Cardiovascular pt 1 Flashcards
Atria
receiving chambers
ventricles
discharging chambers
right and left side act as____
separate pumps
____side receives oxygen-poor blood from tissues
Right
via pulmonary circuit
-pumps blood to lungs to get rid of co2 and pick up o2
____side receives oxygenated blood from lungs
left
via systemic circuit
-pumps blood to body tissues
cardiac muscle cells
-striated, branched, and interconnected
-joined by intercalated discs
cardiac muscle cells depend on
aerobic respiration to make ATP
Coronary arteries
spread over surface, penetrate myocardium
-left CA and right CA branch from aorta
-squeezing of myocardium compresses CAs, blocks blood flow
inner most layer of myocardium is_____
last to receive oxygenated blood
most prone to damage during ischemia
inner most layer of myocardium
collateral circulation
-the heart has connections btwn branches, protects from ischemia
needed for muscle contraction in heart
electrical activity
electrical activity in the heart takes place in
SA- Sinoatrial node (rate of heart beat)
SA sends electric signal to
Right and Left atriums and to Atrioventricular node -AV –>subendocardial branches–> right and left ventricles
innervation of heart originates from
medulla oblongata
Sympathetic NS
Norepinephrine
-leades to incr in Ca2+ release in myocardial cells (accelerated contractions)
-incr ca2+ reuptake (accelerated relaxation)
Parasympathetic NS
Acetylcholine
-opens k+ channels
-hyperpolarizes cell, making it less likely to fire
cardiac output
=stroke volume x heart rate (mL/min)
Stroke volume =
preload, afterload, and contractility
amount leaving with each beat. mL/beat
preload
amount of stretch in a muscle tissue before contraction
-effected by end-dystolic volume and venous return
Afterload
force against muscle, needed to contacts
-effected by aortic pressure and aortic valvular fxn
Contractility
how hard is heart pumping
effected by sympathetic simulation and myocardial oxygen supply
Heart rate
beat/min
-CENTRAL NERVOUS SYSTEM, autonomic NS, neural reflexes, atrial receptors. hormones
Aorta–> capillaries
blood velocity decreases
-further away from heart, are increases, resistance increases.
Capillaries–> vena cava
velocity increases.
-resistance decreases, area decreases
blood pressure
force that blood exerts against the vessel wall
systolic pressure
peak arterial BP, ventricular systole (contraction)
diastolic pressure
minimum arterial BP, diastole (relaxation)
factors effecting blood pressure
-cardiac output (CO= HR X SV)
-resistance to flow
-blood volume (mainly regulated by kidneys and RAAS)
-vessel diameter
HTN =
Incr CO, incr PR
____detect blood pressure
baroreceptors
factors affecting vessel diameter (peripheral resistance)-vasoconstrictors
myogenic- stretch
metabolic- endothelins
neural symph tone
hormonal- epi, norepi, angitensis lll, antidiuretic
Intrinsic factors
distribute blood flow to organs and tissues as needed.
myogenic and metabolic
extrinsic factors
maintains MAP mean artial pressure and redistributes blood during exercise and thermoregulation
neural and hormonal
factors affecting vessel diameter (peripheral resistance)-vasodilators
metabolic-O, CO, H, K, prostaglandins, adenosine, nitric oxide
neural- symph tone
hormonal- atrial natriuretic peptide
Evaluating CV fxn imaging to show structure
-chest radiograph- x-ray
CT
MRI
Gives information about the conduction of the heart muscle and activity of pacemaker cells
Electrical activity
Exercise stress test
Demonstrates how CV system responds to physical stress
Indicators to evaluate CV fxn
Heart rate, cardiac output, cardiac index, stroke volume, oxygen consumption and mean arterial pressure
Hypertension
Consistent elevated blood pressure over time
Systolic
> = 140 mmhg
Diastolic
> = 90mmHg
Hypertension increases risk for
MI, Kidney dx, stroke, other vascular complications
95% of cases are _____and 5% are ______
Primary (essential, idiopathic) secondary
Secondary hypertension can be from
Obesity, drug-induced, hyperthyroidism, drug-induced, aldosteronism, crushing’s syndrome, renal hyper tension
Hypertension risk factors
1.Family hx/ inherited defects: insulin sensitivity, RAAS, renal sodium excretion, insulin, symph NS activity
2. Lifestyle: high Na+, low Ca=, K+ or Mg+, smoking, heavy alcohol consumption
3. Metabolic syndrome; hypertension, dyslipdemia, glucose tolerance
4.Other conditions: obesity, dm, glucose intolerance
“Silent killer”
Hypertension
Effects of hypertension on the body
-damages multiple organs w/o outward symptoms
-results from incr vascular resistance
RAAS
Renin-angiotensin-aldorestrone system
Patho for HTN
-chronic incr in MAP (mean arterial pressure)
-Increased vascular tone (VSM constriction) = increased peripheral resistance
-inc blood volume
activation of SNS temporarily increases______
BP and HR
