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nicks phase 2a flaschards > cardio > Flashcards

cardio Flashcards

1
Q

what is stable angina?

A

a symptom which occurs as a consequence of restricted coronary blood flow which causes a mismatch between oxygen demand and supply

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2
Q

what can cause stable angina?

A

atheroma, anaemia, aortic stenosis, tachyarrythmias, HCM

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3
Q

how does angina present clinically?

A
  • central, crushing chest pain
  • comes on with exertion, relieved at rest
  • exacerbated by cold, anger, excitement
  • radiates to arms and neck
  • dyspnoea, nausea, sweating, fitness
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4
Q

what are some differential diagnoses of angina?

A
  • ACS
  • pericarditis
  • myocarditis
  • aortic dissection
  • PE
  • GORD
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5
Q

How can stable angina be diagnosed?

A
  • ECG- normal- used to differentiate from ACS
  • exercise ECG
  • coronary angiography
  • CT angiography
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6
Q

how is stable angina treated?

A
  • modify risk factors
  • low dose aspirin
  • clopidogrel
  • statins
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7
Q

how can stable angina be managed?

A
  • nitrates- isosorbide, GTN
  • beta blockers
  • calcium channel blockers
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8
Q

what is ACS?

A

acute coronary syndromes- covers a spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving MI

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9
Q

what can cause unstable angina?

A
  • rupture of an atherosclerotic plaque
  • coronary vasospasm
  • drug absue
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10
Q

how does unstable angina present clinically?

A
  • acute central chest pain not relieved by rest
  • chest pain with a crescendo pattern
  • new onset
  • sweating, dyspnoea, palpitations
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11
Q

how is unstable angina treated?

A 
MONA
morphine
Oxygen
Nitrates
Aspirin
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12
Q

how does a patent with a STEMI present clinically?

A
  • central crushing chest pain
  • occurs at rest, lasts several hours
  • sweating, breathlessness, nausea, vomiting, restlessness
  • pale and grey appearance
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13
Q

how does a STEMI appear on an ECG?

A

ST elevation
tall T waves
pathological Q waves

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14
Q

how do you treat a patient with a STEMI?

A 
300mg aspirin
morphine 
oxygen
antiemetic- e.g. metoclopramide
PCI
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15
Q

what is the aetiology of a NSTEMI?

A

partial occlusion of the vessel lumen- ischaemia is limited to the subendocardial zone of the myocardium

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16
Q

how does a NSTEMI present on an ECG?

A

ST depression, T wave inversion

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17
Q

what is heart failure?

A

A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart as a pump is impaired

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18
Q

during heart failure, the body tries to compensate to maintain cardiac output- what are the compensatory mechanisms and what are the consequences of these?

A
  • Activation of sympathetic nervous system- increase HR and contractility, however also leads to arteriolar constriction- increasing afterload so decreasing CO
  • RAAS- activated due to decreased CO, results in oedema and dyspnoea, angiotensin II causes arteriolar constriction, increasing afterload and the work of the heart
  • Ventricular dilatation- failure= reduced volume of blood ejected, so increased vol. remains after systole, stretches fibres, due to Starlings law this restores contractility- in heart failure however compensatory effects are limited- leading to pulmonary and peripheral oedema and increased O2 requirement of myocardium
  • Ventricular remodelling- hypertrophy, loss of myocytes, increased interstitial fibrosis
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19
Q

what is systolic heart failure?

A

inability of ventricles to contract normally- decreased CO, stroke volume is a small fraction of the total filling volume- low ejection fraction (lower than 40%)

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20
Q

what is diastolic heart failure?

A

inability of ventricle to relax and fill normally, causing increased filling pressures, normal ejection fraction- low preload but a normal stroke volume- so the fraction appears higher

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21
Q

how does left ventricular heart failure present clinically?

A

presents with poor exercise tolerance, fatigue, pulmonary oedema

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22
Q

what does right heart failure present with clinically?

A

peripheral oedema, ascites, nausea, raised jugular venous pressure

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23
Q

what is cor pulmonale?

A

right heart failure secondary to lung disease

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24
Q

what is decompensated heart failure?

A

occurs when the heart begins to stop responding to compensatory mechanisms as over activation results in a decreased response

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25
Q

what can cause low output heart failure?

A

pump failure, excessive preload, chronic excessive after load

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26
Q

what can cause high output failure?

A

anaemia, pregnancy, hyperthyroidism

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27
Q

what can cause heart failure?

