Lecture 32 - Cardiovascular Flashcards
Describe the cause and complications of Varicose veins
Etiology: Veins are highly distensible, contain up to 70% of blood at rest; saphenous veins are usually involved (great saphenous vein)
A. Standing for long periods of time without moving
B. Crossing the legs while sitting; it blocks venous flow
C. Wearing restrictive garments
Pathophysiology:
A. Gravity or obstruction causes blood to distend the veins
B. Distension progresses until the valves in the veins are damaged
C. Valves fail, venous pressure rises, and distension worsens to the point that vascular restructuring occurs
Define/Differentiate Thrombus vs Embolus. Delineate the etiology Thrombi vs Emboli and describe the pathophysiologic consequences of the two. Describe the best treatments is for
the prevention of Thrombus formation.
THROMBUS
Thrombus = clot that remains attached to the vessel wall
Etiology: Anything that triggers clotting mechanism
A. Rough intima of vessels –> Artherosclerosis
B. Inflammation/Injury of intima –> Phlebitis from non sterile needle
C. Low blood pressure leading to blood stasis –> Cardiac failure, CHF, or shock
D. Obstruction of blood flow –> crossing your legs, occluding blood flow through veins
note: standing or sitting for long periods of time without moving causes blood stasis leading to clot formation, varicose veins and risk for DVT’s
Pathophysiology:
A. Blocks/Occludes the vessels - in arteries it causes infarction of the tissue distal to the clot
B. Break lose and become and embolus which blocks the first capillary bed it comes in contact with, if venous it causes PE
***Treatment = Low molecular weight Heparin for DVT’s, Streptokinase (enzyme released from streptococcus that bind and activate human plasminogen), tPA (tissue Plasminogen Activator), and Angioplasty (surgical repair or unblocking of a blood vessel)
PREVENTION IS KEY –> MOBILIZE PATIENT AS SOON AS ABLE, THIS IS ESSENTIAL
Define/Differentiate Thrombus vs Embolus. Delineate the etiology Thrombi vs Emboli and describe the pathophysiologic consequences of the two. Describe the best treatments is for
the prevention of Thrombus formation.
EMBOLUS
Embolus = obstruction of a blood vessel by a bolus of matter
Etiology: Dislodged thrombus
In ARTERIAL side usually originates in L heart which is a result from
1. Dysfunctional valves causing turbulent blood flow
2. A fib
3. Stasis in aneurism (ballooning and weakened area in artery)
50% OF EMBOLI GO TO THE LEGS; CAN GO TO CORONARY ARTERIES OR CEREBRAL VASCULATURE –> HEART ATTACK AND STROKES
A. VENOUS side is usually due to phlebitis (inflammation of vein) or stasis or trauma; Highest risk is DVT
*** usually venous embolus goes to lung –> PE
obstructs L –> R flow in lungs
B. Air Embolus - air bubble from IV or from scuba diving
C. Amniotic Embolus - contraction during labor causes a large amount of amniotic fluid to go into mothers blood stream
D. Aggregate of fat - release with Fx of long bones, especially the femur bone; platelets aggregate around fatty emboli and cause it to adhere to endothelial wall
E. Vegetative aggregate of bacteria - usually released from valves during bacterial endocarditis
F. Cluster of cancer cells
Pathophysiology: Embolus floats through circulation until it hits a vessel too small to pass through, then it lodges and obstructs blood flow
Causes-
- Ischemia –> Hypoxia –> Pain from neural hypoxia
- Infarction = death of tissue distal to occlusion
Be prepared to list six different types of emboli, their cause and sources.
