PATH - Cardio Flashcards
alterations of Cardio
A vein in which blood has pooled
Distended, tortuous, and palpable veins
Caused by trauma or gradual venous distention
Varicose Veins
3 Diseases of the veins?
Varicose Veins
Chronic Venous Insufficiency
Deep Venous Thrombosis
stasis
not moving
Deep Venous Thrombosis?
Factors/Causes?
Obstruction of venous flow leading to increased venous pressure
Virchow’s triad – describes causes of DVT:
● Venous stasis
● Venous endothelial damage
● Hypercoagulable states
Chronic Venous Insufficiency
Inadequate venous return over a long period due to varicose veins or valvular incompetence
• Causes pathologic ischemic changes in the vasculature, skin, and supporting tissues.
• Venous stasis ulcers
Venous stasis ulcers
ulcerations of skin that occur due to pressure or trauma.
o Develop as a result of the borderline metabolic state of the cells in the affected extremities
Progressive occlusion of the superior vena cava.
Superior Vena Cava Syndrome
• Leads to venous distention of upper extremities and head.
• Usually caused by bronchogenic cancer and some other cancers.
o As tumors grow they compress the SVC, decreasing its diameter.
Generally considered an oncologic emergency rather than a vascular emergency.
Superior Vena Cava Syndrome
Hypertension
is the consistent elevation of systemic arterial blood pressure resulting from increases in total peripheral resistance, circulating blood volume, or both.
Normal blood pressure is defined as
systolic pressure less than 120 mm Hg and diastolic pressure less than 80 mm Hg.
Hypertension - types
Primary Hypertension (essential or idiopathic) Secondary Hypertension Isolated Systolic Hypertension (ISH) Complicated Hypertension Malignant Hypertension
Affects 92% to 95% of individuals with hypertension
Primary Hypertension (essential or idiopathic)
• Hypertension without a known cause
• Appears to be due to a combination of genetic and environmental factors.
Primary Hypertension • Risk factors include:
o Family history
o Advanced age
o Smoking
o Obesity
o Heavy alcohol consumption (>3 drinks per day)
o Gender (men > women before age 55, women > men after 55)
o Black race
o High dietary sodium intake
o Low dietary intake of potassium, magnesium, and calcium
o Glucose intolerance/diabetes mellitus
Underlying mechanisms of primary hypertension
Overactivity of the sympathetic nervous system (SNS)
Causes increased heart rate and peripheral vasoconstriction.
Overactivity of the renin-angiotensin-aldosterone (RAA) system
High aldosterone levels cause increased retention of sodium and water.
Angiotensin II causes vasoconstriction and vascular remodeling which increases peripheral resistance.
Abnormal secretion of natriuretic hormones
These modulate renal sodium excretion and retention.
Abnormal levels cause sodium and water retention by the kidneys.
Complex interactions involving insulin resistance, inflammation, and endothelial function.
Contribute to vascular remodeling, increased sodium retention, and effects of SNS and RAA.
Caused by a systemic disease process or medication that raises peripheral vascular resistance or cardiac output, such as:
o Renal disease
o Adrenocortical tumors
o Adrenomedullary tumors (pheochromocytoma)
o Drugs (oral contraceptives, corticosteroids, antihistamines).
Secondary Hypertension
• If the cause is identified and removed before permanent structural changes occur, blood pressure returns to normal.
Defined as a sustained systolic BP that is ≥140mm Hg and diastolic BP that is below 90mm Hg.
• Common in older individuals who have stiffer (noncompliant) blood vessels.
Isolated Systolic Hypertension (ISH)
ISH is a risk factor for heart attack, congestive heart failure, and stroke.
Isolated Systolic Hypertension (ISH) - Mechanism:
o As the cardiac output is ejected into the aorta and its branches, they do not stretch to accept this increased blood volume and pressure rises.
o As this volume is distributed to the tissues during diastole, pressure falls back to normal.
Complicated Hypertension
Severe or sustained hypertension that begins to affect many other organs in the body.
• Chronic hypertensive damage occurs in the walls of systemic blood vessels.
• Vascular remodeling occurs
• Clinical manifestations result from damage of organs and tissues
o Smooth muscle cells undergo hypertrophy and hyperplasia.
o Fibrosis occurs in the tunica intima and tunica media.
Vascular remodeling
Complicated Hypertension - Clinical manifestations result from damage of organs and tissues (end organ damage):
o Heart disease
o Renal disease
o Cerebrovascular accidents
o Damage to retina of eye
Malignant Hypertension
- Rapidly progressive hypertension in which diastolic pressure is usually above 140mm Hg.
