cardiovascular disorders Flashcards
hyperlipidemia
elevated lipid content in the blood
cholesterol, triglycerides, phospholipids
what is a apoprotein
a protein that transports lipids
what is a lipoprotein
a apoprotein + a lipid
lipoproteins are named based on
density
low density lipid, high density lipid
what is a chylomicron
lipoproteins that transfer lipids from the digestive tract into circulation
where does atherosclerosis usually occur
highest frequency sites
in the larger arteries
- abdominal aorta
- coronary arteries + carotid arteries
- thoracic aorta, femoral + popliteal arteries
- vertebral, basilar, cerebral arteries
what is an atheroma
a lesion in the intima of the vessel made of lipids and fibrous tissue
what happens as an atheroma forms
the atheroma bulges into the lumen (area of least resistance because it is fluid filled)
obstructs the lumen
what is the progression of an atheroma lesion
- fatty streak
- fibrous atheromatous plaque
- complicated lesion
what is a fatty streak made of
cells
macrophages, foam cells, smooth muscle cells
what is fibrous atheromatous plaque
a lesion made of swelling comprised of fibers
accumulation of lipids, scar tissue, calcification
what is a complicated lesion
hemorrhaging into the plaque
pathogenesis of atherosclerosis stages
- endothelial cell injury (subtle changes - inflm)
- migration of monocytes (monocytes bind/migrate into intima - become macrophages)
- lipid accumulation + s.m. cell proliferation (clot + bulge forms in lumen)
- plaque (atheroma forms = atherosclerotic plaque)
an elevated CRP without underlying inflm indicates
atherosclerosis
4 control mechanisms of BP
- baroreceptors (detect pressure change)
- volume regulation (via kidneys)
- vascular autoregulation (vasoconstriction/dilation)
- RAAS (ADH, aldosterone)
HTN follows what cycle
circadian rhythm
when is BP lowest and highest
lowest = 2-5am highest = first thing in the morning
primary HTN
- 90% cases
- idiopathic - can’t eradicate, just manage
- multifactorial (problem w/ several regulatory mechanisms)
systolic HTN
- systolic > 140, diastolic < 90
- mostly after age 50
- poor vessel compliance - decreased elasticity - increased systolic pressure
- could be d/t atherosclerosis
- heart will compensate (harder+faster) - causes increased CO
secondary HTN
- 5-10%
- renovascular = arteries supplying kidneys occluded
- poor renal perfusion activates RAAS, increases BP systemically
malignant HTN
- diastolic > 120
- emergency situation
manifestations of HTN
- BP may be high unknowingly
- AM headaches
- palpitations
- dizziness, fatigue, blurred vision
- organ failure (kidney, heart, brain)
treatment of HTN
- Lifestyle modification
- DASH diet
- smoking and alcohol cessation
- exercise - 1st line drug = diuretic
- 2nd line drug = add 1/more
- Ca channel blocker (decrease s.m. contraction)
- angiotensin II receptor blocker
- ACE inhibitor
what are the types of peripheral vascular disease
- acute arterial occlusion
- atherosclerotic occlusive disease
what is an acute arterial occlusion caused by
an embolus or thrombus that disrupts perfusion
what is an embolus
something that lodges in a vessel (air, clot, malignant cells)
what is a thrombus
a stationary blood clot
manifestations of acute arterial occlusion
- pain
- pallor
- pistol
- pulselessness
- polar
- paresthesia
- paralysis
diagnosis of acute arterial occlusion
- blood flow assessment
- physical exam
treatment of acute arterial occlusion
- surgery (remove clot)
- thrombolytics (dissolve clot)
- anticoagulants (prevention)
atherosclerotic occlusive disease
- same process as atherosclerosis but occurs mostly in peripheral vessels (femoral + popliteal arteries)
- common in diabetics and elderly
- perfusion is impaired d/t occlusion
- causes inadequate venous return… complications
why does diabetes cause atherosclerotic occlusive disease
diabetes causes vascular damage - causes atherosclerosis
how does the body compensate for atherosclerotic occlusive disease
- vasodilation
- anaerobic metabolism (d/t hypoxic tissue)
- collateralization
manifestations of atherosclerotic occlusive disease
- intermittent claudication
- complications (ulcers, loss of fx)
diagnosis of atherosclerotic occlusive disease
