Exam 3 Flashcards
Vericose Veins
A vein in which blood has pooled.
Distended, tortuous, and palpable veins.
Risk factors of vericose veins
- prolonged standing
- Age
- Family history
- Obesity
- Pregnancy (extra fluid volume)
- History of deep vein thrombosis
Chronic Venous Insufficiency (CVI)
Inadequate venous return over a long period due to varicose veins or valvular incompetence.
Ulcers form as a result of lack of blood flow. Tissues aren’t getting nutrients.
Results of CVI
- Venous hypertension
- Circulatory stasis
- Tissue hypoxia (in low areas of lower extremeties)
These lead to inflammatory reaction in vessels and tissues
This leads to fibrosclerotic remodeling of the skin
This leads to ulcers
Manifestations of CVI
- Edema of lower extremeties
- Hyperpigmentation of the skin of the feet and ankles
- Venous stasis ulcers
Stasis ulcers
Metabolic demands of cells not being met.
Jagged and uneven. Brown pigment
Deep Vein Thrombosis
Obstruction of venous flow leading to increased venous pressure. This happens from an accumulation of platelets and clotting factors, forming a thrombus.
Triad of Virchow
- Venous stasis: immobilty/age
- Venous endothelial damage: trauma or meds
- Hypercoagulable states: cancer/oral contraceptive usage
Thrombus
Clot attached to vessel walls
Embolus
Thrombus that breaks off and travels blood stream
Manifestations of Deep Vein Thrombosis
- Pain
- Redness
- Heat
- Swelling distal to the spot of embolism
Superior Vena Cava Syndrome
Progessive occlusion of the superior vena cava that leads to the venous distension of upper extremities and head.
Number one cause of Superior Vena Cava Syndrome
Bronchogenic cancer. SVCS is an oncology emergency.
Manifestations of Superior Vena Cava Syndrome
- Blood pools in upper extremities and head
- Edema around heart
- Distended veins in the head and neck
- Headaches (cerebral edema)
- Visual disturbances (cerebral edema)
- Purple/red coloration in head and neck
- capillary refill prolonged
- Tight skin
Hypertension
Consistent elevation of systemic arterial blood pressure. All stages of hypertension are associated with increased risk for target organ disease events (MI, kidney disease, stroke) Sustained 140/90+
Types of hypertension
- Primary hypertension
- Secondary hypertension
- Complicated hypertension
- Malignant hypertension
Isolated systolic hypertension
Sustained systolic blood pressure reading that is greater than 140 mmHg and a diastolic measurement that is less than 90 mmHg
Associated with cardiovascular disease (heart failure) and cerebrovascular events (strokes)
Elevations in systolic pressures are caused by
- Increases in cardiac output (more out/pumped harder)
- Total peripheral vascular resistance after the heart
Can be one, the other, or both
Risk factors for primary hypertension
- Family history
- Advancing age
- Gender (Men-younger, women-older)
- Ethnicity
- Excessive salt intake
- Glucose intolerance
- Smoking
- Obesity
- Heavy drinking
- Hypokalemic, Hypocalcemic, Hypomagnesia (chronically)
Progression of hypertension
Genetics and environment can cause:
- Insulin resistance
- Dysfunction of the RAAS system or faulty levels of naturitic peptides
- Inflammations
Which lead to:
- increased peripheral resistance or
- increased blood volume
Which leaves you with
-sustained hypertension
Can be combo of events
Secondary hypertension
Caused by systemic disease process that raises peripheral vascular resistance or cardiac output.
Renal artery stenosis, renal parenchymal disease, pheochromocytoma, drugs (birth control, steroids)
Treat the underlying disease
Complicated hypertension
Chronic severe hypertension that leads to tissue and vessel damage and eventually leads to organ damage.
Organs damaged by complicated hypertension
- Heart
- Kidneys
- Brain
- Eyes
Cardiovascular complications of sustained hypertension
- Left ventricular hypertrophy
- Smooth muscle hypertrophy and hyperplasia
- Fibrosis of the tunica intima and tunica media
- Angina pectoris
- Heart failure
- Coronary artery disease
- Myocardial infarction
- Sudden death
Result of cells being under constant pressure to work and do more
hypertrophy
Mycardial hypertrophy leads to
- Heart failure
- M.I.