- Organ damage resulting from malignant hypertension is life threatening
Malignant Hypertension - Sequelae include:
o Encephalopathy - from profound cerebral edema that disrupts cerebral function and causes loss of consciousness. o Cardiac failure o Uremia o Retinopathy o Cerebrovascular accident
Treatment for Hypertension
- Behavioral changes – weight loss through diet and exercise and salt restriction.
- Antihypertensive drugs
Antihypertensive drugs
a. Diuretics – enhance urinary fluid loss to reduce blood volume.
b. Beta-blockers – block sympathetic input to heart, reducing contraction strength, cardiac output, and thus lowering blood pressure.
c. ACE-inhibitors – block angiotensin converting enzyme in lungs, so less angiotensin II is formed. This reduces vasoconstriction and aldosterone release.
d. Angiotensin-receptor blockers - cause vasodilation, reduced secretion of angiotensin II, and reduced production and secretion of aldosterone.
e. Calcium channel blockers – restrict entry of calcium into arteriolar smooth muscle, thus producing vasodilation, and into cardiac muscle, causing lower cardiac output.
• Multiple types of drugs may be combined to increase effectiveness.
enhance urinary fluid loss to reduce blood volume.
Diuretics
block sympathetic input to heart, reducing contraction strength, cardiac output, and thus lowering blood pressure.
Beta-blockers
ACE-inhibitors
block angiotensin converting enzyme in lungs, so less angiotensin II is formed. This reduces vasoconstriction and aldosterone release.
Angiotensin-receptor blockers
cause vasodilation, reduced secretion of angiotensin II, and reduced production and secretion of aldosterone.
restrict entry of calcium into arteriolar smooth muscle, thus producing vasodilation, and into cardiac muscle, causing lower cardiac output.
Calcium channel blockers
Multiple types of drugs may be combined to increase effectiveness. T/F
True
Antagonists
act against (oppose)
Agonists
increase activity of something
A significant drop in systolic and diastolic blood pressure upon moving from a lying or sitting position to a standing position.
Orthostatic (Postural) Hypotension
Systolic blood pressure decrease of 20 mm Hg (or greater) or diastolic blood pressure decrease of 10 mm Hg (or greater) within the first 3 minutes of standing.
Orthostatic (Postural) Hypotension - Cause
a failure of sympathetic nervous system vasomotor compensatory mechanisms that cause increased heart rate, vasoconstriction, and venous valve closing upon standing.
o Essential to maintaining adequate cerebral perfusion during upright positioning.
Orthostatic (Postural) Hypotension - Clinical Manifestations
dizziness, syncope (fainting), or sudden loss of vision or blurred vision.
Orthostatic (Postural) Hypotension - Types
- Acute orthostatic hypotension – caused by temporary body alterations like drugs and medications, dehydration, venous pooling, and prolonged inactivity.
- Chronic orthostatic hypotension – caused by underlying diseases like endocrine or metabolic disorders. Or it may be a primary condition caused by degeneration of the CNS with age.
Acute orthostatic hypotension
caused by temporary body alterations like drugs and medications, dehydration, venous pooling, and prolonged inactivity
Chronic orthostatic hypotension
caused by underlying diseases like endocrine or metabolic disorders. Or it may be a primary condition caused by degeneration of the CNS with age.
a local dilation or outpouching of a vessel wall or cardiac chamber.
Aneurysm
Aneurysms Primarily develop in the:
o Cerebral arteries (most commonly in the circle of Willis)
o Thoracic or abdominal aorta
Over time __________ grow in size, putting pressure on neighboring structures.
• The wall becomes thinner and weaker, and eventually may rupture, causing stroke or life-threatening hemorrhage.
aneurysms
Dissecting aneurysm (aortic dissection)
o Occurs when the tunica media is weakened and the intima is torn, allowing arterial pressure to force blood into the media, dissecting its layers apart.
o The dissection compresses vessels as they leave the aorta, causing acute ischemia and infarction of vital organs such as the brain and kidney.
o Aortic dissection most commonly involves the thoracic aorta.
o Symptoms - abrupt onset of severe chest pain along with syncope and symptoms of organ ischemia.
Aortic dissection has a very low mortality rate and is not a surgical emergency.
False - high
a clot that remains attached to a vascular wall.
o Can also form on damaged heart valves and in cardiac chambers (atrial fibrillation, ventricular aneurysms).
thrombus
o Activation of the clotting cascade leads to platelet aggregation and formation of a clot (thrombus) within a vessel, on a cardiac valve, or along the wall of a cardiac chamber.
