Cardiac Flashcards
P wave
atrial depolarization
QRS complex
ventricular depolarization and atrial repolarization; contraction of the ventricles
T wave
ventricular repolarization; ventricles return to resting state
ventricular gallop
S3
atrial gallop; rapid firing of the atria
S4
When do you hear S3?
right after S2
When do you hear S4?
right before S1
Systolic murmurs
could or could not be bad;
MR PASS MVP: mitral regurg physiologic aortic stenosis systolic mitral valve prolapse
diastolic murmurs
always bad!
MS ARD: mitral stenosis aortic regurg diastolic
stenosis
- valve is stiff and doesn’t allow blood to get through
- valve will not open all the way
- harder to get blood through
- hear murmur when the valve is open
regurgitation
- blood goes backwards
- the valve doesn’t close all the way
- it leaks when it is closed
- hear murmur when closed
location of the apical pulse
5th or 6th intercostal space at the midclavicular line
Problem with jugular vein distention
right sided HF
bruit in the carotid artery
send to the ER- stroke is imminent
small or weak pulse
hypovolemia, HF, poor circulation
large, bounding pulse
heart block, fever, anemia, compensatory, or lack of O2, hyperthyroidism
bisferiense
double systolic peak in pulse
from aortic regurg, combined aortic stenosis and regurg, or hypertrophic cardiomyopathy
pulsus alternans
- regular rhythm but changes in amplitude
- goes with L sided HF
- should also hear S3 sound
bigeminal pulse
regular irregular rhythm
-very important bc its tells us if someone is having a PVC (premature ventricular contraction)
paradoxical pulse/ pulsus paradox
decreases in strength with inspiration, gets strong with expiration;
- on inspiration, R heart fills with extra blood, then L ventricle is compressed and cannot accept much blood; L ventricle cannot pump much blood on the next heartbeat- systolic pressyre decreases
- COPD or cardiac tamponade
- need thoracentesis STAT
hemostasis
stoppage of blood flow in 5 stages:
1) vessel spasm
2) formation of the platelet plug
3) development of a blood clot
4) clot retraction
5) clot dissolution
normal platelets
150,000-450,000
reasons someone would have thrombocytopenia
Leukemia
HIV
bone marrow disfunction
signs of thrombocytopenia
platelets less than 100,000
petechiae
thrombocytopathia
impaired platelet function
-most commonly from aspirin, NSAIDs, and Von Willobrand
antibody buildup to platelets
-how to treat
ITP- Immune Thrombocytic Pepura
-treat with platelets and steroids to drecrease antibodies that are trying to attack them
COX-1
catalyzes production of thromboxame A2
effects platelets
COX-2
catalyzes production of prostacycline
effects pain and inflammation
Effect of Von Willebrand disease on the platelets
decreased platelet adhesion
DIC
- disseminated intravascular coagulation
- ultimate outcome is bleeding
hemolytic anemia
premature destruction of RBCs; when RBC destruction occurs in the bood
-if there’s too much Hg in the blood, free Hb causes hemoglobinemia and you turn red; excreted Hg in the urine causes urine to be darker in color (hemoglobinuria
why is malaria called “black water fever”
the urine turns so dark from the blood cells bursting intravascularly
RBCs are made in the ___ and destroyed in the ___
bone marrow; spleen
erythropoietin is made in the ___; its function is ___
kidneys, and it stimunates the bone marrow to produce RBCs
how much blood can we loose without symptoms in slow blood loss?
50%
iron deficient anemia
hypochromic and microcytic
megaalobloastic anemia
big cells- people with vitamin b12 deficiency
- if you’re born with it, its pernicious anemia
- most common reason is alcoholism- look at the mean corpuscular volume
what helps sickled cells move along better
fluids
G6PD deficiency
Glucose-6-phosphate dehydrogenase is a RBC ezyme whose function is to protect hemoglobin from oxidation
-deficiency is inherited and leads to hemolytic anemia
Thalassemias
inherited diseases that cause anemia; deficiency in Hb due to decreased synthesis of the effective chain and increased synthesis of the ineffective chain
Alpha thalassemia
defective alpha chain
- 1 to 4 defective genes
- could effect fetus or adult
- most common in asians
Beta thalassemia
beta- defective gene
- > 100 different mutations
- only effects adults
- major type needs regular blood transfusions because of too much iron- give Desperol that will bind to iron or bleed them
aplastic anemia
bone marrow depression; stops the bone marrow from functioning at all- need bone marrow transplant
iron deficiency anemia
blood loss or deficient diet low Hg and hematocrit hypocromic and microcytic erythrocytes Poikilocytosis (irregular shape)- oblong Anisocytosis (irregular size)- microcytic
Polycythemia
increased RBC count and hematocrit >50%
-person would look red
relative polycythemia
loss of plasma colume
absolute polycythemia
increased red cell mass
primary neoplastic polycythemia
making too many RBCs, treated by phlebotomy (remove a lot fo the cells about every 4 months)
Why worry about too many RBCs?