A
  • IHD
  • Valvular disease- mitral regurgitation, aortic stenosis, tricuspid regurgitation, venricular septal defect
  • Pericardial disease- pericarditis, pericardial effusion
  • Drugs- alcohol, cocaine, beta blockers
  • Myocarditis
  • Thyrotoxicosis
  • Arrhythmias
  • Cardiomyopathies- dilated, hypertrophic, restrictive
  • Anaemia
  • Pulmonary hypertension
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28
Q

what are the clinical signs of heart failure?

A

cardiomegaly
3rd heart sound- active filling of the left ventricle
4th heart sound- pathological- heart becomes stiff so vibrates
pleural effusion
elevated JVP

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29
Q

how can heart failure be classified?

A

I.Class I- no limitation to exercise
II.Mild limitation- exercises produces some mild symptoms
III.Marked limitation- symptoms produced on gentle exercise
IV.Symptoms occur at rest and are exacerbated by any activity

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30
Q

how can heart failure be diagnosed?

A
  • CXR- alveolar oedema, cardiomegaly

- ECG- underlying cause

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31
Q

how can heart failure be treated?

A
  • lifestyle modification
  • diuretic
  • spironolactone
  • ACE inhibitor
  • beta blockers
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32
Q

what can cause aortic stenosis?

A
  • Senile calcification
  • Rheumatic heart disease
  • Compensatory heart failure- LVH- results in increased myocardial oxygen demand, ischaemia of myocardium- angina, arrhythmias and LV failure
  • Congenital abnormal valve
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33
Q

how does aortic stenosis present clinically

A
  • asymptomatic
  • angina, syncope, dyspnoea
  • narrow pulse pressure
    systolic ejection murmur
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34
Q

what is the main differential diagnosis of aortic stenos?

A

hypertrophic cardiomyopathy

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35
Q

how can aortic stenosis be diagnosed?

A
  • ECG- P mitrale, LVH, ST depression T wave inversion

- CXR- valvular calcification

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36
Q

how can aortic stenosis be managed?

A
  • dental care

- IE prophylaxis

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37
Q

what can cause mitral regurgitation?

A
  • Backflow through the mitral valve during systole
  • Caused by a volume overload
  • Compensatory mechanisms- left atrial enlargement, LVH and increased contractility
  • Rheumatic heart disease
  • Infective endocarditis
  • LV dilatation
  • Caridomyopathy
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38
Q

how does mitral regurgitation present clinically?

A
  • dyspnoea, fatigue, palpitations

- soft S1

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39
Q

how can mitral regurgitation be diagnosed?

A
  • ECG- AF and P mitrale

- CXR- enlarged LA and LV

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40
Q

what can cause aortic regurgitation?

A
  • Combined pressure and volume overload
  • Compensatory mechanism- LV dilation, LVH- progressive dilation leads to heart failure
  • Rheumatic fever
  • Infective endocarditis
  • Dissection of aorta
  • Severe hypertension
  • Aortic endocarditis
  • Aneurysmal change of the aortic annulus- area surrounding the valve widens so the valve cannot fully close
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41
Q

what are the clinical signs of aortic regurgitation?

A

collapsing pulse
wide pulse pressure
displaced apex beat

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42
Q

how can aortic regurgitation be diagnosed?

A
  • CXR- cardiomegaly
  • pulmonary oedema
  • ECG- LVH
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43
Q

how can aortic regurgitation be treated?

A
  • ACE inhibitors

- valve replacement

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44
Q

what can cause mitral stenosis?

A
  • Rheumatic heart disease
  • Congenital
  • Cardial fibroelastosis
  • Prosthetic valve
  • Infective endocarditis
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45
Q

what are the signs and symptoms of mitral stenosis?

A 
Symptoms:
-Exertional dyspnoea
-Fatigue
-Palpitations
-Chest pain
-Haemoptysis
Signs:
-Malar flush on cheeks
-Low-volume pulse
-Irregular pulse
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46
Q

how can mitral stenosis be diagnosed?

A
  • ECG- AF, P mitrale

- CXR- pulmonary oedema, LVH

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47
Q

what is cardiomyopathy?

A

A cardiomyopathy is a heart muscle disease of uncertain cause, which typically have an autosomal dominant pattern of inheritance

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48
Q

what can cause HCM?

A

sarcomeric gene mutations

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49
Q

what stage of the hearts contraction does HCM affect?

A

diastole- heart cannot relax properly due to thickening of the ventricular walls

50
Q

how does HCM present on an ECG?

A

large QRS, inverted T waves

51
Q

how is HCM treated?

A

beta blockers, calcium channel blockers, septal myectomy

52
Q

how does DCM present clinically?

