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Conditions + definitions > Cardio > Flashcards

Cardio Flashcards

1
Q

What is hypertension?

A

Hypertension is a chronic medical condition in which the blood pressure is elevated > 140/90

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2
Q

What is essential hypertension vs secondary?

A

Primary hypertension = no medical cause is found.

Secondary - other cause

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3
Q

What are the signs and symptoms of hypertension?

A 
Symptoms
- usually asymptomatic
- headaches
- epistaxis
- sweating
Signs
- elevated BP
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4
Q

What are the renal causes of hypertension?

A

Diabetic nephropathy
Chronic glomerulonephritis
Polycistic kidneys
Renal vascular disease

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5
Q

What drugs can cause hypertension?

A

NSAIDs
Oral contraceptives
Steroids
Liquorice

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6
Q

What are the endocrine causes of hypertension?

A

Conn’s syndrome
Phaeochromocytoma
Adrenal hyperplasia
Cushing’s syndrome

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7
Q

What are the risk factors for hypertension?

A

Lifestyle factors - diet, smoking, obeisty, alcohol, no exercise

age, sex, family history
Ethnic group
Diabetes
Kidney disease
High cholesterol
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8
Q

What is the non-pharmacological treatment for hypertension?

A 
Reduce risk factors
Lose weight
Exercise
Reduce salt
Stop drinking/smoking
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9
Q

What is the pharmacological treatment for hypertension?

A

ACI/ARB (first line in under 55s)
CCB/diuretic above (or black/pregnant)
Combination therapy if needed

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10
Q

What are ACEIs?

A 
Angiotensin converting enzyme inhibitors
e.g. Ramipril, Captopril
• Blocks the conversion of angiotensin 1 into angiotensin 2 which is a potent vasoconstrictor.
S/E → Hypotension
Dry cough
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11
Q

What are CCBs?

A 
Calcium channel blockers
e.g. Amlodipine, nifedipine
• Causes arteriole dilatation and reduces the force of heart contractions
S/E → Headaches
>Sweating
>Palpitations
>Flushing
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12
Q

What are diuretics (used for hypertension)?

A

Thiazide type generally used
• Increases water secretion from the body by not absorbing Na therefore Na remains int he filtrate and water follows
S/E → Increases cholesterol levels
>Impaired glucose tolerance

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13
Q

What is malignant hypertension?

A

Malignant hypertension is a complication of hypertension characterized >very elevated blood pressure that occurs rapidly, >organ damage in the eyes, brain, heart and/or kidneys.
Systolic and diastolic blood pressures are usually greater than 220mmHg and 120mmHg, respectively.

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14
Q

What are the signs of malignant hypertension?

A

The eyes may show >papilloedema,
>retinal haemorrhage,
>or exudates

• The brain shows
>increased ICP,

• Patients will usually suffer from left ventricular dysfunction

• The kidneys will be affected,
> haematuria,
>proteinuria,
>and acute renal failure.

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15
Q

What is emergency blood pressure control?

A

Should not bring down the BP too quickly as there is a risk of cerebral, retinal, renal, MI complications

IV Sodium nitroprusside
IV iabetalol

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16
Q

What is angina?

A

Angina: radiating chest pain caused by insufficient blood flow to an area of the heart.

  • STABLE: occurs upon exertion and fades with rest
  • UNSTABLE: occurs suddenly and spontaneously with no exertion
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17
Q

What are the signs and symptoms of angina?

A

Symptoms

  • Tight, dull heavy chest discomfort
  • Retrosternal or radiating to the left arm, neck, back or jaw
  • Breathlessness
  • Nausea
  • Epigastric discomfort that is not relieved with antacidsSigns
  • Usually none!
  • Hypercholesterolaemia (xanthalasma, corneal arcus)
  • Anaemia (pallor, tachy)
  • Thyrotoxicosis (carotid bruits)
  • Hypertension
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18
Q

What is the pathogenesis of atheroma?

A 
Increased lipid levels
Inflammaotry process - infiltration of macrophages
Macrophages form foam cells 
>Through uptake of mdified LDLs
Forms fibrous cap
>Reduces blood flow, can rupture
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19
Q

What is the content of atheromatous plaques?

A

Collagens (produced by smooth muscle cells) in cap provide structural strength

Inflammatory cells (macrophages, lymphocytes, mast cells) reside in fibrous cap: recruited from arterial endothelium

Soft “foamy” macrophages rim (foamy due to uptake)

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20
Q

What are the S&S of major hyperlipidaemia?

