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Patho Mid term

Terms in this set (71)

What part of the heart has the lowest pressure?
Right atrium during relaxation
What part of the heart has the highest pressure?
Left atrium upon contraction
What two things regulate the SYSTEMIC system in terms of control of blood flow?
-Autonomic nervous system: Sympathetic nervous system [SNS]
-Venous and thoracic pumps
What regulates the LOCAL system in terms of control of blood flow?
Intrinsic auto regulatory mechanisms
-Autoregulation is the ability of blood vessels WITHIN ORGANS to maintain a relatively constant blood flow regardless of changes in arterial pressure (Regulates local tissue)
Mechanisms that cause altered blood flow
-Blood vessel obstructions

-Mechanical compression (trauma, compartment syndrome, tight casts)

-Blood vessel Structural Alterations (valvular incompetence, Arteriosclerosis/Atherosclerosis, Aneurisms..)
Thrombosis
Stationary blood clot formed within a vessel or chamber in the heart
Embolus
Material that forms a clot within the bloodstream (breaks off and travels)
Embolus leaving L VENTRICLE
= Ischemic stroke
Embolus leaving R VENTRICLE
= Pulmonary emoblism
Acute Occlusion
Absence of arterial circulation - EMERGENCY
6 P's
Pallor
Paresthesia
Paralysis
Pain
Polar
Pulselessness
Atherosclerosis
Plaque formation, hardening of blood vessel, cause possible blockage
LDL is the worst why?
Because of its size.
-The largeness makes it to where a macrophage can not engulf it and process it.
-Due to its size, it is limited in blood vessel travel.
Types of LDLs
LDL, IDL, VLDL, Chylomicron
Lipids are transported how?
Via apoproteins
HDLs transport cholesterol how?
From peripheral tissue back to the liver, clearing atheromatous plaque
Patho of Atheroclerosis
-Atherosclerotic plaque formation initiated by injury to coronary artery endothelium
-Endothelium recruits leukocytes
-LDL insulations occurs
-Oxidized lipids are damaging to endothelial and smooth muscle cells and stimulate recruitment of macrophages into the vessel
-Macrophages engulf lipids and turn into foam cells which release inflammatory mediators and growth factors attracting more leukocytes
Coronary Heart disease (CHD) includes:
-Angina pectoris
-Myocardial infarction/MI/Heart attack (most sever) [acute occlusion]
-Dysrhythmias
-Heart failure
-Sudden cardiac death
Angina Pectoris
Chest pain associated with intermittent myocardial ischemia
Three patterns of angina pectoris
-Stable or typical angina
-Prinzmetal or variant angina
-Unstable or crescendo angina
Stable angina pectoris
-Onset of ischemia is predictable with certain activities and SUBSIDES WITH REST.
-Treatment: Relieved by REST AND NITRO
-Pt is said to have Chronic Coronary Syndrome
Prinzmetal variant angina
Associated with vasospasm
Unstable or crescendo angina
-Gets worse each time
-If untreated will become an MI
CHD is associated with what?
Coronary atherosclerosis
How does ACS occur?
-Sudden obstruction of coronary blood flow results in acute myocardial ischemia
What may enhance the risk of thrombus formation?
-High fibrinogen level (as occurs with smokers)
-Enhanced platelet level adhesiveness (occurs in hyperlipidemia)
Acute coronary syndrome (ACS)
Can be either Unstable angina or MI
Unstable angina (ACS)
-Occlusion is partial or clot is dissolved before death of myocardial tissue.
Myocardial Infarction (ACS)
-Occlusion is complete and the thrombus persists long enough for development of irreversible damage to myocardial cells resulting in necrosis
Diagnosis of MI is based of what three primary indicators?
-S&S
-ECG changes
-Elevations in levels of specific biomarkers
Three things to look for in ECQ with ACS
Large Q wave
ST elevation
Inverted T wave
Which of the three ECQ changes comes first with an MI?
Large Q wave