- Death
Muscle becomes less effective. Bigger cells need more oxygen, adds to the cycle
Affects on the kidneys by complicated hypertension
- Nephrosclerosis (hardening of the kidneys)
- Renal arterial sclerosis (plaque within renal arteries)
- Renal insufficiency
- Renal failure
- Protienuria from chronic hypertension
Affects on the brain by complicated hypertension
- Cerebral thrombosis
- Ischemia
- Strokes
- Cerebral edema
- Aneurisms
- Hemorrhage
- Vascular dementia
Affects on the eye by complicated hypertension
- Retinal vascular sclerosis
- Increased pressures
- Hemorrhage
Malignant hypertension
Form of complicated hypertension. Progresses rapidly–diastolic pressure is usually more than 140 mmHg.
High arterial pressure of malignant hypertension leads to
- Disregulation of bloodflow to cerebral capillary beds in the brain
- Cerebral edema*
- Cerebral disfunction*
- life threatening
Orthostatic Hypotension
Decrease in both systolic and diastolic blood pressure upon standing. Occurs with rapid position change.
Decrease of 20 mmHg (systolic) and 10 mmHg (diastolic)
Types of orthostatic hypotension
- Acute orthostatic hypotension
- Chronic orthostatic hypotension
Risk for acute orthostatic hypotension
- Alkalosis
- Acidosis
- Meds
- Fluid shift
- Prolonged immobility
- Exhaustion
- Starvation
Risk for Chronic orthostatic hypotension
- Idiopathic
- Could be secondary to an endocrine disorder
Aneurysm
Localized dilation or out-pouching of a vessel wall or cardiac chamber.
Can be true or false.
True aneurysm
Involve all three layers of the arterial wall and are best described as a weakening of the vessel wall.
Weakened portion of the arterial wall, so under pressure, it pops out.
Types of true aneurysm
- Fusiform*
- Saccular
- most common
False aneurysm
Pulsating, encapsulated hematoma attached to the vessel wall. Blood leaks out of small rupture, but gets trapped in layer of vessel wall.
Most susceptible to aneurysm
Aorta (abdominal or thoracic)
—Abdominal aorta aneurysm most common
Manifestations of aneurysm
Depend on location/size/type
- Pain
- Hypotension if ruptured
- Mostly asymptomatic
Fusiform aneurysm
a localized dilation of an artery in which the entire circumference of the vessel is distended. The result is an elongated, tubular, or spindlelike swelling.
Saccular aneurysm
a localized dilation of a small area of an artery, forming a saclike swelling or protrusion.
Dissecting aneurysm
The splitting or dissection of an arterial wall by blood entering through a tear of the inner lining or by interstitial hemorrhage.
Causes of Vericose Veins
- Trauma to sephenous veins (running up thigh) that damages one or more valves (low pressure system)
- Gradual distension. Veins not meant to be flexible. Gravity pooling blood in the veins stretches the vein and it can’t recoil.
Thrombus
Blood vessel that remains attached to the vessel wall
Risk factors for thrombi
- Internal irritation (inflammation)
- Traumatic injury (burns)
- Infection
Threats to circulation from thrombi
- Occlusion
- thromboembolus
Embolism
Detached thrombus that becomes mobile
Types of embolism
- Clots
- Air bubbles
- Fat
- Amniotic fluid
- Aggregate of cancer cells
Pulmonary emboli
Typically originate in the venous system.
DVT emboli
Originate in lower extremeties
Arterial emboli
Originate in left side of the heart
Manifestations of emboli
- Ischemia distal to the site of obstruction.
- Organ disfunction
- Pain
- Infarction may occur with total occlusion of artery or vein
Peripheral vascular disease
Atherosclerotic disease of the arteries that profuses the limbs
Types of peripheral vascular diseases
- Buerger disease
- Raynaud disease/phenomenon
Buerger disease
Inflammatory disease of the peripheral arteries. Characterized by formation of thrombi filled with inflammatory and immune cells with vasospasm.
Over time, thrombi organize and become fibrotic.
Fibrotic thrombi lead to occlusion.
>Occlusion and obliteration of arteries inhibits oxygen to profuse to the extremities.
Obliterates small and medium arteries.