A

Conreal arcus (premature)
Tendon Xanthomata (knuckles, Achilles)
Xanthelasmata (fatty lumps in skin, often in arms)
Risk/premature/family history MI/athermoa

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21
Q

What are the risk factors for atheroma?

A 
Male
Smoking
Drinking
High cholesterol
Obesity
Diabetes
Hypertension
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22
Q

How do you investigate agina?

A

ECG/exercise ECG
Myocardial perfusion scans
CT coronary angiogram

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23
Q

What drugs are used to manage angina?

A

Symptomatic - GTN spray
>Max 3 doses before ambulance should be called

Acute
>Long acting nitrates

Long term
>Betablockers
>Long acting nitrates
>CCBs
>K+ channel activators
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24
Q

What are the S&S of unstable angina?

A

Symptoms:

1) Occurs at rest
2) Severe and new onset
3) Crescendo pattern (more severe & prolonged)

Signs:

1) Heart sound
2) Basal crackles
3) Hypotension
4) Murmurs

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25
Q

What investigations should be done into unstable angina?

A

ECG: May be normal or show ST depression or T wave inversion

Biochem markers: To assess risk of MI

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26
Q

How do you treat unstable angina?

A

B blockers
Nitrates
CCBs

Aspirin
Heparin

Angiography/stent if needed

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27
Q

What are PQRS?

A

P→ atrial depolarisation
QRS → ventricular depolarisation
T → ventricular repolarisation
PR interval → time taken for impulse to pass from SA to AV node.

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28
Q

What are the complications of an MI?

A

Heart failure
Myocardial rupture
VSD – due to infarct in septum
Mitral regurgitation – MI of inferior wall, due to infarct of pappliary muscle
Cardiac arrhythmias- MI of anterior wall
Conduction disturbances – MI of inferior wall presents as heart block

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29
Q

What can cause heart block?

A 
1st/2nd degree 
>Acute infection
>Myocarditis
>Ca blocker/b blocker/digoxin
	3rd degree
>Coronary ischaemia
>SLE
>Drug induced
>endocarditis
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30
Q

What is first degree heart block?

A

Prolonged PR interval >0.22 sec

Asymptomatic

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31
Q

What is type 1 2nd degree heart block?

A

Progressive P-R interval elongation until a P wave fails to conduct at all.
This would show that there is a problem with the A-V node
>Light headedness
>Dizziness
>syncope

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32
Q

What is 3rd degree heart block?

A

no relation between the QRS and P wave i.e. there is no conduction to the ventricles from the atria.
If QRS is narrow = Bundle of His takes over
If QRS is wide = purkinje takes over

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33
Q

What is type 2 2nd degree heart block?

A

No P-R wave elongation but P wave fails to conduct to QRS sometimes at a rate of 3:1
>Light headedness
>Dizziness
>syncope

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34
Q

How do you manage bradycardia?

A

If asymptomatic and rate > 40bpm = no treatment
If rate <40bpm or patient symptomatic:
1) atropine
2) Temporary pacing wire

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35
Q

What are the types of supraventricular tachycardias?

A

Atrial flutter

Atrial fibrillation

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36
Q

What is atrial flutter?

A

Rhythm is still regular (interval between QRS complexes) but there are P waves at a rate of >250/min. There is no flat baseline between P waves

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37
Q

What is atrial fibrilation?

A 
Absent P waves and increased and irregular heart rate
>Palpitations
>Chest pain
>Dizzy
>SOB
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38
Q

What are the causes of atrial flutter?

A

Re entrant rhythm
CAD
Hypertension
cardiomyopathy

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39
Q

What are the causes of AF?

A

Ischaemia
Cardiomyopathy
hypertension

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40
Q

What is VF?

A

Cardiac arrest
Loss of consciousness
There is no QRS complex and ECG is disorganised

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41
Q

What is VT?

A

Severe hypotension

≥ 3 consecutive ventricular beats in all leads and QRS complexes are broad.

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42
Q

How do you manage AF?

A

Maintain sinus rhythym with DC cardioversion
Antiarrhytmic drugs (betablockers 1st line)
Reduce heart rate
Blood thinners to prevent stroke

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43
Q

What are the types of antiarrhythmics?

A

1 - sodium channel blockers (fast, medium, slow for ABC)
2 - B-adrenergic receptor antagonists
3 - prolong refatorinesss
IV - CCBs

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44
Q

What are class 1 antiarrhythmics?