- blood flow assessment
- physical exam
treatment of atherosclerotic occlusive disease
- no clot present - must address manifestations
know complications, prevent, treat
what is an aneurysm
a localized bulge in an artery d/t degenerative change in the vessel wall
(permanent change)
most common arteries for aneurysms
femoral, iliac, popliteal arteries
highest pressure vessels, likely for aneurysms
thoracic, abdominal aorta
risks for aneurysm
- atherosclerosis
- uncontrolled HTN
- congenital defects (weakened vessel walls)
- aging
what is a true aneurysm
vessel wall is intact
50% increase in vessel diameter
what is a false aneurysm
vessel wall is compromised
supported by external structures
what are the types of aneurysms
true
false
what are the forms of aneurysms
fusiform (bilateral)
saccular (unilateral)
dissecting (in vessel walls)
a berry aneurysm is what form of aneurysm
saccular
complications of aneurysms
- rupture (brain=stroke, aorta=death)
- pressure on adjacent structures
- distal embolization (pooling=thrombus -> dislodges)
treatment of aneurysms
- surgery to prevent complications
what is coronary artery disease
one or more branches of the coronary circuit has advanced atherosclerosis
atherosclerosis in the coronary circuit leads to what
ischemia = MI
what are the types of coronary artery disease
- acute coronary syndromes
- chronic ischemic heart disease
characteristics of arteries where aneurysms occur
arteries that:
- bifurcate
- bend
- is not supported externally
acute coronary syndromes result in
- unstable angina
- MI
chronic ischemic heart disease results in
- stable angina
- variant angina
- microvascular angina
- silent myocardial ischemia
what is microvascular angina
occlusion in smaller branches of the coronary circuit = less pressing
called cardiac syndrome X
what is silent myocardial ischemia
myocardial ischemia with no manifestations
what is angina pectoris
chest pain d/t myocardial ischemia
is a manifestation of CAD
what is angina pectoris caused by
- atherosclerosis
- vasospasm
- thrombus
- hemorrhage
how does angina pectoris occur
inadequate perfusion d/t atherosclerosis = ischemia = chest pain
why can’t atherosclerotic vessels dilate
b/c they are already compensating by vasodilating and are at max. dilation
manifestations of angina pectoris
chest pain
types of angina
- stable angina
- unstable angina
- variant/vasospastic/prinzmetals angina
what is stable angina
- fixed plaque w/in the wall of the vessel protrudes into the lumen = partial occlusion
when does pain from stable angina occur
during exertion
= transient pain
what is transient pain
eliminating the trigger makes the pain subside
triggers for stable angina
- physical exertion
- emotional stress
- cold
what is variant angina
spasm of an artery in the coronary circuit
when does pain from variant angina occur
any time; at rest, nocturnal
what causes variant angina
- endothelial dysfunction
- inadequate handling of Ca ions by s.m. cells (intake/output is irregular = spasms)
- hyperactive SNS (stimulation of vessel walls)
- nitric oxide (low concentration = vasoconstriction)
management of variant angina
is difficult because it cannot be triggered
challenges of diagnosing variant angina
ECG must be done during episode (which can’t be triggered)
what is unstable angina
- unstable plaque/atheroma ruptures a vessel wall into the lumen causing bleeding into the wall
- atheroma leaks fibrin, cellular debris = attracts platelets
- thrombus forms in the lumen => occlusion
- platelets release prostaglandins = constriction
===> occlusion + constriction
when does pain from unstable angina occur
any time; is prolonged, severe, can’t withdraw trigger
manifestations of unstable angina
- transient and mild-severe chest pain
- squeezing/burning pain
- pain may radiate to left shoulder/arm, neck, jaw
treatment of unstable angina
- rest, cease activity
- nitroglycerine (nitric oxide = vasodilator)
- prevention (avoid triggers that will lead to MI)
- cease smoking
what is myocardial infarction
an end point/result of CAD
% of MI: STEMI vs NSTEMI
70% STEMI
30% NSTEMI
what is a STEMI
complete occlusion of a larger vessel
what is a NSTEMI
partial occlusion of a distal vessel
primary vessels affected by MI