Thrombus - Causes
o Causes are the same as for venous thrombi: intimal injury, stasis of flow, and hypercoagulable states (although these more commonly cause venous thrombosis).
Types of Arterial Thrombus Formations
- Thrombus
* Thromboembolus
detached portion of a thrombus that travels through the bloodstream
Thromboembolus
If the thrombus or embolus blocks a part of the peripheral circulation, this will cause limb ischemia and tissue infarction (tissue death). T/F
True
o If the thrombus or embolus blocks one of the central arteries, stroke and other types of vital organ infarctions may occur.
o Thromboemboli from the heart valves or chambers frequently travel to the brain, causing stroke.
Raynaud Phenomenon and Raynaud Disease
Peripheral Vascular Disease
• Episodic vasospasm in arteries and arterioles of the fingers, and less commonly the toes.
a primary vasospastic disorder related to an imbalance of endothelium-derived vasodilators and vasoconstrictors.
Raynaud disease
occurs secondary to other systemic diseases or conditions such as:
o Scleroderma, smoking, pulmonary hypertension, myxedema, and environmental factors
Raynaud phenomenon
Vasospasm causes pain and Temperature changes in the skin, especially involving the fingers and toes. T/F
True
• Vasospasm causes pain and color changes in the skin, especially involving the fingers and toes.
• Can occur on exposure to even a small drop in room temperature, or occasionally with vibration or repetitive motion.
Most common form of arteriosclerosis.
Atherosclerosis
Arteriosclerosis
- Chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls.
- Smooth muscle cells and collagen fibers migrate to the tunica intima, gradually narrowing the arterial lumen.
- Part of the normal aging process, but it is a disease state when it occurs to the point of symptom development.
Atherosclerosis is Characterized by
by soft deposits of fat and fibrin in the arterial wall that harden over time (plaques).
Hypertension, diabetes, smoking, high LDL levels, aging, autoimmune injury, and possibly bacterial infection by Chlamydia pneumonia can Cause?
Condition name?
• Plaque development
- begins when there is endothelial injury and inflammation
Atherosclerosis
Atherosclerosis Progression:
o Endothelial injury causes inflammation.
o Macrophages adhere and release cytokines that further injure the wall.
o Low-density lipoprotein (LDL) in the blood is oxidized and engulfed by macrophages (forming foam cells)
o A fatty streak forms as foam cells accumulate in wall of vessel.
o Fibrous plaque - macrophages release growth factors (mitogens) that promote proliferation of smooth muscle cells in the tunica media. These cells migrate over the fatty streak, produce collagen, and form a fibrous cap over the plaque.
o Plaques undergo calcification, grow, and protrude into the lumen of the vessel, obstructing flow.
o Complicated plaque – a plaque that has ruptured. This initiates thrombus formation and instability and vasoconstriction leading to obstruction of the lumen and inadequate oxygen delivery to tissues.
Atherosclerosis is the Secondary risk factor for myocardial infarction, stroke, and peripheral artery disease. T/F
False
• Atherosclerosis is the PRIMARY risk factor for myocardial infarction, stroke, and peripheral artery disease.
any vascular disorder that narrows or occludes the coronary arteries is called
Coronary Artery Disease (CAD)
Coronary Artery Disease (CAD) most common cause.
Atherosclerosis is the most common cause.
o Plaques narrow the coronary arteries.
o May rupture and cause sudden thrombus formation and myocardial ischemia and even infarction.
Risk factors for CAD are Catagorized as
Conventional or major risk factors
Nontraditional or novel risk factors
Conventional or major risk factors for CAD
- Advanced age
- Gender (men > women before age 55, women > men after age 55)
- High cholesterol/LDL levels*
- Hypertension *
- Smoking *
- Diabetes mellitus and insulin resistance
- Obesity
- Sedentary lifestyle
- Metabolic syndrome
- Atherogenic diet (high in saturated and trans fats)
Nontraditional or novel risk factors for CAD
Markers of inflammation o C-reactive protein (CRP) o Fibrinogen o Protein C o Plasminogen activator inhibitor o Interleukins o Others
Hyperhomocysteinemia
Infection
Markers of inflammation
o C-reactive protein (CRP) o Fibrinogen o Protein C o Plasminogen activator inhibitor o Interleukins o Others
Myocardial ischemia types
- Ischemic heart disease
- Angina pectoris
- Silent ischemia
- Acute coronary syndromes
o Local, temporary insufficiency of the coronary blood supply and oxygen.
o Usually occurs when demand for oxygen rises (increased heart rate)
Ischemic heart disease – caused by CAD and the resultant decrease in blood supply.