- Arterial/Venous embolus:
If ARTERIAL it is usually from the L Heart this could be a result of a) Dysfunctional valves causing turbulent blood flow b) A fib or c) blood stasis in aneurism
If VENOUS it is usually from phlebitis, trauma, or injury; the most dangerous type is DVT; usually goes to the lungs and causes PE which bloods L–> R flow of blood in lungs - Air Embolus: usually from air in IV or from scuba diving
- Amniotic Embolus: from labor when a large amount of amniotic fluid enters mother’s blood stream
- Fatty aggregates: from Fx of long bones (usually femur); platelets aggregate around the fatty embolus and it adheres to the endothelial wall
- Accumulation of bacteria
- Cluster of cancer cells
Define/Differentiate: primary hypertension vs secondary hypertension. Describe how
hypertension is diagnosed, the definition of hypertension, and differentiate between:
A) Normal BP C) Stage I hypertension
B) Prehypertension D) Stage II hypertension
HTN = two separate measurements of BP
systolic > 140 mmHg and diastolic > 80 mmHg
Causes:
- Increased CO (either increased HR or SV or both)
- Increased peripheral resistance (greater viscosity of blood or vasoconstriction)
a) NORMAL BP: 160/>100
I. Primary HTN: combined genetic and environmental factors
Genetic =
a) Decreased Na+ excretion and decreased response to aldosterone (causes oversecretion of aldosterone)
- Inherited defects in renal Na+ secretion
- Hypertensive individuals secrete less Na+ in urine
b) Increased production or activation of angiotensin II - this thickens the vasc. smooth mm. (hypertrophy/hyperplasia) thus narrowing the artery; it is a powerful vasoconstrictor; causes cardiac hypertrophy because heart has to work harder
c) Insulin resistance is very common in hypertension
Risk factors = a) age and gender (young males, older women) b) high Na+ intake c) smoking/heavy alcohol consumption d) glucose intolerance (diabetes), microvascular damage e) low intake of K, Ca, Mg f) obesity --> leptin is secreted by adipose cells, meant to suppress appetite Chronically high levels of leptin cause: . insulin resistance (DM II) . increased sympathetic tone . decreased Na+ excretion . stimulates myocyte hypertrophy
Metabolic Syndrome –> Leads to DM II
a) central obesity
b) high normal fasting blood glucose
c) increased LDL and decreased HDL
d) high BP
*** ACE inhibitors and blockers of aldosterone are becoming primary treatment for primary HTN
II. Secondary HTN = altered hemodynamics due to an underlying disease
Tx: treat or remove underlying disease
ex) Renal Atherosclerosis, we would decrease blood flow to kidney
Describe complicated HTN
***Complicated HTN can be either primary or secondary
Pathophysiology:
a) Damage to endothelial membrane. Loss of endothelial vasodilators, NO(relaxes smooth mm.), and prostaglandins (control BP by contracting or dilating)
b) smooth mm. hypertrophy and hyperplasia
c) narrowing of the vessel lumina
d) leads to ischemia –> hypoxia –> organ dysfunction
Complications:
a) Turbulent blood flow –> leads to development of atherosclerosis
b) L ventricular hypertrophy –> stimulated by SNS and angiotensin II
c) CHF
d) CAD and cerebral vascular disease
e) PRIMARY CAUSE for formation of aneurism
f) Malignant HTN causes cerebral edema encephalopathy (general term for any brain disease) which leads to death
Clinical Manifestations: The silent death
No s/s until too late; symptoms are secondary to organ damage
Evaluation: sequential BP readings
Treatment:
Behavioral - exercise, smoking cessation, salt restriction
Pharmacological - . ACE inhibitors . Angi II receptor blocker (natriuretic - process of excretion of Na+ into urine) . B blockers . Ca2+ channel blockers
Delineate the role of each of the following in hypertension:
Metabolic Syndrome
Metabolic Syndrome: Leads to DM II
a) Obesity
b) High normal blood glucose
c) Increased LDL and decreased HDL
d) High BP
This leads to DM II which is seen in Primary HTN
DM is a risk factor for HTN
Delineate the role of each of the following in hypertension:
Leptin
Leptin is secreted by adipose cells. It a) leads to insulin resistance b) reduces Na+ excretion c) induces myocyte hyperplasia and d) increases sympathetic tone
This is a result of obesity which is a risk factor for primary HTN
Delineate the role of each of the following in hypertension:
RAAS system
aka the Renin angiotensin aldosterone system
Renin to angiotensin –> angiotensin II
Angiotensin II leads to powerful vasoconstriction, hypertrophy and hyperplasia of vascular smooth muscle thus narrowing the lumen, and hypertrophy of the L ventricular hypertrophy thus worsening HTN
Angiotensin II –> Aldosterone
Aldosterone causes the kidneys to reabsorb salt water, increasing blood volume and worsens an already hypertensive individual
Delineate the role of each of the following in hypertension:
The Sympathetic nervous system
The sympathetic nervous system causes the vascular smooth mm. to vasoconstrict thus worsening HTN and can lead to L ventricular hypertrophy
Describe the mechanism and benefits of using each of the following to control hypertension.