(ST elevation and Inverted T wave comes later)
Totally ischemic Cells (MI)
-Q waves
-Increased CK-MB and Troponin I&T
-Increased HR
-Vasoconstriction
Partially ischemia Cells (Unstable Angina)
-ST changes on ECG
-Dysrhythmias
-Increased HR
-Vasoconstriction
STEMI diagnosis
ST Elevation
+ Biomarkers (CK-MB and Troponin I&T)
NSTEMI diagnosis
No ST elevation
+ Biomarkers
Unstable angina diagnosis
No ST elevation
- (No) Biomarkers
Compensatory systems for decreased Cardiac Output from MI
-Short term is SNS (Increased HR, contractility, vasoconstriction)
-Long term is RAAS (fluid retention)
SUDDEN CARDIAC DEATH
V-Fib is primary cause
Occurs in younger people, not old people
Karotkoff sounds are what?
thumping sounds you hear when osculating a blood pressure
Atrial Natruretic peptides (ANP)
Causes kidneys to increase sodium and water excretion by increasing glomerular filtration rate.
What does an MI do to the ANP?
ANP goes down to increase Cardiac Output
What does heart failure do to ANP?
ANP goes up to get rid of excess fluid and sodium retention
Does vasoconstriction occur in Angiotensin I or Angiotensin II?
Angiotensin II
ACE inhibitors stop what?
Angiotensin I from converting to Angiotensin II. To cause more water excretion instead of retention.
(ACE INHIBITORS ARE DIURETICS)
Does family history play a role in HTN?
Yes it's a risk factor
Primary HTN
-Idiopathic disorder (unknown cause)
-Most common form of hypertension
Normal BP
Prehypertension
Stage 1 Hypertension
Stage 2 Hypertension
SBP:
<120
120-139
140-159
>or equal 160

DBP:
<80
80-89
90-99
> or equal 100
What is a major risk factor that can lead to a hypertrophic heart and eventually heart failure?
High Systolic blood pressure
IRON DEFICIENCY ANEMIA -> SNS TRIGGERED -> VASOCONSTRICTION -> HTN
(SNS and vasoconstriction occurs because of lack of oxygen and to increase CO)
IRON DEFICIENCY ANEMIA -> SNS TRIGGERED -> VASOCONSTRICTION -> HTN
(SNS and vasoconstriction occurs because of lack of oxygen and to increase CO)
END ORGAN DAMAGE caused by Primary HTN
-Glomerular damage results in kidney failure
-Affects microcirculation of the eyes
-Increased pressure in cerebral vasculature can result in hemorrhage
First and most important prevention and treatment strategy for HTN
Lifestyle modification
Heart failure
Insufficient C.O. over long period of time
-Results from impaired ability of myocardial fibers to contract, relax, or both
Most common cause of Heart failure
Myocardial Ischmia, followed by HTN and dilated cardiomyopathy
Left sided HF
-Low C.O.
-Pulmonary edema/congestion
-Hypoxia
Right sided HF
-Low C.O.
-Superior and inferior vena cava congestion
-Systemic edema
Systolic dysfunction of HF
MI is common dysfunction
-Reduced contractility evidenced by low ejection fraction and reduced isotropy (decreased sympathetic "tone") during ventricular systole
Diastolic dysfunction of HF
Ischemic heart disease and HTN are two main causes
-Disorder of myocardial relaxation such that the ventricle is excessively noncompliant and does not fill effectively
Compensatory mechanisms and remodeling of Heart due to heart failure
OVER LONG TERM THESE ARE DETRIMENTAL TO THE HEART

-SNS Activation
-Increased preload (pressure on left ventricle)
-Myocardial hypertrophy
What are the 3 responses to HF?
Baroreception response
RAS activation, decreased GFR
Increased ventricular wall tension

(All of these are good initially for HF but long term they will damage the system when activated with HF)
Where is HF in the heart most common?
Left ventricle HF because of the highest pressure on it
Forward failure
Insufficient cardiac pumping manifested by poor CO
Backward failure
Congestion of blood behind the pumping chamber
Left sided heart failure
Backwards effect: pulmonary congestion and edema

Forward effect: insufficient CO with diminished delivery of oxygen and nutrients to peripheral tissues and organs
Right sided heart failure
Increased pulmonary vascular resistance

Causes right ventricular hypertrophy (cor pulmonale)

BACKWARDS EFFECT: congestion in the systemic venous system [also the superior and inferior vena cava]

FORWARD EFFECT: Low output to left ventricle leading to low CO
(not enough blood coming from right side of heart and being oxygenated and going to left side of heart to go to the rest of the body)
Biventricular Heart failure
Results primarily fro left sided HF progressing to Right sided HF
-Both pulmonary congestion d/t left sided HF and systemic venous congestion d/t right sided HF
FACES (Stage of heart failure)
FATIGUE, ACTIVITY LIMITATION, CONGESTION, EDEMA, SHORTNESS OF BREATH
Stenosis
Failure of the valve TO OPEN COMPLETELY results in extra pressure work for the heart
Regurgitation
Inability of a valve to CLOSE COMPLETLEY
(Backward flow and eject)
Mitral stenosis
blood flow from the left atrium to the left ventricle is impaired during ventricular diastole
Mitral regurgitation
Backflow of blood from let ventricle to the left atrium during ventricular systole
-LEFT ATRIUM AND VENTRICLE DILATE AND HYPERTROPHY due to extra volume
-May lead to left sided heart failure
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