- R coronary artery
- L coronary descending artery
- L circumflex artery
where does the R coronary artery feed
R atrium + R ventricle
where does the L coronary descending artery feed
R ventricle + L ventricle + interventricular septum
where does the L circumflex artery feed
L atrium + L ventricle
causes of MI
- atherosclerosis
- coronary artery spasms
- hemorrhage
patho of MI
- atherosclerosis = ischemia = hypoxia = anaerobic metablism = metabolic acidosis = arrhythmias = infarction
why does metabolic acidosis cause arrhythmias
decreased oxygen affects conduction
how does arrhythmia affect cardiac output
makes filling/emptying of atria/ventricles off balance
what affects the extent of infarction
- affected vessel (proximal vs distal)
- degree of occlusion (partial vs complete)
- duration of ischemia
- cardiac status (rest/exercise)
- HR, BP, rhythm
- collateral vessels
types of infarcts
- transmural
- subendocardial
what is a transmural infarct
- result of proximal occlusion of an artery
- the entire ventricle wall is affected
- STEMI
what is a subendocardial infarct
- result of distal occlusion
- partial ventricle wall affected (inner 1/2 - 2/3)
- NSTEMI
a STEMI will result in what on an ECG
ST elevation
a NSTEMI will result in what on an ECG
ST depression
manifestations of MI
- crushing chest pain (acute, severe, radiating)
- tachycardia (d/t hypoxia)
- n+v
- anxiety/stress
- dyspnea, dizziness, diaphoresis, palpitations
diagnosis of MI
- ECG
- angiogram
- serum markers (troponin I&T, myoglobin, CKmb)
no R wave indicates what
ventricles are not contracting
treatment of MI
stabilization: - thrombolytics - anticoagulants - anti-arrhythmics - morphine - oxygen post stabilization: - IV diuretic (dec. workload) - vasodilator - inotrope - revascularization surgery (angioplasty, bypass)
what is cardiomyopathy
defective cardiac muscle
3 types of cardiomyopathy
- hypertrophic
- dilated
- restrictive
hypertrophic cardiomyopathy
- thickened septum; obstruction of aorta
- outflow obstruction = dec. CO
- left ventricle hypertrophy = dec. ventricle size = dec. CO
cause of hypertrophic cardiomyopathy
- 50% autosomal dominant
- 50% idiopathic
manifestations of hypertrophic cardiomyopathy
90% asymptomatic
- dyspnea
- angina
- syncope
- palpitations
treatment of hypertrophic cardiomyopathy
- negative inotrope (dec. workload)
- surgery (remove obstruction)
- chemical ablation
dilated cardiomyopathy
ventricle enlargement (d/t loss of elasticity) = congestion = blood pools
causes of dilated cardiomyopathy
- genetic
- viral infection
- alcohol abuse
- chemo drugs
manifestations of dilated cardiomyopathy
- decreased ejection fraction
- cardiac failure
treatment of dilated cardiomyopathy
- decrease cardiac workload (diuretics, beta blockers)
- symptom management
restrictive cardiomyopathy
- worst type, but rare
rigid vessel walls (d/t dec. elasticity) = incomplete filling = decreased CO
what is a typical SA node rhythm
70 bpm
tachycardia rhythm is
> 100
bradycardia rhythm is
< 60
problems happen with the conducting system when
multiple areas attempt to control the pace
what is an arrhythmia
abnormal impulse conduction/generation that alters HR and/or rhythm
=> disrupts the cardiac cycle which affects CO and perfusion
causes of arrythmia
- congenital defects (ex. foramen ovale closure)
- electrolyte imbalance (especially K)
- stimulant drugs
- myocardial ischemia (reversible)
types of arrhythmia
- atrial flutter
- atrial fibrillation
- heart block
- ventricular fibrillation
atrial flutter
- regular but rapid rhythm
- SA node fires repeatedly but ventricles remain slower d/t the refractory period. As the artial rate increases, the ratio will increase
- atrial and ventricle tachycardia
- usually 2:1 ratio (300:150 bpm), could be up to 6:1
atrial fibrillation
- uncoordinated, spontaneous contractions, irregular rhythm
- atrial contractions aren’t effective - atria don’t have enough time to fill
- atrial rate = 300-600 bpm
- irregular ventricular rate = 80-180 bpm
- no distinct P wave
heart block
- migration of the electrical impulse from atria to ventricle are blocked
- not a blockage of a vessel
- 3 types: 1st, 2nd, 3rd degree
first degree heart block
delayed but regular conduction
