP
Home blood pressure monitoring
Other investigations:
Bloods, renin/aldosterone (for hyperaldosteronism), 24 hour urinary catecholamines (phaechromocytoma), TFTs, LFTs
Classification HTN
High normal: 130-139
HTN Grade 1: 140-159
HTN Grade 2: 160-179
HTN Grade 3: >180
HTN Treatments
Lifestyle Advice
Drugs
1st line: ACEi (<55yrs)/ARB or Ca2+ channel blocker (if African/Carribean origin, >55yrs)
2nd line: ACEi + Ca2+ channel blocker
3rd line: ACEi + Ca2+ channel blocker + thiazide diuretic (e.g. bendroflumethiazide)
Resistant HTN: ACEi + Ca2+ thiazide + furthur diuretic, a/b blocker
Aim: <140/90, <130/80 if tolerated