Causes/risk factors of Buerger Disease
· Smoking
· Young age
· Males
· Peripheral ischemia
Manifestations of Buerger disease
·Pain
·Cyanosis via ischemia (bluish/purple coloration of the skin)
·Rubor (redness) of the skin due to dilated capillaries
·Hair loss of affected extremity (due to nutrient loss and physiological prioritizing)
·Thin, shiny skin
·Hardened, malformed nail beds
Advanced disease progress: ·Potential for gangrene and amputation ·Stroke ·Mesenteric disease ·joint pain
Raynaud’s disease/phenomenon
Attacks of vasospasm in the small arteries and arterioles of the fingers and toes.
Blood vessels in affected individuals demonstrate imbalance in vasodialaters and vasoconstricters.
Cause of Raynaud’s disease
Idiopathic. No known cause
Cause of Raynaud’s phenomenon
secondary effect from another disease (collagen vascular disease, vasculitis, hypertension, hypothyroidism) or environmental conditions (smoking, cold)
Causes/Risk factors of Raynaud’s d/p
·Changes in temperature ·Cold temperature ·Emotional stress ·Young age ·Females
Manifestations of Raynaud’s d/p
During attack: ·Pain ·Cyanosis via ischemia (bluish/purple coloration of the skin) ·Numbness due to ischemia ·Pallor ·Cold sensations in affected areas ·Bilateral attacks
As blood flow returns:
·Rubor
·Throbbing pain
·paresthesias (prickling)
Prolonged attacks:
·Thickened skin
·Brittle nails
·Ischemia leads to ulcerations and gangrene
Atherosclerosis
· Characterized by thickening and hardening of the vessel wall via buildup of lipid laden macrophages in the vessel wall
· THE risk factor for every vascular risk factor (PAD, MI, CAD, etc)
· Progressive disease, typically occlusions are throughout the body
Simple description of formation of atherosclerosis
Caused by accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a plaque
Epithelial injury>Accumulation of lipid-laden macrophages>fatty streak>fibrous plaque>complicated plaque
First step of atherosclerosis formation
Atherosclerosis begins with injury to the endothelial cells that line artery walls. Injured cells become inflamed and cannot make normal amounts of anti-thrombic and vasodialating cytokines.
What occurs as a result of endothelial injury in development of atherosclerosis
Macrophages bind to inflamed endothelial cells. (Other types of immune/inflammatory cells bind also.) These macrophages release inflammatory cytokines and enzymes that further injure vessel walls. Oxidation of LDL occurs due to the inflammatory process and recruit monocytes that results in more macrophages. Oxidized LDL feeds macrophages transforming them into lipid-laden macrophages.
Result of lipid-laden macrophage accumulation in development of atherosclerosis
Lipid-laden macrophages accumulate in large amounts to form a lesion on the walls of arteries called a fatty-streak. Fatty streaks produce radicals and additional inflammatory mediations and recruit T-Cells. All these result in progressive damage to the vessel wall.
Development of plaques in progression of atherosclerosis
Macrophages also release growth factors that stimulate smooth muscle cell proliferation. In the damaged area, smooth muscle cells proliferate, produce collagen, and migrate over the fatty streak, forming a fibrous plaque.
Types of plaque formation in atherosclerosis
- Fibrous plaque
- Complicated plaque
Fibrous plaque
Formed after smooth muscle cells in damaged area proliferate and produce collagen. Cover the fatty streak and occlude vessels.
Fatty streak
First grossly visible lesion in the development of atherosclerosis. Formed from accumulation of lipid-laden macrophages. Damage vessel walls.
Lipid-laden macrophages
Macrophages that have engulfed oxidized LDL. Create foam cells that become fatty streaks
Complicated plaque
Fibrous plaques that have ruptured. Thrombi form due to platelet adhesion and the clotting cascade. Thrombi may suddenly occlude affected vessel.
Infarction
a localized area of tissue that is dying or dead, having been deprived of its blood supply because of an obstruction by embolism or thrombosis.
