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my revision > CARDIOVASCULAR > Flashcards

CARDIOVASCULAR Flashcards

1
Q

What contributes to venous return

A
  1. Intermittent skeletal contraction
  2. increase and decrease in thoracic pressure
  3. diaphragm compressing abdnomla veins with each breath
  4. Increase in blood veins closer to heart
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2
Q

Name the different valves and their function

A

function: stop backflow of blood via papillary muscles preventing opening in the wrong direction

AV: Tricuspid (right atrium- right ventricle)
mitral valve (left atrium- eft ventticle)

pulmonary: aortic

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3
Q

briefly describe the contraction of the heart

A
  1. SAN node in right atrium- cels intrinisc timer (dictated by ion permeability
  2. SAN sends signal to AVN
  3. Short delay due to fiborous tissue (allow atria to contract into ventrice)
  4. AVN slows down spread, propogate to left ventricle via purkinje fibres
  5. depolarisation of atria causing contraction
  6. delay of av node
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4
Q

How is Cardiac output measured

A

CO= HR x SV

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5
Q

What is circulation affected

A

use of tissue in exercise
increased metabolsim

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6
Q

How can cardiac output be increased?

A
  • constrict sphelanic circulation so increases redistribution
  • respiratory and skeletal pump (change in thoracic pressure)
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7
Q

How is blood pressure measured

A

Blood pressure= TPR x CO

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8
Q

What is the short term balance of blood pressure

A

parasympathetic & sympathetic nervous sysem

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9
Q

What is long term balancing blood pressure controlled by?

A

Renin-angiotensin system
- blood flow to kidneys & hormone regulation

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10
Q

Describe the renin-angiotensin system

A

persistently low blood pressure causes arteriole constriction & reduced blood flow to kidneys (reduction in sodium and water excretion)

Kidney response:
1. Produce renin
renin converts angiontensin-> angiotensin 1
2. angiotensin 1-> angiotensin 2 (ACE)
3. Angiotensin 2: aldosterone is produced
- bradykinin release

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11
Q

How does cardiopulmonary resuscitation work

A

Heart stops: CPR pumps blood around 1/3 chest, 30:2

  1. 30: 2- 1/3 of chest compressions
  2. creates pressure & each recoil relieves pressure & gives time for heart ro fil

contract: blood taken away from brain : due INCREASE PRESSURE (thorax & head)

Recoil: negative pressure in thorax- perfusion & protects brain

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12
Q

What is a ‘high’ blood pressure

A

135+/ 85mmHg

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13
Q

What are the consequences of hypertension

A
  • damage to walls so epithelium thickens
  • chronic kidney disease
  • retinopathy
  • atheromas, aneurysms,
  • peripheral vascular disease
  • Heart failure
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14
Q

Causes for hypertension

A

non modifiable: age, gender, ethnicity
Modifiable: obesity, alcohol, sodium, smokin,g, stress, low control of kidney/ endocrine disease, drugs

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15
Q

What do diuretics do?
- side effects (oral)

A

Increase secretion of fluid from kidneys( by reducing sodium absorption)- reducing Circulatory volume = Reduced SV

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16
Q

What drugs are ACE inhibitors, what do they do
Side effects (oral)

A

ramipril, apil
- Inhibit ACE enzyme, prevent angiotensin 2 forming
- prevent vasodilation & bradykinin breakdown

Side effects: Dry mouth, glossitis, erythema multiforme, lichenoid reactions

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17
Q

What are calcium channel blockers role & oral side effects

A

Prevent vasoconstriction & reduce contractility (force & rate HR)
- Calcium dependent

side effects: gingival hyperplasia, taste distrubances

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18
Q

What is the mechanism of atherosclerosis

A
  1. Endothelial destruction
  2. Fatty streaks: accumulate in tunica intima- lopi d contained with macrophages (foam cells)
  3. Fibrolipid plaque- smooth muscle proliferation & migration covering fratty plaques form fibrolipid plaque caps over
  4. Complicated plaque: cap is damaged
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19
Q

What is an atheroma and why do they form

A

Mass of platelets, red blood cells, fibrin
- form virchows triad: blood consittutents, turbulent flow of blood, stiff vessel wall

20
Q

How does ACS differ to ACI

A

ACS: Reduced perfusion via coronary artery
ACI: No perfusion to coronary artery

diffferentiate the drs

21
Q

what are the symptoms of ACS

A
  1. Hypoxia
    discomfort
    breathlessness
    nausea
    clammy
    lightheadedness
    arrythmias
22
Q