Angina pectoris -
Types -
- chest pain caused by myocardial ischemia.
o Stable angina - occurs with exercise and relieved with rest.
o Prinzmetal angina – due to vasospasm of coronary vessels without underlying atherosclerosis
Myocardial ischemia occurs unpredictably, often at rest or during sleep.
May result from hyperactivity of the sympathetic nervous system and changes in endogenous vasodilators and vasoconstrictors.
Which type of Angina?
Prinzmetal angina – due to vasospasm of coronary vessels without underlying atherosclerosis
Usually transient, lasting approximately 3 to 5 minutes
Substernal chest discomfort, which may radiate to the neck, lower jaw, left arm, and left shoulder, or occasionally, to the back or down the right arm.
Other symptoms include dizziness, shortness of breath, pallor and sweating.
Which Type of Angina?
Stable angina - occurs with exercise and relieved with rest.
ischemia without symptoms of chest discomfort.
o Can occur with dysfunction of the autonomic nerves that bring efferent messages from the heart to the brain.
o Common in diabetics, since they often suffer autonomic dysfunction.
Silent ischemia
caused by sudden coronary obstruction due to thrombus formation.
Acute coronary syndromes
Unstable angina
– severe chest pain that occurs due to rupture of a plaque in a coronary artery.
Acute coronary syndromes causes anginal pain that occurs at predictable times (for example, at rest) or with less frequency and severity. T/F
False
Causes anginal pain that occurs at UNpredictable times (for example, at rest) or with GREATER frequency and severity.
Unstable angina is a signal of?
Symptom of?
myocardial infarction
Acute coronary syndromes
If the ruptured thrombus is labile and occludes the vessel for no more than 10 to 20 minutes, myocardial ischemia will be severe but will not result in infarction of the heart. T/F
True
Anaerobic metabolism is able to support cell function for about 20 minutes.
Is a Myocardial infarction classified as an acute coronary syndrome?
Yes
Caused by prolonged, unrelieved ischemia that interrupts blood supply to the myocardium.
o Usually due to a ruptured thrombus in a coronary artery.
Myocardial infarction
After about ____ minutes of myocardial ischemia, irreversible hypoxic injury causes cellular death and tissue necrosis due to lack of oxygen.
20 Minutes
Myocardial infarction Classifications:
o Non-STEMI
o STEMI
Non-STEMI
only affects the myocardium just under the endocardium (subendocardial).
STEMI
– damage penetrates all the way from the endocardium to the pericardium (transmural MI). [STEMI = ST-elevated myocardial infarction.] Identifies patients at greatest risk for severe complications and most likely to benefit from rapid intervention
Pathophysiology of MI
Myocardial infarction
o Cellular necrosis results in the release of intracellular enzymes such as troponin I and troponin T, creatinine phosphokinase (CPK-MB), and lactate dehydrogenase (LDH).
o Cellular necrosis is accompanied by release of inflammatory mediators and infiltration of the myocardium with inflammatory cells such as polymorphonucleocytes and macrophages.
Structural and functional changes are defined as?
Neurohumoral changes cause structural and functional alterations that contribute to further dysfunction of heart muscle surrounding the infarction.
Myocardial infarctions Structural and functional changes are?
Myocardial stunning
Hibernating myocardium
Myocardial remodeling
Myocardial stunning
- toxic oxygen radicals and other inflammatory mediators cause temporary loss of contractile function that persists for hours or days after perfusion has been restored.
Hibernating myocardium
- Tissue that survives persistent ischemia through metabolic adaptation to prolong myocyte survival until perfusion can be restored.
Myocardial remodeling
- Myocyte hypertrophy and loss of contractile function of heart muscle distant from the site of infarction. This process is mediated by angiotensin II, catecholamines, aldosterone, adenosine, and inflammatory cytokines. It can be inhibited by the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and beta blockers after an MI.
An increase in plasma enzyme levels is used to diagnose the occurrence of myocardial infarction and indicate its severity. T/F
True
o Elevations of the isoenzymes creatine kinase (CK-MB), troponins, and lactic dehydrogenase (LDH-1) are most predictive of a myocardial infarction.
Myocardial infarction Treatments include:
o Revascularization (thrombolytics or PCI)
o Antithrombotics, ACE inhibitors, and beta-blockers.
o Pain relief and fluid management.
Dysrhythmias and cardiac failure are the most common complications of acute myocardial infarction. T/F
True
