2. Arrythmias, Heart Failure, Hypertension and Valvular Disease Flashcards
- What 2 things determine cardiac output?
2. Name three things that also influence cardiac output
- stroke volume and heart rate
2. venous return, peripheral vascular tone and neurohumoral factors
- What is preload?
2. What is preload determined by? (2)
- end diastolic volume (represents stretch within heart)
2. duration of diastole; venous return
- What is afterload?
2. What is cardiac reserve?
- force resisting myocardial contraction at the start of systole. related to systolic blood pressure
- the ability of the heart to increase performance above resting levels
- What is the mechanism of heart failure with reduced ejection fraction?
- What happens to diastolic volume and pressure in this heart failure?
- What is this type of heart failure common following?
- ventricle contracts poorly and empties inadequately
- both increase
- MI and dilated cardiomyopathy
- What is the mechanism of heart failure with preserved ejection fraction?
- Why is ejection fraction preserved?
- What does this type of heart failure result from?
- ventricles are stiffened, with decreased compliance and impaired relaxation. This causes impaired ventricular filling and thus inadequate stroke volume
- contraction is normal, but the amount of blood in the heart at the end of diastole is reduced so therefore cardiac output is reduced
- increased ventricular stiffness or valvular disease
- how does the myocardium respond to heart failure?
- How does ventricular dilation worsen heart failure?
- How is cardiac reserve lost in heart failure?
- reduction in ejection fraction > increased volume of blood left in the heart following systole > stretch > further reduction in ventricular function
- increased ventricular radius > increased myocardial wall tension > increased work of heart to overcome tension
- heart works harder to meet normal metabolic demands therefore the amount cardiac output increases in times of increased oxygen demand is reduced.
- How does the sympathetic nervous system respond to heart failure?
- What are the consequences of this?
- increased sympathetic output due to reduced systemic BP > Increased HR & myocardial contracility and vasoconstriction
- increased cardiac work, increased preload, increased afterload
- How does the RAAS system respond to heart failure?
2. What are the consequences of this?
- reduced renal perfusion > decreased GFR > activation of RAAS
- vasoconstriction, sodium and water retention, sympathetic stimulation
What is alcoholic cardiomyopathy?
condition where chronic use of alcohol leads to heart failure. Type of dilated cardiomyopathy
Name 4 symptoms of heart failure
- exertional dyspnoea
- orthopnoea
- paroxysmal nocturnal dyspnoea
- fatigue
Name 7 signs of heart failure
- tachycardia
- elevated JVP
- cardiomegaly
- bibasal crackles
- peripheral oedema
- third heart sound
- anasarcia
- How is pulmonary oedema acutely managed?
- In a patient with pulmonary oedema, what is given if they are in cardiogenic shock?
- How is pulmonary oedema managed in the long term
- oxygen, IV furosemode, opiates
- dobutamine
- oral diuretics, ACE inhibitors, beta blockers
Name investigations that are performed for ?Heart failure
- serum electrolytes
- renal function tests
- NT-pro-BNP
- CXR
- Electrocardiogram
What is the triple therapy for the management of chronic heart failure?
ACE inhibitor/ARB
Beta Blocker
Aldosterone antagonist
- What is CRT-P?
2. What is CRT-D?
- internal pacemaker
2. pacemaker + defibrilator
Name the 2 things that determine blood pressure
cardiac output (dependent on heart rate, myocardial contractility and diastolic blood volume) peripheral resistance
- What blood pressure is classified as hypertension?
2. What blood pressure is classified as severe hypertension?
- > 140/90
2. >180/120
- Name 2 types of patients in which isolated systolic hypertension can be seen?
- In what condition cam isolated diastolic hypertension be seen?
- elderly; hyperthyroidism
2. aortic regurgitation
- What is a hypertensive urgency?
- What is a hypertensive emergency?
- What is malignant hypertension?
- severe hypertension, but with no evidence of end organ damage
- severe hypertension, with evidence of end organ damage
- severe hypertension and retinal haemorrhage and/or papilloedema
What 2 criteria describe resistant hypertension?
- blood pressure that remains above target despite 3 different antihypertensive medications, one of which is a diuretic
- blood pressure that is at target with 4 different antihypertensive medications, one of which is a diuretic
- What occurs in the early phase of essential hypertension?