ACE inhibitors
ACE inhibitors will prevent the formation of angiotensin I to angiotensin II thus preventing powerful vasoconstriction, vascular smooth mm. hypertrophy/hyperplasia, and L ventricular hypertrophy.
Describe the mechanism and benefits of using each of the following to control hypertension.
β blockers
B blockers will inhibit the sympathetic nervous response and prevent vasoconstriction of the vascular smooth mm.
Describe the mechanism and benefits of using each of the following to control hypertension.
Ca++ Blockers
Ca++ blockers will prevent the Ca++ from entering the blood vessel walls resulting in lower BP.
Describe the mechanism and benefits of using each of the following to control hypertension.
Salt Restriction diet
A salt restriction diet will prevent HTN, edema in pt’s with kidney failure and hypertension due to reabsorption of water, it will prevent proteins from being excreted into urine, and it will prevent loss of kidney function.
Define aneurism, identify some possible causes of aneurisms and describe the pathological
consequences of aneurisms.
Aneurism = out pouching of the vessel wall or heart wall
Etiology:
a) Constant mechanical stress, once the out pouching occurs, Law of Laplace causes it to accelerate (the larger the radius the less the pressure) P = 2XT/R
b) Artherosclerosis: MOST COMMON CAUSE, causes a weakening of vessel wall leading to aneurism formation
c) Most often occurs in Aorta - aortic arch or abdominal aorta
Pathophysiology:
a) formation of clots due to blood stasis in aneurism
b) hemorrhage due to aneurism rupture
c) dissecting aneurism - will cause much pain and rupture
What is LDL Familial Hypercholesterolemia (FH)?
All cells require cholesterol as a component of their plasma membrane. They can synthesize their own or preferably bring it in via endocytosis on LDL’s. FH is most commonly caused by a reduction of LDL receptors on cell surfaces. Lacking the normal number of LDL receptors cellular cholesterol uptake is reduced and circulating cholesterol is increased.
–> This leads to early artherosclerosis and MI’s
This is a result of more than 1000 mutations in the LDL receptor gene.
Tx:
a) reduce cholesterol in diet
b) take cholesterol reducing agents (statins)
c) Liver transplants (less successful due to lack of donors)
What is atherosclerosis?
Atherosclerosis: thickening and hardening of the blood vessels caused by soft deposits of fat and fibrin; decrease the ability of the vessel to change lumen size (vasoconstrict and vasodilate)
Mechanism: smooth mm. and fibroblasts migrate to the intima, hypertrophy of vascular smooth mm. and collagen deposition causes vessel wall the thicken and stiffen
Pathophysiology: 4 steps in the formation of artherosclerosis
a) endothelial injury
b) fatty streak
c) fibrotic plaque
d) complicated lesion
Define/describe/differentiate between the four levels or stages of atherosclerosis. Describe
the evolution of a normal epithelium from normal to a complicated lesion.
- Endothelial Injury
- Endothelial Injury - little is known about how it is formed but here are some causes
a) Smoking - chemicals cause certain endothelial damage and dysfunction
b) HTN - increased pressure causes mechanical injury to the cells by causing turbulent blood flow
c) Diabetes - glycation and thickening of the basement membrane of microvascular vessels and increased LDL and decreased HDL accelerating fat deposition in large vessels + glycosylation
d) Turbulent blood flow - increased sheer forces and mechanical injury
e) Increased plasma fibrinogen???
