Cardiac and Lymphatic Pathophysiology Flashcards
Cardiovascular and Pulmonary Systems
Circulate oxygenated blood through the arterial system to all cells in the body
Deoxygenated blood is collected from the venous system and delivered….
to the lungs for reoxygenation
What happens when the arteries become narrow or blocked?
Areas of the myocardium supplied by the artery does not receive enough oxygen
Disorders of the myocardium as a result of insufficient blood supply are:
Ischemic heart disease (IHD)
Coronary heart disease (CHD)
Coronary artery disease (CAD)***
Hypertension (HTN)
One of the main risk factors in both CAD and cerebrovascular accidents
What results from HTN?
Cardiac hypertrophy
Heart failure
Aortic dissection
Renal failure
Blood Pressure
Force exerted against the arterial walls
Systolic Pressure
Pressure exerted when the heart contracts
Diastolic Pressure
Pressure when the heart is relaxed between beats
Normal Blood Pressure
Systolic <120
and
Diastolic <80
Pre-hypertensive
High-normal/elevated
Systolic 120-129
and
Diastolic <80
Stage 1 Hypertension
Systolic 130-139
or
Diastolic 80-89
Stage 2 Hypertension
Systolic ≥140
or
Diastolic ≥90
Hypertensive Crisis
(Malignant HTN)
Systolic ≥180
and/or
Diastolic >120
When does HTN happen?
When the relationship between blood volume and peripheral resistance is altered
Primary HTN
(Idiopathic)
Accounts for 90-95%
Modifiable Primary HTN
High sodium
Obesity
DM
Hypercholesterolemia
Non-Modifiable Primary HTN
Family history
Age (>55)
Gender
–>Male (<55)
–>Female (>55)
Ethnicity
*Secondary HTN
Accounts for 5-10%
Renal
Endocrine
ETOH abuse
Drug induced
Pregnancy induced
Acute stress
Blood flow determined by:
Cardiac Output
What is cardiac output?
Ejection of blood (strength, rate, rhythm of heartbeat; blood volume)
BP is regulated by two factors, what are they?
Blood flow and peripheral resistance (vessel diameter, blood viscosity)
Single most common characteristic of HTN
Increased peripheral resistance as a result of the narrowing of the arterioles
How do you control the constriction of peripheral arterioles?
- Autonomic regulation
- Renin-angiotensin system
Autonomic Regulation
(Sympathetic NS activity)
~Norepinephrine is released by the adrenal medulla in response to stress
~Epinephrine is secreted resulting in increased force of cardiac contraction, increased cardiac output, and vasoconstriction
Renin-Angiotensin System
~Vasoconstriction results in decreased blood flow to kidney
~Renin is secreted: angiotensinogen to angiotensin I
~Angio I to Angiotensin II by ACE causes vasoconstriction within renal system - increases peripheral resistance
~Angio II stimulates aldosterone production - promotes sodium and water retention in the kidney = Increase in blood (intravascular) volume
Prolonged HTN leads to
Elastic tissue within the arterioles being replaced with fibrous collagen tissue = arteriosclerosis
Arteriosclerosis
Arteriole becomes less distensible - greater resistance to blood flow
~Accelerates degenerative changes in the walls of the arteries
Narrowing or complete obstruction of the lumina
Progressively - arthrosclerosis
Completely - thrombus (blood clot)
Weakening of the walls
–>dilation
–>rupture
Atherosclerosis
~Generic term for thickening and loss of elasticity of arterial walls
~Refers to the buildup of fats, cholesterol and other substances in and on the artery walls which restrict blood
What is atherosclerosis characterized by?
