Cardiovascular Disorders Flashcards
What are the three most basic components of Cardiovascular system?
Vessels, Blood, Heart
Lymphatic system includes
Lymphatic tissue, vessel and nodes
What is Hyperlipidemia?
What is a Lipoprotein (+ Types)
•Abnormally elevated fats/lipids in blood (cholesterol, phospholipids, and triglycerides)
o Lipids in blood do not move on their own, require carriers (i.e. Apoproteins) - carry lipids/fats
o lipid +apoprotein= lipoprotein
o Lipoprotein vary density
Produced by Liver-
LDL = trouble! since mostly cholesterol
HDL (good) equal parts lipid and protein. Returns cholesterol from peripheral tissue
VLDL (Fig 22-2) + (Fig 22-3) provide lipid transport to skeletal and adipose tissue
Produced in intestinal epithelial cells-
Chylomicrons- largest carry triglycerides
What is Atherosclerosis?
Word Breakdown
A disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls.
Athero- soft and pasty
Osis- generally formation of something, and a deposition of something)
Sclerosis- scaring/hardening
What is plaque?
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. (Generally just means a lesion) Forms progressively, hardens arteries and often leading to a narrowing of the vessel.
What is Atheroma?
An atheroma is an accumulation of degenerative material in the tunica intima (inner layer) of artery walls. The material consists of (mostly) macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
Basically a fibro fatty lesion that forms in the intima of larger arteries
3 lesions associated with the progression of Atherosclerosis?
(see pages 470-471)
1) Fatty streak- deposit of lipids + macrophages, neutrophils, etc
o Macrophages ingest lipids (becoming foam cells) release free radicals/growth factors which encourages further growth
2) Fibrous Atheromatous plaque- cells, platelets, lipids, defence cells, WITH the addition of smooth muscle cells
3) Complicated lesion- Earlier stages were inside the wall, final stage we see changes in the lumen. After bleeding into the plaque a thrombus forms in the vessel
Pathogenesis of Atherosclerosis?
pg 470
- Insidious origin with subtle endothelial injury -> inflm
- Monocytes & other cells associated w/ inflame bind to endothelium (w/ adhesion molecules)
- Monocytes enter intima -> become macropahges -> release free radicals (from oxidizing fat) causing further inflm/injury & engulf lipids (becoming foam cells)
- Foam cells release growth factors and smooth muscle cells proliferate
- Later stages bleeding into plaque
- Atheroma forms
Common sites for atherosclerosis in order of frequency
Abdominal aorta and iliac arteries
proximal coronary arteries
Thoracic aorta, femoral and popliteal arteries
Internal carotid artery
Vertebral, basilar and middle cerebral arteries
Why use C reactive protein in diagnosing atherosclerosis?
CRP is a serum marker for inflm. If there is no specific injury or trauma yet CRP lab value remains high, vessel wall damage/inflm is a common cause of value
What are foam cells?
Foam cells are fat-laden macrophages formed when the body sends them to the location of a fatty deposit on the blood vessel walls.
What compensatory mechanism manages BP
At rest?
On exertion?
BP= CO x PR
• At rest PR changes to maintain BP (CO stable)
• Exertion CO changes
4 major control systems of Bp?
review Fig 23-2
- Arterial baroreceptors (strategically located receptors to detects changes in pressure)
- Renin-angiotensin system
- Vascular Autoregulation
- Regulation of fluid volume
What is the Renin-Angiotensin system?
It’s a paragraph answer that needs to be summarized, so just describe it in general terms
The renin-angiotensin-aldosterone system (RAAS) is a signaling pathway responsible for regulating the body’s blood pressure.
Stimulated by low blood pressure or certain nerve impulses (e.g. in stressful situations), the kidneys release an enzyme called renin. This triggers a signal transduction pathway: renin splits the protein angiotensinogen, producing angiotensin I. This is converted by another enzyme, the angiotensin-converting enzyme (ACE), into angiotensin II.
