CARDIOVASCULAR Flashcards
What contributes to venous return
- Intermittent skeletal contraction
- increase and decrease in thoracic pressure
- diaphragm compressing abdnomla veins with each breath
- Increase in blood veins closer to heart
Name the different valves and their function
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
briefly describe the contraction of the heart
- SAN node in right atrium- cels intrinisc timer (dictated by ion permeability
- SAN sends signal to AVN
- Short delay due to fiborous tissue (allow atria to contract into ventrice)
- AVN slows down spread, propogate to left ventricle via purkinje fibres
- depolarisation of atria causing contraction
- delay of av node
How is Cardiac output measured
CO= HR x SV
What is circulation affected
use of tissue in exercise
increased metabolsim
How can cardiac output be increased?
- constrict sphelanic circulation so increases redistribution
- respiratory and skeletal pump (change in thoracic pressure)
How is blood pressure measured
Blood pressure= TPR x CO
What is the short term balance of blood pressure
parasympathetic & sympathetic nervous sysem
What is long term balancing blood pressure controlled by?
Renin-angiotensin system
- blood flow to kidneys & hormone regulation
Describe the renin-angiotensin system
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
How does cardiopulmonary resuscitation work
Heart stops: CPR pumps blood around 1/3 chest, 30:2
- 30: 2- 1/3 of chest compressions
- 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
What is a ‘high’ blood pressure
135+/ 85mmHg
What are the consequences of hypertension
- damage to walls so epithelium thickens
- chronic kidney disease
- retinopathy
- atheromas, aneurysms,
- peripheral vascular disease
- Heart failure
Causes for hypertension
non modifiable: age, gender, ethnicity
Modifiable: obesity, alcohol, sodium, smokin,g, stress, low control of kidney/ endocrine disease, drugs
What do diuretics do?
- side effects (oral)
Increase secretion of fluid from kidneys( by reducing sodium absorption)- reducing Circulatory volume = Reduced SV
What drugs are ACE inhibitors, what do they do
Side effects (oral)
ramipril, apil
- Inhibit ACE enzyme, prevent angiotensin 2 forming
- prevent vasodilation & bradykinin breakdown
Side effects: Dry mouth, glossitis, erythema multiforme, lichenoid reactions
What are calcium channel blockers role & oral side effects
Prevent vasoconstriction & reduce contractility (force & rate HR)
- Calcium dependent
side effects: gingival hyperplasia, taste distrubances
What is the mechanism of atherosclerosis
- Endothelial destruction
- Fatty streaks: accumulate in tunica intima- lopi d contained with macrophages (foam cells)
- Fibrolipid plaque- smooth muscle proliferation & migration covering fratty plaques form fibrolipid plaque caps over
- Complicated plaque: cap is damaged
What is an atheroma and why do they form
Mass of platelets, red blood cells, fibrin
- form virchows triad: blood consittutents, turbulent flow of blood, stiff vessel wall
How does ACS differ to ACI
ACS: Reduced perfusion via coronary artery
ACI: No perfusion to coronary artery
diffferentiate the drs
what are the symptoms of ACS
- Hypoxia
discomfort
breathlessness
nausea
clammy
lightheadedness
arrythmias
What is the mx of ACS
- Clot breakdown: thrombolysis, angioplasty,place a stent
- removal of blood clot
- replace vessel with another vein
mx: statins(reduce LDL), Beta blockers & ACE inhbitior (reduce BP & strain on the heart), antiplatelets, anticoagulant
What is the cause of peripheral vascular disease
atheroscleorsis- reduced perfusion: causing pain
What is meant by claudication
symptom of peripheral vascular disease
- pain in legs, worsen on elevation
- better with rest
in severe: can cause ulcers, gangrea
What is a varicose vein
swollen tortuous vein: due to incompetent valve in veins: blood flow is slow & causes swelling tortous veins
- causes vascular ulcers: arterial ulcers/ venous ulcers
What are the causes of arrythmias
- rhythm elsewhere
- circuit elsewhere (congential, electrolyte imbalance)
Why would tachyarrythmia cause a low cardiac output & what is its management
Reduced stroke volume
mx: cardioversion (shock therapy to reset heart)
- rate controlling medication
Why might bradyarrythmias cause a low cardiac output- Why might it occur?>
reduces HR
causes of bradyarrythmias:
- sinus bradycardia
- heart block due to conduction issue
-ventricular escape
What is atrial fibrilartion and what are its risks & managemebt
discoordinated fibrilation (not SAN node)
risks:
- irregular control: risk of stroke, thrombous and clot formation
mx:
DOAC
Warfarin
How does disarrytmias affect dentistry
- Avoid bupivacaine (cardiotoxic- alter consciousness (syncope),
- b-blockers: control ventricular rate (exaggerated gag reflex)
What is red flag syncopoe
- excess 5 mins
- reoccurence when upright
- cardiac history
- no warning signs
- syncope from surpine
How does digoxin impact dentist
pain similar to trigeminal neuralgia
NSAIDS, erythromuycosin increase plasma concentration
how do antifungals impact heart conditions
risk of ventricular arrythmias
What are the potential side effects of procainamide, quinidine
produce angioedema
What are the 2 types of valve disease
- stenosis
- regurgitation
What is the consequence of stenosis
reduced blood flow as valve cannot open
What is the consequence of regurgitation
larger contractions to push blood onwards
causes of valve disease
- calcification causing stenosis
- damage to papillary muscles
- endocarditis: damage to heart valve (from rheumartic fever a streptococcal infection- immune system damages valve)
What is endocarditis
inflammation of heart (including heart valves)
What is heart failure
heart’s inability to pump blood strongly enough to meet body’s needs
What are the causes of heart failure
Hypertension (hypertrophy as reduces room in ventricles)
Myocardial infarction (cannot pump as hard)
Valve disease
Arrhythmia (reduce stroke volume)
Other diseases→ cardiomyopathy
lung disease
how does cardiomyopathy cause heart failure
disease of heart muscles (mudcles fibres are stretched, chambers enlarged, left hypertrophy)
- occurs due to drugs, alcohol, nutritional deficiencies, infections
symptoms of left sided heart failure
lower cardiac output
fainting
tiredness
kidney disease- reduced perfusion
breathlessness (pulmonary oedema so reduced perfusion)
Symptoms of right sided heart failure
Lungs receive less blood to be oxygenated
Leg swelling
liver and spleen swelling
impaired gastric absorption
Why should caution be taken when prescribing NSAIDs in patients with oedema
NSAIDS→ may cause fluid retention & acute reneal failure in patients who take diuetics and ACE inhbitiors
Why does oedema occur in heart failure
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
How does valve disease cause heart failure
stenosis- narrowing of valve causes pressure overload causing left ventricular hypertrophy to
eject
regurgitation: volume overload- stretches heart- heart is dialated-> frank starling mechanism