A

Membrane-stabilizing agents
A - quinidine
B - lidocaine
C - flecainide

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45
Q

What are the signs of digoxin toxicity?

A 
Nausea and vomiting
Xanthopsia
Bradycardia
Tachycardia
Arrhythmias: VT and VF
46
Q

What is the clinical presentation of cardiac failure?

A

Symptoms:

  • dysopnea/orthopnea
  • Fatigue

Signs:

  • Cardiomegaly
  • 3rd/4th heart sounds
  • ↑ JVP
  • Tachycardia/Hypotension
  • Bi basal crackles
  • ascities
  • Pleural effusion
  • ankle odema
  • Hepatomegaly
47
Q

What can cause left sided heart failure?

A

Commonly IHD but can also occur with
valvular heart disease &
hypertension,
dilated cardiomyopathy.

Mainly IHD, cardiomyopathy and hypertension

48
Q

What can cause right sided heart failure?

A

Left sided heart failure
right ventricular cardiomyopathy,
right ventricular infarction,
pulmonary hypertension.

Mainly IHD, cardiomyopathy and hypertension

49
Q

What drugs affect preload?

A

Diuretics decrease

50
Q

What drugs affect aferload?

A

ACEI decrease by vasodilation
ARBs decrease
CCBs

51
Q

What drugsd affect cardiac contracability?

A

Anti-arrhytmics

52
Q

What are the types of shock?

A 
Hypovolaemic
Septic
Anaphylactic
Disruptive
Obstructive
53
Q

What are the signs of shock?

A 
↓BP, 
Pale, 
Clammy hands, 
Tachycardia, 
Tachypnoea, 
Confusion, 
↓Urine output, 
↑ Capillary refill
54
Q

What drugs are used to treat shock?

A

Adrenaline/neuroadrenaline
Dopamine (precurosor to adrenaline)
Dobutamine (increases CO)

55
Q

What are the clinical signs of infective carditis?

A 
Valve destruction:  heart failure +/- new heart murmurs
• Vascular phenomena:  embolisation of vegetation + metastatic abscess formation in brain, spleen +kidney
• Immune complex deposition: 
>Vascalitis
>petechia
>Splinter haemorrhage
>Roth spots
>Oslers nodes
>arthralgia 
>glomerulonephritis
56
Q

What causes infective carditis?

A

Staph A
Alpha haemolytic strep. viridans

Due to prosthetic valve/valve surgery
Soft tissue infections
IV drug users
Prolonged catheter/antibiotic use

57
Q

What is the pathogenesis of infective carditis?

A

Endocarditis is usually the consequence of two factors:
• The presence of organism in the blood stream
• Abnormal cardiac endothelium facilitating adherence and growth

> Damaged endocardium promotes platelet and fibrin deposition which allows organisms to adhere and grow leading to an infected vegetation.
Valvular lesions may create non laminar flow and jet lesions from septal defects or patent ductus arteriosus
Aortic and mitral valves are usually affected
>IV drug users – tricuspid!

58
Q

What are the complications of infective carditis?

A

Cardiac failure (destruction of heart valve)
• Embolism
• Glomerulonephritis

59
Q

How do you investigate infective carditis?

A 
Blood cultures (Before antibiotics)
>3 different sites in 24 hours
Echo
Serological tests if blood cultures negative
Chest X-ray
ECG
Blood count (WBC raised)
60
Q

What are the indications for a valve replacement?

A

Severe heart failure
• Infection of prosthetic material
• Worsening renal failure
• Extensive damage to valve

61
Q

What are the characteristics of pericardial disease?

A

Sharp central chest pain which is exacerbated by movement, respiration and lying down and is characteristically relieved by leaning forward

62
Q

What are the causes of pericarditis?

A

Most commonly due to viral infection & MI

  • viral: Cox sackle B
  • post MI
  • bacterial: Staph aureus in HIV
  • Malignant: carcinoma of the bronchus, breasts and hodgkins lymphoma
63
Q

What are the clinical features of pericarditis?

A

Sharp chest pain
• Pericardial friction rub
• +- fever

64
Q

What are the ECG changes in pericarditis?

A

Concave upwards, (saddle shaped) ST segment elevation which then changes to T wave flattening or inversion – then normalizes

65
Q

How do you treat pericarditis?

A

Underlying cause

Then NSAIDs, if no improvement corticosteroids

66
Q

What causes Pericardial Effusion?