f) Autoimmunity - Type III Hypersensitivity responses; antigen-antibody complexes precipitate out of blood and trigger neutrophils to attach and degranulate, digesting the endothelial cells
g) Bacteria and Viruses - lysis of endothelial cells through digestion; phlebitis
Steps of Endothelial Injury:
a) Cessation of synthesis of antithrombin factors and vasodilatory substances such a NO, prostaglandins, and vasodilatory cytokines
b) Release of inflammatory cytokines (IL-1, TNF alpha, Interferon, oxygen free radicals)
c) Release of growth factors stimulating mitosis and proliferation of vascular smooth mm. and fibroblasts –> collagen
ex) Angi II, Fibroblast growth factor, Platelet growth factors
d) Margination of macrophages
–> enter lesion and phagocytize oxidized LDL’s = foam cells, release toxic oxygen free radicals and further damage vessel wall
e) Accumulation of LDL in lesion, oxidation of LDL’s phagocytized by macrophages attracts more macrophages
f) Accumulation of foam cells (macrophages full of LDL’s) which penetrate further into lesion –> now called fatty streak
Define/describe/differentiate between the four levels or stages of atherosclerosis. Describe
the evolution of a normal epithelium from normal to a complicated lesion.
- Fatty Streak
Fatty streaks are found in most people and can be reversed by lowering LDL intake and increasing HDL intake.
- Increases formation of oxygen free radicals (Vit A,C,E) which trigger inflammatory changes
- Activation of fibroblast to secrete fibrous connective tissue in an attempt to heal the lesion –> forms a fibrous plaque made of collagen protein also at this point a risk of triggering the clotting mechanism
Define/describe/differentiate between the four levels or stages of atherosclerosis. Describe
the evolution of a normal epithelium from normal to a complicated lesion.
Fibrous plaque
Smooth mm. migrate, proliferate; Fibroblasts secrete collagen forming a cover over the lesion –> Decreases the size of the lumen and increases resistance to blood flow
This area of the vessel is no longer responsive to vasodilation, and may cause ischemia to tissue distal to occlusion especially if there is increased O2 demand
The fibrous tissue can ulcerate or rupture due to
a) Sheer forces on the vessel
b) Continued necrosis of the tissue
*** The fibrous plaque can cause platelet aggregation due to exposed collagen on ruptured plaque thus triggering the clotting cascade
–> This is now called a complicated lesion
Define/describe/differentiate between the four levels or stages of atherosclerosis. Describe
the evolution of a normal epithelium from normal to a complicated lesion.
Complicated Lesion
Complicated lesions can occur quite rapidly and result in infarction (obstruction of blood flow to tissue)
Clinical manifestation:
a) Ischemia - ST segment depression of T wave inversion
b) Angina - chest pain or pressure
- this is due to decreased blood flow to the heart
c) Transient ischemic events
d) Assume that if this has occurred in one area, then it has probably occurred in other areas ex) coronary, cerebral, and other arteries
Evaluation:
a) complete health history including risk factors
b) ECG either resting or stress test
c) Nuclear scanning
d) Angiography - can see where blockage is on x ray
e) CT or MRI - for coronary aa.
Tx: Primary goal is to restore adequate blood supply
a) Remove initial cause of lesion
- smoking cessation
- control HTN
- control DM
- Reduce LDL/cholesterol
- Remove US diet
- Exercise
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Smoking
Smoking causes endothelial cell damage which can lead to atherosclerotic disease
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Hypertension
HTN also damages endothelial cells by increased pressure which results in mechanical injury through turbulent blood flow.
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Diabetes Mellitus
DM causes glycosylation of the endothelial cells as well as LDL increase and deposition and HDL decrease –> Thickens the basement membrane
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Bacteria or viral infections
Bacteria/Viral infections cause release of damaging toxins that digest the endothelial cells or cause them to lyse –> phlebitis
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Turbulent blood flow
Increased sheer forces and mechanical injury.
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Type III hypersensitivity reactions
Antigen-antibody deposition on the endothelial cells causes neutrophils to come in and release chemicals that damage the endothelium.
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Sedentary life style
Sedentary life style may lead to obesity which can lead to DM and HTN and increased LDL levels. This also can cause blood stasis which worsens the clotting mechanisms and further occludes the vessels.
Be prepared to list and explain the mechanisms of endothelial injury leading to
atherosclerotic disease for each of the following etiologies.
Atherogenic diet
Atherogenic diet contributes to the formation of plaque in the arteries which causes CAD.
This decreases the lumen size and can rupture which worsens clotting and leads to complicated lesion.