-fight of flight
-maintains BP and tissue perfusion
Prolonged activation promotes _______
Vascular remodeling
-insulin resistance, endothelial dysfunction
-procoagulant effects
Prolonged activation may be due to:
-incr production of Epi and NE
-incr receptor reactivity to Epi and NE
Role of RAAS
-Maintains BP, tissue perfusion
-Contributes to atherosclerosis, renal dx, cardiac hypertrophy
Over activation of RAAS
-Salt and water retention
-incr in vascular resistance
- lots of angiotensin II (Ang II)
Ang II
A potent vasoconstrictor
High levels of Ang II lead to :
-Endothelial dysfunction
-athsclerotic plaque formation
-platelet aggregation
-risk of thrombus
Vascular remodeling —>
Further promotes hypertension
Natriuretic hormones
-Atrial natriuretic peptide (ANP)
-Brain natriuretic peptide (BNP)
natriuretic peptides……
-modulate real Na2+ excertion by enhancing renal blood flow and GFR
-induced systemic vasodilation
-suppress aldosterone (of RAAS0
-Inhibit SNS
-require adequate Ca2+, Mg2+, K+ to fxn properly
In HTN Increase serum levels of ANP and BNP
-heart failure
-atherosclerosis
-ventricular hypertrophy
Contributors to hypertension
-inflammation -kidneys suffer damage —> initiates inflammatory response
-endothelial dysfunction- release of inflamm cytokines, decrease prod of vasodilators and incr vasoconstrictors
-obesity-linked to inflamm, vascular remodeling, endothelial dysfunction, insulin resistance. Changes in leptin
-DM/insulin resistance- insulin resistance even in pts w/o DM, decr vasodilator realest by ECs. Incr salt, water retention, activity of RAAS and SNS
Complicated HTN
HTN that is sustained and causes organ damage
Vascular remodeling
-VSM cells undergo hypertrophy, hyperplasia
-fibrosis in the vessel wall
-decr blood flow, causing damage to organs
Heart
-LV hypertrophy—>bigger heart means more O2 demand, impaired contractility
-congestive heart failure
-coronary artery dx
-Myocardial infarction
-Aorta and other large vessels prone to aneurysms
-damage to vessel walls from high pressure can initiate clotting cascade (thrombus)
Vascular beds cannot stand pressure. Capillaries ____and cause____
Rupture, ischemia
HTN Treatments-lifestyle
-less sodium
-less saturated fat
-adjust caloric intake to reach optimal weight
-exercise that promotes endurance
-smoking cessation, reduced alcohol
Pharmacological treatments
-Diuretics
-Beat-blockers
-ACE inhibitors
Diuretics
-decrease blood volume by increasing urine production
-classes defined by site of action in nephron
Beta-blockers
Slow HR, reduce workload of heart
Beta-adrenergic antagonists-block action of Epi and nE on the heart
ACE inhibitors
ACE=angiotensin-converting enzyme) inhibitors
-prevent conversion of Ang I and Ang II
Aneurysm
Dilation or outward ballooning of vessel wall or cardiac chamber
Aneurysm characteristics
-thoracic or abdominal aorta- conduit arteries that endure high stress/pressure
-weak point in vessel or ventricular wall (necrotic muscle) becomes stretched by high pressure
-wall continues to weaken, becomes more fibrotic
Aneurysm risk factors/causes
-arteriosclerosis and hypertension found in half of patients bc of vascular remodeling
-infection (syphilis)
-injury/truama to the chest
-genetic susceptibility
Aneurysm treatment
-goal is to reduce blood volume and blood pressure to prevent rupture
-diuretics, beat-blockers
-surgery : stent placement for rapid, growing over 5 cm
Aneurysms diagnosed with ____
Imaging, CT, MRI, etc
Thrombus
Blood clot in a vessel; healthy response to injury intended to stop bleeding
Embolus
Any thing that is circulating in the bloodstream
Two threats if arterial thrombus
-Grows large enough to occlude vessel, cause ischemia and infract
-may dislodge and become thrombembolus
thrombembolus
Clot that travels until it occludes a vessel
Arterial thrombus/ embolism risk factors/causes
-inappropriate activation of the clotting cascade
-the heart
Inappropriate activation of the clotting cascade bc of :
-endothelial damage
-inflammation
-infection
-traumatic injury
-obstructions that cause blood pooling
-may be bc of HTN, Atherosclerosis
Most common cause of thromboembolus is___
The heart.
-valve dx of heart arrhythmias disturb blood flow
-cause formation of thrombus
-dislodged clot usually ends up in lower extremities
-may also go to coronary arteries or cerebral circulation
Endothelium
NO and PGI2 maintain blood flow and inhibition platelet activity
Platelets
-activation causes them to clump together, stopping bleeding
Pharmacological treatments for arterial thrombus
-indirect clotting inhibitors (warfarin, heparin)
-direct thrombin inhibitors (hirudin)
-thromolytics-administered with clotting inhibitors
Surgical treatments for arterial thrombus
-ballon-tipped catheter to remove or compress thrombus
-catheter may also directly deliver thrombolytic drug