What is the mx of ACS

A
  1. Clot breakdown: thrombolysis, angioplasty,place a stent
  2. removal of blood clot
  3. replace vessel with another vein

mx: statins(reduce LDL), Beta blockers & ACE inhbitior (reduce BP & strain on the heart), antiplatelets, anticoagulant

23
Q

What is the cause of peripheral vascular disease

A

atheroscleorsis- reduced perfusion: causing pain

24
Q

What is meant by claudication

A

symptom of peripheral vascular disease
- pain in legs, worsen on elevation
- better with rest

in severe: can cause ulcers, gangrea

25
Q

What is a varicose vein

A

swollen tortuous vein: due to incompetent valve in veins: blood flow is slow & causes swelling tortous veins

  • causes vascular ulcers: arterial ulcers/ venous ulcers
26
Q

What are the causes of arrythmias

A
  • rhythm elsewhere
  • circuit elsewhere (congential, electrolyte imbalance)
27
Q

Why would tachyarrythmia cause a low cardiac output & what is its management

A

Reduced stroke volume

mx: cardioversion (shock therapy to reset heart)
- rate controlling medication

28
Q

Why might bradyarrythmias cause a low cardiac output- Why might it occur?>

A

reduces HR

causes of bradyarrythmias:
- sinus bradycardia
- heart block due to conduction issue
-ventricular escape

29
Q

What is atrial fibrilartion and what are its risks & managemebt

A

discoordinated fibrilation (not SAN node)

risks:
- irregular control: risk of stroke, thrombous and clot formation

mx:
DOAC
Warfarin

30
Q

How does disarrytmias affect dentistry

A
  1. Avoid bupivacaine (cardiotoxic- alter consciousness (syncope),
  • b-blockers: control ventricular rate (exaggerated gag reflex)
31
Q

What is red flag syncopoe

A
  • excess 5 mins
  • reoccurence when upright
  • cardiac history
  • no warning signs
  • syncope from surpine
32
Q

How does digoxin impact dentist

A

pain similar to trigeminal neuralgia
NSAIDS, erythromuycosin increase plasma concentration

33
Q

how do antifungals impact heart conditions

A

risk of ventricular arrythmias

34
Q

What are the potential side effects of procainamide, quinidine

A

produce angioedema

35
Q

What are the 2 types of valve disease

A
  1. stenosis
  2. regurgitation
36
Q

What is the consequence of stenosis

A

reduced blood flow as valve cannot open

37
Q

What is the consequence of regurgitation

A

larger contractions to push blood onwards

38
Q

causes of valve disease

A
  • calcification causing stenosis
  • damage to papillary muscles
  • endocarditis: damage to heart valve (from rheumartic fever a streptococcal infection- immune system damages valve)
39
Q

What is endocarditis

A

inflammation of heart (including heart valves)

40
Q

What is heart failure

A

heart’s inability to pump blood strongly enough to meet body’s needs

41
Q

What are the causes of heart failure

A

Hypertension (hypertrophy as reduces room in ventricles)
Myocardial infarction (cannot pump as hard)
Valve disease
Arrhythmia (reduce stroke volume)
Other diseases→ cardiomyopathy
lung disease

42
Q

how does cardiomyopathy cause heart failure

A

disease of heart muscles (mudcles fibres are stretched, chambers enlarged, left hypertrophy)
- occurs due to drugs, alcohol, nutritional deficiencies, infections

43
Q

symptoms of left sided heart failure

A

lower cardiac output
fainting
tiredness
kidney disease- reduced perfusion
breathlessness (pulmonary oedema so reduced perfusion)

44
Q

Symptoms of right sided heart failure

A

Lungs receive less blood to be oxygenated
Leg swelling
liver and spleen swelling
impaired gastric absorption

45
Q

Why should caution be taken when prescribing NSAIDs in patients with oedema

A

NSAIDS→ may cause fluid retention & acute reneal failure in patients who take diuetics and ACE inhbitiors

46
Q

Why does oedema occur in heart failure

A

low blood pressure & tissue perfusion causes ittle forward flow in arterial circulation

  • venous circulation: congested with blood, increasing capillary pressure forcing fluid from circulation into tissues causing oedema
47
Q

How does valve disease cause heart failure

A

stenosis- narrowing of valve causes pressure overload causing left ventricular hypertrophy to
eject

regurgitation: volume overload- stretches heart- heart is dialated-> frank starling mechanism

my revision (13 decks)

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