cardiac output- too many RBCs increases resistance and decreases afterload
can you have polycythemia and shock? why?
yes. you usually do bc you’re losing volume but maybe not cells- most commonly in distributive shock
all types of polycythemia can be caused by….
high altitude, chronic lung disease, smoking
LDL transports cholesterol from ____ to ___
the liver to the cells
HDL transports cholesterol from ____ to ____
the cells to the liver
atherosclerosis
LDLs are oxidized and deposited and become plaque
unstable plaques
have thin, fibrous caps
- plaques can rupture —> clot forms
- may completely block the artery
- may break free and become an embolus
PAD (peripheral arterial disease
atherosclerotic blockages of the large arteries in the peripheries
-lots of amputations with PAD
thromboangitis obliterans (Buerger disease)
nonatherosclerotic inflammation and thrombosis
-small and medium sized arteries and veins
Raynauds
intense vasospasms
aneurysm
wall of the vessel stretches and weakens
true aneurysm
wall is weak but intact
false aneurysm
there is a tear in the artery and the aneuysm is actually a tear and clot that forms
berry aneurism
dilation of bifurcation
-happens in the circle of willis- you have a stroke and possibly death
fusiform aneurism
has to do with the shape
-involves the entire circumference of the cessels
dissecting aneurysm
nearly always fatal because blood is just pouring out
pulse pressure
systolic-diastolic
- normal is 30 to 40
- if pressure is higher, the heart is working much harder
lower or more narrow PP
decreased stroke volume and CO
higher or wider PP
increased stroke volume or CO
-can be from stiff arteries, aortic regurg, pregnancy, increased cranial pressure
mean arterial pressure
1/3 systolic + 2/3 diastolic
- mean arterial pressure of 120/80 is 93
- normal is 70-105
cardiac output
HR x stroke volume
- stroke colume- 1cc/kh… about 70 avg
- normal CO is about 5 liters/min
blood pressure
CO x peripheral resistance
hypertensive urgency
high BP , but not to 180/120… no organ damage
hypertensive emergency
BP greater than 180/20… organ damage
Preeclampsia
HT after 20 weeks, proteinuria, and PT 140/90
- seizures from eclampsia lead to death
- deliver is the only safe cure
proteinuria
protein spilling into urine
gestational hypertension
BP 140/90, no proteinuria
worried about preeclampsia being developed
enzyme that points to MI
elevated troponin
acute coronary syndrome (ACS)
- ECG changes- T-wave inversion (different from MI, which has abnormal Q wave)
- troponin released from necrotic cells
acute myocardial infarction
chest pain, sympathic response (GI upset, tachy, vasoconstriction, anxiety, doom), hypotension, shock
widow maker
having an dMI in the lateral ascending artery, which supplies blood to the septum of the heart
chronic ischemic heart disease
imbalance in the blood supply and the hearts demand for oxygen
- less blood- atherosclerosis and vasospasm
- higher O2 demand- stress, cold, exercise
chronic stable angina
- pain when the heart’s oxygen demand rises
- you’re fine unless you run to your car
- treat with rest and nitro
silent myocardial ischemia
myocardial ischemia without pain
variant/ vasospastic angina
- pain when coronary arteries spasm
- usually occurs at rest
- when pt says “i woke up with pain in my chest”
which side of the heart is failing with pitting edema
Right
which side of the heart is failing with paroxysmal nocturnal dyspnea
left- mitral stenosis
which side of the heart is failing with congested liver
right
which side of the heart is failing with distended jugular vein
right
which side of the heart is failing with productive cough with frothy, pink sputum
Left
pericarditis manifestations
inflammation of the pericardium:
- pain and exudate and subsequent restriction of the heart’s movement
- pain when pt moves position
- ECG changes
- FEVER (different from MI)
- cough
serous exudate in pericarditis
cardiac tamponade: rapid accumulation of exudate compresses the heart
fibrous exudate in pericarditis
causes friction rub; adhesions
-sounds like rubbing fingers up to your ear
pericardial effusion
serous exudate filling the pericardial cavity
–>restricts the heart’s expansion
–>L ventricle cannot accept enough blood
–>decrease CO
–>decreased BP and shock
OR
–>R ventricle cannot accept enough blood
–>increased venous pressure