Three layers of vessel walls
- Tunica intima (thin layer of endothelium)
- Tunica Media (smooth muscle that constricts/dilates in arteries)
- Tunica Adventitia (connective tissue)
Risk factors for atherosclerosis (or any vascular disease: CAD, PAD, MI)
· Smoking · Hypertension · Family history · Diabetes mellitus · Autoimmune disorders · Obesity · Sedentary lifestyle · Increased Low Density Lipoprotiens/Decreased High Density Lipoproteins · Age · Males or females post-menopause
Manifestations of atherosclerosis
Result from inadequate perfusion of tissues because of obstruction
· Pain
· Disability
· Transient ischemic events (associated with stress or exersize)
· Tissue infarction (in presence of complicated plaque)
Peripheral arterial disease
PAD
Atherosclerotic disease of arteries that perfuse the limbs, particularly lower extremities.
Risk factors of Peripheral Arterial Disease
Same as atherosclerosis. Can’t have PAD without atherosclerosis
Manifestations of Peripheral Arterial Disease
At first, may be asymptomatic.
Hallmark sign: intermittent claudication. (Pain with ambulation that’s relieved with rest.)
Complete obstruction of blood flow may occur, causing:
- Pain
- Loss of pulse
- Skin color changes
Someone has pain while walking. The pain gets better when they sit and rest. What disease could they have?
Peripheral arterial disease
Coronary Artery Disease
atherosclerotic occlusion (or ANY lesion that causes a narrowing) of the coronary arteries (The arteries that supply the heart with its Oxygen to continue to pump)
(it is mostly due to atherosclerosis. So for my studying purposes, CAD is an atherosclerotic PARTIAL occlusion of the Coronary Arteries)
-Christine Morton
Effects of Coronary Artery Disease
Atherosclerotic plaque #1 cause:
- Ischemia (temporary)
- Persistent ischemia can lead to infarction (death of tissues)
- Imbalance between myocardial demand and blood supply to coronary arteries.
- Lack of oxygen to heart
Risk factors of Coronary Artery Disease
Same as atherosclerosis.
Ischemic attack
Tissues without oxygen for up to 20 minutes. Reversible
Cause breaks in electrical conduction of impulses: dysrhythmia/failure to contract/heart failure.
Causes of myocardial ischemia
Atherosclerosis (Coronary artery disease)
- Hypovolemia/hypotension (not enough blood supply)
- Dysrhythmia
- Increased demand of the heart
Events that occur due to myocardial ischemia
- Stable angina pectoris
- Prinzmetal angina
- Silent ischemia
Stable angina pectoris
Recurrent/predictable chest pain that. Rest repairs blood flow, alleviates pain.
Pathophysiology of stable angina pectoris
- Gradual narrowing of the coronary vessels due to plaque.
- Artery is hardened because of plaque
Body can not respond to increase of myocardial demand.
Manifestations of stable angina pectoris
- Substernal chest discomfort (pain or pressure)
- Profuse sweating
- Pain radiates
- Dyspnia (short of breath due to pain)
- Pallor (pale due to pain)
Prinzmetal angina
Abnormal vasospasm of coronary vessels. Results in unpredictable chest pain (often at rest or at night) and has a cyclical pattern of occurrence.
Relatively benign.
Silent ischemia
Seldom detectable symptoms. Could be linked with diabetes millitus or chronic stress.
Manifestations of silent ischemia
Few detectable symptoms. The ones that do appear are vague.
- fatigue
- malaise
- Can form into unstable angina
EKG signs of ischemia
- ST segment depression
- T wave inversion
- ST segment elevation (most serious)
Acute coronary syndromes
- Transient ischemia
- Unstable angina
- Sustained ischemia
- M.I. (STEMI/nonSTEMI)
Result of stable plaque
Stable angina
Paths of acute coronary syndromes
Transient ischemia>Unstable angina>Sustained ischemia>Myocardial infarction (non-STEMI or STEMI)>Myocardial inflammation and necrosis
Transient ischemia
- Unpredictable.
- Precursor to a stroke.
Unstable angina EKG reading
ST segment depression
T wave inversion
Myocardial infarction categories
- STEMI
- non-STEMI
non-STEMI
non-ST elevated myocardial infarction. Only damage to the myocardium (middle layer of heart tissue.)
STEMI
ST elevation myocardial infarction. More serious because there’s an indication of damage to all three layers of the heart tissue.
Requires immediate intervention.