A

breathlessness, tiredness, oedema

53
Q

what is the most common cause of restrictive CM?

A

Amyloidosis- extra-cellular deposition of an insoluble fibrillar protein (amyloid)

54
Q

what can cause arryhthmogenic right/left ventricular CM?

A

desmosome gene mutations- Desmosomes attach cells via intermediate filaments, mutation leads to myocytes being pulled apart and ventricles are replaced by fatty fibrous tissue

55
Q

how does arryhthmogenic right/left ventricular CM present on an ECG?

A

ventricular tachycardia and epsilon waves

56
Q

what is a ventricular septal defect?

A

This an abnormal connection between the 2 ventricles- since there is high pressure in the left ventricle and low pressure in the right ventricle blood flows from left to right.

57
Q

what can cause a VSD?

A

congenital, post MI (acquired)

58
Q

how does VSD present clinically?

A
  • symptoms- severe in infants, detected later in adults

- signs- loud murmurs= small hole, large hole= pulmonary hypertension

59
Q

how does a large VSD present on ECG and CXR?

A

ECG- LVH and RVH

CXR- cardiomegaly, large pulmonary arteries

60
Q

what is an atrial septal defect?

A

hole that connects the atria- classified as either ostium secundum (high in the septum) or ostium primum (opposing the endocardial cushions)

61
Q

how does an atrial septal defect present clinically?

A
  • pulmonary hypertension
  • cyanosis
  • arrhythmia
  • haemoptysis
  • chest pain
  • AF, raised JVP, pulmonary ejection systolic murmur
62
Q

how does an atrial septal defect present on an ECG?

A

RBBB with LAD and prolonged PR interval

63
Q

how does the presentation of an atrioventricular septal defect differ between a complete and a partial defect?

A 
•Complete defect
oBreathless as neonate
oPoor weight gain
oPoor feeding
oTorrential pulmonary blood flow
oNeeds repair or PA band in infancy
oRepair is surgically challenging

•Partial defect
oCan present in adulthood
oPresents like small ASD/VSD
oMay be left alone if no right heart dilatation

64
Q

what is a patent ductus arteriosus?

A

Persistent communication between the proximal left pulmonary artery and the descending aorta – continuous left to right shunt

65
Q

what are the clinical signs of a patent ductus arteriosus?

A

bounding pulse, continuous ‘machinery murmur’, pulmonary hypertension in a large PDA

66
Q

how does coarctation of the aorta present clinically?

A

radio femoral delay, weak femoral pulse, high BP, systolic murmur

67
Q

what are the 4 key feats fo the tetralogy of fallot?

A
  1. Ventricular septal defect
  2. Pulmonary stenosis
  3. Right ventricular hypertrophy
  4. The aorta overriding the VSD
68
Q

how does the tetralogy of fallot present clinically?

A
  • gradually becomes cyanotic due to decreasing. blood flow to lungs
  • hypoxic spells
  • toddlers may squat
69
Q

how can tetralogy of fallot be diagnosed?

A
  • CXR- boot shaped heart

- echo shows degree of stenosis

70
Q

what is cardiac tamponade?

A

when fluid in the pericardium builds up, resulting in compression of the heart.

71
Q

why does chronic pericarditis rarely cause cardiac tamponade?

A

In chronic pericarditis, chronic accumulation of fluid in the pericardial sac allows for adaptation of the parietal pericardium- this compliance reduces the effect on diastolic filling of the chambers

72
Q

what can cause pericarditis?

A
  • Usually idiopathic
  • Dressler’s syndrome- occurs after an MI
  • Viral- e.g. EBV, influenza, herpes simplex
  • Bacterial- e.g. mycobacterium tuberculosis
  • Autoimmune- rheumatoid arthritis, systemic lupus erythematosus
  • Neoplastic- secondary metastatic tumours
73
Q

how does pericarditis present clinically?

A

Chest pain- severe, sharp, pleuritic, rapid onset, radiates to arm, relieved by sitting forward

74
Q

how can you diagnose pericarditis?

A
  • examination- pericardial rub, sinus tachycardia
  • ECG- diffuse ST segment elevation
  • ESR, CRP raised
75
Q

how is pericarditis treated and managed?

A
  • anti-inflammatory drugs
  • avoid strenuous activity
  • NSAIDs/ aspirin
  • colchicine for 6-8 weeks
76
Q

what is Dressler’s syndrome?

A

secondary form of pericarditis- Myocardial injury stimulates formation of autoantibodies against the heart. Cardiac tamponade may occur
- occurs 2-10 weeks after and MI

77
Q

how does Dressler’s syndrome present clinically?