2. What occurs in the chronic phase of essential hypertension?
- increased blood volume and cardiac output drives hypertension
- thickened wall of resistance vessels increases vascular resistance; blood volume and cardiac output normal
Name 5 causes of secondary hypertension
- renal artery stenosis - poor renal perfusion > activation of RAAS
- chronic renal disease - increase in BP to restore GFR
- primary hyperaldosteronism - overproduction of aldosterone > sodium and water retention
- phaeochromocytoma - adrenal medulla tumours secrete catecholamines > alpha mediated vasoconstriction and beta mediated cardiac stimulation
- Coarctation of the aorta - results in renal hypoperfusion
Name 4 instances where you should be suspicious of secondary hypertension
- renal dysfunction
- young
- severe treatment resistnace
- hypokalaemia (indicates mineralocorticoid excess)
describe the ECG trace of normal sinus rhythm (P waves)
- upright p waves in leads I and III
- inverted p waves in aVR and V1
Describe the pathophysiology of atrial fibrillation
rapid activation of the atria by multiple foci; no co-ordinated mechanical function
only a proportion of atrial impulses are conducted to the ventricles
Name causes of AF (6)
- any condition resulting in raised atrial pressure, increased atrial mass or atrial fibrosis
- heart failure
- hypertension - idiopathic
- hyperthyroidism
- alcohol intoxication
Describe some clinical features of AF
- asymptomatic (30%)
- palpatations
- chest pain
- dyspnoea
- irregularly irregular pulse
Describe the ECG waveform of AF
- no distinct P wave
- Atrial rate >300bpm
- irregular and rapid QRS
- fine oscillations of baseline (F waves)
- What scoring system is used to determine stroke risk in a patient with AF?
- Describe some features of this scoring system
- CHA2DS2-VASc
- congestive heart failure
hypertension
age
diabetes
stroke, tia or vte
vaascular disease
female
- What scoring system is used to determine risk of bleeding with anti-coagulation?
- Name some features of this scoring system
- HASBLED
- hypertension
abnormal renal/liver function
previous stroke
previous major bleed or predisposition
labile INR
alcohol use
drugs which predispose to bleeding
- How is unstable AF managed?
2. How is stable AF managed? (3)
- cardioversion
- anticoagulation with doacs
rate control - b blocker/digoxin/non-dihydropyridine calcium channel blockers
rhythm control - cardioversion; class I or III antiarrythmics
describe the pathophysiology of atrial flutter
- 2 foci of electrical activity that creates a re-entrant circuit within the atria
- only some electrical activity is conducted to the ventricles
- no-co-ordinated mechanical function
what is the ECG of atrial flutter?
saw tooth appearance
block may be 2”1, variable or 1:1
- What is supraventricular tachycardia?
2. What is characteristic of ECG of supraventricular tachycardia
- tachycardia which arises from the atrium or AV junction
2. QRS <120 msec/3 small squares wide
Describe the 2 mechanisms of supraventricular tachycardia
- AV nodal re-entrant tachycardia
- two functioning and anatomically different pathways WITHIN the AV node with different refractory periods and conduction velocities. creates re-entry circuit - AV re-entrant tachycardia
- accessory pathway near AV node creates a re-entry circuit. Atrial activation occurs after ventricular activation. P wave is seen between QRS and T waves
- Describe clinical features of supraventricular tachycardia
- How is SVT managed? (4)
- rapid, regular palpitations. Anxiety, dizziness, dyspnoea, central chest pain, hypotension, syncope
- emergency cardioversion if haemodynamically unstable
valsalva manouvre
IV adenosine (blocks AV node)
verapamil/beta blockers
- What is ventricular tachycardia?
- name 3 causes of VT
- how is VT managed if the patient is:
a) haemodynamically unstable
b) haemodynamically stable
- wide, regular, rapid QRS complexes
- electrolyte disturbances, ischaemic, fibrotic scar tissue within the myocardium
3a) emergency cardioversion
3b) IV beta blockers and amiodarone
- What is ventricular fibirilation?
- What does it require?
- What is the long term risk and how is this managed?
- very rapid, irregular ventricular activation with no mechanical effect; results in arrested cardiac pump function and immediate death
- emergency, immediate defibrilation
- high risk of sudden cardiac death. Implatable defibrilator.
- Describe 1st degree heart block.
- ECG?
- how is it managed?
- slower conduction through AV node
- regular QRS; P wave always present. PROLONGED PR INTERVAL
- IV atropine
- describe second degree heart block type 1
- ECG
- management
- only some atrial activity is conducted to the ventricles
- progressively prolonged PR interval until a P wave fails to conduct
- pacing
- describe second degree heart block type 2
- ECG
- management
- only some atrial activity is conducted to the ventricles
- P waves are not always followed by a QRS (e.g 2 P waves to every 1 QRS; 2:1 block)
- pacing
- describe third degree heart block
- ECG
- management
- all atrial activity fails to conduct to the ventricles
- regular, wide, QRS; no relationship between P waves and QRS
- pacing
- What is hypertrophic cardiomyopathy?