A

Most commonly due to pericarditis
Viral
Post MI
And malignant

67
Q

What are the clinical features of pericardial effusion?

A

Heart sounds soft and distant
• Apex beat obscured
• Cardiac tamponade: ↑JVP, ↓BP, ↑HR

68
Q

What is the treatment for pericardial effusion?

A

Treat underlying cause

PERICARDIOCENTESIS – When fluid is aspirated from the pericardium with US guidance

69
Q

What are the causes of constrictive pericarditis?

A

Infection– TB
-Inflammation– Chronic pericarditis
Usually - IDIOPATHIC

70
Q

What are the clinical features of constrictive pericarditis?

A 
↑JVP
	• Ascites
	• Hepatomegaly
	• Dyspnoea
	• Cough
	• Orthopnoea
	• ↓BP
• fatigue
71
Q

How do you treat constrictive pericarditis?

A

Complete resection of pericardium

72
Q

What is the presentation of myocarditis?

A 
Chest pain
Palpitations
Fatigue
Dysopnea
Congestive heart failure 
Soft heart sounds
3rd heart sound
Tachycardia
Pericardial friction rub
73
Q

What is cardiomyopathy, and what are its types?

A

Cardiomyopathy: is a group of diseases of the myocardium that affect the mechanical or electrical function of the heart. They are not secondary to anything and frequently genetic
Dilated, hypertrophic and restrictive

74
Q

What can cause dilated cardiomyopathy?

A

Hypertension
Ischaemia
Congenital heart disease
Infections

75
Q

What is the presentation of dilated cardiomyopathy?

A
  • SOB
  • Embolism
  • Arrhythmia
  • Heart failure symptoms (dyspnoea, orthopnoea, fatigue)
76
Q

How do you investigate dilated cardiomyopathy?

A

CXR: Cardiac enlargement
ECG: ST segment and T wave changes
ECHO: dilated ventricles
“dilated left ventricle which contracts poorly”

77
Q

How do you manage dilated cardiomyopathy?

A

Treat heart failure and arrhythmias

- Disease progression is slowed down with ACE, ARB’s, spironolactone and B-blockers.
- ICD’s given if risk of VT
78
Q

What are the causes of hypertrophic cardiomyopathy?

A

genetic disorder caused by mutations in genes coding for proteins that regulate contractions

79
Q

What is the presentation of hypertrophic cardiomyopathy?

A 
Usually asymptomatic
• SOB, chest pain, syncope
• Jerky carotid pulse
• Ejection systolic murmur
• Pansystolic murmur
80
Q

How do you investigate hypertrophic cardiomyopathy, and its results?

A

ECG: Let ventricular hypertrophy
ECHO: ventricular hypertrophy with involvement of the septum

81
Q

How do you manage hypertrophic cardiomyopathy?

A

If increased risk of sudden death then implant ICD

- If ok the give amiadarone
- Treat symptoms with b-blockers and verapamil
82
Q

What are the causes of restrictive cardiomyopathy?

A

amyloidosis
sarcoidosis.
famlial

83
Q

What is the presentation of restrictive cardiomyopathy?

A 
Dyspnoea
	• Fatigue and embolitic symptoms
	• ↑JVP
	• Hepatomegaly
	• Ascites
• 3rd and 4th heart sounds
84
Q

What are the investigations for restrictive cardiomyopathy?

A

Cardiac catheter: Characteristic pressure changes

“rigid myocardium”

85
Q

What are the systolic murmurs?

A

Aortic stenosis
Pulmonary stenosis
Mitral regurgitation
Tricuspid regurgitation

86
Q

What are the septal defects?

A

VSD - left ventricular pressure greater than right, leads to central cyanosis
ASD - left atrial pressure greater than right, blood moves left to right
>Increases overload and leads to heart failure

87
Q

What is aortic stenosis?

A

Outflow of blood from LV is obstructed
>increases LV pressure –> causing LV hypertrophy

Caused by
•Congenital stenotic valve
• Rheumatic fever
• Calcific valvular disease

88
Q

What is the presentation of aortic stenosis?

A

Mid systolic murmur in aortic area
Radiates to carotid

  • usually no symptoms until severe
  • Syncope (exercise)
  • Angina
  • Dyspnoea
  • slow rising carotid pulse
89
Q

What is pulmonary stenosis?

A

Outflow of blood from the RV obstructed by pulmonary valve
>reduces blood flow to lungs, –>leads to RV hypertrophy

Caused by
• Congenital
• Carcinoid syndrome
• Rubella during pregnancy

90
Q

How does pulmonary stenosis present?