A
  • Fever
  • Chest pain
  • Pericardial rub
78
Q

what is the definition of hypertension?

A

BP over 140/90mmHg based on over 2 readings on separate occasions

79
Q

what is the aetiology of hypertension?

A

Essential hypertension (hypertension with no known underlying cause):

  • Genetics
  • Low birth weight
  • Obesity
  • Excess alcohol intake
  • High salt intake
  • Metabolic syndrome

Secondary hypertension (result of a specific, treatable cause)

  • Renal disease
  • Diabetic neuropathy
  • Endocrine disease- Conns, adrenal hyperplasia, phaeochromocytoma, Cushing’s syndrome, acromegaly
  • Coarctation of the aorta
  • Pregnancy
  • OCP
80
Q

how can hypertension be diagnosed?

A
  • Fasting glucose and cholesterol tests
  • U&E’s and Ca2+ checked to rule out underlying causes
  • 24H ambulatory BP monitoring-
81
Q

what is the pharmacological treatment of hypertension?

A
  • ACE inhibitors- prevent production of angiotensin II (potent vasoconstrictor), also prevent degradation of bradykinin (a vasodilator)
  • Diuretics- increase sodium and water retention
  • Beta blockers- reduce renin production and sympathetic nervous activity
  • ARBS- selectively block receptors for angiotensin II
  • Calcium channel blockers- dilate peripheral arterioles
82
Q

what is the first line of treatment for a patient under 55 and over 55?

A 
under= ACE inhibitor 
over= CCB
83
Q

what is atrial fibrillation?

A

The atrial muscle fibres contract independently- producing no P waves- as a result of this the ventricles contract irregularly due to the ‘all-or-nothing’ principle- however QRS complexes are of normal shape as the conduction through the ventricles passes by the same route, however QRS complexes are irregular

84
Q

what is the aetiology of atrial fibrillation?

A
  • Heart failure/ ischaemia
  • Hypertension
  • MI
  • PE
  • Mitral valve disease
  • Pneumonia
  • Hyperthyroidism
  • Caffeine
  • Alcohol
  • Hypokalaemia
  • Hypomagnaesaemia
85
Q

how can atrial fibrillation be diagnosed?

A
  • ECG- absent P waves, irregular QRS complexes ‘irregularly irregular’
  • Bloods- U&E, cardiac enzymes, thyroid function tests
86
Q

how can atrial fibrillation be treated?

A

acute- O2, cardioversion, LMWH

chronic- warfarin, beta blocker, calcium channel blocker

87
Q

how does an atrial flutter present on an ECG?

A

sawtooth baseline

88
Q

what can cause heart block?

A

oCoronary artery disease
oCardiomyopathy
oFibrosis of conducting tissue (elderly people)

89
Q

what is first degree AV block?

A

delayed AV condition resulting in a prolonged PR interval

90
Q

what is mobtiz type 1 heart block?

A

progressive PR elongation until a P wave fails to conduct, the PR interval then returns to normal

91
Q

what is a Mobitz Type 2 block?

A

dropped QRS isn’t preceded by progressive PR prolongation

92
Q

what is a 3:1 advanced heart block?

A

o When only every third P wave conducts to ventricles- so the ratio of P waves to QRS complexes

93
Q

what is third degree heart block?

A

P waves and QRS complexes occur independently of eachother

94
Q

what is a RBBB?

A

oSequential spread of an impulse from L to R
oRemember MaRRoW (m shape in VI, W shape in v6)
oProduces late activation of right ventricle

95
Q

What is a LBBB?

A 
oProduces a deep S wave in VI and tall R in leads I and V6
oRemember WiLLiaM (W in V1, M in V6)
96
Q

What can cause sinus tachycardia?

A

exercise, fever, anaemia, heart failure, acute pulmonary thromboembolism, hypovolaemia

97
Q

how can ventricular tachycardia be managed?

A 
oConnect to monitor, have defib to hand
oHigh flow O2
oIV access – U&Es, cardiac enzymes, Ca2+, Mg2+
oABG
oAmiodarone IV
98
Q

what can cause prolonged QT syndrome?

A

Congenital – mutations in sodium/potassium channel genes
Electrolyte disturbances – hypokalaemia, hypocalcaemia, hypomagnesaemia
Drugs – tricyclic antidepressants

99
Q

what can cause Wolf-Parkinson-White syndrome?

A

Due to congenital accessory conduction pathway between atria and ventricles

100
Q

what is the most common cause of a dissecting aortic aneurysm?