2. describe its pathophys
- group of genetic conditions that produce myocardial hypertrophy in absence of other cause
- septal thickening due to myocytic hypertrophy - may lead to LV outflow tract obstruction
myocardial ischaemic due to increased O2 demand, increased wall distension and coronary vascular resistance
How does hypertrophic cardiomyopathy present?
- mostly asymptomatic
- chest pain, dyspnoea, syncope; typically worse on exertion
- systolic ejection murmur
- How is hypertrophic cardiomyopathy investigated (2)
2. how is it managed?
- ECG and echo
- implantable cardioverter-defibrilator
amiodarone
beta blockers
verapamil
- What is dilated cardiomyopathy?
2. How may it present?
- dilatation of the ventricular chambers and systolic dysfunction, with preserved wall thickness
- heart failure, arrhythmia, thromboembolism, sudden death
- What is myocarditis?
- Name the 2 most common causative agents in western society
- What are symptoms of myocarditis related to?
- inflammation of the myocardium
- coxsackie virus or adenovirus
- reduced cardiac output due to cardiomyopathy (palpatations, chest pain, dyspnoea, tachycardia, elevated JVP)
Name 5 investigations of myocarditis
- CXR - may show cardiac enlargement
- ECG
- Cardiac enzymes - elevated
- Echocardiogram
- Cardiac MRI
- What is pericarditis?
2. name some clinical features of pericardiitis
- inflammation of the pericardium
- sharp central chest pain. signs of heart failure. systemic symptoms of inflammation. pericardial rub
may be accompanied by pericardial effusion:
- soft heart sounds
- obscured apex beat
signs of cardiac tamponade
What is constrictive pericarditis?
pericardium becomes thick, fibrous and calcified in response to inflammation.
it is inelastic, thus interferes with diastolic filling. Changes are more chronic so body able to compensate to some extent.
Describe the cardiac cycle, with particular respect to the closure of the 4 heart valves
- DIASTOLE - atria and ventricles relaxed. Mitral and Tricuspid valves open. Ventricles fill passively
- atrial systole
- VENTRICULAR SYSTOLE - ventricular pressure exceeds atrial pressure thus mitral and tricuspid valves close
Aortic and pulmonary valves forced open by increased ventricular pressures - VENTRICULAR DIASTOLE - blood flow back down the aorta/pulmonary artery closes aortic/pulmonary valves
Atrial pressure exceeds ventricular pressure thus mitral and tricuspid valves open
HEART SOUNDS what causes the following sounds? 1. S1 2. S2 3. S3 4. S4
- tricuspid and mitral valve closure
- aortic and pulmonary valve closure
- added heart sound; indicates volume overload
- added heart sound; indicates pressure overload (e.g uncontrolled hypertension)
What type of murmurs do the following produce?
- mitral/tricuspid regurgitation
- aortic/pulmonary stenosis
- mitral/tricuspid stenosis
- aortic/pulmonary regurgitation
- (pan)systolic murmur (these valves close during ventricular systole)
- (ejection) systolic murmur (these valves open during ventricular systole)
- (mid to late) diastolic murmur (these valves open during diastole)
- (early) diastolic murmur (these valves close during diastole)
- Describe the sound of a systolic murmur
2. describe the sound of a diastolic murmur
- lub shh dub (felt with pulse)
2. lub dub shh (felt after/inbetween pulses)
What are the three most common valvular pathologies?
- aortic stenosis
- mitral regurgitation
- tricuspid regurgitation
How are heart murmurs primarily investigated?
- ECG
- echocardiogram
How can valvular stenosis lead to heart failure?
Increase in pressure proximal chamber to affected valve in order to maintain CO
How can valvular regurgitation lead to heart failure?
regurgitation of blood causes dilatation of proximal chamber
What is endocarditis?
inflammation of the endocardium, characterised by VEGETATIONS (mass of platelets, fibrin, micro-colonies of micro-organisms, and inflammatory cells)
Endocarditis is a consequence of which 2 factors?
- bacteremia
2. abnormal cardiac endothelium that facilitates the adherence and growth of bacteria
- Name the 3 clinical signs specific for endocarditis
2. Name 2 other clinical features which could indicate endocarditis
- Osler’s nodes, Splinter haemorrhages, Janeway lesions
- embolic events of unknown origin
new murmur
- Which criteria is used in the diagnosis of endocarditis?
2. Name some features of this scoring criteria.
- Duke criteria
- positive blood culture (2 separate samples obtained 12 hrs apart)
echo evidence of endocardial involvement
predisposing heart condition of IVDU
fever
vascular phenomena - embolic event; janeway lesion