= longer PR interval
second degree heart block
intermittent loss of conduction
some activity passes through, some doesn’t
third degree heart block
no conduction between artia and ventricle
= safety net activated => ventricles self pace (atria + ventricles are not syncronized)
= independent, regular atrial + ventricle paces
ventricular fibrillation
worst case, no contractions, heart quivers (no filling/emptying) = no CO
ECG goes flat
diagnosis of arrhythmia
ECG
treatment of arrhythmia
- defibrillation
- antiarrhythmics
- pacemaker
- ablation (part that is blocking conduction)
- cardioversion
what is cardioversion
defibrillation that is synchronised to the QRS complex
what does defibrillation do
extinguishes all existing electrical activity in the heart, allows the pace maker to take on pacing function to establish a sinus rhythm
what do valves do
ensure unidirectional flow of blood
when are atria-ventricular valves open/closed
open normally, close during ventricular contraction
when are the semilunar valves open/closed
normally closed, open during ventricular contraction
which valves are most susceptible to damage and why
the aortic and mitral valves
d/t the high pressure of the left ventricle
2 forms of damage/disease to valves
- regurgitant valve
- stenotic valve
causes of valvular disease
- trauma/inflammation
- ischemia
- aging
- congenital defects
stenotic valve
stiff valve
causes narrowing which impedes flow
regurgitant valve
floppy valve
improper closure causes regurgitation
valvular diseases causes what
changes to intra-cardiac blood flow which increases the workload => persistently high workload will cause HF
treatment of valvular disease
- pharmacological (maintain fx to prevent failure)
- surgery (repair/replace valve)
non modifiable risk factors for coronary heart disease
- men > 45
- women > 55 (or postmenopausal)
- family hx CVD: women < 65, men < 55
- first nations, african, south asian
modifiable risk factors for coronary heart disease
- HTN
- smoking
- dyslipidemia (low HDL, elevated LDL)
- diabetes mellitus
- obesity
- alcohol
- low activity
target organ damage of coronary heart disease
- LV hypertrophy
- CAD
- HF
- stroke/TIA
- nephropathy
- peripheral arterial disease
what is infectious endocarditis
a bacterial infection of the endocardium and valves causing inflammation
what are the 2 requirements of bacteria during infectious endocarditis
- enter and survive the cardiovascular system
- adhere to the intra-cardiac surface
what makes it difficult for bacteria to adhere to the intra-cardiac surface
- high pressure
- smooth surface
- turbulent flow
bacterial adherence to the intra-cardiac surface leads to what
proliferation which attracts platelets which will create fibrin strands which bacteria will colonize
manifestations of infectious endocarditis
- local + systemic infection
- manifestations of impaired valve function
- heart murmur
complications of infectious endocarditis
distal embolization
diagnosis of infectious endocarditis
- history
- ECG
- C+S and other labs over 24 hours
- serology
treatment of infectious endocarditis
- antibiotics
- treat the complications
what is rheumatic fever
an immune-mediated and multi-system inflammatory disease
who is affected most by rheumatic fever
3% of children aged 5-15
rheumatic fever is what kind of genetic abnormality
complex trait:
must have strep throat + predisposition
rheumatic fever starts as what
strep throat
how does rheumatic fever cause damage
1-4 weeks after having strep throat, antibodies persist and target self-antigens in the heart, joints, CNS, and integument
= molecular mimicry
what is rheumatic heart disease
the effect rheumatic fever has on the heart
= immune-mediated inflammation of the valves, myocardium and pericardium
acute form of RHD
- self-limiting
- no intervention required
- monitor and treat symptoms
chronic form of RHD
leads to severe heart damage
manifestations of RHD
- cold/cough symptoms
- valvular dysfunction (SOBOE, weakness, fatigue, edema, chest pain)
diagnosis of RHD
- strep throat test
- CBC, CRP, ESR, serology
- echo
treatment of RHD
- penicillin, erythromycin (strep)
- anti-inflammatories
- steroids
- 4-5 weeks bed rest
- treat complications
