alterations of cardiovascular function Flashcards
resistance to flow is determined by
length of tube
viscosity (thickness) (low rbc volume= thin so moves quick)
radius: 1 unit change in radius results in a fourfold change
laminar flow vs turbulent flow
usually due to radius or anemia
laminar:
smooth and streamlined
turbulent:
irregular and choatic
factors regulating cardiovascular function
preload
afterload
contractility
heart rate : recall CO=HR x SV
preload
provided by the degree of ventricular filling (End-Diastolic Volume (EDV)
preload reflects myocardial muscle length before contraction
*(degree of muscle stretch and relationship between actin and myosin fibers)
why is it left venticular EDV?
how do we assess ventrular EDV?
left side of the heart has a greater workload
ventricular EDV can be assessed thru:
echocardiography
afterload
resistance to outflow from the heart
(typically the left ventricular afterload is greater concern unless pt has pulmonary vascular problem with high V/Q ratio)
determined by the degree of systemic vascular resistance (SVR)
SVR is assessed by the mean arterial pressure (MAP)
what is MAP more influenced by?
diastolic pressure more than systolic
*bc more time is spent in diastolic filling phase
*due to this MAP is not a mean average of Systolic over diastolic BPS
contractility
strength of contraction at any given end diastolic volume (EDV)
a more forcefull contraction can cause a increase SV by causing greater ejection of blood (better emptying of ventricules)
how is contractility assessed
by ejection fraction (EF) of the left ventricle
EF = SV/EDV
normal 60-75%
EF can be assessed with an echocardiogram
heart rate
measure by pulse, apical HR or HR by monitor
CO=HR x SV which means increased HR will increase CO
capillaries
the presence of multiple parallel capillary channels reduces the effect of the small radius of each individual capillary
therefore the overall resistance to flow thru the capillary bed is low
arterial disorders:
atherosclerosis
formation of an atheroma (atherosclerotic plaque) within artery
AKA: arteriosclerosis
(hardening of arteries)
patho if atherosclerosis
atheroma formation is related to:
*blood vessel injury
*inflammation
*blood lipid levels
Hyperlipidemia
Increased lipids in blood
Dyslipidemia
Abnormal lipid levels but also reflects that levels of some lipid components can also be too low:
Triglycerides
Total cholesterol
HDL cholesterol
LDL cholesterol
Lipid panel
Triglycerides
Total cholesterol:
*uses protein transporter bc it can not dissolve into the plasma
HDL cholesterol: good (return lipids to liver)
LDL cholesterol: bad (for plaque)
Both are either high or low density lipoproteins so they carry proteins
Patho how atherosclerosis occurs
Platelets and monocytes try to fix injury
If LDL is increased then they will be engulfed by macrophages
Macrophages die and inflammation increased
Macrophage accumultion and we get plaques
Common sites for atherosclerotic vascular disease
Carotid artery
Cerebral artery
Coronary arter
Abdominal aorta
Iliac artery
Thoracic aorta
Femoral
Popiteal artery
Aneurysm
Weaking of aterial wall
Usually due to atherosclerosis
Common locations of aneurysms
Same locations as atheroscleotic plaque due to them being the main cause of aneuysms
Aneurysms with increased risk for mortality
Brain (cerebral aneurysm)
*increased incidence in arterial branching locations (circle of willis)
Aorta (aortic aneurysm)
*In the arch
*Increased risk to become a dissecting aneurysm due to highest presures
*high risk for people with marfan syndrome
*abdominal aortic aneurism (AAA)
Other Arterial disorders
Arterial vasculitis Aka: arteritis (or angitis)
Acute arterial occlusion
Peripheral artery disease (chronic)
Raynaud phenomenon (raynaud syndrome)
Peripheral artery disease (chronic)
Primary cause is atherosclerosis of peripheral arteries
Primary symptom is intermittent claudication
Raynaud phenomenon (raynaud syndrome)
Arterial vasospactic disorder (caused by the vasospastic)
Characterized bu intermittent arterial spasms
Triggers include cold exposure, strong emotions
Venous disorders
Venous thrombosis
And
Venous inflammation
Thrombosis:
Deep venous thrombosis (DVT)