A

results from a tear in the intima- blood under high pressure creates a false lumen in the diseased media

101
Q

how does a dissecting aortic aneurysm present clinically?

A
  • Severe, tearing central chest pain which radiates through the back
  • Involvement of branch arteries may result in neurological signs, absent pulses and unequal BP in both arms
102
Q

what can cause an aortic aneurysm?

A
  • atherosclerosis

- connective tissue diseases

103
Q

what are the symptoms of an aortic aneurysm?

A
  • Epigastric/ back pain due to pressure effects
  • May rupture- presents with epigastric pain and hypovolaemic shock
  • asymptomatic
104
Q

how would you treat an aortic aneurysm?

A

if abdominal- surgical replacement with prosthetic graft

105
Q

how would you manage an aortic aneurysm?

A

hypotensives to keep systolic BP at 100-110mmHg- e.g. lanetalol

106
Q

how can PVD present clinically?

A
  • Intermittent claudication- cramping pain felt in calf, thigh or buttock after walking a given distance which is relieved at rest
  • Critical ischaemia- ulceration, gangrene and foot pain at rest
  • Acute limb ischaemia (sudden limb ischaemia)- pain, pale, paralysis, paraesthesia, perishing cold, pulseless
107
Q

how can PVD be diagnosed?

A
  • ESR/ CRP can exclude diabetes mellitus
    FBC- anaemia and polycythaemia
    thrombophillia screen
    MRI and CT angiography
108
Q

how would you treat PVD?

A
  • risk factor modification
  • clopidogrel- prevent progression and reduce CV risk
  • revascularisation- percutaneous balloon angioplasty
109
Q

what are the 3 stages of ischaemia?

A
  • Stress- induced physiological malfunction (exercise-induced angina, intermitted claudication)
  • Structural and functional breakdown (ischaemic cardiac failure, critical limb ischaemia, vascular dementia)
  • Infarction- gangrene
110
Q

what are some risk factors for infective endocarditis?

A

poor dental hygiene, systemic sepsis, diabetes mellitus, long-term haemodialysis, immunosuppression

111
Q

what is the aetiology of IE?

A
  • GRAM-POSITIVE BACTERIA
  • Mostly staphylococcus
  • Some streptococcus- e.g. strep. Viridans
  • Dental treatments increase the risk of bacteria being introduced into the blood stream- results in bacteraemia
  • Candida on skin can be introduced into the blood stream via cannulation
112
Q

how does IE present clinically?

A
  • Fever
  • Weight loss
  • Malaise
  • Clubbing
  • Signs- splinter haemorrhages (small haemorrhages seen on the nails- like red lines), osler’s nodes (tender nodules in the digits of the patient), janeway lesions (haemorrhages and nodules in the fingers- dark red dots), roth spots, heart murmurs
113
Q

what is shock?

A

Shock is the term used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion- meaning there is inadequate oxygen and glucose for aerobic cellular respiration. This results in generalised hypoxia and an inability of cells to utilise oxygen

114
Q

what is haemorrhagic shock and what can cause it?

A

-Shock due to blood loss

AETIOLOGY

  • Caused by an internal or external haemorrhage
  • Increased vascular permeability
  • Loss of fluid- dehydration, burns, vomiting, pancreatitis
115
Q

what are the classes of haemorrhagic shock?

A 
Class I:
• 15% blood loss
• Pulse below 100 bpm
• BP normal
• Pulse pressure normal
• Resp rate; 14-20
• Urine output greater than 30ml/hr
• Slightly anxious
Class II:
• 15-30% blood loss
• Pulse greater than 100 bpm (tachycardia - earliest sign)
• BP normal due to autonomic response (increased sympathetic activity)
• Pulse pressure decreased
• Resp rate; 20-30
• Urine output: 20-30ml/hr
• Mental status: mildly anxious

Class III:

  • 30-40% blood loss
  • Pulse above 120 bpm
  • BP decreased
  • Pulse pressure decreased
  • Resp rate; 30-40
  • Urine output: 5-15ml/hr
  • Mental status: confused
116
Q

what can cause cardiogenic shock?

A
  • cardiac tamponade
  • PE
  • acute MI
  • myocarditis
117
Q

what can cause neurogenic shock?

A
  • spinal cord injury
  • epidural
  • spinal anaestheisa
118
Q

what is an anaphylactic shock?

A

the release of IgE due to an allergic response

119
Q

how does a patent with anaphylactic shock present clinically?

A

warm peripheries, hypotension, urticarial, angio-oedema

120
Q

what is septic shock?

A

Septic shock exists when sespsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

nicks phase 2a flaschards (15 decks)

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