- Cell death (infarction)
- Can lead to heart failure due to formation of scar tissue
Three layers of heart tissue
- Epicardium (outer)
- Myocardium
- Endocardium (inner)
Changes in the heart due to myocardial infarction
- Myocardium becomes cyanotic with ischemia after 10 seconds
- Oxygen demand increases leading to anaerobic metabolism causing acidic environment
- Cell death occurs in 20 minutes
- Myocardial stunting in area of infarction (stops contracting) that lasts hours to days
- Hibernating myocardium. Area stops in an attempt to lower demand.
- Myocardial remodeling occurs once tissue blood flow is restored. Hypertrophy/loss of contraction of the heart distal to the infarction. Trying to compensate.
- Wound repair: 10-14 days after infarction
Biomarker from myocardial infarction (one example)
Triponin
Manifestations of MI
First signs:
- Sudden, severe chest pain (crushing, radiating, etc)
- Sweating
- Dyspnia
- Nausea/vomiting
Men:
- Chest pain
- Arm pain
- Shortness of breath
Women:
- Nausea/vomiting
- Jaw pain
- Fatigue
- Back pain
Complications of MI
- Death (depending on area of infarction)
- Electrical instability
Left ventricular failure is
- also called congestive heart failure
- can be further categorized into systolic and diastolic failure
- most causes of heart failure result from dysfunction of the left ventricle
Three types of pericardial disorders:
- acute pericarditis
- pericardial effusion
- constrictive pericarditis
Causes of acute pericarditis
unknown or viral
Manifestations of acute pericarditis
- sudden on set of chest pain with fever
- difficulty swallowing
- restlessness
- irritability
- tachycardia
- friction rub with stethoscope
- pulsus paradoxus
Pulsus paradoxus is a
decrease in systolic blood pressure of >10 mmHg with inspiration
it is suggestive of cardiac tamponade, which is life- threatening
Pericardial effusion
accumulation of fluid in pericardial cavity
Causes of pericardial effusion
could be infection or underlying issue
Pulsus paradoxus can also be defined as
when arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10 mm Hg
Manifestations of pericardial effusion
- muffled heart waves
- weak and thready pulse
- dull chest pain
- dyspnea
Cardiac tamponade
fluid compresses heart so much that it can’t beat, which leads to circulatory stoppage
this is connected with pericardial effusion
Constrictive pericarditis
heart is not as flexible; fibrous scarring with occasional calcification causes layers of pericardium to adhere, obliterating the pericardial cavity and subsequently lowering cardiac output
develops gradually
Causes of constrictive pericarditis
commonly idiopathic
Manifestations of constrictive pericarditis
- exercise intolerance
- dyspnea on exertion
- fatigue
- anorexia
Clinical assessments show:
- edema
- jugular vein distention
- hepatic congestion
- T wave inversion
Disorders of the myocardium: cardiomyopathies
-occur on left side of heart
-are a result of remodeling after effect of neurohumoral response to ischemic heart disease or hypertension
diabetes can also be a cause
-often idiopathic, but may be secondary to other disease
Types of cardiomyopathies
- Dilated
- Hypertrophic
- Restrictive
Dilated cardiomyopathy
- causes impaired systolic function
- the extra blood in the heart leads to dilation and we end up with systolic heart failure
- left ventricle because rounder
Manifestations of dilated cardiomyopathy
- dyspnea
- fatigue
- jugular vein distention
- edema
- weakened LV
Hypertrophic cardiomyopathy
is a hypertrophy of septum walls which cause restriction and leads to thickened wall and smaller cavity
can have LA dilation
Manifestations of hypertrophic cardiomyopathy
- dysrhythmias
- angina, syncopy (fainting)
- dsypnea on exertion
- palpitations
Restrictive cardiomyopathy
Restrictive filling and increased diastolic pressure of either or both ventricles
LV cavity is normal size, but LA is dilated because of reduced diastolic compliance
It’s called restrictive because it’s restricting diastole so the decreased diastolic function doesn’t let LV relax
Cause is often idopathic
Manifestations of restrictive cardiomyopathy
similar to constrictive pericarditis because we have hardening and stiffening of myocardium
Manifestations of constrictive peri are
- exercise intolerance
- dyspnea on exertion
- fatigue
- anorexia
Rheumatic fever
systemic, inflammatory disease which can ultimately lead to rheumatic heart disease if left untreated
causes scarring and deformity of cardiac structures when untreated
Cause of rheumatic fever