Explain how and why endothelial injury leads to atherosclerosis and complicated lesions (thrombosis). Describe how higher levels of HDLs slow or prevent the development of
atherosclerosis.
Endothelial injury leads to atherosclerosis because the endothelial cells:
a) stop producing antithrombin factors and vasodilators
b) endothelial injury causes the release of inflammatory cytokines
c) endothelial injury causes the release of Growth Factors which cause proliferation of the smooth mm. and narrow the lumen (angi II)
d) endothelial injury causes macrophages to come into lesion and digest oxidized LDLs, further chemicals are released from the now foam cells
e) more LDL’s deposit which attracts more macrophages
f) more foam cells are formed which causes fatty streak
Fatty streaks then cause the formation of more oxygen free radicals and activated fibrinogen to form more collagen which can worsen the clotting cascade
The fatty streaks if they continue to worsen become fibrous plaques which cause proliferation of smooth mm. which narrows the lumen of the vessel. Ultimately increased pressure on these narrowed vessels can cause them to rupture thus exposing platelets to collagen. Now we have a complicated lesion.
HIGH LEVELS OF HDLS REMOVE THE LDL’S BOUND TO CHOLESTEROL AND TAKE THEM TO THE LIVER TO BE EXCRETED
*** Fewer HDL’s = fewer macrophages that come into lesion = less fatty streak = no formation of plaque = no risk for complicated lesion
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
ECG S-T segment depression
This is seen within complicated lesion. The clotting cascade is further activated which causes occlusion of the vessels and leads to ischemia. This is seen as an ECG S-T segment depression.
It indicates subendocardial ischemia –> just extended to the endocardium
The heart mm. is hypoxic at this point, O2 supply doesn’t meet demand of heart
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
ECG S-T segment elevation
This indicates transmural ischemia
This is ischemic necrosis of all the mm. layers form the endocardium to the myocardium to the epicardium
The person is currently under an MI
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
ECG T Wave inversion
A T wave inversion indicated subendocardial ischemia which means the ischemia is just limited to the endocardium.
The person has ischemia/hypoxia
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
Stable Angina
Stable angina - chest pain that does not occur at rest but upon exercise or strenuous activities
It is a result of the inability of the coronary arteries to dilate during periods of physical activity - increases O2 demand
It is predictable
May be accompanied by pallor and diaphoresis
This decreases blood flow and the person may feel chest pain radiating along jaw, left arm, left shoulder, and neck
Relief of pain is felt upon resting
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
Unstable angina
Unstable angina - chest pain that is UNPREDICTABLE, occurs without warning, and is not associated with one particular activity
Cause by rupture or the plaque and platelet aggregation –> thrombus formation
Aggravated platelets release thromboxane a3 and serotonin which causes vasoconstriction
Need to get to ER immediately!!!
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
Prenzmetal angina
Prenzmetal angina: this is UNPREDICTABLE but occurs mostly at rest
Caused by vasospasms from platelet aggregation and release of thromboxane a3, serotonin and endothelin
May resolve but may persist in infarction
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
PVC’s - premature ventricular contraction
AS we decrease the O2 supply we decrease ATP which slows the Na/K pump
Na+ and H20 will accumulate in the cells, as the sodium accumulated, resting membrane potential increases
When it hits threshold before SA node that is when we start seeing PVC’s
When threshold is being hit consistently before the SA node, it becomes the new pacemaker = V tac
List and describe the pathology and clinical manifestations of myocardial ischemia and the
mechanisms that cause them in terms of the following:
V. Tac
Threshold consistently is being hit before the SA node and there is a new pacemaker –> leads to V tac
In V. Tac hypoxia is getting worse –> V. Fib –> asystole
As the quantity of Na+ increases resting membrane potential increases and the heart can’t repolarize, there is no longer an action potential.
Describe the difference between the symptoms and pathophysiology of a fibrous plaque and
a complicated lesion. Identify the medial interventions be for each.
Fibrous plaque occurs from the foam cells activating the fibroblasts which increase their collagen secretion
The lumen size decreases because of the secretion of collagen and the smooth mm. proliferating and migrating
The area becomes less responsive to vasodilation and may cause ischemia to the distal tissue
Fibrous plaques can ulcerate and rupture which exposes collagen to platelets. In this case the platelets stick and don’t leave thus forming a complicated lesion.