Angiotensin II not only causes blood vessels to narrow (vasoconstriction), it also simultaneously stimulates the secretion of the water-retaining hormone vasopressin (also called AVP) in the pituitary gland (hypophysis) as well as the release of adrenaline, noradrenaline and aldosterone in the adrenal gland.
Whereas adrenaline and noradrenaline enhance vasoconstriction, aldosterone influences the filtration function of the kidneys. The kidneys retain more sodium and water in the body and excrete more potassium. The vasopressin from the pituitary gland prevents the excretion of water without affecting the electrolytes sodium and potassium.
In this way, the overall volume of blood in the body is increased: more blood is pumped through constricted arteries, which increases the pressure exerted on the artery walls – the blood pressure.
What is the difference between primary and secondary HTN?
1* HTN (140/90)
• essential or idiopathic
• about 90% of cases
• Et: multifactorial (kidney implicated)
2* HTN (>140/90) identifiable Et (eg renal disease) about 10% of cases
What is Systolic HTN?
Systolic HTN
• Systolic p* >140, diastolic p* reduced elasticity -> increased systolic pressure but not diastolic pressure
What is malignant HTN
o Diastolic >120
Not referring to cancer, just a serious issue
Can pregnancy cause HTN
Yes, Gestational HTN
What is White Coat HTN
Refers to Bp measuring higher then usual when individual is in a clinical setting
What is the only Mnft of HTN
High BP, everything else is a complication related to HTN
What are the complications associated with HTN?
o Fatigue,
o palpitations (sensation of a forceful irregular heartbeat)
o AM headaches (Bp has circadian rhythm, highest in the AM)
o Blurred visions (damage from aneurism in retina capillaries)
o Dizziness
• *** Those of progressive organ damage (heart, kidney, eyes, vessels)
Tx for Stage 1 and (maybe) Stage 2 HTN
Tx often includes only mngmt, not tx of underlying cause
• Life style modification- diet, exercise, body weight
Tx for Stage 2 to Stage 3 HTN (Pharmaceutical)
1rst and 2nd line of defence?
• 1st line- diuretics
• 2nd line : if req add 1 or more of
o Ca channel blockers (prevents Ca from crossing cell membrane, inhibits cardiac muscle contraction, reduces Bp)
o Angiotensin ll receptor blocker (Angiotension loop) blocking receptor
o ACE (Ace inhibitor) Prevents formation
What is Peripheral Vascular Disease (PVD)?
Two sub categories?
A common circulatory problem in which narrowed arteries reduce blood flow to your limbs. Your extremities — usually your legs — don’t receive enough blood flow to keep up with demand. This causes symptoms, most notably leg pain when walking (intermittent claudication)
Separated into Acute Arterial Occlusion (thrombus) and Artherosclerotic Arterial Occlusion (gradual dev and intermittent)
PVD- Atherosclerotic occlusive disease
Who is at risk? Common Mnfts?
Anyone with chronic vascular damage (Elderly and Diabetics)
Intermittent claudication (ischemic pain while walking)
o impedes perfusion -> ischemia -> tissue damage
o venous or lymphatic stasis – fluid and waste accumulation in legs
PVD- What happens when body tries to compensate?
Likely outcome w/o tx?
- Body attempts compensation w/ vasodilation (Quick response, but vessel already damaged, already dialated) anaerobic metb & collateralization occur
- W/O effective tx -> ulceration & gangrene -> amputation
What is an Aneurysm and where is it likely to occur?
Risk Factors?
- Localized dilation of artery (bulge)
- Permanent (not reversible)
- Increases near corners or bifurcation of vessels
- d/t degeneration/damage change in vessel wall
Risk factors
• HTN, atherosclerosis, congenital defects
Three types of Aneurysms?
(Fig 22-10)
- Saccular- One sided- forms a pouch or sac
- Fusiform- Both sides or around the vessel completely
- Dissecting- Blood flows between two layers of blood wall
Specific common sites of an aneurysm?
