Cardiology (Exam 2) Flashcards
Functions of CV System
Delivery and removal of substances
Right Heart
Pulmonary circulation
Pumps blood through lungs
Left Heart
Systemic circulation
Pumps blood through body
Flow of blood
Artery –> arteriole –> capillary –> venule –> vein
Major difference between veins and arteries
Arteries have much thicker tunica media to tolerate higher forces of pressure
Hypertension
Damages blood vessels
Hypertension is usually…?
Asymptomatic until organ damage occurs
Systole
Heart contraction
Diastole
Heart relaxation
Normal Blood Pressure
<120/<80
Blood pressure
Cardiac output x peripheral resistance
Cardiac output
Amount of blood the heart pumps per minute
Alpha1 Receptors
Vasoconstriction
Beta1 Receptors
Vasodilation
Vasodilator Hormones
Prostacylin
Natriuretic peptides
Nitric oxide
Vasoconstrictor Hormones (2)
Angiotensin II
Vasopressin
Blood Viscosity
Increase in RBCs increases viscosity
Blood Volume
RAAS activation increases blood volume
ACE
Converts angiotensin I to angiotensin II
found in lungs
ADH
Antidiuretic Hormone
Vasopressin
Renin
Converts angiotensinogen to angiotensin I
Release of ADH
Leads to water reabsorption and increase in blood volume
Release of aldosterone
Reabsorption of NaCl and water, excretion of K+ –> increased blood volume
Renin release is increased by (2)
Activation of renal beta1 receptors
Decrease in renal perfusion
Primary Hypertension
no single identifiable cause
Genetic or environmental factors
Secondary Hypertension
Specific medical condition
arteries have
low volume and high pressure
veins have
high volume and low pressure
purpose of muscle pumps and valves in veins
to keep blood flow in the correct direction
the most common cardiovascular disease
hypertension
renin release is increased by
activation of beta 1 receptors
decrease in renal perfusion
hypertension is associated with
an increased peripheral resistance of the arterial system
4 factors that may contribute to hypertension
over activation of RAAS
over activation of the sympathetic nervous system
vascular endothelial dysfunction
sodium retention
overactivation of the sympathetic nervous system
E/NE released from sympathetic neurons and adrenal medulla will activate beta 1 receptors in the heart, kidneys or alpha 1 in the arteries
vascular endothelial dysfunction
damage to blood vessels and impaired vascular relaxation
biggest factor for HTN
sodium retention leads to
increased blood volume
organs most effected from hypertension
eyes
heart
kidneys
brain
damage of HTN on the brain
ischemic or hemorrhagic stoke
damage of HTN on the kidneys
chronic kidney disease
damage of HTN on the heart
heart failure, arrhythmia, myocardial infarction
damage of HTN on the eyes
retinopathy
dyslipidemia
abnormal blood lipid levels
hyperlipidemia
increased blood lipid levels
patients with dyslipidemia are initially
asymptomatic
dyslipidemia can lead to
atherosclerosis
atherosclerosis
disease of arterial system characterized by fatty plaques within vasculature
plaques lead to stenosis then ischemia
what is a major contributor to atherosclerosis
elevated LDL
atherosclerotic cardiovascular disease (ASCVD) includes
cerebrovascular disease
peripheral artery disease
coronary artery disease
cerebrovascular disease
plaques in cerebral vasculature
can lead to ischemic stroke or transient ischemic attack
peripheral artery disease
plaques in peripheral arteries (lower limbs) reducing blood flow and oxygen supply
coronary artery disease (ischemic heart disease)
plaques in coronary arteries
can lead to myocardial infarction
familial hypercholesterolemia
most common genetic disorder leading to dyslipidemia
autosomal dominant disorder, mutations of uptake of LDL by the liver, leading to more in the blood
which form of familial hypercholesterolemia is more severe?
homozygous
lipoproteins
lipid protein complexes
made up of triglycerides, cholesterol, phospholipids and proteins
lipoproteins are classified by
what protein they contain
Apo-B containing lipoprotein
chylomicrons
VLDL, IDL, and LDL
Apo-A1 containing lipoprotein
HDL (tissues to liver)
chylomicrons
transports dietary TH and cholesterol from intestines to tissues
three cholesterol pathways
exogenous
endogenous
reverse
exogenous cholesterol pathway
cholesterol from the diet is digested and absorbed in GI tract
endogenous cholesterol pathway
cholesterol synthesized in the liver
LDL transports cholesterol to tissues and excess LDL is taken up by vasculature or returned to liver for reuptake
reverse cholesterol pathway
removal by HDL and degradation of cholesterol by bile
pathophysiology of atherosclerosis
in liver cells
cholesterol and triglycerides packaged into VLDL particles –> exported to blood –> converted to IDL–> LDL
hypertriglyceridemia
dyslipidemia that is caused by a number of drugs or conditions
elevated TG associated with increased CV risk
extreme elevations of hypertriglycedemia can lead to
acute pancreatitis
patho of acute pancreatitis
excessive breakdown of TG into free fatty acids –> toxicity and inflammatory response
symptoms of acute pancreatitis
persistent severe epigastric abdominal pain, nausea, and vomiting
symptoms of peripheral artery disease
skin loses integrity, pain in the affected area
may be asymptomatic
intermittent claudication (PAD)
pain caused by ischemia to the limbs
usually during exercise, resolved at rest
pain at rest = severe PAD
main symtptom of ischemic heart disease
angina (chest pain due to inadequate supply of oxygen)
stable ischemic heart disease
stable angina
occurs in a predictable manner and lasts a short time
gradual stenosis over time
acute coronary syndrome
acte obstruction in blood flow to the heart
due to plaque rupture followed by thrombus formation
can lead to heart attack
types of acute coronary syndrome
unstable angina
non-ST elevation myocardial infarction
ST elevation myocardial infarction
infarction
death of tissue
unstable angina
markers not present
ST segment not elevated
NSTEMI
markers present
ST segment not elevated
STEMI
markers present
ST segment elevated
most severe acute coronary syndrome
STEMI = complete blockage
after MI, what forms and what is different about it?