–>jugular distension
constrictive paricarditis
fibrous scar tissue making the pericardium stick to the heart
cardiomyopaty
chronic disease of the heart muscle
hypertrophic cardiomyopathy
genetic; defects in contractile proteins make cells too weak
- cells hypertrophy to do the same amt of work as other cells
- needs more oxygen and performs less effeiciently
- sudden death of many young athletes
- tell if your kid has it if their PMI is in the 6th or 7th intercostal space instead of 4th or 5th
arrhythmogenic cardiomyopathy
genetic;
causes right ventricular tachycardia
dilated cardiomyopathy
genetic and aquired;
most common cause of HF and heart transplant;
big, floppy heart, walls are not very muscular and very poor pump
restrictive cardiomyopathy
genetic and acquired;
heart becomes stiff
radiation and tumors
myocarditis
acquired cadiomyopathy;
inflammation of the heart
peripardum cardiomyopathy
acquired;
1 month before or after giving birth; at risk if older when giving birth or if taking supplements to get pregnant
takotsubo
acquired cardiomyopathy; caused by stress, often seen in women;
ventricle balloons out
shunt
opening or connection that lets blood move from one side of the circulation to the other
ductus venosus
lets blood flow from the visceral veins to the vena cava, bypassing the liver;
left to right
foramen ovale
lets blood flow from the right atrium to the left atrium bypassing the lungs;
right to left
ductus arteriosus
lets blood flow from the pulmonary trunk to the aorta to bypass the lungs;
right to left
in left to right shunts…
less blood goes to the body
more blood goes to the lungs
in right to left shunts…
deoxygenated blood goes to the body
less blood to the lungs
arterial septal defects
blood will flow from high to low pressure;
left to right
ventricular septal defects
blood will flow from high to low pressure;
left to right
pulmonary stenosis
increased right sided pressure bc blood can’t get out of the pulmonary valve
coarctation of the aorta
narrowing of the aorta;
- symptomatic is L sided HF
- BP is high in arms and low in legs
- causes intermittent claudication (low blood supply to lets and feet, causing them to be painful and cold, esp when exercising)
frank starling
if the CO goes down the body with compensate- good for a moment, but bad long term
ejection fraction
net volume of blood per beat
- divide stroke volume by the end diastolic volume
- normal is about half the blood in the ventricle… need at least half to get out or you have HF
- systolic measure
chain stoke breathing
start with shallow breaths and get deeper and deeper, then shallow, then no breathing, and over again
manifestations of HF
- dependent edema and ascites
- anorexia, GI distress, weight loss
- impaired liver function
- activity intolerance and signs of decreased tissue perfusion
- cyanosis and signs of hypoxia
- cough with frothy sputum
- orthopnea
- parolysmal nocturnal dyspnea
manifestations of left sided HF
body lacks blood
lungs fill with blood (pulmonary edema)
manifestations of right sided HF
body fills with blood
lungs do not oxygenate enough blood
hypovolemic shock
most common kind of shock;
- acute blood loss volume (15%)
- anything than causes fluid loss
- huge sympathetic trigger
- if we lose more than 40% of volume- death
cardiogenic shock
heart fails to pump blood adequately
- bc of MI, sustained arrhythmias, cardiac surgeries
- “normal volume shock”
- decreased CO lowers BP
- sympathetic response, but vasoconstriction increases resistance causing increase work on the heart, furthering HF
distributive or vasodilatory shock
blood vessels dilate- massive dilation= loss of tone
- loss of tone from neurogenic shock or nanphylaxis (all fluid goes to the skin)
- not enough blood to fill the circulatory system
- blood flow decreases
- less blood is returned to the heart
- less blood is circulated to the body
- if you don’t have a changein BP after fluids, you’re going to die
septic shock
infection gets into blood stream
- fever… **key to sepsis
- increased HR
- hypotension
- hypoxia
- increased WBCs
- – give antibiotics
do this with all types of shock except cardiogenic
give fluids
5 major complications of shock
- acute respiratory distress syndrome
- acute kidney injury
- GI complications
- Disseminated Intravascular Coagulation (DIC)
- Multiple Organ Dysfunction Syndrome