- Abdominal and thoracic aorta, femoral iliac and popliteal
* Vessels which lack external support, bends and bifurcation
The rules fro addressing complications
o Potential to develop (may not)
o Be aware of what they are
o Avoid them, if they develop, deal with them
Complications r/t aneurisms
- Aneurysms will apply pressure to any adjoining structure which may cause problems
- Aneurysms- Rupture (most pressing complication)
- Thrombosis (potential for clotting around low pressure aneurysm) Emboli could then break off from thrombus (distal embolization)
What is Coronary Artery Disease (CAD)?
Arteries that supply blood to heart muscle become hardened and narrowed (Potentially not only the coronary artery) As it grows, less blood can flow through the arteries. As a result, the heart muscle can’t get the blood or oxygen it needs.
• Major cause of death- most common heart disease
• Often d/t atherosclerosis/plaque build up
Two types of CAD
• Acute coronary syndromes (ACS)
o MI
• STEMI (st segment elevation)
o Unstable angina ( unstable lesion w/ plaque)
o Sudden cardiac death
• Chronic ischemic heart disease
o Stable angina (fixed lesion, only with exertion, up to about 50% occluded )
o CHF (congestive heart failure)
What is Angina Pectoris
ET?
Patho?
Mnfts?
• Angina is a Mnft of coronary artery disease
o Et.
• mostly Atherosclerosis
• Vasospasm
• Thrombosis
• Patho
o Inadequate perfusion -> myocardial ischemia -> chest pain
o Generally arteries will dilate on demand. Atherosclerosis -> unable to dilate on demand
• Mnfts
o Chest Pain (Triggered by exertion, emotion, cold)
• Transient, mild to moderate chest pain
o Squeezing, burning, (heartburn, indigestion misdiagnosis often prevents individual seeking care)
• Can radiate to L shoulder and U arm
What is the difference between stable and Unstable Angina?
Stable Angina
• Fixed plaque
• Perfusion impeded short term– ischemia (transient pain)
• Triggered by exertion only, relieved by rest
Unstable Plaque
• Unstable plaques
• Plaque collects platelets, fibrin and cellular debris
• If ruptured -> thrombosis
• Platelets aggregate -> prostaglandin release -> vasospasm
• Pain: severe, longer, also at rest and/or even nocturnal trigger, -> ACS
Is prostaglandin generally a local or systemic acting hormone?
• Prostaglandins are local hormones, act differently in different areas
Angina Variant?
Variant/Vasospastic/Prinzmetals’s angina
• Often nocturnal, at rest
• d/t spasm of the coronary artery
• can’t trace spasm with ECG unless it mnfst during exertion ECG test
Tx for Angina?
Tx • Reduce activity • Nitroglycerin o May not work during an MI because the vessel may already be dilated fully • Prevention to reduce MI risk
What is a MI?
STEMI?
ET?
Occurs when blood flow stops to a part of the heart causing damage to the heart muscle
• End point of CAD
• Life threatening
• Acute Onset
Stemi- A kind of MI characterized by a S-T segment elevation (see ECG)
ET-
• Atherosclerosis (mostly)
• Hemorrhage
• Coronary a. spasm
Common MI pathology?
fig 24-8
Artherosclerosis -> Complicated lesion ->ischemia -> cardiac hypoxia -> anaerobic metb -> metabolic acidosis -> arrhythmias -> inability to fx and infarction
Size of Infarction based on?
- Vessel involved – how much tissue affected
- Extent of occlusion
- Duration
- Metb status of the heart
- HR, Bp and Rhythm
- Collateral circulation
Two general categories of MI?
Subendocardial Infarction
• Inner 1/3 to ½ of vessel wall
• A distal occlusion
• ST segment depression
Transmural (epicardial) injury
• ST segment elevation
• Proximal branch or 1* artery obstruction (larger vessel)
Muftis of MI?