A

Mid systolic ejection murmur
Left of sternum 2nd intercostals space

fatigue

  • syncope
  • right heart failure
  • raised JVP
  • thrill
91
Q

What is mitral regurgitation?

A

Regurg into LA causes LA dilatation.
causes LV hypertrophy and pulmonary congestion

Caused by
• Rheumatic fever
• Prolapsing miitral valve
• Rupture of pap muscle or chordate due to MI

92
Q

How does mitral regurgitation present?

A

Pan systolic murmur
loudest at the apex and radiates to the axilla

palpitations

  • dyspnoea
  • Fatigue
  • Displaced apex
93
Q

What is tricupsid regurgitation?

A

Occurs when there is RV dilatation leading to a change in anatomy

Caused by
• Cor pulmonale
• MI
• Pulmonary hypertension
• Infective endocarditis
94
Q

How does tricupsid regurgitation present?

A

Pan systolic murmur
Best heard on inspiration

right heart failure

  • raised JVP
  • palpable liver
95
Q

What are the diastolic murmurs, what causes them?

A

Mitral stenosis
>Rheumatic fever

Aortic regurgitation
>Rhemuatic fever + infective endocarditis

96
Q

What is mitral stenosis?

A

Outflow of blood form the LA is obstructed
>causes LA hypertrophy as pressure increases.
pulmonary pressure then increases
>Causes right heart failure

97
Q

How does mitral stenosis present?

A

Mid diastolic murmur with opening snap
low pitched rumbling with bell at apex with patient on the left side

Pulmonary hypertension: malar flush, dyspnoea, cough, haemoptysis
• Right heart failure: fatigue, oedema, raised JVP (a wave)
• AF: palpitations

98
Q

What is aortic regurgitation?

A 
Reflux of blood from aorta into the LV.
 LV has to work harder to pump blood 
>LV hypertrophy 
>increases demand of cardiac perfusion 
>leads to cardiac ischaemia
99
Q

How does aortic regurgitation present?

A

Early diastolic murmur
High pitched
Left sternal edge (4th intercostals space) patient leaning forward and holding breath in expiration

Increased pulsation/pounding of the heart
• Angina
• dyspnoea

100
Q

What are the risk factors for congenital cardiac disease?

A 
Maternal rubella (PDA)
Foetal alcohol syndrome
Maternal SLE
Downs syndrome (trisomy 21)
Turner’s syndrome (coarctation of the aorta)
101
Q

What are the common congenital heart diseases?

A 
VSD
ASD
PDA
Fallots tetralogy
Coarcation of aorta
102
Q

What is the presentation of VSD?

A

Small VSD: Asymptomatic
Moderate VSD: Fatigue, dyspnoea, cardiac enlargement
Pan systolic murmur

103
Q

What is the presentation of ASD?

A

Palpatations/AF
Dyspnoea
Pulmonary infection

104
Q

What is the presentation of PDA?

A

No signs

The ductus arteriosus conncets the pulmonary artery to the descending aorta. If it remains patent = LV hypertrophy

105
Q

What is the presentation of fallots tetraology?

A 
Dyspnoea
	Fatigue
	Cyanotic
	Syncope
	Squatting
	Clubbing
polycythaemia
106
Q

What is fallot’s tetraology?

A

1)Overriding aorta
2) RV outflow obstruction
3) Ventricular septal defect
4) RV hypertrophy
= right to left shunt

107
Q

What is coarctation of aorta?

A

Hypertension
Weak delayed pulses
Radial to radial delay

108
Q

What are the types of aortic aneurysm?

A

Saccular
Fusiform
False
Dissecting

109
Q

What are the symptoms of a PE?

A 
Severe dyspnoea of sudden onset
Collapse
Blue lips and tongue- cyanosis
Tachycardia
Low blood pressure
Raised jugular venous 
	pressure
Altered heart sounds
110
Q

What are the risk factors for AAA?

A

male sex
advancing age
smoking
COAD

111
Q

What is the presentation of AAA?

A

Asymptomatic
- incidental finding on examination
>Or on ultrasound
Emergency - imending/actual rupture

112
Q

What is the presentation of aortic dissection?

A

Tearing, severe chest pain (radiating to back)
Collapse (tamponade, acute AR, external rupture)
Beware inferior ST elevation
Hypotension (severe)
Pulmonary odema

Conditions + definitions (68 decks)

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