Inflammation:
Phlebitis
Thrombophlebitis
Systemic hypertension
Increased BP in the systemic CV circulation
Primary (essential) hypertension
And
Secondary hypertension
Primary (essential) hypertension
No specifically identifies physiologic cause
Secondary hypertension
Most causes originate outside the CV system
Causes include:
Renal disease
(high blood volume due to decreased UO)
Adrenocortical hormone excess
(aldosterone excess causes NA and water retention)
Pheochromocytoma
(Adrenal medulla catecholamine excess)
Coarctation of the aorta
(Congential narrowing of aortic arch)
Complications of systemic HTN
Bc of End-Organ damage
HTN retinopathy
HTN cardiovascular disease
HTN cerebrovascular disease
Renal insufficiency & chronic kidney disease
(chronic renal failure)
Orthostatic Hypotension
Rapid decrease in BP that occurs with change in position
Fall risk
Action potential of myocardial cells
A: cells of electrical conducting system (SA node)
*with “automaticity” (self gen of action potential thru slow leak of Ca into cell)
B: atrial muscle cells
C: ventricular muscle cells
*have a plateau phase during depolarization
(So ventricles can contract the blood out
EKG
Is a summated view of the movement of action potentials (electrical wave) thru heart
Diastole and systole
Diastole
1. Refractory period
2.atrial depolarization (P wave)
3. Atrial contraction and ejection (between P-Q segment)
4. Ventricular depolarization (QRS)
Systole
5. S-T segment (venticular start to contract)
6.ventricular repolarization (T wave)
4 limb leads
Green is the electrical ground
In 3 lead ecg monitoring the leg lead needs to be placed on the left leg
Case models: cardiac dysrhythmias
Artial dysrhythmias:
*premature atrial contraction
*supraventricular tachycardia
*atrial fibrillation
Ventricular dysrhythmias:
*premature ventricular contration
*ventricular tachycardia
*ventricular fibrillation
*long QT interval
*Torsades de pointe
Premature atrial contration (PAC)
Early atrial contraction (stress)
Pwave too early
Premature ventricular contraction (PVC)
Early ventricle contraction
Abnormal QRS (Stress)
Supraventricular tachycardia (SVT)
Causes decreased CO
Fast HR triggered from atrium (abnormal Rythm)
Ventricular tachycardia
Vtach
Looks like shark teeth
Atrial fibrillation a-fib
Muscle of atrium are quivering and not contracting
Fast irregular HR
Tx: meds to decrease HR and anticoagulats due to blood stasis in atrium
Ventricular fibrillation
V-fib
No QRS (no perfusion/CO)
Long QT interval
QT is the time from beginning of the QRS to the end of the T wave
Associated with increase risk of a special life threatening type of ventricular tachycardia called (torsades de pointes)
Torsades de pointes
No cardiac output
Other causes of cardiac dysrhythmias
Acute coronary syndromes
Electrolyte imbalances:
Potassium
Calcium
Coronary artery disease (CAD)
Aka:
coronary heart disease (CHD)
atherosclerotic heart disease (ASHD)
Due to imbalance between myocardial oxygen supply vs demand
Ischemia:
Decreased tissue perfusion
Inadequate perfusion to meet cell need for o2 and waste product removal leads to cell damage
Infarction:
Death of tissue caused bu ischemia
Myocardial ischemia
2 patterns of presentation
*Chronic ischemic heart disease (partial blockage)
*Acute coronary syndromes (sudden blockage or chronic becomes too much)
Angina pectoris:
Myocardial pain caused by ischemica
Severe crushing pain
Women often under diagnosed due to having different symptoms
Chronic ischemic heart disease
Main cause: atherosclerosis and vasospasm
Presentations:
Stable angia =
*predictable pattern (trigger is increased activity, stress)
Variant (vasopastic) angina =
*associated with vasospasm and is unpredictable
Silent myocardial ischemia =
*myocardial tissue is ischemic but pt not experiencing symptoms
Actue coroncary syndromes
Signs of ventricular ischemia (ekg)
Due to progressive (chronic) or sudden obstruction of cornoary blood flow, producing myocardial ischemia
Signs of ischemia of ventricular muscle in ECG are changes to:
ST segment
T wave
*these tell us ventricular cells are experiencing hypoxic-ischmic cell injury
What is happening in the cardiac cycle during ST segment and T wave ?