Mnfts of MI
• Severe chest pain d/t ischemia (often radiates to L arm, neck or Jaw
• Anxiety, tachycardia
• Nausea, vomiting, fatigue (Pain center located nearby vomit reflex center (often associated with eachother)
3 Key diagnostic to Dx MI
ECG, Angiogram, serum marker
How is angiogram used in DX of MI
o Enter artery, often through wris , with catheter follow vessel to heart and release medium. Allows visual of blockages in arterial system and left side of the heart.
o Can also look at venous system and right side of heart
What are serum markers and which are used in MI Dx
• Serum markers- when cardiac muscle is damaged they released known proteins which we can use to identify cardiac injury
o Troponin I and T - markers for cardiac damage, first to appear 3-10 hrs (There is also C)
o Myoglobin (serves as storage of 02 in muscle), also released in cardiac injury but peak in later on. Least Important of 3
o CKmb (AKA CPK)- Heart injury specific (Note same enzymes, different subclass)
• Ck BB- specific for brain injury
• Ck mm- specific cardiac and skeletal
Tx for MI
• Requires Stat attention (life preservation)
• Medications
o Thrombolytics (will be a thrombus, clot busters, dissolve to fragments, caution because of spread to distal branches)
o Anti Arrhythmics- return cardiac rhythm to normal
o Anticoagulants- no more build up on thrombus
- 02 therapy for hypoxia
- Morphine PRN (helps reduce anxiety)
• Once STABLE
o IV Diuretics (decrease heart workload)
o Inotrope (Positive- increase force of contraciton Negative- decrease force of contraction)
o Vasodilator (decrease workload on the heart)
• Revascularization SX (angioplasty, bypass) STINT
o Angioplastly
• Balloon angioplasty- blow up in lumen to open it up
• Stent (Eluting- release medication to prevent clotting
o Bypass
• Graft a vessel around the obstruction (from lymphatic)
Describe Hypertrophic Cardiomyopathy
Include ET, MNFTS, TX
NOTES: Cardiomyopathy • 1* and 2* forms (2* d/t another conditions) • muscle disorder • Several types
Hypertrophic (60% of cases) (1*) Ventrical wall patho
• Excessive hypertrophy of Ventrical (Walls become thick, creating smaller chamber size, reducing volume)
• Thick InterVentricular septum
ET
o Genetic (50%) Autosomal dominant
o Idiopathic (50%)
• Usually systolic Fx remains normal and many pts are asymptomatic
• MNFTS
o Dyspnea (caused by Hypoxia systemically), angina, syncope, palpitations
o Sudden Death?
• Tx
o Negative inotrope
o Alcohol sepal Ablation (Shave off septum thickness)
How do dilated and restrictive cardiomyopathy differ?
Dilated Cardiomyopathy
• Cardiac enlargement (esp. Ventricals)
o Increased size, casuing decrease contractility
o Weak contractions -> decreased ejection fraction
o Associated with alcohol abuse
Restrictive Cardiomyopathy
• Least common type
• Very rigid Ventricle wall (decreased contractility)
• Incomplete ventrical filling -> decreased Cardiac Output
• Usually leads to CHF
What is an Arrhythmia?
ET?
• Abnormal heart rate and/or rhythm
• Can be present normal and diseased hearts
• Alters cardiac cycle (filling and emptying)
o CO and perfusion affected
• ET o Heart defects (congenital) o Myocardial ischemia o MI o Drugs o Fluid electrolyte balance
How do arrhythmias most commonly progress?
Escalation runs from A flutter, to A Fib, to Heart Block
Describe an Atrial Flutter
• Regular, Atrial tachycardia (~300bpm)
o Problems with atrium rhythm will inevitably extend the problem to septum/ventricles
• Regular, Ventical tachycardia (~150bpm)
• Usual 2:1 ratio in bpm (A:V)
Describe Atril Fibrillation
- Irreg chaotic contractions (400-600bpm)
* Irreg rapid ventricle rate (~80-180)
Describe Heart Block
1* to 3*
• Abnormal or no impulse conduction from A to V
o 1st degree- delayed conduction, regular rhythms
• delay before ventricals contract
o 2nd degree – intermittent failure of conduction
o 3rd degree- no conduction, independent AR & VR
Describe ventricular fibrillation
- Quivering, no contraction
* Can cause death in minutes
Function of heart valves?