The complicated lesion leads to ischemia –> hypoxia –> infarction
Interventions: Primary goal is to allow return of blood supply and remove the initial cause of lesion by…
a) smoking cessation
b) control HTN
c) control DM
d) Reduce LDL and cholesterol
e) Remove US diet
f) Exercise
List the risk factors for atherosclerosis and delineate which are “modifiable” and which ones are “not modifiable”.
Non- modifiable risk factors:
a) Genetic Propensity
b) Age
c) Gender
Modifiable risk factors:
a) HTN
b) Familial Hyperlipidemia
c) DM I/II
d) smoking cigarettes
e) sedentary lifestyle
f) obesity (metabolic syndrome)
g) US diet (Atherogenic diet)
Other risk factors not as common:
a) inflammation
b) infection
c) adipokines
d) thrombosis
What is an MI?
Myocardial infarction: death to cardiac mm cells second to ischemia
Pathophysiology:
a) 20 min of extreme ischemic condition
b) Anaerobic metabolism (increased lactic acid) –> H+ accumulation injures cells
c) ATP production stops - Na/K and Ca fail
d) Na+ accumulates in the cell, H20 enters cells causing swelling and lysis
e) Ca++ moves into mitochondria causing irreversible damage
f) Loss of membrane integrity causes the loss of myocardial cytoplasmic enzymes - CK (creatinine kinase), LH (lactate dehydrogenase), and troponin I
** note: serial measurement of these enzymes in the plasma will indicate the extent the infarction has occurred
More pathophysiology:
Acute - for 1-2 weeks there is a high risk of fatal ECG dysrhythmias
a) Hypoxic region around infarct is slow to depolarize and repolarize
b) Leads to circus conduction –> fibrillation
c) Remodeling of heart –> thinning of heart wall possibly rupture or formation of cardiac aneurism
Acute and Chronic:
a) Decreased ventricular strength and contractility
b) Decreased CO
c) Reduced O2 delivery to all tissues
d) Reduced functional capacity
Symptoms:
a) Sudden Death
b) Severe and sudden onset of pain “truck on my chest”
c) pallor
d) diaphoresis
e) N/V
Be prepared to outline the medical interventions for an MI from the onset of symptoms to the resolution of the problem. (Not counting death as a resolution)
for unstable angina and MI:
- Oxygen - increased O2 delivery
- Aspirin - prevent further platelet adhesions and thromboxane
- Morphine sulfate - relieve pain/vein and artery dilation
- Nitroglycerin - dilates EVERYTHING, coronary arteries
- Lidocaine - may control dysrhythmias
- Re-establish coronary blood flow - time to cath lab is critical!!!
- -> streptokinase/urokinase/tPA –> all work to break down blood clots if thrombus is suspected
- -> PTCA, ballooning procedure to dilate the artery, place stent
- -> Bypass surgery (CABG)
Describe the role and efficacy of using the following types of medications in the treatment of Coronary artery disease or an MI.
Beta blockers
This is used to reduce cardiac contractility
Blocks B1 receptors and reduces sympathetic stimulation of heart rate and contractility
*For CAD
Describe the role and efficacy of using the following types of medications in the treatment of Coronary artery disease or an MI.
Ca++ blockers
Ca++ blockers prevent the movement of calcium into the smooth mm. and cardiac mm. to reduce afterload and decrease peripheral resistance
(Verapamil) reduces contractility of the heart but little HR control
*** For CAD
Describe the role and efficacy of using the following types of medications in the treatment of Coronary artery disease or an MI.
Streptokinase
Streptokinase is produced by streptococci and it prevents clot formation by activating plasminogen.
This is used to treat and MI to re-establish blood flow to heart.
Describe the role and efficacy of using the following types of medications in the treatment of Coronary artery disease or an MI.
Nitroglycerin
Nitro is used for CAD and MI because it dilates everything!!! –> coronary arteries especially in MI
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
Oxygen
Oxygen is used in MI and unstable angina to increase O2 delivery
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
Plasminogen activators
Used in MI (streptokinase is an example) –> for decreasing blood clot formation if thrombus is suspected.