Intimal lesions that protrude into and obstruct the vascular lumina
–>weakens the underlying media
Atherosclerosis primarily affects
Elastic arteries, and large / medium muscular arteries
Atherosclerotic plaque
~Intimal thickening and lipid accumulation giving rise to an atheroma
3 principal components of Atherosclerotic plaque
~Smooth muscle cells, macrophages, and leukocytes
~ECM with collagen, elastic fibers
~Intra and extracellular lipids
~foam cells - large lipid laden cells derived from monocytes
Atherosclerosis Epidemiology
Genetic predisposition
Hyperlipidemia (>200mg/dL)
HTN
Cigarette smoking
Diabetes
Atherosclerosis Pathogenesis
Chronic inflammatory response of the arterial wall initiated by injury to the endothelium
–>harmful substances in the blood or the result of high BP
Ischemic Heart Disease (IHD)
~group of closely related syndromes caused by an imbalance between myocardial oxygen demand and blood supply
IHD most common cause of
narrowing of the lumina of the coronary arteries - most often termed coronary artery disease (CAD)
Myocardial Infarction (MI)
(Aka Heart attack)
~development of myocardial necrosis caused by local ischemia (occurs when a blood clot blocks blood flow to the heart; no blood =tissue loses O2 and dies)
Syndromes that may develop due to CAD
~Angina pectoris
~Acute myocardial infarction
~Sudden cardiac death
~Chronic IHD with congestive heart failure
MI Pathogenesis
~Coronary artery thrombus
~Atherosclerotic plaque serves as the source for the generation of the thrombus
~location of the MI determined by the site of vascular occlusion
MI Morphology
LAD (40-50%) - widow maker
R coronary artery (30-40%)
Left circumflex (15-20%)
MI Pain Patterns
Sudden sensation of pressure; crushing chest pain radiating to arms, throat, neck, and back
Pain lasts 30min to hours
Women - shortness of breath (midnight) and chronic fatigue
Congestive Heart Failure (CHF)
~Multisystem derangement that occurs when the heart is no longer able to eject the blood delivered to it by the venous system
~Inadequate cardiac output accompanied by congestion of the venous circulation
CHF
~Failing ventricle unable to eject normal volume of venous blood delivered to it
~Increases blood in the ventricle at the end of a diastole
–>Increased end diastolic pressure
–>Elevated venous pressure
Systolic CHF
Contractile failure of the myocardium
Diastolic CHF
Increased pressures are required to maintain adequate cardiac output despite normal contractile function
—>Heart failure with preserved ejection fraction
Left and Right CHF
Left - left ventricle can no longer maintain normal cardiac output
Right - right ventricular dysfunction due to left sided failure or pulmonary disease (cor pulmonale)
Ejection Fraction
~Amount, percentage, of blood that is pumped (or ejected) out of the ventricles with each contraction
Normal: 55-70%
Vicious Cycle of CHF - Positive Feedback
When there is a decreased blood pressure
Kidney releases renin, which starts process to retain sodium and water
LV dysfunction still exists, unable to eject blood
Kidney keeps retaining fluid
Peripheral Vascular Disease (PVD)
or
Peripheral Artery Disease (PAD)
~Diseases of the blood vessels supplying the extremities and major abdominal organs
~PVD encompasses disorders affecting both the arterial and venous blood vessels
PADS
Functional:
Doesn’t have an organic cause
Doesn’t involve defects in blood vessels’ structure, usually short-term effects and come and go
Organic:
Caused by structural changes in the blood vessels, such as inflammation
Arteriosclerosis Obliterans
~In PAD, fatty deposits build up in the inner linings of the artery walls
~Early stages: cramping, fatigue in the legs/buttocks during activity
Intermittent Claudication
Muscle pain (ache, cramp, numbness or sense of fatigue), usually in the calf muscle during exercise and is relieved by a short rest
Buerger Disease
~Segmental, thrombosing, acute and chronic inflammation of medium and small arteries
~Occurs in smokers
Raynaud Disease
~Intense vasospasm of small arteries or arterioles
~Paroxysmal pallor or cyanosis of the digits or feet
Anuerysms
~Localized abnormal dilation of a blood vessel or the heart
~Causes:
—->Atherosclerosis and degeneration of the arterial media
—->Trauma
Abdominal Aortic Anuerysm (AAA)
~Rupture into peritoneal cavity
~Obstruction of iliac, renal, mesenteric, or vertebral branches
~Embolism from atheroma or thrombus
~Impingement of adjacent structure (ureter)
Varicose Veins
~Abnormally dilated, tortuous veins produced by prolonged, intraluminal pressure w/loss of vessel wall support
~Venous stasis, congestion, edema, pain, and thrombosis
~Usually form in the LEs
~Thrombus formation can lead to embolism
Edema
Fluid excess in the tissues due to overload of interstitial or intracellular fluid causing congestion
Non-pitting Edema
Skin that is stretched, shiny, with hardness of underlying tissue
Deep Vein Thrombosis (DVT)
~Immobilization (bed rest, travel, Fx stabilization)
~Injuries to LEs
~Increased age
~Clotting disorders
~Infections and inflammatory diseases
~Orthopedic pts - post THA, TKA
Lymphedema
Swelling of the soft tissues that results from the accumulation of protein-rich fluid in the extracellular spaces
Lymphedema Facts
23-45% pts after breast cancer (post-surgery)
21% pt after ovarian cancer
28% pt after endometrial cancer
Up to 70% pt after prostate cancer
Lymphedema Chief Complaints
Limb heaviness, paresthesias, achiness, skin tightness, poor fitting clothes, altered cosmesis, decreased ADLs and ROM
Primary Lymphedema
(Idiopathic)
~Less common
~10% of all cases
~Congenital malformation / impairment of lymphatics
~LE affected most often
Secondary Lymphedema
(Acquired)
~Most common
~Acquired
~Disruption of or damage to lymphatics
~Filariasis (parasitic infection)
~Cancer treatment
~Chronic venous insufficiency
Stage 0 Lymphedema
Latent
No edema
Reduced lymph system transport capacity
Most commonly due to radiation or surgery
Stage 1 Lymphedema
Reversible
Pitting edema
Greatly or completely reduces with elevation
No 2ary skin changes
Stage 2 Lymphedema
Spontaneously irreversible
Does not pit
Does not substantially reduce with elevation
Skin becomes brawny and fibrotic
May have frequent skin infections
Stage 3 Lymphedema
Lymphostatic elephantiasis
Extreme increase in limb volume
Deep skin folds
Papillomas present
Frequent skin infections