a delayed immune response due to group A hemolytic streptococcus
Characteristics of acute rheumatic fever
is a febrile illness
shows inflammation of joints, skin, nervous system and heart
Manifestation of acute rheumatic fever
- fever
- enlarged lymph nodes
- joint pain
- nausea
- vomiting
Aschoff bodies
a form of granulomatous inflammatory lesions within the heart, seen in acute rheumatic fever
Most common cause of valvular injury
Rheumatic fever
Valvular dysfunctions
are disorders of the endocardium
Valvular stenosis
is when valve is restricted leading to myocardial hypertrophy
Types of valvular stenosis
Aortic
Mitral
Aortic stenosis
most common type of valvular abnormality. Orifice of the aortic valve narrows causing resistance to clood flow from the left ventricle into the aorta. Develops gradually
Three common causes of aortic stenosis
- congenital bicuspid valve problems
- degeneration with aging
- inflammation damage caused by rheumatic heart disease
Manifestations of aortic stenosis
- angina
- syncopy
- dyspnea
- decreased stroke volume
- Narrowed pulse pressure
- Slowed heart rate
- Delayed pulse
Mitral stenosis
impairs blood flow from LA to LV
valve leaflets harden and become fibrous and fuse, LA pressure increases if LA is backed up
Causes of mitral stenosis
occurs in patients with history of Rheumatic heart disease and autoimmunity to strep
Manifestations of mitral stenosis
- pulmonary congestion
- pulmonary edema
Types of valvular regurgitation
Aortic
Mitral
Tricuspid
Aortic regurgitation
inability of aortic valve leaflets to close properly during diastole
ejected blood flows back into LV, causing hypertrophy, dilation of LV
continued hypertrophy causes heart failure
Manifestations of aortic regurgitation
- widened pulse pressure resulting from increased stroke volume and diastolic backflow
- dysrhythmias
Pulse pressure
is the difference btwn systolic and diastolic blood pressures, normally 30 to 50 mmHg
Causes of aortic regurgitation
- congenital (bicuspid valvue)
- acquired (often idopathic)
Mitral regurgitation
permits backflow of blood from LV to LA during ventricular systole
Causes of mitral regurgitation
many possibilities, including:
- mitral valve prolapse
- rheumatic heart disease
- infective endocarditis
- MI
Manifestations of mitral regurgitation
- pulmonary hypertension
- heart failure
Tricuspid regurgitation
usually associated with dilation and failure of RV
leads to volume overload in RA and RV
Causes of tricuspid regurgitation
secondary to pulmonary hypertension
less commonly caused by rheumatic heart disease and infective endocarditis
Manifestations of tricuspid regurgitation
- peripheral edema
- jugular vein distention
Infective endocarditis
infection and inflammation of the endocardium - especially the cardiac valves
Pathophysiology and development of infective endocarditis
- Endocardial damage from trauma, congenital heart disease or valvular heart disease
- leads to inflammation and thrombus formation
- then blood-borne microorganism (bacteremia) have much better chance at adherence and increase in clotting factor
- which leads to fibrin and thrombus formation, proliferation of microorganisms
- then microorganisms aggregate into infective endocardial vegetations
Manifestations of infective endocarditis
- fever
- malaise
- weight loss
- changed cardiac murmur
- petechial lesions on skin
- conjuctive and oral mucosa
- Janeway lesions
- Osler nodes
Dysrhythmias
disturbance of hearth rhythm
ranges from occasional “missed” or rapid beats to severe disturbance that affects the pumping ability of the heart
Cause of dysrhythmias
- abnormal rate of impulse generation or abnormal impulse conduction
- MI causes scar tissue in purkinje fibers
Types of dysrhythmias
Sinus Bradycardia
Atrial Tachycardia
Ventricular Standstill (Asystole)
Sinus Bradycardia
effect is increased preload and decreased mean arterial pressure (MAP)
slow heartbeat
Mean Arterial Pressure (MAP)
we want it above 60
normal heart beat range is between 60 and 100
Causes of sinus bradycardia
- hyperkalemia
- vagal nerve stimulation
- age
Atrial Tachycardia
effect is decreased filling time, decreased MAP and increased myocardial oxygenation demand
rapid heartbeat
Causes of atrial tachycardia
- electrolyte disturbances (mostly potassium)
- hypoxia
- elevated preload
- age
Ventricular standstill (asystole)
effect is no heartbeat and no cardiac output
Causes of ventricular standstill
- profound ischemia
- MI
- hyperkalemia
- acidosis
Zone of ischemia
- Wider than zone of infarction.