What happens when valves are damaged and which are most susceptible?
• Main function of a valve is to provide unidirectional flow (prevents regurgitation)
• Damaged valves -> impeded flow or regurgitation
• Aortic & mitral valve more susceptible
o Why? These valves are exposed to the highest pressure
Valvular disease ET?
o Valve trauma
o Degenerative change (with age)
o Ischemic damage
o Congenital effects
Two main dysfunctioning valve characteristics
- Stenosis – stiff valve, narrow orifice -> impeded flow
* Incompetent valve- distorted valve -> improper closure -> regurgitation
Is there ay treatment for Valvular disease?
Yes
o Need to maintain and improve fx (prevents failure)
o Sx? Synthetic valve
o Fig 24-18 and 24-21
Which valves is valvular disease most likely to effect?
Mitral and aortic d/t higher pressure
Triggers of RAAS?
- Drop in BP
- Drop in Na of Kidney
- Sympathetic response
RAAS described
Not done
Prostaglandin is local messenger to Juxtalur glomural cells in kidney. Kidney releases Renin. Interacts w/ angiotensinogen to form angiotensin 1. Interacts with ACE (enzyme from lungs) to form angiotensin 2.
Angiotensin 2 acts on
smooth muscles to cause vasoconstriction
Reacts with pituitary gland releasing ADH (AKA vasopressin) Encourages fluid retention no electrolytes
adrenal gland producing aldosterone (and adrenalin and noradrenaline )
Kidney reabsorb Na and water (aldosterone)
Increases BP. RAAS start and ends in kidney.
Tx of MI
Stat attention (prevent death of person & salvage myocardium)
- 02
- pain control (narcotics) →less anxiety, reduced
tachycardia→helps problem Remove obstruction via:
- Anticoagulants (prevent more platelets from
coagulating)
- Antiarrhythmics (re-establish heart rhythm gets
heart to work better) Break down clot via:
- thrombolytics (breakdown the thrombus) Revascularization interventions: (blood through the area)
- angioplasty (insert a stent)
- bypass (Sx, put a vein from the leg and attach it
around the block in the vessel)
Where does ACE come from
Lungs
How electrical impulse moves through heart
SA node, AV node, AV bundle (HIS), AV branch, PRUKINJE fibres (Ventrical)
What is endocarditis?
Inflm of of the endocardium and valves. Normally caused by bacterial infection
What are the 3 challenges for bacteria causing an infection in the heart?
1) bacteria must enter into the circulation CVS (Cardio Vascular system)
2) and must survive (your defenses must be compermised)
3) must have an adherence/adhesion surface (because the heart is smooth muscle)
What might allow bacteria to adhere in the heart. Where are they likely to grow
Sutures/ trauma/ defective valves
Likely to colonize amongst platelets and fibrin
What are the mnfts of endocarditis?
- Those of infect (local and systemic)
- Impaired heart fx
- Valvular dysfunction
- Murmur (whooshing sound)
- Distal embolization
How might you Dx and Tx endocarditis?
Dx • C&S to identify microbe (blood) • Echocardiogram Tx • Eradicate microbe (Antibiotics) • Deal with complication associate with heart dysfunction
What causes rheumatic heart disease?
Rheumatic fever
What is rheumatic fever?
Mediator? What is effected?
1) acute immune-mediated, multi system inflm disease
2) ∼ 3% incidences (5-15 year olds mostly)
3) preceded (1-4 wks) by strep infection (pharynx)
4) Abs and T cells attack strep
5) Also attack antigens in heart and joints (molecular
mimicry Auto Immune Attack
6) Also affects joints, CNS, and integument
difference between acute and chronic RHD?
inflm of valves, myocardium, pericardium The acute form is self-limiting but you must closely monitor and treat the infection otherwise death
What is the Tx for RHD?
- Penicillin or erythromycin (no infection in heart- autoimmunity and inflm)
- Decrease cardiac work load (bed rest)
- Symptomatic management (pain, swelling)
- Monitor for cardiac failure