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
Aspirin
Aspirin is used in an MI to prevent coagulation (platelet aggregation and release of thromboxane)
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
Morphine
Morphine is used in MI to reduce pain and to vasodilate the arteries and veins.
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
ACE inhibitors
ACE inhibitors prevent the formation of angiotensin II which helps CAD because it decrease vasoconstriction as well as smooth mm. proliferation.
Describe the role and efficacy of using the following types of medications in the treatment of
Coronary artery disease or an MI.
Diuretics
This is to decrease the after load of the heart by decreasing blood pressure and decreasing peripheral resistance.
It also decreases preload.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
Graded exercise test
Graded exercise test (GXT) is used to determine stable angina. Stable agina is evident upon exercise and shows us decreased coronary blood flow.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
Thallium exercise test
This shows cold spots, areas of decreased diffusion.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
Angiography
Shows coronary artery obstruction.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
Angioplasty
surgical repair or unblocking of a blood vessel.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD
Stents
Used to establish coronary blood flow in an MI.
- Ballooning procedure that dilates the artery
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
Bypass surgery
Used to establish coronary blood flow in an MI.
Be prepare to briefly discuss the use of the following in diagnosing or treating of CAD.
a) creatinine kinase
b) lactate dehydrogenase
c) troponin I
measurement of these enzymes in the plasma helps determine the extent of the infarction
Define/differentiate; and be prepared to describe different etiologies that might lead to each of the following cardiomyopathies. Explain how each causes heart failure. (Reduces cardiac output). Describe the state of the art treatment for each of these myopathies.
Dilated cardiomyopathy
Just as note: dilated cardiomyopathy has no issues filling the heart with blood during preload, it just has a difficult time ejecting it during systole
A cardiomyopathy is the disease of the myocardium itself
Dilated cardiomypathy: ventricular dilation and decreased systolic function aka decreased myocardial contractility; BP will elevate initially but then go hypotensive
Etiology -
a) 50% is idiopathic
b) Most common cause is ischemic heart disease or valvular disease
c) Cancer chemotherapy
d) Alcohol
e) Bacterial, viral, or parasitic infection of the myocardium
f) fluid overload, excessive IV infusion
Pathophysiology -
a) Dilated heart failure –> severely diminished myocardial contractility
b) Heart overstretched due to original weakness of mm.
c) The heart becomes weak due to the overstretch of the mm. and it loses the ability to form myosin cross bridges; the heart is overstretched and can’t generate pressure
Symptoms:
a) Pulmonary congestion
b) Dyspnea and fatigue
Treatment:
a) salt restriction to reduce blood volume
b) digitalis to increase contractility
c) vasodilators to reduce afterload
d) anti-coagulants
e) bed rest to decrease work load
Define/differentiate; and be prepared to describe different etiologies that might lead to each of the following cardiomyopathies. Explain how each causes heart failure. (Reduces cardiac output). Describe the state of the art treatment for each of these myopathies.
Hypertrophic Cardiomyopathy
Def: increased size of the mm. due to increased levels of work; hallmark is disproportionate septal hypertrophy even though on the outside the heart looks fine
*** remember! hypertrophy goes inward not outward.
Etiology: overwork due to
a) Chronic HTN
b) Valvular stenosis or mitral regurgitation
Pathophysiology:
a) Decreased ventricular volume and compliance (unable to stretch as well)
b) –> deminished preload
c) –> normal or diminished stroke volume
d) –> normal or diminished CO
e) increased O2 demand without increase in coronary vessels
f) Increased susceptibility to ischemia and infarction
g) Systolic failure to to decreased stroke volume
Tx:
a) B blockers (inhibit effects of NE and Epi)
b) Ca++ channel blockers
c) surgical resection of hypertrophic tissue
Define/differentiate; and be prepared to describe different etiologies that might lead to each of the following cardiomyopathies. Explain how each causes heart failure. (Reduces cardiac output). Describe the state of the art treatment for each of these myopathies.