- Reversible, can heal
Zone of hypoxic injury
- Damage to cell, but no cell death.
- Might or might not totally heal.
Zone of infarction
- Localized.
- Unable to heal.
- Area of scar tissue after infarction.
Conventional or major risk factors for atherosclerotic disease that are non-modifiable
- Advanced age
- Male gender or women after menopause
- -Family history
Modifiable risk factors for Atherosclerotic disease
- Dislipidemia (abnormal concentrations of lipoproteins)
- Hypertension
- Cigarette smoking
- Diabetes/insulin resistance
- Obesity
- Sedentary lifestyle
- Atherogenic diet
Heart failure
The heart is unable to generate an adequate cardiac output, causing inadequate perfusion of tissues
Types of heart failure:
- Left systolic
- Left diastolic
- Right side heart failure
Causes of left systolic heart failure
Contractility reduced by:
-M.I. (most common)
Cardiac output
Depends on the heart rate and stroke volume. Amount ejected from the heart.
Stroke volume
Influenced by three major determinants:
- Contractility
- Preload
- Afterload
Left Systolic Heart Failure
An inability of the heart to generate and adequate cardiac output to perfuse vital tissues. Contractility is reduced by diseases that disrupt myocyte activity, namely MI due to scar tissue formation.
-Walls of the heart become distended with increased volume, which further disrupts contractility.
Ejection fraction
The fraction of blood that is ejected from ventricles with each heartbeat. Given in a percentage. Marker: 40%
Manifestations of Left Side Heart Failure
- pulmonary congestion
- Dyspnea
- Orthopnia (shortness of breath when lying flat)
- Cough with pink frothy sputum
- Pulmonary edema causes crackle sounds in the lung
- Cyanosis
- Fatigue
- Decreased cardiac output
- Inadequate perfusion of tissues in the system
- Variable BP
- Abnormal heart sounds
Diastolic Heart Failure
Heart failure with preserved ejection fraction. Normal stroke volume and cardiac output.
Decreased compliance of the LV ending with too much volume in LV after relaxation as a result of thickening of ventricular walls.
Causes of diastolic heart failure
- Myocardial hypertrophy
- Ischemia
- Valve dysfunction
- Pericardial disease
Right Side Heart Failure
Inability of the RV to provide adequate blood flow into the lungs. As pressure in the pulmonary circulation rises, the resistance to right ventricular emptying increases. The right ventricle is poorly prepared to compensate for this increased afteload and will dilate and fail.
Manifestations of right side heart failure
- Dilation of RV
- Peripheral maifestations
- peripheral edema
- Fluid buildup in the abdomen
- Jugular vein distension
- Enlarged liver or spleen
Shock
Cardiovascular system fails to perfuse the tissues adequately, thus impairing cellular metabolism.
Types of shock
- Cardiogenic
- Hypovolemic
- Septic
Final common pathway in all types of shock
Impaired cellular metabolism—Cells switch from aerobic to anaerobic metabolism. Energy stores drop, and cellular mechanisms relative to membrane permeability, action potentials, and lysozome release fail.
Results of anaerobic metabolism
- Activation of the inflammatory response
- Decreased circulatory volume
- Acidosis
Predictive route of MODS
Lungs>liver/kidney>GI>Heart
Transient ischemia
Temporary ischemia, less than 20 minutes, that leads to unstable angina
Unstable angina
Reversible; shows that atherosclerotic plaque has become complicated and you are at risk for an MI
Sustained ischemia
Lasts more than 20 minutes. Leads to myocardial infarction (STEMI/nonSTEMI)
Aortic stenosis leads to
- Hypertrophic cardiomyopathy
- Dysrhythmias
- MI
- Heart failure
Mitral stenosis leads to
- Pulmonary hypertension
- RV failure
- Pulmonary edema