ST: venticular depolarization
T: ventrical repolarization
Substances released from injured myocardial cells
*Potassium ion (alter resting membran potention)
*Hydrogen ion (from lactic acid production by injured myocardial cells due to anaerobic metabolism)
*intracellular enzymes and molecules
These can lead to:
*Injury of cells in the surrounding tissue
*Distrubances of electrical membran potentail and electrical conduction problems
*Systemic chemcial and electrolyte imbalances
Serum biomarkers for acute coroncary syndrome
(cardiac panel)
Cardiac-specific troponin
*troponin I
*troponin T
Increase in these we know are from heart bc their specific to cardiac muscle
Creatinine kinase MK (CK-MB)
*MB isoenzyme form is specific to cardiac muscle
Myoglobin
*not specific to cardiac muscle (in skeletal muscle too)
What cardiac bio markers are specific and not
Specific:
Troponin I
Troponin T
Creatinine kinase MB
Not specific:
Myoglobin
Types of acute coronary syndrome
Unstable angina (UA)
Non-ST segment elevation myocarial infarction (NSTEMI)
ST segment elevation myocardial infarction (STEMI)
Unstable angina (UA)
ECG:
Non-ST segment elevation
Changes:
*ST depression
*T wave changes
Location of damage:
Subendocardial
Serum biomarkers not present
Effect on cell: ischemia
(functional changes from reduced perfusion)
Non-ST segment elevation myocarial infarction (NSTEMI)
ECG:
Non-ST segment elevation
Changes:
*ST depression
*T wave changes
Location of damage:
Subendocardial
Serum biomarkers are present
Effect on cell: ischemic injury
(Both structural (biomarkers) and functional changes)
ST segment elevation myocardial infarction (STEMI)
ECG: ST segment elevation
Changes:
*may have T wave changes
*may progress to prolonged Q wave
Location of damage: transmural
Serum biomarkers are present
Effect on cells: infarction
(Necrotic death caused by ischemia)
Typical pattern of myocardial damage
Ischemia:
*inversion of the T wave
Injury:
ST segment depression (subendocardial injury)
ST segment elevation (transmural injury)
Necrosis:
Prolonged Q wave
Permanent EKG change:
indicating large are of myocardial cell death
Risks of myocardial ischemia
Risk for actual ischemic death of myocardial cell
(Myocardial cells cannot regenerate)
Therefore when they die cells are replaced with scar tissue with permanent impairements of myocardial function
Fibrous scar tissue:
Cannot conduct electrical impulses or contract
Clincial manifestation of MI
Pain and autonomic (SNS) responses related to ischemia
Symtoms R/T impaired myocardial fucntion
Symptoms R/T changes in electrical conduction
Symtpoms R/T inflammation
Potential complications of MI
Sudden death
Cardiogenic shock (circulatory failure/ can deliver)
Congestive heart failure (due to scar tissue)
Thromboembolism
Strole
Pericarditis
Myocardial rupture
Ventricular aneurysm
Dysrhythmia
Myocardial disorders
Myocarditis (inflammation of heart)
Cardiomyopathies:
Dilated: stretches/cant contract
Hypertrophic: growth of muscle
*cant full bc muscle is too big (not due to afterload)
Constrictive (restrictive)
*becomes rigid on the outside
