Cardiovascular anatomy Flashcards
What is the blood supply of the SA Node?
Commonly supplied by RCA (blood supply independent of dominance)
What is the blood supply of the AV Node?
Supplied by the PDA
Describe effects of PDA infarct
Infarct may cause AV nodal dysfunction (bradycardia or heart block)
Describe the prevalence and features of a right-dominant circulation
85% of people PDA arises from RCA
Describe the prevalence and features of a left-dominant circulation
8% of people, PDA arises from LCX
Describe the prevalence and features of a Codominant circulation
7% of people, PDA arises from both LCX and RCA
What is the most common site of coronary artery occlusion?
Coronary artery occlusion most commonly occurs in the LAD
When does coronary blood flow peak?
Coronary blood flow peaks in early diastole
The left circumflex coronary artery supplies?
Supplies lateral and posterior walls of left ventricle, anterolateral papillary muscle
LCX AKA
Left circumflex coronary artery
LAD AKA
Left anterior descending coronary artery
LAD supplies
Anterior 2/3 of interventricular septum, anterolateral papillary muscle, anterior surface of the left ventricle
PDA AKA
Posterior descending/interventricular artery
PDA supplies
AV node, posterior 1/3 of interventricular septum, posterior 2/3 walls of ventricles and posteromedial papillary muscle
Right acute marginal artery supplies
Right ventricle
What is the most posterior part of the heart?
Left atrium
Left atrial enlargement can cause?
Dysphagia, (due to compression of the esophagus), or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus nerve)
What are the layers of the pericardium?
From outer to inner Fibrous pericardium Parietal layer of serous pericardium Visceral layer of serous pericardium
Where is the pericardial cavity?
Lies between parietal and visceral layers of the pericardium
Innervation of the pericardium
Phrenic nerve
Pericarditis pain location
Can cause referred pain to the shoulder
CO equation
SV x HR = CO
Fick Principle
Rate of O2 consumption / (arterial O2 content - venous O2 content)
MAP equation
MAP = CO x TPR
MAP at resting HR
(2/3 diastolic + 1/3 systolic)
Pulse pressure equation
Systolic pressure - diastolic pressure
Pulse pressure is proportional to?
SV
Pulse pressure is inversely proportional to?
Arterial compliance
SV equation
EDV - ESV
Describe CO control in exercise
During the early stages of exercise CO is maintained by Increased HR and increased SV During the late stages of exercise CO is maintained only by increased HR as SV plateaus
Increased HR effect on SV
Diastole is shortened with increased HR because there is less filling time so CO is decreased such as in ventricular tachycardia)
Causes of increased pulse pressure
- Hyperthyroidism
- Aortic regurgitation
- Aortic stiffening (isolated systolic hypertension in the elderly)
- Obstructive sleep apnea (increased sympathetic tone)
- Anemia
- Exercise (transient)
Causes of decreased pulse pressure
- Aortic stenosis
- Cardiogenic shock
- Cardiac tamponade
- Advanced heart failure
SV is increased by
- Increased contractility
- Increased preload
- Decreased afterload
SVCAP
Stroke volume is affected by contractility, afterload and preload
Contractility (and SV) are increased with
- Catecholamine stimulation via B1 receptor
- Increased intracellular Ca2+
- Decreased extracellular Na+ (reduced activity of Na/Ca exchanger)
- Digitalis (bocks Na/K pump -> increased intracellular Na -> decreased Na/Ca exchanger activity -> increased intracellular Ca
Describe the pathway of B1 stimulation
- Ca channels phosphorylated -> increased Ca entry -> increased Ca-induced Ca-release and increased Ca storage in the sarcoplasmic reticulum
- Phospholamban phosphorylation results in active CaATPase -> increased Ca storage in the sarcoplasmic reticulum
Describe Phospholamban phosphorylation
results in active CaATPase -> increased Ca storage in the sarcoplasmic reticulum
Describe the function of digitalis
Digitalis blocks the Na/K pump -> increased intracellular Na -> decreased Na/Ca exchanger activity -> increased intracellular Ca and thereby increasing contractility
Contractility is decreased by
- B1 blockade (decreased cAMP)
- HF with systolic dysfunction
- Acidosis Hypoxia/hypercapnia (decreased PO2/ increased PCO2)
- Non-dihydropyridine Ca2 channel blockers
How is preload determined?
It is approximated by ventricular EDV and depends on venous tone and circulating blood volume
Venous vasodilators effect on preload
Decrease preload
Nitroglycerin effect on venous circulation
Venous vasodilation and decreased preload through reduced venous return
How is afterload determined?
Afterload is approximated by MAP Increased afterload -> increased pressure -> increased wall tension per Laplace’s Law
What is the adaptive response to increased afterload?
The left ventricle compensates for increased afterload by thickening (hypertrophy) in order to reduce wall tension
Arterial vasodilators affect on afterload
Decrease afterload
ACE inhibitors affect on afterload and preload
Decrease afterload and preload
Chronic hypertension (MAP) leads to what heart changes?
LV hypertrophy
Myocardial O2 demand is increased by?
- Increased contractility
- Increased afterload
- Increased heart rate
- Increased diameter of the ventricle (increased wall tension)
Wall tension principle
LaPlace’s Law