Restrictive Cardiomyopathy
Etiology: caused by an infiltrative disease
ex) fatty infiltration, amyloidosis (build up of amyloid proteins), glycogen storage disease, schleroderma
*remember glucose doesn’t need insulin to go into mm.
Pathophysiology:
a) myocardium becomes stiff and noncompliant
b) –> decreased preload, increased ventricular filling pressure, and pulmonary edema
c) –> decreased stroke volume
d) –> systolic and diastolic failure
Symptoms:
a) CHF especially of right heart
Tx:
a) there is no treatment other than to fix the underlying disease!!!
Define/differentiate; and describe different etiologies for and consequences of the two types of failure. Identified heart diseases or events which might lead to one or the other or both.
Systolic V. Diastolic
Heart failure - cardiac dysfunction resulting in inadequate tissue perfusion
Left heart failure is identified as systolic v. diasolic failure with an ejection fraction less than 40%. Normally should be 60%. Yikes!
Left systolic failure = inability for the heart to generate enough systolic pressure to perfuse tissues; depends on…
- contracility - decreased contractility = decreased ejection fraction
- Preload is not ejected = ventricular dilation
- Afterload - resistance to ejection is too great thus decreasing stroke volume
Etiology:
a) MI is the most common - loss of enough of the L ventricle to reduce CO; remodeling after MI causes collagen deposition which decreases contractility
b) myocarditis
c) cardiomyopathy
d) decreased CO leads to
- -> sympathetic stimulation and ADH secretion, both cause vasoconstriction
- -> activation of renin –> angi1/2–> aldosterone
- -> angi II stimulates cardiac and vascular smooth mm. hypertrophy
- -> peripheral vasoconstriction (increased preload and afterload)
- -> increased afterload = decreased SV
- -> viscious + feed back loop
Symptoms
a) inadquate perfusion
b) pulmonary vascular congestion and edema
c) dyspnea
d) wet cough with frothy pink sputum
e) decreased urine output due to decreased CO
Tx: Digoxin = increased contractility as well as doputamine
ACE inhibitors - prevents angi ii formation which helps to decrease BP, to decrease vasoconstriction, and to prevent proliferation of vascular endothelium
Define/differentiate; and describe different etiologies for and consequences of the two types of failure. Identified heart diseases or events which might lead to one or the other or both.
Systolic V. Diastolic continued
Diastolic discussed here
Def: decreased compliance of L ventricle, abnormal diastolic relaxation - decrease preload
Etiology:
a) Primary cause: Cardiac Hypertrophy caused by HTN
b) Restrictive cardiomyopathy
c) Restrictive pericarditis
d) Valvular disease
Pathophysiology:
a) Decreased preload –> decreased SV –> decreased CO
b) Pulmonary vascular congestions –> pulmonary edema
c) May lead to right heart failure
Tx:
a) Increase diastolic filling time
b) Ca++ channel blockers
c) B blockers
d) ACE inhibitors or Angi II receptors blockers if due to HTN
Define/differentiate; and describe different etiologies for and consequences of the two types of failure. Identified heart diseases or events which might lead to one or the other or both.
Left heart failure v. Right heart failure
Right Heart Failure:
Etiology -
- results from L heart failure due to..
a) Increased L ventricular filling pressure
b) Pulmonary vascular congestion
c) Either dilates R ventricle or over stretches the myomeres
d) Causes right ventricular hypertrophy –> Cardiomyopathy - Primary pulmonary vascular HTN
- Pulmonary diseases specifically cor pulmonale or cystic fibrosis
a) dilates the R ventricle overstretching the myomeres
b) Causes R ventricular hypertrophy –> cardiomyopathy
Pathophysiology:
a) Thinner ventricular wall –> Doesn’t handle increased pressure well
b) peripheral edema
c) hepatomegaly
Left heart failure is from either systolic or diastolic failure. Ejection fraction is less than 40%.
Left systolic failure - the heart is unable to generate enough systolic pressure to perfuse tissues; this depends on
- -> contracility decreases –> decreased ejection fraction ( preload isn’t ejected –> ventricular dilation
- -> afterload has increased peripheral resistance –> reduced stroke volume
Left diastolic failure - decreased compliance of the left ventricle which causes abnormal diastolic relaxation –> decreased preload
