Cardiovascular Flashcards
What are 3 determinants of blood flow resistance?
- length of artery
- viscosity of blood
- radius of artery
3 equations relevant to blood flow
- Flow ∝ 1/R
- R ∝ 1/r4 (double radius = 16x ↑ flow)
- Mean arterial pressure ∝ CO x PR
Histology of the Myocardium (heart muscle tissue)
- involuntary
- striated (has sarcomeres)
- may mitochondria (very good at using O2)
- gap junctions so cells can communicate
- very fatigue resistant
- no neuromuscular junctions
- independent contractions
Excitation-contration coupling and relaxation in cardiac muscle
1) A.P enters from adjacent cell
2) voltage-gated Ca channels open, Ca into cell
3) Ca release from sarcoplasmic reticulum through Ca gated ryanodine receptor channels (RyR)
4) Ca binds to troponin and removes tropomyosin
5) relaxation occurs when Ca unbinds troponin
6) active pump (use ATP) Ca back into S.R
7) Na-Ca pump moves left over Ca out of cell (1Ca out, 3Na in)
8) Na-K-ATPase the pumps 3Na out to maintain gradient
Action potential and histology of a cardiac contractile cell
- resting membrane potential -90mV
- Na passes trough double-gated voltage channels
- plateau is decreased K and increased Ca
- syncytium
- pacemaker cells don’t have sarcomeres
1) Na channels open
2) Na channels close
3) Ca channels open, fast K channels close
4) Ca channels close, slow K channels open
The electrocardiogram
- gives info on HR, heart rhythm, conduction velocity and heart condition
- Three major waves
- P wave, QRS complex, T wave
Short Term regulation of MAP
- involves neural reflexes (neg feedback loops)
- baroreceptors detect increased MAP (located carotid artery and aortic arch & measure through arterial wall stretch)
- stimulate Medulla
- send signals to the heart and blood vessels (PSNS)
- causes bradycardia & vasodilation
predominant organ and mechanism for long term control of MAP
- Kidneys are the predominant organ in long term control of MAP
- regulated through GFR
- GFR needs to be auto-regulated
- remains relatively constant so we don’t have to pee heaps when increased MAP (exercise)
2 major auto-regulatory mechanism that control GFR
Myogenic Tone
- is a property of arteriolar smooth muscle (in afferent arteriole)
- it involves contraction of the muscle in response to stretch
- when MAP increases, muscle contracts and reduces diameter of arteriole
- therefore, more resistance and decrease blood flow to limit increase of glomerular capillary pressure
Tubuloglomerular feedback
- increased MAP leads to increased flow and filtration in glomerulus (increased GFR)
- therefore increased Na and Cl reaching the macula densa
- JGA senses lots on Na and Cl
- Macula densa resorbs Na and Cl into efferent tubule
- MD also releases adenosine which constricts afferent arteriole smooth muscle
- therefore decreasing pressure in bowman capsule and decreased GFR
regulation of GFR when experiencing decreased MAP can override the auto-regulatory mechanisms
- baroreceptors detect reduced MAP
- Increased SNS activity
- vasoconstriction
- afferent arteriole constriction reduces GFR
- reduced urine volume
- conservation of water and salt
Actions of Aldosterone
Release
- released from adrenal cortex
- increased plasma K directly stimulates aldosterone release from adrenal cortex
- Also released during RAAS
- decrease Na also causes release
Actions
- steroid hormone
- binds to mineralocorticoid receptor (MR)
- increases transcription or ENaC (Na channels) and activates the Na-K pumps in the collecting tubule
- leads to increased Na resorption and increase K secretion
Consequences of hypertension (high blood pressure)
- left ventricular hypertrophy
- stroke - rupture of cerebral/coronary blood vessels
- renal failure - high pressure leads to damaged glomerulus & reduced integrity of filtration barrier
- retinal damage - damage to retinal blood vessels