scar tissue
can’t contract and relax like healthy tissue
2 cardiac markers
creatine phosphokinase MB
Troponins (cardiac troponin 1)
heart failure
cardiomyopathy
heart is unable to pump enough blood to meet the metabolic demands of the body
heart failure =
a reduction in cardiac output
heart failure typically refers to
left side heart failure
systolic heart failure
heart failure with reduced ejection fraction
diastolic heart failure
heart failure with preserved ejection fraction
CV symptoms of heart failure
tachycardia
peripheral edema and ascites (swelling in abdomen)
pulmonary symptoms of heart failure
pulmonary edema (fluid in lungs)
dyspnea (difficulty breathing)
cough
other symptoms of heart failure
sudden weight gain
fatigue
preload
pressure within the ventricle or stretching of the myocytes at the end of diastole
afterload
resistance to ejection of blood from the ventricle
contractility
force of contraction
cardiac output =
stroke volume x heart rate
heart rate is primarily dependent on the
autonomic nervous system
preload is dependent on
venous return
venous return is dependent on
fluid volume and venous tone
after load is dependent on
arterial tone (BV diameter)
contractility is dependent on
ANS, Ca2+ and preload
HFpEF (diastolic HF)
heart is unable to fill normally
associated with stiffening myocardium
HFrEF (systolic HF)
heart is unable to contract normally
associated with dilation of heart chambers (ventricles)
what helps us classify heart failure?
ejection faction (EF) = stoke volume/ end diastolic volume
Hypertension pathophysiology
increase in after load –> stress on myocardium -> ventricle walls thicken/dilate –> inefficient pumping
ischemic heart diseases pathophysiology
reduced blood flow to myocardium over time –> ischemia/angina and weakening of myocardium (thin walls)
most common cause of heart failure
myocardial infarction
conditions that can lead to HF
abnormal heart valves or congenital heart defects
cardiotoxic medications (ex: chemotherapies)
other conditions (ex: diabetes)
compensatory mechanisms activated to increase cardiac output
activation of RAAS
activation of SNS
activation of RAAS and SNS –> cardiac remodeling
activation of RAAS
increases blood volume –> increases preload –> increases stroke volume
problem of activation of RAAS
causes edema and increases afterload
activation of SNS
activation of beta1 on the heart –> increases HR and contractility
problem with activation of SNS
increases after load and workload of the heart
activation of RAAS and SNS –> cardiac remodeling
cardiac hypertrophy to increase contractility
problem of activation of RAAS and SNS –> cardiac remodeling
scarring and tissue damage which impairs cardiac function
compensatory mechanisms can help maintain cardiac output initially but
overtime lead to worsening of heart failure
acute decompensated HF
sudden worsening of HF, leads to need for hospitalization
ADHF occurs due to
- excessive fluid overload –> severe dyspnea
- excessive reduction in cardiac output –> hypotension
patients with ADHF are categorized by
tissue perfusion and fluid status
tissue perfusion
warm = stable
cold = hypoperfusion
fluid volume
dry = stable
wet = fluid overload
fluid status is measured by
pulmonary capillary wedge pressure
perfusion Status is measured by
cardiac index
cardiac index
cardiac output/ body surface area
arrythmia
disturbance of electrical signals in the heart leadings to an irregular rate or rhythm
arrhythmia can occur due to
damage/structural change, electrolyte alteration or drugs that alter cardiac function
symptoms of arrhythmia
palpitations, lightheadedness, syncope, fatigue, cardiac arrest
arrhythmias range from
asymptomatic to life-threatening
arrhythmias can be classified by
where they originate, how they affect heart rate and type of impulse abnormaility
cardiac conduction system
pacemaker cells generate action potential without input from the nervous system
sinoatrial node
primary pacemaker of the heart
atrioventricular node
spontaneously generates 40-60 action potentials per minute
If SA node fails,
AV node can take over
heart block
failure in the normal propagation of action potentials from atrium to ventricle
heart block results in
bradycardia or skipped beats
reentry (accessory pathway)
impulse reenters and excites areas of the heart more than once due to dysfunction of the refractory period
atrial fibrillation
most common type of arrhythmia
unpredictable
complications of chronic A-fib
stoke and heart failure
ventricular fibrillation
electrical signals fire from multiple locations in the ventricular leading to inability of the ventricles to pump properly
ventricular fibrillation is
life threatening and a form of cardiac arrest
shock
CV system fails to refuse the tissues adequately resulting in widespread impairment of cellular metabolism
shock leads to
organ failure and death
types of shock
hypovolemic shock
cariogenic shock
distributive shock
hypovolemic shock
low fluid volume
cardiogenic shock
damage or dysfunction of the heart
unable to pump blood forward
distributive shock
leaky blood vessels and excessive vasodilation
examples of distributive shock
septic shock, anaphylactic shock and neurogenic shock
pathophysiology of arryhthmias
due to damage or structural change in cardiac tissue, electrolyte alteration or drugs that alter cardiac function
most arrhythmias are
tachyarrythmias
if another tissue spontaneously depolarizes more frequently than the SA node,
it controls heart rate and rhythm
atypical automaticity (ectopic pacemaker)
group of cardiac cells that gain automaticity and begin spontaneously depolarizing
